FEED Validator

Congratulations!

This is a valid RSS feed.

Recommendations

This feed is valid, but interoperability with the widest range of feed readers could be improved by implementing the following recommendations.

• line 7, column 299: Self reference doesn't match document location [help]

  ... amp;v=2.18.0.post9+e462414" rel="self"/>
                                               ^

• line 18, column 0: content:encoded should not contain xmlns:xlink attribute (142 occurrences) [help]

        <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Patient Re ...
  

• line 18, column 0: content:encoded should not contain xmlns:mml attribute (142 occurrences) [help]

        <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Patient Re ...
  

• line 18, column 0: content:encoded should not contain xmlns:p1 attribute (142 occurrences) [help]

        <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Patient Re ...
  

• line 28, column 6: An item should not include both pubDate and dc:date (50 occurrences) [help]

        <dc:date>2024-04-26</dc:date>
        ^

Source: http://www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib

1. <?xml version='1.0' encoding='UTF-8'?>
2. <rss xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:atom="http://www.w3.org/2005/Atom" xmlns:content="http://purl.org/rss/1.0/modules/content/" version="2.0">
3.  <channel>
4.    <title>ischemic stroke</title>
5.    <link>https://pubmed.ncbi.nlm.nih.gov/rss-feed/?feed_id=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;ff=20240426165415&amp;utm_source=Feedvalidator&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;utm_medium=rss&amp;v=2.18.0.post9+e462414</link>
6.    <description>ischemic stroke: Latest results from PubMed</description>
7.    <atom:link href="https://pubmed.ncbi.nlm.nih.gov/rss-feed/?feed_id=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;ff=20240426165415&amp;utm_source=Feedvalidator&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;utm_medium=rss&amp;v=2.18.0.post9+e462414" rel="self"/>
8.    <docs>http://www.rssboard.org/rss-specification</docs>
9.    <generator>PubMed RSS feeds (2.18.0.post9+e462414)</generator>
10.    <language>en</language>
11.    <lastBuildDate>Fri, 26 Apr 2024 20:54:17 +0000</lastBuildDate>
12.    <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
13.    <ttl>120</ttl>
14.    <item>
15.      <title>Exploring patients' experience using PROMs within routine post-discharge follow-up assessment after stroke: a mixed methods approach</title>
16.      <link>https://pubmed.ncbi.nlm.nih.gov/38668901/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
17.      <description>CONCLUSIONS: Completing PROMs appears to be feasible for patients with stroke attending post-discharge consultation; the vast majority of patients experienced added value for themselves or the healthcare provider. We recommend that healthcare providers discuss the PROM results with their patients to improve the value of PROMs for the patient. This could also improve the willingness to complete PROMs in the future.</description>
18.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Patient Rep Outcomes. 2024 Apr 26;8(1):46. doi: 10.1186/s41687-024-00724-w.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Patient Reported Outcomes Measures (PROMs) are being used increasingly to measure health problems in stroke clinical practice. However, the implementation of these PROMs in routine stroke care is still in its infancy. To understand the value of PROMs used in ischemic stroke care, we explored the patients' experience with PROMs and with the consultation at routine post-discharge follow-up after stroke.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: In this prospective mixed methods study, patients with ischemic stroke completed an evaluation questionnaire about the use of PROMs and about their consultation in two Dutch hospitals. Additionally, telephone interviews were held to gain in-depth information about their experience with PROMs.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: In total, 63 patients completed the evaluation questionnaire of which 10 patients were also interviewed. Most patients (82.2-96.6%) found completing the PROMs to be feasible and relevant. Half the patients (49.2-51.6%) considered the PROMs useful for the consultation and most patients (87.3-96.8%) reported the consultation as a positive experience. Completing the PROMs provided 51.6% of the patients with insight into their stroke-related problems. Almost 75% of the patients found the PROMs useful in giving the healthcare provider greater insight, and 60% reported discussing the PROM results during the consultation. Interviewed patients reported the added value of PROMs, particularly when arranging further care, in gaining a broader insight into the problems, and in ensuring all important topics were discussed during the consultation.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Completing PROMs appears to be feasible for patients with stroke attending post-discharge consultation; the vast majority of patients experienced added value for themselves or the healthcare provider. We recommend that healthcare providers discuss the PROM results with their patients to improve the value of PROMs for the patient. This could also improve the willingness to complete PROMs in the future.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38668901/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38668901</a> | DOI:<a href=https://doi.org/10.1186/s41687-024-00724-w>10.1186/s41687-024-00724-w</a></p></div>]]></content:encoded>
19.      <guid isPermaLink="false">pubmed:38668901</guid>
20.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
21.      <dc:creator>B M P Mourits</dc:creator>
22.      <dc:creator>S J den Hartog</dc:creator>
23.      <dc:creator>J A de Graaf</dc:creator>
24.      <dc:creator>B Roozenbeek</dc:creator>
25.      <dc:creator>M W M Post</dc:creator>
26.      <dc:creator>J M A Visser-Meily</dc:creator>
27.      <dc:creator>E W M Scholten</dc:creator>
28.      <dc:date>2024-04-26</dc:date>
29.      <dc:source>Journal of patient-reported outcomes</dc:source>
30.      <dc:title>Exploring patients' experience using PROMs within routine post-discharge follow-up assessment after stroke: a mixed methods approach</dc:title>
31.      <dc:identifier>pmid:38668901</dc:identifier>
32.      <dc:identifier>doi:10.1186/s41687-024-00724-w</dc:identifier>
33.    </item>
34.    <item>
35.      <title>Is time really brain in stroke therapy?: A meta-analysis of mechanical thrombectomy up to 155 h post ictus</title>
36.      <link>https://pubmed.ncbi.nlm.nih.gov/38668855/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
37.      <description>CONCLUSION: Our meta-analysis provides evidence that supports the need of further randomized and prospective clinical trials to better assess the effectiveness and safety of MT in these patients.</description>
38.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Acta Neurochir (Wien). 2024 Apr 26;166(1):195. doi: 10.1007/s00701-024-06070-6.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND AND OBJECTIVES: Mechanical thrombectomy (MT) has been established as the gold standard of treatment for patients with Acute Ischemic Stroke (AIS) who present up to 6 h after the onset of the stroke. Recently, the DEFUSE-3 and DAWN trials established the safety of starting the MT procedure up to 16 and 24 h after the patient was last seen well, respectively. The purpose of this study is to assess the safety and functional effects of thrombectomy in individuals with AIS detected at a late stage (&gt; 24 h).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">MATERIALS AND METHODS: PubMed, Web of Science, Embase, and Cochrane databases were thoroughly searched for research on MT in patients in the extremely late time window after AIS. The primary outcomes were symptomatic cerebral hemorrhage, 90-day mortality, Thrombolysis in Cerebral Infarction (TICI) 2b-3, and Modified Rankin Scale (mRS) 0-2.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Our study included fifteen studies involving a total of 1,221 patients who presented with AIS and an extended time window. The primary outcome of interest was the favorable functional outcome, mRS 0-2 at 90 days. The pooled proportion for this outcome was 45% (95% confidence interval 34-58%). Other outcomes included the TICI 2b or 3 (successful recanalization), which was reported in 12 studies and had a 79% incidence in the study population (95% CI 68-87%). Complications included: symptomatic intracranial hemorrhage (sICH), which revealed an incidence of 7% in the study population (95% CI 5-10%); and 90-day mortality, which reported a 27% incidence (95% CI 24-31%). In addition, we conducted a comparative analysis between endovascular treatment and standard medical therapy.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Our meta-analysis provides evidence that supports the need of further randomized and prospective clinical trials to better assess the effectiveness and safety of MT in these patients.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38668855/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38668855</a> | DOI:<a href=https://doi.org/10.1007/s00701-024-06070-6>10.1007/s00701-024-06070-6</a></p></div>]]></content:encoded>
39.      <guid isPermaLink="false">pubmed:38668855</guid>
40.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
41.      <dc:creator>Anna Laura Lima Larcipretti</dc:creator>
42.      <dc:creator>Fernando Cotrim Gomes</dc:creator>
43.      <dc:creator>Caroline Serafim Dagostin</dc:creator>
44.      <dc:creator>Gabriela Borges Nager</dc:creator>
45.      <dc:creator>Ofonime Chantal Udoma-Udofa</dc:creator>
46.      <dc:creator>Julia Pereira Muniz Pontes</dc:creator>
47.      <dc:creator>Jéssica Sales de Oliveira</dc:creator>
48.      <dc:creator>Matheus de Andrade Bannach</dc:creator>
49.      <dc:date>2024-04-26</dc:date>
50.      <dc:source>Acta neurochirurgica</dc:source>
51.      <dc:title>Is time really brain in stroke therapy?: A meta-analysis of mechanical thrombectomy up to 155 h post ictus</dc:title>
52.      <dc:identifier>pmid:38668855</dc:identifier>
53.      <dc:identifier>doi:10.1007/s00701-024-06070-6</dc:identifier>
54.    </item>
55.    <item>
56.      <title>AZD1390, an ataxia telangiectasia mutated inhibitor, attenuates microglia-mediated neuroinflammation and ischemic brain injury</title>
57.      <link>https://pubmed.ncbi.nlm.nih.gov/38668740/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
58.      <description>CONCLUSION: AZD1390 suppressed NF-κB signaling pathway to alleviate ischemic brain injury in experimental stroke, and attenuated microglia activation and neuroinflammation, which indicated that AZD1390 might be an attractive agent for the treatment of ischemic stroke.</description>
59.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">CNS Neurosci Ther. 2024 Apr;30(4):e14696. doi: 10.1111/cns.14696.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">AIMS: Excessive neuroinflammation mediated mainly by microglia plays a crucial role in ischemic stroke. AZD1390, an ataxia telangiectasia mutated (ATM) specific inhibitor, has been shown to promote radio-sensitization and survival in central nervous system malignancies, while the role of AZD1390 in ischemic stroke remains unknown.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Real-time PCR, western blot, immunofluorescence staining, flow cytometry and enzyme-linked immunosorbent assays were used to assess the activation of microglia and the release of inflammatory cytokines. Behavioral tests were performed to measure neurological deficits. 2,3,5-Triphenyltetrazolium chloride staining was conducted to assess the infarct volume. The activation of NF-κB signaling pathway was explored through immunofluorescence staining, western blot, co-immunoprecipitation and proximity ligation assay.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: The level of pro-inflammation cytokines and activation of NF-κB signaling pathway was suppressed by AZD1390 in vitro and in vivo. The behavior deficits and infarct size were partially restored with AZD1390 treatment in experimental stroke. AZD1390 restrict ubiquitylation and sumoylation of the essential regulatory subunit of NF-κB (NEMO) in an ATM-dependent and ATM-independent way respectively, which reduced the activation of the NF-κB pathway.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: AZD1390 suppressed NF-κB signaling pathway to alleviate ischemic brain injury in experimental stroke, and attenuated microglia activation and neuroinflammation, which indicated that AZD1390 might be an attractive agent for the treatment of ischemic stroke.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38668740/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38668740</a> | DOI:<a href=https://doi.org/10.1111/cns.14696>10.1111/cns.14696</a></p></div>]]></content:encoded>
60.      <guid isPermaLink="false">pubmed:38668740</guid>
61.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
62.      <dc:creator>Zhen Lan</dc:creator>
63.      <dc:creator>Long-Jie Qu</dc:creator>
64.      <dc:creator>Ying Liang</dc:creator>
65.      <dc:creator>Li-Qiu Chen</dc:creator>
66.      <dc:creator>Shuai Xu</dc:creator>
67.      <dc:creator>Jian-Wei Ge</dc:creator>
68.      <dc:creator>Zhi-Wei Xue</dc:creator>
69.      <dc:creator>Xin-Yu Bao</dc:creator>
70.      <dc:creator>Sheng-Nan Xia</dc:creator>
71.      <dc:creator>Hai-Yan Yang</dc:creator>
72.      <dc:creator>Jing Huang</dc:creator>
73.      <dc:creator>Yun Xu</dc:creator>
74.      <dc:creator>Xiao-Lei Zhu</dc:creator>
75.      <dc:date>2024-04-26</dc:date>
76.      <dc:source>CNS neuroscience &amp; therapeutics</dc:source>
77.      <dc:title>AZD1390, an ataxia telangiectasia mutated inhibitor, attenuates microglia-mediated neuroinflammation and ischemic brain injury</dc:title>
78.      <dc:identifier>pmid:38668740</dc:identifier>
79.      <dc:identifier>doi:10.1111/cns.14696</dc:identifier>
80.    </item>
81.    <item>
82.      <title>Impact of immediate postrecanalization cooling on outcome in acute ischemic stroke patients with a large ischemic core: prospective cohort study</title>
83.      <link>https://pubmed.ncbi.nlm.nih.gov/38668659/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
84.      <description>CONCLUSIONS: Postrecanalization cooling is feasible in patients with a large ischemic core. Future randomized clinical trials are warranted to validate its efficacy.</description>
85.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Int J Surg. 2024 Apr 1;110(4):2065-2070. doi: 10.1097/JS9.0000000000001127.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Patients with large acute ischemic strokes (AIS) often have a poor prognosis despite successful recanalization due to multiple factors including reperfusion injury. The authors aim to describe our preliminary experience of endovascular cooling in patients with a large AIS after recanalization.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: From January 2021 to July 2022, AIS patients presenting with large infarcts (defined as ASPECTS ≤5 on noncontrast CT or ischemic core ≥50 ml on CT perfusion) who achieved successful recanalization after endovascular treatment were analyzed in a prospective registry. Patients were divided into targeted temperature management (TTM) and non-TTM group. Patients in the TTM group received systemic cooling with a targeted core temperature of 33° for at least 48 h. The primary outcome is 90-day favorable outcome [modified Rankin Scale (mRS) 0-2]. The secondary outcomes are 90-day good outcome (mRS 0-3), mortality, intracranial hemorrhage and malignant cerebral edema within 7 days or at discharge.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Forty-four AIS patients were recruited (15 cases in the TTM group and 29 cases in the non-TTM group). The median Alberta Stroke Program Early CT Score (ASPECTS) was 3 (2-5). The median time for hypothermia duration was 84 (71.5-147.6) h. The TTM group had a numerically higher proportion of 90-day favorable outcomes than the non-TTM group (46.7 vs. 27.6%, P=0.210), and no significant difference were found regarding secondary outcomes (all P&gt;0.05). The TTM group had a numerically higher rates of pneumonia (66.7 vs. 58.6%, P=0.604) and deep vein thrombosis (33.3 vs. 13.8%, P=0.138). Shivering occurred in 4/15 (26.7%) of the TTM patients and in none of the non-TTM patients (P=0.009).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Postrecanalization cooling is feasible in patients with a large ischemic core. Future randomized clinical trials are warranted to validate its efficacy.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38668659/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38668659</a> | DOI:<a href=https://doi.org/10.1097/JS9.0000000000001127>10.1097/JS9.0000000000001127</a></p></div>]]></content:encoded>
86.      <guid isPermaLink="false">pubmed:38668659</guid>
87.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
88.      <dc:creator>Xuesong Bai</dc:creator>
89.      <dc:creator>Xin Qu</dc:creator>
90.      <dc:creator>Raul G Nogueira</dc:creator>
91.      <dc:creator>Wenhuo Chen</dc:creator>
92.      <dc:creator>Hao Zhao</dc:creator>
93.      <dc:creator>Wenbo Cao</dc:creator>
94.      <dc:creator>Peng Gao</dc:creator>
95.      <dc:creator>Bin Yang</dc:creator>
96.      <dc:creator>Yabing Wang</dc:creator>
97.      <dc:creator>Jian Chen</dc:creator>
98.      <dc:creator>Yanfei Chen</dc:creator>
99.      <dc:creator>Yuxin Wang</dc:creator>
100.      <dc:creator>Feng Shang</dc:creator>
101.      <dc:creator>Weitao Cheng</dc:creator>
102.      <dc:creator>Yueqiao Xu</dc:creator>
103.      <dc:creator>Meng Qi</dc:creator>
104.      <dc:creator>Lidan Jiang</dc:creator>
105.      <dc:creator>Wenjin Chen</dc:creator>
106.      <dc:creator>Jie Lu</dc:creator>
107.      <dc:creator>Qingfeng Ma</dc:creator>
108.      <dc:creator>Ning Wang</dc:creator>
109.      <dc:creator>Liqun Jiao</dc:creator>
110.      <dc:date>2024-04-26</dc:date>
111.      <dc:source>International journal of surgery (London, England)</dc:source>
112.      <dc:title>Impact of immediate postrecanalization cooling on outcome in acute ischemic stroke patients with a large ischemic core: prospective cohort study</dc:title>
113.      <dc:identifier>pmid:38668659</dc:identifier>
114.      <dc:identifier>doi:10.1097/JS9.0000000000001127</dc:identifier>
115.    </item>
116.    <item>
117.      <title>The Water Extract of Rhubarb Prevents Ischemic Stroke by Regulating Gut Bacteria and Metabolic Pathways</title>
118.      <link>https://pubmed.ncbi.nlm.nih.gov/38668344/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
119.      <description>Rhubarb (RR), Chinese name Dahuang, is commonly used in the treatment of ischemic stroke (IS). However, its potential mechanism is not fully elucidated. This study intended to verify the effect of RR on IS and investigate the possible mechanism of RR in preventing IS. IS in male rats was induced by embolic middle cerebral artery occlusion (MCAO) surgery, and drug administration was applied half an hour before surgery. RR dramatically decreased the neurological deficit scores, the cerebral...</description>
120.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Metabolites. 2024 Apr 12;14(4):216. doi: 10.3390/metabo14040216.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Rhubarb (RR), Chinese name Dahuang, is commonly used in the treatment of ischemic stroke (IS). However, its potential mechanism is not fully elucidated. This study intended to verify the effect of RR on IS and investigate the possible mechanism of RR in preventing IS. IS in male rats was induced by embolic middle cerebral artery occlusion (MCAO) surgery, and drug administration was applied half an hour before surgery. RR dramatically decreased the neurological deficit scores, the cerebral infarct volume, and the cerebral edema rate, and improved the regional cerebral blood flow (rCBF) and histopathological changes in the brain of MCAO rats. The 16S rRNA analysis showed the harmful microbes such as <i>Fournierella</i> and <i>Bilophila</i> were decreased, and the beneficial microbes such as <i>Enterorhabdus</i>, <i>Defluviitaleaceae</i>, <i>Christensenellaceae</i>, and <i>Lachnospira</i> were significantly increased, after RR pretreatment. <sup>1</sup>H-nuclear magnetic resonance (<sup>1</sup>H-NMR) was used to detect serum metabolomics, and RR treatment significantly changed the levels of metabolites such as isoleucine, valine, N6-acetyllysine, methionine, 3-aminoisobutyric acid, N, N-dimethylglycine, propylene glycol, trimethylamine N-oxide, myo-inositol, choline, betaine, lactate, glucose, and lipid, and the enrichment analysis of differential metabolites showed that RR may participate in the regulation of amino acid metabolism and energy metabolism. RR exerts the role of anti-IS via regulating gut bacteria and metabolic pathways.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38668344/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38668344</a> | DOI:<a href=https://doi.org/10.3390/metabo14040216>10.3390/metabo14040216</a></p></div>]]></content:encoded>
121.      <guid isPermaLink="false">pubmed:38668344</guid>
122.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
123.      <dc:creator>Xiaoyao Liu</dc:creator>
124.      <dc:creator>Yuxi Wang</dc:creator>
125.      <dc:creator>Yuan Tian</dc:creator>
126.      <dc:creator>Jiahui Hu</dc:creator>
127.      <dc:creator>Zhen Liu</dc:creator>
128.      <dc:creator>Yuncheng Ma</dc:creator>
129.      <dc:creator>Wenhui Xu</dc:creator>
130.      <dc:creator>Weiling Wang</dc:creator>
131.      <dc:creator>Jian Gao</dc:creator>
132.      <dc:creator>Ting Wang</dc:creator>
133.      <dc:date>2024-04-26</dc:date>
134.      <dc:source>Metabolites</dc:source>
135.      <dc:title>The Water Extract of Rhubarb Prevents Ischemic Stroke by Regulating Gut Bacteria and Metabolic Pathways</dc:title>
136.      <dc:identifier>pmid:38668344</dc:identifier>
137.      <dc:identifier>doi:10.3390/metabo14040216</dc:identifier>
138.    </item>
139.    <item>
140.      <title>Carotid Artery Calcification Detected on Panoramic Radiography Is Significantly Related to Cerebrovascular Accident, Coronary Artery Disease, and Poor Oral Health: A Retrospective Cross-Sectional Study</title>
141.      <link>https://pubmed.ncbi.nlm.nih.gov/38668011/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
142.      <description>Panoramic radiography imaging modality is widely used by dentists for diagnosing dental and jaw conditions. It can also detect carotid artery calcification (CAC), indicative of calcified atherosclerotic plaques in the carotid arteries. This cross-sectional retrospective study at the University of Tennessee Health Science Center investigated the link between CAC identified on panoramic radiograph (PR) and cerebrovascular accident (CVA), coronary artery disease (CAD), and poor oral health. Data...</description>
143.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Dent J (Basel). 2024 Apr 10;12(4):99. doi: 10.3390/dj12040099.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Panoramic radiography imaging modality is widely used by dentists for diagnosing dental and jaw conditions. It can also detect carotid artery calcification (CAC), indicative of calcified atherosclerotic plaques in the carotid arteries. This cross-sectional retrospective study at the University of Tennessee Health Science Center investigated the link between CAC identified on panoramic radiograph (PR) and cerebrovascular accident (CVA), coronary artery disease (CAD), and poor oral health. Data from 314 CAC patients collected from 2014 to 2023 included age at diagnosis, gender, and clinical histories of hypertension, hyperlipidemia, diabetes mellitus, CVA, CAD, and the decay, missing, and filled permanent teeth (DMFT) index. These patients were age- and gender-matched with non-CAC patients for analysis. The findings revealed high prevalences of hypertension (86.2%), hyperlipidemia (57.6%), diabetes mellitus (30.7%), CVA (15.5%), and CAD (28.7%) amongst CAC patients and the average DMFT index was 26.6. A comparative analysis of 276 matched controls demonstrated significant differences in hypertension (85.9% vs. 57.6%), hyperlipidemia (58.3% vs. 33.7%), diabetes (32.6% vs. 22.1%), CVA history (14.9% vs. 5.1%), CAD (26.1% vs. 9.8%), and DMFT scores (26.3 vs. 23.7), all indicating strong associations between CAC and these health conditions. The adjusted analysis showed that hypertension (aOR: 3.20 [95% CI: 2.06-5.07]), hyperlipidemia (aOR: 1.70 [95% CI: 1.14-2.50]), CVA (aOR: 2.20 [95% CI: 1.13-4.30]), and CAD (aOR: 2.10 [95% CI: 1.28-3.60]) were significantly associated with CAC. Notably, only 41.7% of the patients received a medical consultation after CAC detection on PR. It is crucial for dentists to refer patients for further evaluation.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38668011/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38668011</a> | DOI:<a href=https://doi.org/10.3390/dj12040099>10.3390/dj12040099</a></p></div>]]></content:encoded>
144.      <guid isPermaLink="false">pubmed:38668011</guid>
145.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
146.      <dc:creator>Anmol Brar</dc:creator>
147.      <dc:creator>Katherine DeColibus</dc:creator>
148.      <dc:creator>D Shane Rasner</dc:creator>
149.      <dc:creator>Angela R Haynes</dc:creator>
150.      <dc:creator>Frank Pancratz</dc:creator>
151.      <dc:creator>Oreoluwa Oladiran</dc:creator>
152.      <dc:creator>Semiu O Gbadamosi</dc:creator>
153.      <dc:creator>Adepitan A Owosho</dc:creator>
154.      <dc:date>2024-04-26</dc:date>
155.      <dc:source>Dentistry journal</dc:source>
156.      <dc:title>Carotid Artery Calcification Detected on Panoramic Radiography Is Significantly Related to Cerebrovascular Accident, Coronary Artery Disease, and Poor Oral Health: A Retrospective Cross-Sectional Study</dc:title>
157.      <dc:identifier>pmid:38668011</dc:identifier>
158.      <dc:identifier>doi:10.3390/dj12040099</dc:identifier>
159.    </item>
160.    <item>
161.      <title>Thrombus Imaging Characteristics to Predict Early Recanalization in Anterior Circulation Large Vessel Occlusion Stroke</title>
162.      <link>https://pubmed.ncbi.nlm.nih.gov/38667725/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
163.      <description>The early management of transferred patients with a large vessel occlusion (LVO) stroke could be improved by identifying patients who are likely to recanalize early. We aim to predict early recanalization based on patient clinical and thrombus imaging characteristics. We included 81 transferred anterior-circulation LVO patients with an early recanalization, defined as the resolution of the LVO or the migration to a distal location not reachable with endovascular treatment upon repeated...</description>
164.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Cardiovasc Dev Dis. 2024 Mar 29;11(4):107. doi: 10.3390/jcdd11040107.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">The early management of transferred patients with a large vessel occlusion (LVO) stroke could be improved by identifying patients who are likely to recanalize early. We aim to predict early recanalization based on patient clinical and thrombus imaging characteristics. We included 81 transferred anterior-circulation LVO patients with an early recanalization, defined as the resolution of the LVO or the migration to a distal location not reachable with endovascular treatment upon repeated radiological imaging. We compared their clinical and imaging characteristics with all (322) transferred patients with a persistent LVO in the MR CLEAN Registry. We measured distance from carotid terminus to thrombus (DT), thrombus length, density, and perviousness on baseline CT images. We built logistic regression models to predict early recanalization. We validated the predictive ability by computing the median area-under-the-curve (AUC) of the receiver operating characteristics curve for 100 5-fold cross-validations. The administration of intravenous thrombolysis (IVT), longer transfer times, more distal occlusions, and shorter, pervious, less dense thrombi were characteristic of early recanalization. After backward elimination, IVT administration, DT and thrombus density remained in the multivariable model, with an AUC of 0.77 (IQR 0.72-0.83). Baseline thrombus imaging characteristics are valuable in predicting early recanalization and can potentially be used to optimize repeated imaging workflow.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38667725/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38667725</a> | DOI:<a href=https://doi.org/10.3390/jcdd11040107>10.3390/jcdd11040107</a></p></div>]]></content:encoded>
165.      <guid isPermaLink="false">pubmed:38667725</guid>
166.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
167.      <dc:creator>Nerea Arrarte Terreros</dc:creator>
168.      <dc:creator>Jeffrey Stolp</dc:creator>
169.      <dc:creator>Agnetha A E Bruggeman</dc:creator>
170.      <dc:creator>Isabella S J Swijnenburg</dc:creator>
171.      <dc:creator>Ricardo R Lopes</dc:creator>
172.      <dc:creator>Laura C C van Meenen</dc:creator>
173.      <dc:creator>Adrien E D Groot</dc:creator>
174.      <dc:creator>Manon Kappelhof</dc:creator>
175.      <dc:creator>Jonathan M Coutinho</dc:creator>
176.      <dc:creator>Yvo B W E M Roos</dc:creator>
177.      <dc:creator>Bart J Emmer</dc:creator>
178.      <dc:creator>Ludo F M Beenen</dc:creator>
179.      <dc:creator>Diederik W J Dippel</dc:creator>
180.      <dc:creator>Wim H van Zwam</dc:creator>
181.      <dc:creator>Ed van Bavel</dc:creator>
182.      <dc:creator>Henk A Marquering</dc:creator>
183.      <dc:creator>Charles B L M Majoie</dc:creator>
184.      <dc:creator>MR CLEAN Registry investigators</dc:creator>
185.      <dc:date>2024-04-26</dc:date>
186.      <dc:source>Journal of cardiovascular development and disease</dc:source>
187.      <dc:title>Thrombus Imaging Characteristics to Predict Early Recanalization in Anterior Circulation Large Vessel Occlusion Stroke</dc:title>
188.      <dc:identifier>pmid:38667725</dc:identifier>
189.      <dc:identifier>doi:10.3390/jcdd11040107</dc:identifier>
190.    </item>
191.    <item>
192.      <title>Racial Disparities in Selected Complications and Comorbidities among People with Type 2 Diabetes</title>
193.      <link>https://pubmed.ncbi.nlm.nih.gov/38667608/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
194.      <description>Type 2 diabetes (T2D) is a growing public health concern, disproportionately impacting racial and ethnic minorities. Assessing disparities is the first step towards achieving the translation goal to reduce disparities in diabetes outcomes, according to the Centers for Disease Control and Prevention (CDC)'s Division of Diabetes. We analyzed the data of patients (18+ years) diagnosed with T2D between 1 January 2012 and 31 March 2017, using the electronic health records of the University of Texas...</description>
195.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Healthcare (Basel). 2024 Apr 17;12(8):846. doi: 10.3390/healthcare12080846.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Type 2 diabetes (T2D) is a growing public health concern, disproportionately impacting racial and ethnic minorities. Assessing disparities is the first step towards achieving the translation goal to reduce disparities in diabetes outcomes, according to the Centers for Disease Control and Prevention (CDC)'s Division of Diabetes. We analyzed the data of patients (18+ years) diagnosed with T2D between 1 January 2012 and 31 March 2017, using the electronic health records of the University of Texas Medical Branch at Galveston. We compared the crude rate and age-standardized rate (using direct method) of selected micro- and macrovascular complication rates, associated obesity, and insulin dependence among racial and ethnic groups. Our sample included 20,680 patients who made 394,106 visits (9922 non-Hispanic White patients, 4698 non-Hispanic Black patients, and 6060 Hispanic patients). Our results suggest a higher risk of acquiring macrovascular (hypertension, ischemic disease, and stroke) and microvascular (renal, ophthalmic, and neurological) complications in Black patients compared to non-Hispanic White and Hispanic patients. The rates of stage I or II obesity were higher in Black patients compared with White and Hispanic patients. The rates of insulin use rather than oral hypoglycemics were also higher in Black patients than White and Hispanic patients. The disparities in terms of the higher susceptibility to complications among Black patients are possibly linked to the socioeconomic disadvantages of this population, leading to poorer management. Prevention strategies are warranted to reduce the incidence of T2D complications in racial minorities.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38667608/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38667608</a> | DOI:<a href=https://doi.org/10.3390/healthcare12080846>10.3390/healthcare12080846</a></p></div>]]></content:encoded>
196.      <guid isPermaLink="false">pubmed:38667608</guid>
197.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
198.      <dc:creator>Caitlin M Hackl</dc:creator>
199.      <dc:creator>Wei-Chen Lee</dc:creator>
200.      <dc:creator>Hanaa S Sallam</dc:creator>
201.      <dc:creator>Hani Jneid</dc:creator>
202.      <dc:creator>Kendall M Campbell</dc:creator>
203.      <dc:creator>Hani Serag</dc:creator>
204.      <dc:date>2024-04-26</dc:date>
205.      <dc:source>Healthcare (Basel, Switzerland)</dc:source>
206.      <dc:title>Racial Disparities in Selected Complications and Comorbidities among People with Type 2 Diabetes</dc:title>
207.      <dc:identifier>pmid:38667608</dc:identifier>
208.      <dc:identifier>doi:10.3390/healthcare12080846</dc:identifier>
209.    </item>
210.    <item>
211.      <title>Human-Induced Pluripotent Stem Cell-Derived Neural Progenitor Cells Showed Neuronal Differentiation, Neurite Extension, and Formation of Synaptic Structures in Rodent Ischemic Stroke Brains</title>
212.      <link>https://pubmed.ncbi.nlm.nih.gov/38667286/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
213.      <description>Ischemic stroke is a major cerebrovascular disease with high morbidity and mortality rates; however, effective treatments for ischemic stroke-related neurological dysfunction have yet to be developed. In this study, we generated neural progenitor cells from human leukocyte antigen major loci gene-homozygous-induced pluripotent stem cells (hiPSC-NPCs) and evaluated their therapeutic effects against ischemic stroke. hiPSC-NPCs were intracerebrally transplanted into rat ischemic brains produced by...</description>
214.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cells. 2024 Apr 12;13(8):671. doi: 10.3390/cells13080671.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Ischemic stroke is a major cerebrovascular disease with high morbidity and mortality rates; however, effective treatments for ischemic stroke-related neurological dysfunction have yet to be developed. In this study, we generated neural progenitor cells from human leukocyte antigen major loci gene-homozygous-induced pluripotent stem cells (hiPSC-NPCs) and evaluated their therapeutic effects against ischemic stroke. hiPSC-NPCs were intracerebrally transplanted into rat ischemic brains produced by transient middle cerebral artery occlusion at either the subacute or acute stage, and their in vivo survival, differentiation, and efficacy for functional improvement in neurological dysfunction were evaluated. hiPSC-NPCs were histologically identified in host brain tissues and showed neuronal differentiation into vGLUT-positive glutamatergic neurons, extended neurites into both the ipsilateral infarct and contralateral healthy hemispheres, and synaptic structures formed 12 weeks after both acute and subacute stage transplantation. They also improved neurological function when transplanted at the subacute stage with γ-secretase inhibitor pretreatment. However, their effects were modest and not significant and showed a possible risk of cells remaining in their undifferentiated and immature status in acute-stage transplantation. These results suggest that hiPSC-NPCs show cell replacement effects in ischemic stroke-damaged neural tissues, but their efficacy is insufficient for neurological functional improvement after acute or subacute transplantation. Further optimization of cell preparation methods and the timing of transplantation is required to balance the efficacy and safety of hiPSC-NPC transplantation.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38667286/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38667286</a> | DOI:<a href=https://doi.org/10.3390/cells13080671>10.3390/cells13080671</a></p></div>]]></content:encoded>
215.      <guid isPermaLink="false">pubmed:38667286</guid>
216.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
217.      <dc:creator>Yonehiro Kanemura</dc:creator>
218.      <dc:creator>Atsuyo Yamamoto</dc:creator>
219.      <dc:creator>Asako Katsuma</dc:creator>
220.      <dc:creator>Hayato Fukusumi</dc:creator>
221.      <dc:creator>Tomoko Shofuda</dc:creator>
222.      <dc:creator>Daisuke Kanematsu</dc:creator>
223.      <dc:creator>Yukako Handa</dc:creator>
224.      <dc:creator>Miho Sumida</dc:creator>
225.      <dc:creator>Ema Yoshioka</dc:creator>
226.      <dc:creator>Yutaka Mine</dc:creator>
227.      <dc:creator>Ryo Yamaguchi</dc:creator>
228.      <dc:creator>Masayasu Okada</dc:creator>
229.      <dc:creator>Michihiro Igarashi</dc:creator>
230.      <dc:creator>Yuko Sekino</dc:creator>
231.      <dc:creator>Tomoaki Shirao</dc:creator>
232.      <dc:creator>Masaya Nakamura</dc:creator>
233.      <dc:creator>Hideyuki Okano</dc:creator>
234.      <dc:date>2024-04-26</dc:date>
235.      <dc:source>Cells</dc:source>
236.      <dc:title>Human-Induced Pluripotent Stem Cell-Derived Neural Progenitor Cells Showed Neuronal Differentiation, Neurite Extension, and Formation of Synaptic Structures in Rodent Ischemic Stroke Brains</dc:title>
237.      <dc:identifier>pmid:38667286</dc:identifier>
238.      <dc:identifier>doi:10.3390/cells13080671</dc:identifier>
239.    </item>
240.    <item>
241.      <title>Rhoa/ROCK, mTOR and Secretome-Based Treatments for Ischemic Stroke: New Perspectives</title>
242.      <link>https://pubmed.ncbi.nlm.nih.gov/38666949/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
243.      <description>Ischemic stroke triggers a complex cascade of cellular and molecular events leading to neuronal damage and tissue injury. This review explores the potential therapeutic avenues targeting cellular signaling pathways implicated in stroke pathophysiology. Specifically, it focuses on the articles that highlight the roles of RhoA/ROCK and mTOR signaling pathways in ischemic brain injury and their therapeutic implications. The RhoA/ROCK pathway modulates various cellular processes, including...</description>
244.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Curr Issues Mol Biol. 2024 Apr 18;46(4):3484-3501. doi: 10.3390/cimb46040219.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Ischemic stroke triggers a complex cascade of cellular and molecular events leading to neuronal damage and tissue injury. This review explores the potential therapeutic avenues targeting cellular signaling pathways implicated in stroke pathophysiology. Specifically, it focuses on the articles that highlight the roles of RhoA/ROCK and mTOR signaling pathways in ischemic brain injury and their therapeutic implications. The RhoA/ROCK pathway modulates various cellular processes, including cytoskeletal dynamics and inflammation, while mTOR signaling regulates cell growth, proliferation, and autophagy. Preclinical studies have demonstrated the neuroprotective effects of targeting these pathways in stroke models, offering insights into potential treatment strategies. However, challenges such as off-target effects and the need for tissue-specific targeting remain. Furthermore, emerging evidence suggests the therapeutic potential of MSC secretome in stroke treatment, highlighting the importance of exploring alternative approaches. Future research directions include elucidating the precise mechanisms of action, optimizing treatment protocols, and translating preclinical findings into clinical practice for improved stroke outcomes.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666949/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666949</a> | DOI:<a href=https://doi.org/10.3390/cimb46040219>10.3390/cimb46040219</a></p></div>]]></content:encoded>
245.      <guid isPermaLink="false">pubmed:38666949</guid>
246.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
247.      <dc:creator>Elena Anca Pinoșanu</dc:creator>
248.      <dc:creator>Denisa Pîrșcoveanu</dc:creator>
249.      <dc:creator>Carmen Valeria Albu</dc:creator>
250.      <dc:creator>Emilia Burada</dc:creator>
251.      <dc:creator>Andrei Pîrvu</dc:creator>
252.      <dc:creator>Roxana Surugiu</dc:creator>
253.      <dc:creator>Raluca Elena Sandu</dc:creator>
254.      <dc:creator>Alina Florina Serb</dc:creator>
255.      <dc:date>2024-04-26</dc:date>
256.      <dc:source>Current issues in molecular biology</dc:source>
257.      <dc:title>Rhoa/ROCK, mTOR and Secretome-Based Treatments for Ischemic Stroke: New Perspectives</dc:title>
258.      <dc:identifier>pmid:38666949</dc:identifier>
259.      <dc:identifier>doi:10.3390/cimb46040219</dc:identifier>
260.    </item>
261.    <item>
262.      <title>Nationwide Incidence and Trends in Central Retinal Arterial Occlusion Management: A 5000-Patient Analysis</title>
263.      <link>https://pubmed.ncbi.nlm.nih.gov/38666795/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
264.      <description>Central retinal artery occlusion (CRAO) is a rare and visually debilitating vascular condition characterized by sudden and severe vision loss. CRAO is a compelling target for intravenous alteplase (tPA) and endovascular mechanical thrombectomy (MT) due to pathophysiological similarities with acute ischemic stroke; however, the utility of these interventions in CRAO remains dubious due to limited sample sizes and potential risks. To assess usage and outcomes of tPA and MT in CRAO, we queried the...</description>
265.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cardiol Rev. 2024 Apr 26. doi: 10.1097/CRD.0000000000000682. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Central retinal artery occlusion (CRAO) is a rare and visually debilitating vascular condition characterized by sudden and severe vision loss. CRAO is a compelling target for intravenous alteplase (tPA) and endovascular mechanical thrombectomy (MT) due to pathophysiological similarities with acute ischemic stroke; however, the utility of these interventions in CRAO remains dubious due to limited sample sizes and potential risks. To assess usage and outcomes of tPA and MT in CRAO, we queried the National Inpatient Sample database using International Classification of Disease, Ninth and Tenth edition for patients with CRAO and acute ischemic stroke between 2010 and 2019. Our cohort of 5009 CRAO patients were younger with higher rates of obesity, hypertension, long-term anticoagulant use, and tobacco use compared to acute ischemic stroke patients. CRAO patients had lower rates of tPA administration (3.41% vs 6.21%) and endovascular MT (0.38% vs 1.31%) but fewer complications, including deep vein thrombosis, pneumonia, urinary tract infection, acute kidney injury, and acute myocardial infarction (all P &lt; 0.01). CRAO patients had lower rates of poor functional outcome (31.74% vs 58.1%) and in-hospital mortality (1.2% vs 5.64%), but higher rates of profound blindness (9.24% vs 0.58%). A multivariate regression showed no relationship between tPA and MT and profound blindness, although the limited sample size of patients receiving interventions may have contributed to this apparent insignificance. Further investigation of larger patient cohorts and alternative treatment modalities could provide valuable insights for revascularization therapies in CRAO to optimize visual restoration and clinical outcomes.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666795/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666795</a> | DOI:<a href=https://doi.org/10.1097/CRD.0000000000000682>10.1097/CRD.0000000000000682</a></p></div>]]></content:encoded>
266.      <guid isPermaLink="false">pubmed:38666795</guid>
267.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
268.      <dc:creator>Galadu Subah</dc:creator>
269.      <dc:creator>Patricia Xu</dc:creator>
270.      <dc:creator>Sabrina Zeller</dc:creator>
271.      <dc:creator>Bridget Nolan</dc:creator>
272.      <dc:creator>Aiden Lui</dc:creator>
273.      <dc:creator>Michael Fortunato</dc:creator>
274.      <dc:creator>Eric Feldstein</dc:creator>
275.      <dc:creator>Martin Kafina</dc:creator>
276.      <dc:creator>Daniel Elefant</dc:creator>
277.      <dc:creator>Ji Chong</dc:creator>
278.      <dc:creator>Chirag Gandhi</dc:creator>
279.      <dc:creator>Fawaz Al-Mufti</dc:creator>
280.      <dc:date>2024-04-26</dc:date>
281.      <dc:source>Cardiology in review</dc:source>
282.      <dc:title>Nationwide Incidence and Trends in Central Retinal Arterial Occlusion Management: A 5000-Patient Analysis</dc:title>
283.      <dc:identifier>pmid:38666795</dc:identifier>
284.      <dc:identifier>doi:10.1097/CRD.0000000000000682</dc:identifier>
285.    </item>
286.    <item>
287.      <title>Thrombectomy in ischemic stroke patients with large core but minor ischemic changes on non-enhanced computed tomography</title>
288.      <link>https://pubmed.ncbi.nlm.nih.gov/38666480/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
289.      <description>CONCLUSIONS: In patients with ASPECTS≥6, core volumes did not significantly modify outcomes following recanalization. Reperfusion and higher core volume were significantly associated with core overestimation which may explain the treatment effect of MT for patients with a large ischemic core but minor ischemic changes on non-enhanced CT.</description>
290.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Int J Stroke. 2024 Apr 26:17474930241249588. doi: 10.1177/17474930241249588. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">PURPOSE: The Alberta Stroke Program Early CT Score (ASPECTS) is regularly used to guide patient selection for mechanical thrombectomy (MT). Similarly, penumbral imaging based on computed tomography perfusion (CTP) may serve as neuroimaging tool to guide treatment. Yet, patients with a large ischemic core on CTP may show only minor ischemic changes resulting in a high ASPECTS.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">AIM: We hypothesized twofold: 1) the treatment effect of vessel recanalization in patients with core volume &gt;50ml but ASPECTS≥6 is not different compared to high ASPECTS patients with core volume &lt;50ml, and 2) recanalization is associated with core overestimation.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We conducted an observational study analyzing ischemic stroke patients consecutively treated with MT after triage by multimodal-CT. Functional endpoint was the rate of functional independence at day-90 defined as modified Rankin Scale (mRS) 0-2. Imaging endpoint was core overestimation, which was considered when CTP-derived core was larger than final infarct volume assessed on follow-up imaging. Recanalization was evaluated with the eTICI (extended Thrombolysis in Cerebral Infarction) scale. Multivariable logistic regression analysis and prospensity score matching (PSM) were used to assess the association of recanalization (eTICI≥2b) with functional outcome and core overestimation.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Of 630 patients with ASPECTS≥6, 91 patients (14.4%) had a large ischemic core. Following 1:1 PSM, the treatment effect of recanalization was not different in patients with large core and ASPECTS≥6 (+25.8%,95%CI: 16.3-35.4,p&lt;0.001) compared to patients with ASPECTS≥6 and core volume &lt;50 ml (+14.9%,95%CI: 5.7-24.1,p=0.002). Recanalization (aOR: 3.87, 95%CI: 1.66-9.00, p=0.002) and higher core volume (aOR: 1.04,95%CI: 1.02-1.05,p&lt;0.001) were significantly associated with core overestimation.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: In patients with ASPECTS≥6, core volumes did not significantly modify outcomes following recanalization. Reperfusion and higher core volume were significantly associated with core overestimation which may explain the treatment effect of MT for patients with a large ischemic core but minor ischemic changes on non-enhanced CT.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666480/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666480</a> | DOI:<a href=https://doi.org/10.1177/17474930241249588>10.1177/17474930241249588</a></p></div>]]></content:encoded>
291.      <guid isPermaLink="false">pubmed:38666480</guid>
292.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
293.      <dc:creator>Gabriel Broocks</dc:creator>
294.      <dc:creator>Helge Kniep</dc:creator>
295.      <dc:creator>Rosalie McDonough</dc:creator>
296.      <dc:creator>Matthias Bechstein</dc:creator>
297.      <dc:creator>Christian Heitkamp</dc:creator>
298.      <dc:creator>Laurens Winkelmeier</dc:creator>
299.      <dc:creator>Susan Klapproth</dc:creator>
300.      <dc:creator>Tobias Djamsched Faizy</dc:creator>
301.      <dc:creator>Maximilian Schell</dc:creator>
302.      <dc:creator>Gerhard Schön</dc:creator>
303.      <dc:creator>Uta Hanning</dc:creator>
304.      <dc:creator>Susanne Gellißen</dc:creator>
305.      <dc:creator>André Kemmling</dc:creator>
306.      <dc:creator>Panagiotis Papanagiotou</dc:creator>
307.      <dc:creator>Jens Fiehler</dc:creator>
308.      <dc:creator>Lukas Meyer</dc:creator>
309.      <dc:date>2024-04-26</dc:date>
310.      <dc:source>International journal of stroke : official journal of the International Stroke Society</dc:source>
311.      <dc:title>Thrombectomy in ischemic stroke patients with large core but minor ischemic changes on non-enhanced computed tomography</dc:title>
312.      <dc:identifier>pmid:38666480</dc:identifier>
313.      <dc:identifier>doi:10.1177/17474930241249588</dc:identifier>
314.    </item>
315.    <item>
316.      <title>Adaptive Metabolic Responses Facilitate Blood-Brain Barrier Repair in Ischemic Stroke via BHB-Mediated Epigenetic Modification of ZO-1 Expression</title>
317.      <link>https://pubmed.ncbi.nlm.nih.gov/38666466/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
318.      <description>Adaptive metabolic responses and innate metabolites hold promising therapeutic potential for stroke, while targeted interventions require a thorough understanding of underlying mechanisms. Adiposity is a noted modifiable metabolic risk factor for stroke, and recent research suggests that it benefits neurological rehabilitation. During the early phase of experimental stroke, the lipidomic results showed that fat depots underwent pronounced lipolysis and released fatty acids (FAs) that feed into...</description>
319.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Adv Sci (Weinh). 2024 Apr 26:e2400426. doi: 10.1002/advs.202400426. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Adaptive metabolic responses and innate metabolites hold promising therapeutic potential for stroke, while targeted interventions require a thorough understanding of underlying mechanisms. Adiposity is a noted modifiable metabolic risk factor for stroke, and recent research suggests that it benefits neurological rehabilitation. During the early phase of experimental stroke, the lipidomic results showed that fat depots underwent pronounced lipolysis and released fatty acids (FAs) that feed into consequent hepatic FA oxidation and ketogenesis. Systemic supplementation with the predominant ketone beta-hydroxybutyrate (BHB) is found to exert discernible effects on preserving blood-brain barrier (BBB) integrity and facilitating neuroinflammation resolution. Meanwhile, blocking FAO-ketogenesis processes by administration of CPT1α antagonist or shRNA targeting HMGCS2 exacerbated endothelial damage and aggravated stroke severity, whereas BHB supplementation blunted these injuries. Mechanistically, it is unveiled that BHB infusion is taken up by monocarboxylic acid transporter 1 (MCT1) specifically expressed in cerebral endothelium and upregulated the expression of tight junction protein ZO-1 by enhancing local β-hydroxybutyrylation of H3K9 at the promoter of TJP1 gene. Conclusively, an adaptive metabolic mechanism is elucidated by which acute lipolysis stimulates FAO-ketogenesis processes to restore BBB integrity after stroke. Ketogenesis functions as an early metabolic responder to restrain stroke progression, providing novel prospectives for clinical translation.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666466/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666466</a> | DOI:<a href=https://doi.org/10.1002/advs.202400426>10.1002/advs.202400426</a></p></div>]]></content:encoded>
320.      <guid isPermaLink="false">pubmed:38666466</guid>
321.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
322.      <dc:creator>Ruijie Li</dc:creator>
323.      <dc:creator>Yilin Liu</dc:creator>
324.      <dc:creator>Jihao Wu</dc:creator>
325.      <dc:creator>Xiong Chen</dc:creator>
326.      <dc:creator>Qiying Lu</dc:creator>
327.      <dc:creator>Kai Xia</dc:creator>
328.      <dc:creator>Congyuan Liu</dc:creator>
329.      <dc:creator>Xin Sui</dc:creator>
330.      <dc:creator>Yixuan Liu</dc:creator>
331.      <dc:creator>Yiling Wang</dc:creator>
332.      <dc:creator>Yuan Qiu</dc:creator>
333.      <dc:creator>Jinsi Chen</dc:creator>
334.      <dc:creator>Yi Wang</dc:creator>
335.      <dc:creator>Ruijun Li</dc:creator>
336.      <dc:creator>Yucheng Ba</dc:creator>
337.      <dc:creator>Jiayun Fang</dc:creator>
338.      <dc:creator>Weijun Huang</dc:creator>
339.      <dc:creator>Zhengqi Lu</dc:creator>
340.      <dc:creator>Yanbing Li</dc:creator>
341.      <dc:creator>Xinxue Liao</dc:creator>
342.      <dc:creator>Andy Peng Xiang</dc:creator>
343.      <dc:creator>Yinong Huang</dc:creator>
344.      <dc:date>2024-04-26</dc:date>
345.      <dc:source>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</dc:source>
346.      <dc:title>Adaptive Metabolic Responses Facilitate Blood-Brain Barrier Repair in Ischemic Stroke via BHB-Mediated Epigenetic Modification of ZO-1 Expression</dc:title>
347.      <dc:identifier>pmid:38666466</dc:identifier>
348.      <dc:identifier>doi:10.1002/advs.202400426</dc:identifier>
349.    </item>
350.    <item>
351.      <title>Voacangine protects hippocampal neuronal cells against oxygen-glucose deprivation/reoxygenation-caused oxidative stress and ferroptosis by activating the PI3K-Akt-FoxO signaling</title>
352.      <link>https://pubmed.ncbi.nlm.nih.gov/38666302/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
353.      <description>Voacangine, a naturally occurring alkaloid, has been testified to display beneficial effects on a variety of human diseases, but its role in ischemic stroke is unclear. The impacts of voacangine on oxygen-glucose deprivation/reoxygenation (OGD/R)-tempted hippocampal neuronal cells are investigated. The bioinformatics analysis found that voacangine is a bioactive ingredient that may have good effects on ischemic stroke. KEGG pathways analysis found that voacangine may regulate ischemic stroke...</description>
354.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Appl Toxicol. 2024 Apr 26. doi: 10.1002/jat.4615. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Voacangine, a naturally occurring alkaloid, has been testified to display beneficial effects on a variety of human diseases, but its role in ischemic stroke is unclear. The impacts of voacangine on oxygen-glucose deprivation/reoxygenation (OGD/R)-tempted hippocampal neuronal cells are investigated. The bioinformatics analysis found that voacangine is a bioactive ingredient that may have good effects on ischemic stroke. KEGG pathways analysis found that voacangine may regulate ischemic stroke through modulating the PI3K-Akt-FoxO signaling pathway. Voacangine could mitigate OGD/R-tempted cytotoxicity in HT22 cells. Voacangine mitigated OGD/R-tempted oxidative stress in HT22 cells by diminishing reactive oxygen species level and enhancing superoxide dismutase level. Voacangine mitigated OGD/R-tempted ferroptosis in HT22 cells. Voacangine promoted activation of the PI3K-Akt-FoxO signaling in OGD/R-induced HT22 cells. Inactivation of the PI3K-Akt-FoxO signaling pathway reversed the protective effects of voacangine against OGD/R-tempted oxidative stress, cytotoxicity, and ferroptosis in HT22 cells. In conclusion, voacangine protects hippocampal neuronal cells against OGD/R-caused oxidative stress and ferroptosis by activating the PI3K-Akt-FoxO signaling.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666302/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666302</a> | DOI:<a href=https://doi.org/10.1002/jat.4615>10.1002/jat.4615</a></p></div>]]></content:encoded>
355.      <guid isPermaLink="false">pubmed:38666302</guid>
356.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
357.      <dc:creator>Ying Li</dc:creator>
358.      <dc:creator>Yan Sun</dc:creator>
359.      <dc:creator>Jianghong Wang</dc:creator>
360.      <dc:creator>Xiaolong Wang</dc:creator>
361.      <dc:creator>Wenjie Yang</dc:creator>
362.      <dc:date>2024-04-26</dc:date>
363.      <dc:source>Journal of applied toxicology : JAT</dc:source>
364.      <dc:title>Voacangine protects hippocampal neuronal cells against oxygen-glucose deprivation/reoxygenation-caused oxidative stress and ferroptosis by activating the PI3K-Akt-FoxO signaling</dc:title>
365.      <dc:identifier>pmid:38666302</dc:identifier>
366.      <dc:identifier>doi:10.1002/jat.4615</dc:identifier>
367.    </item>
368.    <item>
369.      <title>Anticoagulation Therapy in a Patient who had two Consecutive Strokes After Antibiotic Therapy for Infective Endocarditis: A Case Report</title>
370.      <link>https://pubmed.ncbi.nlm.nih.gov/38666280/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
371.      <description>A 77-year-old male presented with altered mentation and was diagnosed with infective endocarditis. Echocardiography revealed aortic valve vegetations. While receiving inpatient antibiotic therapy, the patient experienced an acute ischemic stroke. Magnetic resonance imaging of the brain showed punctate embolic-appearing infarcts in the right cerebellum and in the left occipital, frontal, and parietal lobes. Anticoagulation was not initiated due to a high risk of hemorrhagic transformation. He was...</description>
372.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Neurohospitalist. 2024 Apr;14(2):204-207. doi: 10.1177/19418744231224061. Epub 2023 Dec 22.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">A 77-year-old male presented with altered mentation and was diagnosed with infective endocarditis. Echocardiography revealed aortic valve vegetations. While receiving inpatient antibiotic therapy, the patient experienced an acute ischemic stroke. Magnetic resonance imaging of the brain showed punctate embolic-appearing infarcts in the right cerebellum and in the left occipital, frontal, and parietal lobes. Anticoagulation was not initiated due to a high risk of hemorrhagic transformation. He was readmitted after being discharged due to another episode of altered mentation. Repeat echocardiography indicated increased size of aortic valve vegetations. The patient was then transferred to our hospital for surgical intervention of enlarging vegetations, however was deemed unsuitable for surgery. During hospitalization, he suffered another embolic stroke in the right frontal lobe. By this time, the patient had completed a full course of antibiotics for infective endocarditis, and additional antibiotics were deemed unnecessary by our infectious disease specialists. Literature review highlighted that residual vegetations carry a higher risk for stroke, but no clear guidelines were found on how to intervene or assess the risk of hemorrhage with anticoagulation in this population. Consequently, a decision was made to initiate anticoagulation, Follow-up imaging revealed no evidence of hemorrhagic transformation. Subsequently, the patient remained stable and was discharged to a rehabilitation center, where he did not experience any further events.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666280/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666280</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11040627/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11040627</a> | DOI:<a href=https://doi.org/10.1177/19418744231224061>10.1177/19418744231224061</a></p></div>]]></content:encoded>
373.      <guid isPermaLink="false">pubmed:38666280</guid>
374.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
375.      <dc:creator>Abdalla Jamal Albanna</dc:creator>
376.      <dc:creator>Ammar Jumah</dc:creator>
377.      <dc:creator>Utkarsh Agarwal</dc:creator>
378.      <dc:creator>Michael Fana</dc:creator>
379.      <dc:creator>Samer Abdul Kareem</dc:creator>
380.      <dc:creator>Daniel Miller</dc:creator>
381.      <dc:date>2024-04-26</dc:date>
382.      <dc:source>The Neurohospitalist</dc:source>
383.      <dc:title>Anticoagulation Therapy in a Patient who had two Consecutive Strokes After Antibiotic Therapy for Infective Endocarditis: A Case Report</dc:title>
384.      <dc:identifier>pmid:38666280</dc:identifier>
385.      <dc:identifier>pmc:PMC11040627</dc:identifier>
386.      <dc:identifier>doi:10.1177/19418744231224061</dc:identifier>
387.    </item>
388.    <item>
389.      <title>Evaluation of Paroxysmal Events in Critically Ill Patients: Relationship of Primary Diagnosis to Long-Term Electroencephalogram Yield</title>
390.      <link>https://pubmed.ncbi.nlm.nih.gov/38666279/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
391.      <description>Continuous EEG (cEEG) is indicated for the workup of paroxysmal events. We aimed to assess whether primary admission diagnoses predict the yield of cEEG when ordered for evaluating paroxysmal events. We identified patients in the ICU who underwent at least 6 hours of cEEG monitoring to evaluate paroxysmal events. Primary admission diagnoses were categorized into neurological or non-neurological conditions. cEEG results were dichotomized into presence or absence of epileptiform discharges. We...</description>
392.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Neurohospitalist. 2024 Apr;14(2):178-181. doi: 10.1177/19418744231215958. Epub 2023 Nov 28.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Continuous EEG (cEEG) is indicated for the workup of paroxysmal events. We aimed to assess whether primary admission diagnoses predict the yield of cEEG when ordered for evaluating paroxysmal events. We identified patients in the ICU who underwent at least 6 hours of cEEG monitoring to evaluate paroxysmal events. Primary admission diagnoses were categorized into neurological or non-neurological conditions. cEEG results were dichotomized into presence or absence of epileptiform discharges. We identified 159 recordings that were obtained for the evaluation of paroxysmal events. Most patients (n = 100, 63%) were admitted with primary admission diagnoses of neurological disorders, such as ischemic stroke, or intracranial hemorrhage. We found that patients with primary neurological conditions were more likely to have brain surgeries, abnormal brain imaging, and focal neurological deficits on examination compared to those with primary non-neurological conditions. However, there was no significant difference in the prevalence of epileptiform discharges in cEEG among patients with primary diagnoses of neurological or non-neurological disorders. These results suggest that cEEG is often necessary to evaluate paroxysmal events, even among patients without primary neurological disorders.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666279/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666279</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11040618/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11040618</a> | DOI:<a href=https://doi.org/10.1177/19418744231215958>10.1177/19418744231215958</a></p></div>]]></content:encoded>
393.      <guid isPermaLink="false">pubmed:38666279</guid>
394.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
395.      <dc:creator>Hai Chen</dc:creator>
396.      <dc:creator>Andrew Becker</dc:creator>
397.      <dc:creator>Eugenie Atallah</dc:creator>
398.      <dc:creator>Jennifer Pauldurai</dc:creator>
399.      <dc:creator>Mohamad Koubeissi</dc:creator>
400.      <dc:date>2024-04-26</dc:date>
401.      <dc:source>The Neurohospitalist</dc:source>
402.      <dc:title>Evaluation of Paroxysmal Events in Critically Ill Patients: Relationship of Primary Diagnosis to Long-Term Electroencephalogram Yield</dc:title>
403.      <dc:identifier>pmid:38666279</dc:identifier>
404.      <dc:identifier>pmc:PMC11040618</dc:identifier>
405.      <dc:identifier>doi:10.1177/19418744231215958</dc:identifier>
406.    </item>
407.    <item>
408.      <title>Clinical Decision Support for Patients Presenting With Large Vessel Occlusion</title>
409.      <link>https://pubmed.ncbi.nlm.nih.gov/38666277/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
410.      <description>A single center had a collaborative, multidisciplinary review to determine how to best implement new acute ischemic stroke trials involving large vessel occlusions. A flow diagram process map was created for clinical decision support. Patients were divided into four groups based upon size of infarct and timing of presentation. The process map, available in the electronic health record (EHR) for clinicians to reference, guides the selection of patients for endovascular therapy with neuroimaging....</description>
411.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Neurohospitalist. 2024 Apr;14(2):182-185. doi: 10.1177/19418744231220699. Epub 2023 Dec 10.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">A single center had a collaborative, multidisciplinary review to determine how to best implement new acute ischemic stroke trials involving large vessel occlusions. A flow diagram process map was created for clinical decision support. Patients were divided into four groups based upon size of infarct and timing of presentation. The process map, available in the electronic health record (EHR) for clinicians to reference, guides the selection of patients for endovascular therapy with neuroimaging. In addition, the process map offers guidance for discussions with families and patients experiencing large vessel occlusions with both small and large core infarcts. This manuscript describes the process of creating the process map through a multidisciplinary review and discussion, with points of controversy and how these were addressed.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666277/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666277</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11040614/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11040614</a> | DOI:<a href=https://doi.org/10.1177/19418744231220699>10.1177/19418744231220699</a></p></div>]]></content:encoded>
412.      <guid isPermaLink="false">pubmed:38666277</guid>
413.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
414.      <dc:creator>Jennifer R Simpson</dc:creator>
415.      <dc:creator>Russell J VanCoevering</dc:creator>
416.      <dc:creator>Kerri Jeppson</dc:creator>
417.      <dc:creator>David Case</dc:creator>
418.      <dc:creator>Joshua Seinfeld</dc:creator>
419.      <dc:creator>Christopher Roark</dc:creator>
420.      <dc:creator>Sharon N Poisson</dc:creator>
421.      <dc:date>2024-04-26</dc:date>
422.      <dc:source>The Neurohospitalist</dc:source>
423.      <dc:title>Clinical Decision Support for Patients Presenting With Large Vessel Occlusion</dc:title>
424.      <dc:identifier>pmid:38666277</dc:identifier>
425.      <dc:identifier>pmc:PMC11040614</dc:identifier>
426.      <dc:identifier>doi:10.1177/19418744231220699</dc:identifier>
427.    </item>
428.    <item>
429.      <title>Lateral Medullary Syndrome With Ipsilateral Upper Motor Neuron Facial Palsy</title>
430.      <link>https://pubmed.ncbi.nlm.nih.gov/38666275/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
431.      <description>Lateral medullary syndrome is a common presentation of posterior circulation ischemia that presents with ipsilateral Horner syndrome, ipsilateral facial numbness, contralateral body numbness, vestibular symptoms, ataxia, dysphagia, and dysarthria. Here, we describe an 84-year-old who presented to the hospital with right upper motor neuron facial weakness and gait abnormality found to have a right lateral medullary ischemic stroke. Multiple MRI's, including with thin brainstem slices, were...</description>
432.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Neurohospitalist. 2024 Apr;14(2):195-198. doi: 10.1177/19418744231220175. Epub 2023 Dec 2.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Lateral medullary syndrome is a common presentation of posterior circulation ischemia that presents with ipsilateral Horner syndrome, ipsilateral facial numbness, contralateral body numbness, vestibular symptoms, ataxia, dysphagia, and dysarthria. Here, we describe an 84-year-old who presented to the hospital with right upper motor neuron facial weakness and gait abnormality found to have a right lateral medullary ischemic stroke. Multiple MRI's, including with thin brainstem slices, were without evidence of pontine, midbrain or cerebral ischemia outside the medulla. We postulate that the patient's ipsilateral upper motor neuron facial weakness was caused by involvement of aberrant corticobulbar fibers in the medulla ascending to the facial nucleus.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666275/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666275</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11040634/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11040634</a> | DOI:<a href=https://doi.org/10.1177/19418744231220175>10.1177/19418744231220175</a></p></div>]]></content:encoded>
433.      <guid isPermaLink="false">pubmed:38666275</guid>
434.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
435.      <dc:creator>Dylan Ryan</dc:creator>
436.      <dc:creator>Rahul Gaini</dc:creator>
437.      <dc:creator>Michael Snider</dc:creator>
438.      <dc:creator>Janie Qing</dc:creator>
439.      <dc:creator>Wuwei Feng</dc:creator>
440.      <dc:date>2024-04-26</dc:date>
441.      <dc:source>The Neurohospitalist</dc:source>
442.      <dc:title>Lateral Medullary Syndrome With Ipsilateral Upper Motor Neuron Facial Palsy</dc:title>
443.      <dc:identifier>pmid:38666275</dc:identifier>
444.      <dc:identifier>pmc:PMC11040634</dc:identifier>
445.      <dc:identifier>doi:10.1177/19418744231220175</dc:identifier>
446.    </item>
447.    <item>
448.      <title>Extended Window Thrombolytics for Ischemic Stroke: A Telestroke versus In-person Experience</title>
449.      <link>https://pubmed.ncbi.nlm.nih.gov/38666267/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
450.      <description>CONCLUSIONS: In patients eligible for extended window acute stroke treatment with thrombolytics, there was no difference in adverse events between telestroke and in-person care.</description>
451.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Neurohospitalist. 2024 Apr;14(2):170-173. doi: 10.1177/19418744231211968. Epub 2023 Nov 11.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND AND PURPOSE: Telestroke evaluation of patients with acute ischemic stroke is supported by American Heart and Stroke Association Guidelines. However, there is no data on outcomes or safety of administering IV thrombolytic stroke therapy using extended window criteria (&gt;4.5 h since onset of symptoms with a hyperacute MRI diffusion T2/FLAIR mismatch) via telestroke. Here, we report adverse events and outcomes of extended-window thrombolysis by telestroke vs in-person care.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We performed a retrospective cohort review from 2020 to 2022 of prospectively collected multinstitutional databases from a large, not-for-profit health system with both in-person stroke and telestroke care. The primary outcome was frequency of symptomatic intracranial hemorrhage (sICH). Secondary outcomes were favorable functional outcome at hospital discharge (modified Rankin Scale, mRS, 0-3) and discharge disposition.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: A total of 33 patients were treated with extended-window thrombolysis (n = 20 in-person, n = 13 telestroke). The median NIH stroke scale was 6, and time since last known normal was similar (median [95% CI]: in-person 13 h [11-15 h] vs telestroke 12 h [9-16 h], <i>P</i> = .33). The sICH frequency was low and occurred in one patient (4.8% in-person vs 0% by telestroke). Favorable outcome at discharge was not different between in-person and telestroke care (median mRS [95% CI]: 2 [1-3] vs 1 [0-2], OR .0 [.0-1.8], <i>P</i> = .27), and discharge deposition was also similar.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: In patients eligible for extended window acute stroke treatment with thrombolytics, there was no difference in adverse events between telestroke and in-person care.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666267/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666267</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11040611/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11040611</a> | DOI:<a href=https://doi.org/10.1177/19418744231211968>10.1177/19418744231211968</a></p></div>]]></content:encoded>
452.      <guid isPermaLink="false">pubmed:38666267</guid>
453.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
454.      <dc:creator>Nick M Murray</dc:creator>
455.      <dc:creator>Paul Johnson</dc:creator>
456.      <dc:creator>Marilyn McKasson</dc:creator>
457.      <dc:creator>Julie Martinez</dc:creator>
458.      <dc:creator>Stephen Chatwin</dc:creator>
459.      <dc:creator>Adrian Püttgen</dc:creator>
460.      <dc:date>2024-04-26</dc:date>
461.      <dc:source>The Neurohospitalist</dc:source>
462.      <dc:title>Extended Window Thrombolytics for Ischemic Stroke: A Telestroke versus In-person Experience</dc:title>
463.      <dc:identifier>pmid:38666267</dc:identifier>
464.      <dc:identifier>pmc:PMC11040611</dc:identifier>
465.      <dc:identifier>doi:10.1177/19418744231211968</dc:identifier>
466.    </item>
467.    <item>
468.      <title>Parent Artery Occlusion for a Dissecting Posterior Cerebral Artery Aneurysm in the P4 Segment Presenting with Ischemic Stroke and Rapid Growth: A Case Report</title>
469.      <link>https://pubmed.ncbi.nlm.nih.gov/38666033/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
470.      <description>A dissecting aneurysm in the P4 segment of the posterior cerebral artery (PCA) is extremely rare, and its treatment is sometimes challenging. Endovascular parent artery occlusion (PAO) was performed for an unruptured P4 segment dissecting PCA aneurysm presenting with ischemic stroke and rapid growth. A 70-year-old man was rushed to our emergency department due to a right-sided headache and a visual field defect. Head magnetic resonance imaging showed a right occipital lobe ischemic stroke, with...</description>
471.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">NMC Case Rep J. 2024 Apr 5;11:103-108. doi: 10.2176/jns-nmc.2023-0267. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">A dissecting aneurysm in the P4 segment of the posterior cerebral artery (PCA) is extremely rare, and its treatment is sometimes challenging. Endovascular parent artery occlusion (PAO) was performed for an unruptured P4 segment dissecting PCA aneurysm presenting with ischemic stroke and rapid growth. A 70-year-old man was rushed to our emergency department due to a right-sided headache and a visual field defect. Head magnetic resonance imaging showed a right occipital lobe ischemic stroke, with right PCA occlusion and aneurysm formation in the P4 segment. The diagnosis was PCA dissection in the calcarine artery, and oral aspirin was started. Within a week, the dissecting aneurysm had enlarged progressively to 6.2 mm in diameter. Thus, PAO with coils was performed as a preventive measure against aneurysm rupture, assuming that complication risks were low because the tributary area of the dissecting PCA had already infarcted. A 6-Fr guiding sheath was introduced from the right brachial artery to the right vertebral artery, and a microcatheter/microguidewire was placed into the true lumen of the calcarine artery distal to the aneurysm. PAO with coils was performed, and the blood flow to the aneurysm was completely obliterated. After the treatment, the known infarction in the right occipital lobe was enlarged, but no new neurological symptoms developed. The patient was discharged independently on postoperative day 3. Treatment for a distal PCA dissecting aneurysm is challenging. PAO with coils is one of the reasonable choices, especially when a visual field defect has already developed.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666033/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666033</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11043799/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11043799</a> | DOI:<a href=https://doi.org/10.2176/jns-nmc.2023-0267>10.2176/jns-nmc.2023-0267</a></p></div>]]></content:encoded>
472.      <guid isPermaLink="false">pubmed:38666033</guid>
473.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
474.      <dc:creator>Kotaro Ishimoto</dc:creator>
475.      <dc:creator>Jo Matsuzaki</dc:creator>
476.      <dc:creator>Ryoichi Iwata</dc:creator>
477.      <dc:creator>Naoki Yamamoto</dc:creator>
478.      <dc:creator>Toru Yamagata</dc:creator>
479.      <dc:creator>Hiromichi Ikuno</dc:creator>
480.      <dc:creator>Misao Nishikawa</dc:creator>
481.      <dc:creator>Takeo Goto</dc:creator>
482.      <dc:date>2024-04-26</dc:date>
483.      <dc:source>NMC case report journal</dc:source>
484.      <dc:title>Parent Artery Occlusion for a Dissecting Posterior Cerebral Artery Aneurysm in the P4 Segment Presenting with Ischemic Stroke and Rapid Growth: A Case Report</dc:title>
485.      <dc:identifier>pmid:38666033</dc:identifier>
486.      <dc:identifier>pmc:PMC11043799</dc:identifier>
487.      <dc:identifier>doi:10.2176/jns-nmc.2023-0267</dc:identifier>
488.    </item>
489.    <item>
490.      <title>Exploring the multifaceted potential of (R)-ketamine beyond antidepressant applications</title>
491.      <link>https://pubmed.ncbi.nlm.nih.gov/38666026/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
492.      <description>(R, S)- and (S)-ketamine have made significant progress in the treatment of treatment-resistant depression (TRD) and have become a research focus in recent years. However, they both have risks of psychomimetic effects, dissociative effects, and abuse liability, which limit their clinical use. Recent preclinical and clinical studies have shown that (R)-ketamine has a more efficient and lasting antidepressant effect with fewer side effects compared to (R, S)- and (S)-ketamine. However, a recent...</description>
493.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Front Pharmacol. 2024 Apr 11;15:1337749. doi: 10.3389/fphar.2024.1337749. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">(<i>R</i>, <i>S</i>)- and (<i>S</i>)-ketamine have made significant progress in the treatment of treatment-resistant depression (TRD) and have become a research focus in recent years. However, they both have risks of psychomimetic effects, dissociative effects, and abuse liability, which limit their clinical use. Recent preclinical and clinical studies have shown that (<i>R</i>)-ketamine has a more efficient and lasting antidepressant effect with fewer side effects compared to (<i>R</i>, <i>S</i>)- and (<i>S</i>)-ketamine. However, a recent small-sample randomized controlled trial found that although (<i>R</i>)-ketamine has a lower incidence of adverse reactions in adult TRD treatment, its antidepressant efficacy is not superior to the placebo group, indicating its antidepressant advantage still needs further verification and clarification. Moreover, an increasing body of research suggests that (<i>R</i>)-ketamine might also have significant applications in the prevention and treatment of medical fields or diseases such as cognitive disorders, perioperative anesthesia, ischemic stroke, Parkinson's disease, multiple sclerosis, osteoporosis, substance use disorders, inflammatory diseases, COVID-19, and organophosphate poisoning. This article briefly reviews the mechanism of action and research on antidepressants related to (<i>R</i>)-ketamine, fully revealing its application potential and development prospects, and providing some references and assistance for subsequent expanded research.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666026/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666026</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11043571/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11043571</a> | DOI:<a href=https://doi.org/10.3389/fphar.2024.1337749>10.3389/fphar.2024.1337749</a></p></div>]]></content:encoded>
494.      <guid isPermaLink="false">pubmed:38666026</guid>
495.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
496.      <dc:creator>Senbing Zhang</dc:creator>
497.      <dc:creator>Yanzhu Pu</dc:creator>
498.      <dc:creator>Jianning Liu</dc:creator>
499.      <dc:creator>Lewen Li</dc:creator>
500.      <dc:creator>Chibing An</dc:creator>
501.      <dc:creator>Yumin Wu</dc:creator>
502.      <dc:creator>Wenjie Zhang</dc:creator>
503.      <dc:creator>Wenxia Zhang</dc:creator>
504.      <dc:creator>Song Qu</dc:creator>
505.      <dc:creator>Wenjun Yan</dc:creator>
506.      <dc:date>2024-04-26</dc:date>
507.      <dc:source>Frontiers in pharmacology</dc:source>
508.      <dc:title>Exploring the multifaceted potential of (R)-ketamine beyond antidepressant applications</dc:title>
509.      <dc:identifier>pmid:38666026</dc:identifier>
510.      <dc:identifier>pmc:PMC11043571</dc:identifier>
511.      <dc:identifier>doi:10.3389/fphar.2024.1337749</dc:identifier>
512.    </item>
513.    <item>
514.      <title>Risk of Long-Term Ischemic Stroke in Patients With Traumatic Brain Injury and Incident Hypertension</title>
515.      <link>https://pubmed.ncbi.nlm.nih.gov/38666008/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
516.      <description>Traumatic brain injury (TBI) is independently associated with hypertension and ischemic stroke. The goal of this study was to determine the interplay between TBI and incident hypertension in the occurrence of post-TBI stroke. This prospective study used a hospital-based registry to identify patients without pre-existing comorbidities. TBI patients (n = 3664) were frequency matched on age, sex, and race to non-TBI patients (n = 1848). Follow-up started 6 months post-TBI or study entry and...</description>
517.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Neurotrauma Rep. 2024 Apr 22;5(1):462-466. doi: 10.1089/neur.2024.0015. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Traumatic brain injury (TBI) is independently associated with hypertension and ischemic stroke. The goal of this study was to determine the interplay between TBI and incident hypertension in the occurrence of post-TBI stroke. This prospective study used a hospital-based registry to identify patients without pre-existing comorbidities. TBI patients (<i>n</i> = 3664) were frequency matched on age, sex, and race to non-TBI patients (<i>n</i> = 1848). Follow-up started 6 months post-TBI or study entry and extended up to 10 years. To examine hypertension's role in post-TBI stroke, we used logistic regression models to calculate the effect estimates for stroke in four exposure categories that included TBI or hypertension in isolation and in combination. Second, we calculated the conditional direct effect (CDE) of TBI in models that considered hypertension as intermediary. Third, we examined whether TBI effect was modified by antihypertensive medication use. The 10-year cumulative incidence of stroke was higher in the TBI group (4.7%) than the non-TBI group (1.3%; <i>p</i> &lt; 0.001). TBI patients who developed hypertension had the highest risk of stroke (odds ratio [OR] = 4.83, 95% confidence interval [CI] = 2.53-9.23, <i>p</i> &lt; 0.001). The combined effect estimates were less than additive, suggesting an overlapping biological pathway. The total effect of TBI (OR = 3.16, 95% CI = 1.94-5.16, <i>p</i> &lt; 0.001) was higher than the CDE that accounted for hypertension (OR = 2.45, 95% CI = 0.93-6.47, <i>p</i> = 0.06). Antihypertensives attenuated the TBI effect, suggesting that the TBI effect on stroke is partially mediated through hypertension. TBI is an independent risk factor for long-term stroke, and the underlying biological pathway may partly operate through TBI-precipitated hypertension. These findings suggest that screening for hypertension may mitigate stroke risk in TBI.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38666008/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38666008</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11044850/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11044850</a> | DOI:<a href=https://doi.org/10.1089/neur.2024.0015>10.1089/neur.2024.0015</a></p></div>]]></content:encoded>
518.      <guid isPermaLink="false">pubmed:38666008</guid>
519.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
520.      <dc:creator>Farid Radmanesh</dc:creator>
521.      <dc:creator>Saef Izzy</dc:creator>
522.      <dc:creator>Ran S Rotem</dc:creator>
523.      <dc:creator>Zabreen Tahir</dc:creator>
524.      <dc:creator>Quinn J Rademaker</dc:creator>
525.      <dc:creator>Taha Yahya</dc:creator>
526.      <dc:creator>Ahmad Mashlah</dc:creator>
527.      <dc:creator>Herman A Taylor</dc:creator>
528.      <dc:creator>Marc G Weisskopf</dc:creator>
529.      <dc:creator>Ross D Zafonte</dc:creator>
530.      <dc:creator>Aaron L Baggish</dc:creator>
531.      <dc:creator>Rachel Grashow</dc:creator>
532.      <dc:date>2024-04-26</dc:date>
533.      <dc:source>Neurotrauma reports</dc:source>
534.      <dc:title>Risk of Long-Term Ischemic Stroke in Patients With Traumatic Brain Injury and Incident Hypertension</dc:title>
535.      <dc:identifier>pmid:38666008</dc:identifier>
536.      <dc:identifier>pmc:PMC11044850</dc:identifier>
537.      <dc:identifier>doi:10.1089/neur.2024.0015</dc:identifier>
538.    </item>
539.    <item>
540.      <title>Joint effect of ischemic stroke and obesity on the risk of venous thromboembolism: the Tromso Study</title>
541.      <link>https://pubmed.ncbi.nlm.nih.gov/38665865/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
542.      <description>CONCLUSION: The combination of obesity and ischemic stroke did not yield an excess risk of VTE. Our findings suggest that obese subjects with ischemic stroke do not have a more than additive risk of VTE.</description>
543.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Res Pract Thromb Haemost. 2024 Mar 27;8(3):102392. doi: 10.1016/j.rpth.2024.102392. eCollection 2024 Mar.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Patients with ischemic stroke have increased risk of venous thromboembolism (VTE). Obesity is prevalent in stroke patients and a well-established risk factor for VTE. Whether obesity further increases the VTE risk in patients with stroke remains unclear.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVES: We investigated the joint effect of ischemic stroke and obesity on the risk of incident VTE in a population-based cohort.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Participants (<i>n</i> = 29,920) were recruited from the fourth to sixth surveys of the Tromsø Study (1994-1995, 2001, and 2007-2008) and followed through 2014. Incident events of ischemic stroke and VTE during follow-up were recorded. Hazard ratios (HRs) of VTE with 95% CIs were estimated according to combined categories of ischemic stroke and obesity (body mass index ≥ 30 kg/m<sup>2</sup>), with exposure to neither risk factors as reference.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: During a median follow-up of 19.6 years, 1388 participants experienced ischemic stroke and 807 participants developed VTE. Among those with stroke, 51 developed VTE, yielding an incidence rate of VTE after stroke of 7.2 per 1000 person-years (95% CI, 5.5-9.5). In subjects without stroke, obesity was associated with a 1.8-fold higher VTE risk (HR, 1.76; 95% CI, 1.47-2.11). In nonobese subjects, stroke was associated with a 1.8-fold higher VTE risk (HR, 1.77; 95% CI, 1.27-2.46). Obese subjects with stroke had a 2-fold increased VTE risk (HR, 2.44; 95% CI, 1.37-4.36).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: The combination of obesity and ischemic stroke did not yield an excess risk of VTE. Our findings suggest that obese subjects with ischemic stroke do not have a more than additive risk of VTE.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38665865/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38665865</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11043863/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11043863</a> | DOI:<a href=https://doi.org/10.1016/j.rpth.2024.102392>10.1016/j.rpth.2024.102392</a></p></div>]]></content:encoded>
544.      <guid isPermaLink="false">pubmed:38665865</guid>
545.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
546.      <dc:creator>Birgitte G Tøndel</dc:creator>
547.      <dc:creator>Joakim K Sejrup</dc:creator>
548.      <dc:creator>Vânia M Morelli</dc:creator>
549.      <dc:creator>Maja-Lisa Løchen</dc:creator>
550.      <dc:creator>Inger Njølstad</dc:creator>
551.      <dc:creator>Ellisiv B Mathiesen</dc:creator>
552.      <dc:creator>Tom Wilsgaard</dc:creator>
553.      <dc:creator>John-Bjarne Hansen</dc:creator>
554.      <dc:creator>Sigrid K Brækkan</dc:creator>
555.      <dc:date>2024-04-26</dc:date>
556.      <dc:source>Research and practice in thrombosis and haemostasis</dc:source>
557.      <dc:title>Joint effect of ischemic stroke and obesity on the risk of venous thromboembolism: the Tromso Study</dc:title>
558.      <dc:identifier>pmid:38665865</dc:identifier>
559.      <dc:identifier>pmc:PMC11043863</dc:identifier>
560.      <dc:identifier>doi:10.1016/j.rpth.2024.102392</dc:identifier>
561.    </item>
562.    <item>
563.      <title>Discovery of novel positive allosteric modulators targeting GluN1/2A NMDARs as anti-stroke therapeutic agents</title>
564.      <link>https://pubmed.ncbi.nlm.nih.gov/38665828/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
565.      <description>Excitotoxicity due to excessive activation of NMDARs is one of the main mechanisms of neuronal death during ischemic stroke. Previous studies have suggested that activation of either synaptic or extrasynaptic GluN2B-containing NMDARs results in neuronal damage, whereas activation of GluN2A-containing NMDARs promotes neuronal survival against ischemic insults. This study applied a systematic in silico, in vitro, and in vivo approach to the discovery of novel and potential GluN1/2A NMDAR positive...</description>
566.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">RSC Med Chem. 2024 Jan 4;15(4):1307-1319. doi: 10.1039/d3md00455d. eCollection 2024 Apr 24.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Excitotoxicity due to excessive activation of NMDARs is one of the main mechanisms of neuronal death during ischemic stroke. Previous studies have suggested that activation of either synaptic or extrasynaptic GluN2B-containing NMDARs results in neuronal damage, whereas activation of GluN2A-containing NMDARs promotes neuronal survival against ischemic insults. This study applied a systematic <i>in silico</i>, <i>in vitro</i>, and <i>in vivo</i> approach to the discovery of novel and potential GluN1/2A NMDAR positive allosteric modulators (PAMs). Ten compounds were obtained and identified as potential GluN1/2A PAMs by structure-based virtual screening and calcium imaging. The neuroprotective activity of the candidate compounds was demonstrated <i>in vitro</i>. Subsequently, compound 15 (<b>aegeline</b>) was tested further in the model of transient middle cerebral artery occlusion (tMCAO) <i>in vivo</i>, which significantly decreased cerebral infarction. The mechanism by which <b>aegeline</b> exerts its effect on allosteric modulation was revealed using molecular dynamics simulations. Finally, we found that the neuroprotective effect of <b>aegeline</b> was significantly correlated with the enhanced phosphorylation of cAMP response element-binding protein (CREB). Our study discovered the neuroprotective effect of <b>aegeline</b> as a novel PAM targeting GluN1/2A NMDAR, which provides a potential opportunity for the development of therapeutic agents for ischemic stroke.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38665828/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38665828</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11042165/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11042165</a> | DOI:<a href=https://doi.org/10.1039/d3md00455d>10.1039/d3md00455d</a></p></div>]]></content:encoded>
567.      <guid isPermaLink="false">pubmed:38665828</guid>
568.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
569.      <dc:creator>Hongyu Zhu</dc:creator>
570.      <dc:creator>Xin Chen</dc:creator>
571.      <dc:creator>Lu Zhang</dc:creator>
572.      <dc:creator>Xuequan Liu</dc:creator>
573.      <dc:creator>Ji Chen</dc:creator>
574.      <dc:creator>Han-Ting Zhang</dc:creator>
575.      <dc:creator>Mingxin Dong</dc:creator>
576.      <dc:date>2024-04-26</dc:date>
577.      <dc:source>RSC medicinal chemistry</dc:source>
578.      <dc:title>Discovery of novel positive allosteric modulators targeting GluN1/2A NMDARs as anti-stroke therapeutic agents</dc:title>
579.      <dc:identifier>pmid:38665828</dc:identifier>
580.      <dc:identifier>pmc:PMC11042165</dc:identifier>
581.      <dc:identifier>doi:10.1039/d3md00455d</dc:identifier>
582.    </item>
583.    <item>
584.      <title>Health behavior outcomes in stroke survivors prescribed wearables for atrial fibrillation detection stratified by age</title>
585.      <link>https://pubmed.ncbi.nlm.nih.gov/38665288/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
586.      <description>CONCLUSION: Stroke survivors demonstrated a willingness to use smartwatches for AF monitoring. Importantly, among these study participants, the majority did not experience negative health behavior outcomes or decreased engagement as age increased.</description>
587.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Geriatr Cardiol. 2024 Mar 28;21(3):323-330. doi: 10.26599/1671-5411.2024.03.005.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Smartwatches have become readily accessible tools for detecting atrial fibrillation (AF). There remains limited data on how they affect psychosocial outcomes and engagement in older adults. We examine the health behavior outcomes of stroke survivors prescribed smartwatches for AF detection stratified by age.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We analyzed data from the Pulsewatch study, a randomized controlled trial that enrolled patients (≥ 50 years) with a history of stroke or transient ischemic attack and CHA2DS2-VASc ≥ 2. Intervention participants were equipped with a cardiac patch monitor and a smartwatch-app dyad, while control participants wore the cardiac patch monitor for up to 44 days. We evaluated health behavior parameters using standardized tools, including the Consumer Health Activation Index, the Generalized Anxiety Disorder questionnaire, the 12-Item Short Form Health Survey, and wear time of participants categorized into three age groups: Group 1 (ages 50-60), Group 2 (ages 61-69), and Group 3 (ages 70-87). We performed statistical analysis using a mixed-effects repeated measures linear regression model to examine differences amongst age groups.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Comparative analysis between Groups 1, 2 and 3 revealed no significant differences in anxiety, patient activation, perception of physical health and wear time. The use of smartwatch technology was associated with a decrease in perception of mental health for Group 2 compared to Group 1 (β = -3.29, <i>P</i> = 0.046).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Stroke survivors demonstrated a willingness to use smartwatches for AF monitoring. Importantly, among these study participants, the majority did not experience negative health behavior outcomes or decreased engagement as age increased.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38665288/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38665288</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11040051/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11040051</a> | DOI:<a href=https://doi.org/10.26599/1671-5411.2024.03.005>10.26599/1671-5411.2024.03.005</a></p></div>]]></content:encoded>
588.      <guid isPermaLink="false">pubmed:38665288</guid>
589.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
590.      <dc:creator>Joanne Mathew</dc:creator>
591.      <dc:creator>Jordy Mehawej</dc:creator>
592.      <dc:creator>Ziyue Wang</dc:creator>
593.      <dc:creator>Taylor Orwig</dc:creator>
594.      <dc:creator>Eric Ding</dc:creator>
595.      <dc:creator>Andreas Filippaios</dc:creator>
596.      <dc:creator>Syed Naeem</dc:creator>
597.      <dc:creator>Edith Mensah Otabil</dc:creator>
598.      <dc:creator>Alex Hamel</dc:creator>
599.      <dc:creator>Kamran Noorishirazi</dc:creator>
600.      <dc:creator>Irina Radu</dc:creator>
601.      <dc:creator>Jane Saczynski</dc:creator>
602.      <dc:creator>David D McManus</dc:creator>
603.      <dc:creator>Khanh-Van Tran</dc:creator>
604.      <dc:date>2024-04-26</dc:date>
605.      <dc:source>Journal of geriatric cardiology : JGC</dc:source>
606.      <dc:title>Health behavior outcomes in stroke survivors prescribed wearables for atrial fibrillation detection stratified by age</dc:title>
607.      <dc:identifier>pmid:38665288</dc:identifier>
608.      <dc:identifier>pmc:PMC11040051</dc:identifier>
609.      <dc:identifier>doi:10.26599/1671-5411.2024.03.005</dc:identifier>
610.    </item>
611.    <item>
612.      <title>Statin utilization and cardiovascular outcomes in a real-world primary prevention cohort of older adults</title>
613.      <link>https://pubmed.ncbi.nlm.nih.gov/38665251/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
614.      <description>CONCLUSION: Lack of statin use was associated with increased cardiovascular events and mortality in high-risk older adults. Given the benefits appreciated, statin use may need to be strongly considered for primary ASCVD prevention among high-risk older adults. Future studies will assess the risk-benefit ratio of statin intervention in older adults.</description>
615.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Am J Prev Cardiol. 2024 Apr 5;18:100664. doi: 10.1016/j.ajpc.2024.100664. eCollection 2024 Jun.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Statins are a cost-effective therapy for prevention of atherosclerotic cardiovascular disease (ASCVD). Guidelines on statins for primary prevention are unclear for older adults (&gt;75 years).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVE: Investigate statin utility in older adults without ASCVD events, by risk stratifying in a large healthcare network.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We included 8,114 older adults, without CAD, PVD or ischemic stroke. Statin utilization based on ACC/AHA 10-year ASCVD risk calculation, was evaluated in intermediate (7.5%-19.9%) and high-risk patients (≥ 20%); and categorized using low and 'moderate or high' intensity statins with a follow up period of ∼7 years. Cox regression models were used to calculate hazard ratios for incident ASCVD and mortality across risk categories stratified by statin utilization. Data was adjusted for competing risk using Elixhauser Comorbidity Index.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Compared with those on moderate or high intensity statins, high-risk older patients not on any statin had a significantly increased risk of MI <i>[HR 1.51 (1.17-1.95); p</i><i>&lt;</i><i>0.01]</i>, stroke <i>[HR 1.47 (1.14-1.90); p</i><i>&lt;</i><i>0.01]</i> and all-cause mortality <i>[HR 1.37 (1.19-1.58); p</i><i>&lt;</i><i>0.001]</i> in models adjusted for Elixhauser Comorbidity Index<b>.</b> When comparing the no statin group versus the moderate or high intensity statin group in the intermediate risk cohort, although a trend for increased risk was seen, it did not meet statistical significance thresholds for MI, stroke or all-cause mortality.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Lack of statin use was associated with increased cardiovascular events and mortality in high-risk older adults. Given the benefits appreciated, statin use may need to be strongly considered for primary ASCVD prevention among high-risk older adults. Future studies will assess the risk-benefit ratio of statin intervention in older adults.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38665251/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38665251</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11043821/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">PMC11043821</a> | DOI:<a href=https://doi.org/10.1016/j.ajpc.2024.100664>10.1016/j.ajpc.2024.100664</a></p></div>]]></content:encoded>
616.      <guid isPermaLink="false">pubmed:38665251</guid>
617.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
618.      <dc:creator>Aaron J Walker</dc:creator>
619.      <dc:creator>Jianhui Zhu</dc:creator>
620.      <dc:creator>Floyd Thoma</dc:creator>
621.      <dc:creator>Oscar Marroquin</dc:creator>
622.      <dc:creator>Amber Makani</dc:creator>
623.      <dc:creator>Martha Gulati</dc:creator>
624.      <dc:creator>Eugenia Gianos</dc:creator>
625.      <dc:creator>Salim S Virani</dc:creator>
626.      <dc:creator>Fatima Rodriguez</dc:creator>
627.      <dc:creator>Steven E Reis</dc:creator>
628.      <dc:creator>Christie Ballantyne</dc:creator>
629.      <dc:creator>Suresh Mulukutla</dc:creator>
630.      <dc:creator>Anum Saeed</dc:creator>
631.      <dc:date>2024-04-26</dc:date>
632.      <dc:source>American journal of preventive cardiology</dc:source>
633.      <dc:title>Statin utilization and cardiovascular outcomes in a real-world primary prevention cohort of older adults</dc:title>
634.      <dc:identifier>pmid:38665251</dc:identifier>
635.      <dc:identifier>pmc:PMC11043821</dc:identifier>
636.      <dc:identifier>doi:10.1016/j.ajpc.2024.100664</dc:identifier>
637.    </item>
638.    <item>
639.      <title>Safety and efficacy of endovascular treatment for acute ischemic stroke of large-vessel occlusion beyond the time window based on imaging evaluation</title>
640.      <link>https://pubmed.ncbi.nlm.nih.gov/38665125/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
641.      <description>CONCLUSIONS: The safety and effectiveness of EVT treatment for selected AIS-LVO patients with symptom onset of 24-72 h are not inferior to those treated within 6-24 h of onset, especially in a short term based on the pre-treatment advanced neuroimaging computed tomography perfusion even though further investigations are necessary to prove this finding.</description>
642.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Interv Neuroradiol. 2024 Apr 26:15910199241250081. doi: 10.1177/15910199241250081. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">PURPOSE: Endovascular treatment (EVT) of acute ischemic stroke caused by large-vessel occlusion (AIS-LVO) over 24 h of onset remains controversial. This study was to explore the safety and efficacy of EVT for patients with AIS-LVO between 24 and 72 h of symptom onset after rigorous imaging evaluation.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Patients with AIS-LVO treated with EVT were retrospectively enrolled and divided into two groups according to the time from symptom onset to groin puncture: 64 in the over-time group (&gt;24 h) and 257 in the within-time group (≤24 h). Outcomes included 3-month modified Rankin Scale (mRS) score, functional independence (defined as mRS 0-2), successful cerebral reperfusion, symptomatic intracranial hemorrhage (sICH), and 3-month mortality.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Patients in the over-time group had no significant differences in the functional independence (40.6% vs 42.5%, odds ratio or OR 0.91, 95% confidence interval or CI 0.52-1.60, <i>p</i> = 0.753), successful reperfusion (96.7% vs 95.8%, OR 0.76, 95% CI 0.36-1.59, <i>p</i> = 0.467), sICH (8.3% vs 6.7%, OR 1.20, 95% CI 0.42-3.38, <i>p</i> = 0.735), 3-month mortality (13.3% vs 10.8%, OR 1.17, 95% CI 0.51-2.70, <i>p</i> = 0.716) compared with patients in the within-time group. After matching adjustment, the results did not change significantly.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: The safety and effectiveness of EVT treatment for selected AIS-LVO patients with symptom onset of 24-72 h are not inferior to those treated within 6-24 h of onset, especially in a short term based on the pre-treatment advanced neuroimaging computed tomography perfusion even though further investigations are necessary to prove this finding.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38665125/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38665125</a> | DOI:<a href=https://doi.org/10.1177/15910199241250081>10.1177/15910199241250081</a></p></div>]]></content:encoded>
643.      <guid isPermaLink="false">pubmed:38665125</guid>
644.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
645.      <dc:creator>Shi-Dun Chen</dc:creator>
646.      <dc:creator>Cheng-Bao Yang</dc:creator>
647.      <dc:creator>Yong-Xiang Wang</dc:creator>
648.      <dc:creator>Yue-Han Yin</dc:creator>
649.      <dc:creator>Bu-Lang Gao</dc:creator>
650.      <dc:creator>Chun-Guang Chen</dc:creator>
651.      <dc:date>2024-04-26</dc:date>
652.      <dc:source>Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences</dc:source>
653.      <dc:title>Safety and efficacy of endovascular treatment for acute ischemic stroke of large-vessel occlusion beyond the time window based on imaging evaluation</dc:title>
654.      <dc:identifier>pmid:38665125</dc:identifier>
655.      <dc:identifier>doi:10.1177/15910199241250081</dc:identifier>
656.    </item>
657.    <item>
658.      <title>Gamma-glutamyl transferase and the risk of all-cause and disease-specific mortality in patients with diabetes: A nationwide cohort study</title>
659.      <link>https://pubmed.ncbi.nlm.nih.gov/38664890/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
660.      <description>CONCLUSIONS: Serum gamma-glutamyl transferase levels may be useful for the risk assessment of all-cause and disease-specific mortality among patients with type 2 diabetes mellitus.</description>
661.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Diabetes. 2024 May;16(5):e13551. doi: 10.1111/1753-0407.13551.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: There exists a paucity of data regarding whether gamma-glutamyl transferase is associated with disease-specific mortality in patients with type 2 diabetes mellitus. This study aimed to investigate the association of serum gamma-glutamyl transferase levels with all-cause and disease-specific mortality in patients with diabetes mellitus using a Korean nationwide health-screening database.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: A total of 9 687 066 patients without viral hepatitis or liver cirrhosis who underwent health examination in 2009 were included. These patients were divided into four groups according to sex-specific quartiles of serum gamma-glutamyl transferase levels.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: During a median follow-up period of 8.1 years, 222 242 deaths were identified. The all-cause mortality rate increased as the serum gamma-glutamyl transferase levels became higher (highest quartile vs lowest quartile: hazard ratio [HR], 1.57; 95% confidence interval [CI], 1.55-1.59; p for trend &lt;.001). Similar trends were observed for cardiovascular disease (HR, 1.57; 95% CI, 1.53-1.62), ischemic heart disease (HR, 1.40; 95% CI, 1.33-1.48), and stroke (HR, 1.72; 95% CI, 1.60-1.85) in the highest quartile, as compared with the lowest quartile (p for trend &lt;.001). As the gamma-glutamyl transferase quartiles became higher, mortality rates related to cancer (HR, 1.56; 95% CI, 1.52-1.60), liver disease (HR, 9.42; 95% CI, 8.81-10.07), respiratory disease (HR, 1.55; 95% CI, 1.49-1.62), and infectious disease (HR, 1.73; 95% CI, 1.59-1.87) also increased in the highest quartile, compared with the lowest quartile (p for trend &lt;.001).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Serum gamma-glutamyl transferase levels may be useful for the risk assessment of all-cause and disease-specific mortality among patients with type 2 diabetes mellitus.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38664890/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38664890</a> | DOI:<a href=https://doi.org/10.1111/1753-0407.13551>10.1111/1753-0407.13551</a></p></div>]]></content:encoded>
662.      <guid isPermaLink="false">pubmed:38664890</guid>
663.      <pubDate>Fri, 26 Apr 2024 06:00:00 -0400</pubDate>
664.      <dc:creator>Goh Eun Chung</dc:creator>
665.      <dc:creator>Su-Min Jeong</dc:creator>
666.      <dc:creator>Su Jong Yu</dc:creator>
667.      <dc:creator>Jeong-Ju Yoo</dc:creator>
668.      <dc:creator>Yuri Cho</dc:creator>
669.      <dc:creator>Kyu-Na Lee</dc:creator>
670.      <dc:creator>Dong Wook Shin</dc:creator>
671.      <dc:creator>Yoon Jun Kim</dc:creator>
672.      <dc:creator>Jung-Hwan Yoon</dc:creator>
673.      <dc:creator>Kyungdo Han</dc:creator>
674.      <dc:creator>Eun Ju Cho</dc:creator>
675.      <dc:date>2024-04-26</dc:date>
676.      <dc:source>Journal of diabetes</dc:source>
677.      <dc:title>Gamma-glutamyl transferase and the risk of all-cause and disease-specific mortality in patients with diabetes: A nationwide cohort study</dc:title>
678.      <dc:identifier>pmid:38664890</dc:identifier>
679.      <dc:identifier>doi:10.1111/1753-0407.13551</dc:identifier>
680.    </item>
681.    <item>
682.      <title>Stroke incidence increases with diabetic retinopathy severity and macular edema in type 1 diabetes</title>
683.      <link>https://pubmed.ncbi.nlm.nih.gov/38664827/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
684.      <description>CONCLUSIONS: Stroke incidence increases with the severity of diabetic retinopathy independently of comorbid conditions, including diabetic kidney disease.</description>
685.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cardiovasc Diabetol. 2024 Apr 25;23(1):136. doi: 10.1186/s12933-024-02235-w.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: As the retina is suggested to mirror the brain, we hypothesized that diabetic retinopathy and macular edema are indicative of stroke risk in type 1 diabetes and sought to assess this association in individuals with type 1 diabetes.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We included 1,268 adult FinnDiane Study participants with type 1 diabetes (age 38.7 ± 11.8 years, 51.7% men vs. 48.3% women, and 31.5% had diabetic kidney disease), data on baseline diabetic retinopathy severity, and first stroke during our observational follow-up. Retinopathy was graded by the Early Treatment Diabetic Retinopathy Study (ETDRS) scale, and macular edema as clinically significant (CSME) or not. Strokes identified from registries were confirmed from medical files. Adjusted hazard ratios (HR) for stroke by retinopathy severity and CSME were calculated by Cox models adjusted for clinical confounders, including diabetic kidney disease.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: During median 18.0 (14.1-19.3) follow-up years, 130 strokes (96 ischemic, 34 hemorrhagic) occurred. With no-very mild (ETDRS 10-20) retinopathy as reference, the adjusted HR for stroke was 1.79 (95%CI 1.02-3.15) in non-proliferative (ETDRS 35-53), and 1.69 (1.02-2.82) in proliferative (ETDRS 61-85) retinopathy. Corresponding adjusted HR for ischemic stroke was 1.68 (0.91-3.10) in non-proliferative and 1.35 (0.77-2.36) in proliferative retinopathy. The adjusted HR for hemorrhagic stroke was 2.84 (0.66-12.28) in non-proliferative and 4.31 (1.16-16.10) in proliferative retinopathy. CSME did not increase HR for any stroke type after adjustment for clinical confounders (data not shown).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Stroke incidence increases with the severity of diabetic retinopathy independently of comorbid conditions, including diabetic kidney disease.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38664827/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38664827</a> | DOI:<a href=https://doi.org/10.1186/s12933-024-02235-w>10.1186/s12933-024-02235-w</a></p></div>]]></content:encoded>
686.      <guid isPermaLink="false">pubmed:38664827</guid>
687.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
688.      <dc:creator>Marika I Eriksson</dc:creator>
689.      <dc:creator>Kustaa Hietala</dc:creator>
690.      <dc:creator>Paula Summanen</dc:creator>
691.      <dc:creator>Valma Harjutsalo</dc:creator>
692.      <dc:creator>Jukka Putaala</dc:creator>
693.      <dc:creator>Anni Ylinen</dc:creator>
694.      <dc:creator>Stefanie Hägg-Holmberg</dc:creator>
695.      <dc:creator>Per-Henrik Groop</dc:creator>
696.      <dc:creator>Lena M Thorn</dc:creator>
697.      <dc:creator>FinnDiane Study</dc:creator>
698.      <dc:date>2024-04-25</dc:date>
699.      <dc:source>Cardiovascular diabetology</dc:source>
700.      <dc:title>Stroke incidence increases with diabetic retinopathy severity and macular edema in type 1 diabetes</dc:title>
701.      <dc:identifier>pmid:38664827</dc:identifier>
702.      <dc:identifier>doi:10.1186/s12933-024-02235-w</dc:identifier>
703.    </item>
704.    <item>
705.      <title>A dynamic nomogram for predict individual risk of malignant brain edema after endovascular thrombectomy in acute ischemic stroke</title>
706.      <link>https://pubmed.ncbi.nlm.nih.gov/38664433/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
707.      <description>The aim of this study was to develop a dynamic nomogram combining clinical and imaging data to predict malignant brain edema (MBE) after endovascular thrombectomy (EVT) in patients with large vessel occlusion stroke (LVOS). We analyzed the data of LVOS patients receiving EVT at our center from October 2018 to February 2023, and divided a 7:3 ratio into the training cohort and internal validation cohort, and we also prospectively collected patients from another stroke center for external...</description>
708.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Sci Rep. 2024 Apr 25;14(1):9529. doi: 10.1038/s41598-024-60083-w.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">The aim of this study was to develop a dynamic nomogram combining clinical and imaging data to predict malignant brain edema (MBE) after endovascular thrombectomy (EVT) in patients with large vessel occlusion stroke (LVOS). We analyzed the data of LVOS patients receiving EVT at our center from October 2018 to February 2023, and divided a 7:3 ratio into the training cohort and internal validation cohort, and we also prospectively collected patients from another stroke center for external validation. MBE was defined as a midline shift or pineal gland shift &gt; 5 mm, as determined by computed tomography (CT) scans obtained within 7 days after EVT. A nomogram was constructed using logistic regression analysis, and its receiver operating characteristic curve (ROC) and calibration were assessed in three cohorts. A total of 432 patients were enrolled in this study, with 247 in the training cohort, 100 in the internal validation cohort, and 85 in the external validation cohort. MBE occurred in 24% (59) in the training cohort, 16% (16) in the internal validation cohort and 14% (12) in the external validation cohort. After adjusting for various confounding factors, we constructed a nomogram including the clot burden score (CBS), baseline neutrophil count, core infarct volume on CTP before EVT, collateral index, and the number of retrieval attempts. The AUCs of the training cohorts were 0.891 (95% CI 0.840-0.942), the Hosmer-Lemeshow test showed good calibration of the nomogram (P = 0.879). And our nomogram performed well in both internal and external validation data. Our nomogram demonstrates promising potential in identifying patients at elevated risk of MBE following EVT for LVOS.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38664433/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38664433</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-60083-w>10.1038/s41598-024-60083-w</a></p></div>]]></content:encoded>
709.      <guid isPermaLink="false">pubmed:38664433</guid>
710.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
711.      <dc:creator>Huiyuan Wang</dc:creator>
712.      <dc:creator>Chenghua Xu</dc:creator>
713.      <dc:creator>Yu Xiao</dc:creator>
714.      <dc:creator>Panpan Shen</dc:creator>
715.      <dc:creator>Shunyuan Guo</dc:creator>
716.      <dc:creator>Yafei Shang</dc:creator>
717.      <dc:creator>Xinyi Chen</dc:creator>
718.      <dc:creator>Jie Xu</dc:creator>
719.      <dc:creator>Chunrong Li</dc:creator>
720.      <dc:creator>Mingming Tan</dc:creator>
721.      <dc:creator>Sheng Zhang</dc:creator>
722.      <dc:creator>Yu Geng</dc:creator>
723.      <dc:date>2024-04-25</dc:date>
724.      <dc:source>Scientific reports</dc:source>
725.      <dc:title>A dynamic nomogram for predict individual risk of malignant brain edema after endovascular thrombectomy in acute ischemic stroke</dc:title>
726.      <dc:identifier>pmid:38664433</dc:identifier>
727.      <dc:identifier>doi:10.1038/s41598-024-60083-w</dc:identifier>
728.    </item>
729.    <item>
730.      <title>Molecular Imaging of Fibroblast Activation in Rabbit Atherosclerotic Plaques: a Preclinical PET/CT Study</title>
731.      <link>https://pubmed.ncbi.nlm.nih.gov/38664355/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
732.      <description>CONCLUSIONS: We successfully achieve molecular imaging of fibroblast activation in atherosclerotic lesions of rabbits, suggesting Al^(18)F-NOTA-FAPI-04 PET/CT may be a potentially valuable tool to identify plaques.</description>
733.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Mol Imaging Biol. 2024 Apr 25. doi: 10.1007/s11307-024-01919-9. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">AIM: Atherosclerosis remains the pathological basis of myocardial infarction and ischemic stroke. Early and accurate identification of plauqes is crucial to improve clinical outcomes of atherosclerosis patients. Our study aims to evaluate the potential value of fibroblast activation protein inhibitor (FAPI)-04 PET/CT in identifying plaques via a preclinical rabbit model of atherosclerosis.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: New Zealand white rabbits were fed high-fat diet (HFD), and randomly divided into the model group injured by the balloon, and the sham group only with incisions. Ultrasound was performed to detect plaques, and FAPI-avid was determined through Al<sup>18</sup>F-NOTA-FAPI-04 PET/CT. Mean standardized uptake values (SUVmean) in lesions were compared, and biodistribution of Al<sup>18</sup>F-NOTA-FAPI-04 and target-to-background ratios (TBRs) were calculated. Histological staining was performed to display arterial plaques, and autoradiography (ARG) was employed to measure the in vitro intensity of Al<sup>18</sup>F-NOTA-FAPI-04. At last, the correlation among FAP levels, plaque area, SUVmean values and fibrous cap thickness was assessed.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: The rabbit carotid and abdominal atherosclerosis model was established. Al<sup>18</sup>F-NOTA-FAPI-04 showed a higher uptake in carotid plaques (SUVmean 1.32 ± 0.11) and abdominal plaques (SUVmean 0.73 ± 0.13) compared to corresponding controls (SUVmean 1.07 ± 0.06; 0.46 ± 0.03) (P &lt; 0.05). Biodistribution analysis of Al<sup>18</sup>F-NOTA-FAPI-04 revealed that the bigger plaques were delineated with higher TBRs. Pathological staining showed the formation of arterial plaques, and ARG staining exhibited a higher intensity of Al<sup>18</sup>F-NOTA-FAPI-04 in the bigger plaques. Lastly, plaque area was found to be positively correlated to FAP expression and SUVmean, while FAP expression was negatively correlated to fibrous cap thickness of plaques.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: We successfully achieve molecular imaging of fibroblast activation in atherosclerotic lesions of rabbits, suggesting Al<sup>18</sup>F-NOTA-FAPI-04 PET/CT may be a potentially valuable tool to identify plaques.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38664355/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38664355</a> | DOI:<a href=https://doi.org/10.1007/s11307-024-01919-9>10.1007/s11307-024-01919-9</a></p></div>]]></content:encoded>
734.      <guid isPermaLink="false">pubmed:38664355</guid>
735.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
736.      <dc:creator>Tianxiong Ji</dc:creator>
737.      <dc:creator>Chunfang Zan</dc:creator>
738.      <dc:creator>Lina Li</dc:creator>
739.      <dc:creator>Jianbo Cao</dc:creator>
740.      <dc:creator>Yao Su</dc:creator>
741.      <dc:creator>Hongliang Wang</dc:creator>
742.      <dc:creator>Zhifang Wu</dc:creator>
743.      <dc:creator>Min-Fu Yang</dc:creator>
744.      <dc:creator>Kefei Dou</dc:creator>
745.      <dc:creator>Sijin Li</dc:creator>
746.      <dc:date>2024-04-25</dc:date>
747.      <dc:source>Molecular imaging and biology</dc:source>
748.      <dc:title>Molecular Imaging of Fibroblast Activation in Rabbit Atherosclerotic Plaques: a Preclinical PET/CT Study</dc:title>
749.      <dc:identifier>pmid:38664355</dc:identifier>
750.      <dc:identifier>doi:10.1007/s11307-024-01919-9</dc:identifier>
751.    </item>
752.    <item>
753.      <title>Safety and effectiveness assessment of the surpass evolve (SEASE): a post-market international multicenter study</title>
754.      <link>https://pubmed.ncbi.nlm.nih.gov/38663997/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
755.      <description>CONCLUSION: These results demonstrate that SE has a consistently high effectiveness and favorable safety for the treatment of iAs.</description>
756.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Neurointerv Surg. 2024 Apr 25:jnis-2024-021503. doi: 10.1136/jnis-2024-021503. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Flow diverters are the first-line treatment for specific intracranial aneurysms (iA). Surpass Evolve (SE) is a new-generation 64-wire flow diverter with a high braid angle. Current literature on the SE is limited. We aimed to report the first international real-world experience evaluating the safety and effectiveness of the SE.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: The Safety and Effectiveness Assessment of the Surpass Evolve (SEASE) was a multicenter retrospective international post-marketing cohort study including consecutive patients treated with SE for iAs between 2020 and 2022. Demographic, clinical, and angiographic data were collected. Primary effectiveness was independent core lab adjudicated complete occlusion rates (Raymond-Roy Class 1) at last follow-up. Primary safety were major ischemic/hemorrhagic events and mortality.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: In total, 305 patients with 332 aneurysms underwent SE implantation. The patients had a median age of 59 [50-67] years, and 256 (83.9%) were female. The baseline modified Rankin scale score was 0-2 in 291 patients (96.7%). Most aneurysms were unruptured (285, 93.4%) and saccular (309, 93.1%). Previous treatment was present in 76 (22.9%) patients. The median aneurysm size was 5.1 [3.4-9.0] mm, and the median neck width was 3.6 [2.7-5.1] mm. Most aneurysms were in the internal carotid artery C6 ophthalmic segment (126, 38.0%), followed by the communicating segment (58, 17.5%). At median 10.2 [6.4-12.9] months follow-up, 233 (73.0%) aneurysms achieved complete occlusion. After adjusting for confounders, complete occlusion remained consistent. Major stroke and procedure-related mortality were reported in 6 (2%) and 2 (0.7%) cases, respectively.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: These results demonstrate that SE has a consistently high effectiveness and favorable safety for the treatment of iAs.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38663997/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38663997</a> | DOI:<a href=https://doi.org/10.1136/jnis-2024-021503>10.1136/jnis-2024-021503</a></p></div>]]></content:encoded>
757.      <guid isPermaLink="false">pubmed:38663997</guid>
758.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
759.      <dc:creator>Juan Vivanco-Suarez</dc:creator>
760.      <dc:creator>Mahmoud Dibas</dc:creator>
761.      <dc:creator>Demetrius Klee Lopes</dc:creator>
762.      <dc:creator>Ricardo A Hanel</dc:creator>
763.      <dc:creator>Mario Martínez-Galdámez</dc:creator>
764.      <dc:creator>Aaron Rodriguez-Calienes</dc:creator>
765.      <dc:creator>Gustavo M Cortez</dc:creator>
766.      <dc:creator>Johanna T Fifi</dc:creator>
767.      <dc:creator>Alex Devarajan</dc:creator>
768.      <dc:creator>Gabor Toth</dc:creator>
769.      <dc:creator>Thomas Patterson</dc:creator>
770.      <dc:creator>David Altschul</dc:creator>
771.      <dc:creator>Vitor M Pereira</dc:creator>
772.      <dc:creator>Eileen Liu</dc:creator>
773.      <dc:creator>Ajit S Puri</dc:creator>
774.      <dc:creator>Anna Luisa Kuhn</dc:creator>
775.      <dc:creator>Waldo R Guerrero</dc:creator>
776.      <dc:creator>Priyank Khandelwal</dc:creator>
777.      <dc:creator>Ivo Bach</dc:creator>
778.      <dc:creator>Peter Kan</dc:creator>
779.      <dc:creator>Gautam Edhayan</dc:creator>
780.      <dc:creator>Curtis Given</dc:creator>
781.      <dc:creator>Sandra Narayanan</dc:creator>
782.      <dc:creator>Bradley A Gross</dc:creator>
783.      <dc:creator>Mudassir Farooqui</dc:creator>
784.      <dc:creator>Milagros Galecio-Castillo</dc:creator>
785.      <dc:creator>Shahram Derakhshani</dc:creator>
786.      <dc:creator>Santiago Ortega-Gutierrez</dc:creator>
787.      <dc:date>2024-04-25</dc:date>
788.      <dc:source>Journal of neurointerventional surgery</dc:source>
789.      <dc:title>Safety and effectiveness assessment of the surpass evolve (SEASE): a post-market international multicenter study</dc:title>
790.      <dc:identifier>pmid:38663997</dc:identifier>
791.      <dc:identifier>doi:10.1136/jnis-2024-021503</dc:identifier>
792.    </item>
793.    <item>
794.      <title>Assessing the Performance of Artificial Intelligence Models: Insights from the American Society of Functional Neuroradiology Artificial Intelligence Competition</title>
795.      <link>https://pubmed.ncbi.nlm.nih.gov/38663992/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
796.      <description>CONCLUSIONS: To assess the performance of AI models in real-world clinical scenarios, we analyzed their performance in the ASFNR AI Competition. The first ASFNR Competition underscored the gap between expectation and reality; the models largely fell short in their assessments. As the integration of AI tools into clinical workflows increases, neuroradiologists must carefully recognize the capabilities, constraints, and consistency of these technologies. Before institutions adopt these algorithms,...</description>
797.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">AJNR Am J Neuroradiol. 2024 Apr 25:ajnr.A8317. doi: 10.3174/ajnr.A8317. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND AND PURPOSE: Artificial intelligence (AI) models in radiology are frequently developed and validated using datasets from a single institution and are rarely tested on independent, external datasets, raising questions about their generalizability and applicability in clinical practice. The American Society of Functional Neuroradiology (ASFNR) organized a multi-center AI competition to evaluate the proficiency of developed models in identifying various pathologies on NCCT, assessing age-based normality and estimating medical urgency.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">MATERIALS AND METHODS: In total, 1201 anonymized, full-head NCCT clinical scans from five institutions were pooled to form the dataset. The dataset encompassed normal studies as well as pathologies including acute ischemic stroke, intracranial hemorrhage, traumatic brain injury, and mass effect (detection of these-task 1). NCCTs were also assessed to determine if findings were consistent with expected brain changes for the patient's age (task 2: age-based normality assessment) and to identify any abnormalities requiring immediate medical attention (task 3: evaluation of findings for urgent intervention). Five neuroradiologists labeled each NCCT, with consensus interpretations serving as the ground truth. The competition was announced online, inviting academic institutions and companies. Independent central analysis assessed each model's performance. Accuracy, sensitivity, specificity, positive and negative predictive values, and receiver operating characteristic (ROC) curves were generated for each AI model, along with the area under the ROC curve (AUROC).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: 1177 studies were processed by four teams. The median age of patients was 62, with an interquartile range of 33. 19 teams from various academic institutions registered for the competition. Of these, four teams submitted their final results. No commercial entities participated in the competition. For task 1, AUROCs ranged from 0.49 to 0.59. For task 2, two teams completed the task with AUROC values of 0.57 and 0.52. For task 3, teams had little to no agreement with the ground truth.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: To assess the performance of AI models in real-world clinical scenarios, we analyzed their performance in the ASFNR AI Competition. The first ASFNR Competition underscored the gap between expectation and reality; the models largely fell short in their assessments. As the integration of AI tools into clinical workflows increases, neuroradiologists must carefully recognize the capabilities, constraints, and consistency of these technologies. Before institutions adopt these algorithms, thorough validation is essential to ensure acceptable levels of performance in clinical settings.<b>ABBREVIATIONS:</b> AI = artificial intelligence; ASFNR = American Society of Functional Neuroradiology; AUROC = area under the receiver operating characteristic curve; DICOM = Digital Imaging and Communications in Medicine; GEE = generalized estimation equation; IQR = interquartile range; NPV = negative predictive value; PPV = positive predictive value; ROC = receiver operating characteristic; TBI = traumatic brain injury.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38663992/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38663992</a> | DOI:<a href=https://doi.org/10.3174/ajnr.A8317>10.3174/ajnr.A8317</a></p></div>]]></content:encoded>
798.      <guid isPermaLink="false">pubmed:38663992</guid>
799.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
800.      <dc:creator>Bin Jiang</dc:creator>
801.      <dc:creator>Burak Berksu Ozkara</dc:creator>
802.      <dc:creator>Guangming Zhu</dc:creator>
803.      <dc:creator>Derek Boothroyd</dc:creator>
804.      <dc:creator>Jason W Allen</dc:creator>
805.      <dc:creator>Daniel P Barboriak</dc:creator>
806.      <dc:creator>Peter Chang</dc:creator>
807.      <dc:creator>Cynthia Chan</dc:creator>
808.      <dc:creator>Ruchir Chaudhari</dc:creator>
809.      <dc:creator>Hui Chen</dc:creator>
810.      <dc:creator>Anjeza Chukus</dc:creator>
811.      <dc:creator>Victoria Ding</dc:creator>
812.      <dc:creator>David Douglas</dc:creator>
813.      <dc:creator>Christopher G Filippi</dc:creator>
814.      <dc:creator>Adam E Flanders</dc:creator>
815.      <dc:creator>Ryan Godwin</dc:creator>
816.      <dc:creator>Syed Hashmi</dc:creator>
817.      <dc:creator>Christopher Hess</dc:creator>
818.      <dc:creator>Kevin Hsu</dc:creator>
819.      <dc:creator>Yvonne W Lui</dc:creator>
820.      <dc:creator>Joseph A Maldjian</dc:creator>
821.      <dc:creator>Patrik Michel</dc:creator>
822.      <dc:creator>Sahil S Nalawade</dc:creator>
823.      <dc:creator>Vishal Patel</dc:creator>
824.      <dc:creator>Prashant Raghavan</dc:creator>
825.      <dc:creator>Haris I Sair</dc:creator>
826.      <dc:creator>Jody Tanabe</dc:creator>
827.      <dc:creator>Kirk Welker</dc:creator>
828.      <dc:creator>Chris Whitlow</dc:creator>
829.      <dc:creator>Greg Zaharcuk</dc:creator>
830.      <dc:creator>Max Wintermark</dc:creator>
831.      <dc:date>2024-04-25</dc:date>
832.      <dc:source>AJNR. American journal of neuroradiology</dc:source>
833.      <dc:title>Assessing the Performance of Artificial Intelligence Models: Insights from the American Society of Functional Neuroradiology Artificial Intelligence Competition</dc:title>
834.      <dc:identifier>pmid:38663992</dc:identifier>
835.      <dc:identifier>doi:10.3174/ajnr.A8317</dc:identifier>
836.    </item>
837.    <item>
838.      <title>Guidezilla Catheter in Neuroendovascular Interventions: A Case Series Study</title>
839.      <link>https://pubmed.ncbi.nlm.nih.gov/38663737/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
840.      <description>CONCLUSION: Although helpful in overcoming challenging anatomy, the Guidezilla™ guide extension catheter should be used with caution when used as a bailout device.</description>
841.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">World Neurosurg. 2024 Apr 23:S1878-8750(24)00679-X. doi: 10.1016/j.wneu.2024.04.106. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Neuroendovascular procedures can be challenging due to severe angulation of the cervical and cranial vessels. Typical approaches for overcoming this tortuosity involve using multiple telescoping catheter systems to provide proximal support for therapeutic device delivery. While this approach can be effective, it does have limitations.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We describe the utility of the Guidezilla™ (Boston Scientific, Natick, MA) guide extension catheter, a device designed for coronary interventions, in the treatment of three patients undergoing neuroendovascular procedures. In the following cases, the decision to use a guide extension catheter had varied, but mainly were due to severe tortuosity, heavy calcifications, and failure to introduce stents into distal locations.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Although helpful in overcoming challenging anatomy, the Guidezilla™ guide extension catheter should be used with caution when used as a bailout device.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38663737/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38663737</a> | DOI:<a href=https://doi.org/10.1016/j.wneu.2024.04.106>10.1016/j.wneu.2024.04.106</a></p></div>]]></content:encoded>
842.      <guid isPermaLink="false">pubmed:38663737</guid>
843.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
844.      <dc:creator>Ammar Jumah</dc:creator>
845.      <dc:creator>Michael Fana</dc:creator>
846.      <dc:creator>Hassan Aboul-Nour</dc:creator>
847.      <dc:creator>Abdalla Jamal Albanna</dc:creator>
848.      <dc:creator>Owais K AlSrouji</dc:creator>
849.      <dc:creator>Alex Chebl</dc:creator>
850.      <dc:date>2024-04-25</dc:date>
851.      <dc:source>World neurosurgery</dc:source>
852.      <dc:title>Guidezilla Catheter in Neuroendovascular Interventions: A Case Series Study</dc:title>
853.      <dc:identifier>pmid:38663737</dc:identifier>
854.      <dc:identifier>doi:10.1016/j.wneu.2024.04.106</dc:identifier>
855.    </item>
856.    <item>
857.      <title>A Systematic Review of the Epidemiology and The Public Health Implications of Stroke in Sub-Saharan Africa</title>
858.      <link>https://pubmed.ncbi.nlm.nih.gov/38663647/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
859.      <description>CONCLUSION: The increasing incidence/prevalence, lifestyle factors and interactions with other diseases, including major communicable diseases, stroke is becoming a pressing public health problem for SSA. Reducing the incidence of stroke in Africa will surely lower mortality, morbidity, disability, and the neurological as well as cognitive aftereffects of stroke, as is clear from the experience of higher-income nations. We recommend a collective intervention involving the governments of nations,...</description>
860.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Stroke Cerebrovasc Dis. 2024 Apr 23:107733. doi: 10.1016/j.jstrokecerebrovasdis.2024.107733. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: With approximately 11 million strokes occurring annually worldwide, and over 6.5 million deaths annually, stroke has made its place as one of the major killers in the world. Although developing countries make up more than 4/5 of the global stroke burden, well-grounded information on stroke epidemiology remains lacking there.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">AIMS: This systematic review study aimed to provide a synthesis of studies on the incidence and prevalence of stroke among adults in sub-Saharan Africa (SSA), subsequently deduce the associated risk factors and public health implications (mortality rates and economic costs) of the disease on the population of this region.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: A systematic review of studies carried out in the region and published on PUBMED. Eligibility criteria were established using the PEO (Population/Patient, Exposure, Outcome) format. Research articles investigating either (or all) of the following: ischemic or haemorrhagic stroke, incidence, prevalence, and risk factors of stroke in adults (≥ 18 years old), in at least one region of SSA were included. Exclusion criteria comprised studies involving populations younger than 18 years old, research conducted outside the designated research region, and articles inaccessible in full text. The PRISMA guidelines were used for the search strategy.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Fifty-two studies were included review. Among them, over 11 studies investigated the prevalence of the disease. Some older studies within the continent (Nigeria, 2011) showed a prevalence of 1.3 per 100 while more recent studies (Zambia, 2021) showed a prevalence of 4.3 per 1000. The highest prevalence noted in this region was in Madagascar (2017) with 48.17 per 100, while the lowest was recorded in (Zimbabwe, 2017) with 0.61 per 100. The study in Tanzania showed a crude incidence of 94·5 per 100 000 (76·0-115·0) while the study in Ghana in 2018 showed an incidence of 14.19 events per 1000 person-years [10.77-18.38]. The identified risk factors included hypertension, diabetes, smoking, alcohol consumption, physical inactivity, poor diets (more salt, less vegetables), dyslipidaemia, HIV/AIDS co-infection, heart disease (cardiomyopathies, cardiac arrhythmias), obesity, previous stroke and/or family history of stroke. Over 21 studies investigated the mortality rates due to stroke in SSA, with most of the studies being in West Africa. These studies revealed mortality rates as high as 43.3% in Ghana, and as low as 10.9% in Cameroon. Few studies reported on the economic costs of stroke in the region; two in Benin, two in Nigeria and one in Tanzania.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: The increasing incidence/prevalence, lifestyle factors and interactions with other diseases, including major communicable diseases, stroke is becoming a pressing public health problem for SSA. Reducing the incidence of stroke in Africa will surely lower mortality, morbidity, disability, and the neurological as well as cognitive aftereffects of stroke, as is clear from the experience of higher-income nations. We recommend a collective intervention involving the governments of nations, international organizations, civil society, and the private sector for greater impact and sustainable outcomes reducing the epidemiology and implications of stroke in SSA.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38663647/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38663647</a> | DOI:<a href=https://doi.org/10.1016/j.jstrokecerebrovasdis.2024.107733>10.1016/j.jstrokecerebrovasdis.2024.107733</a></p></div>]]></content:encoded>
861.      <guid isPermaLink="false">pubmed:38663647</guid>
862.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
863.      <dc:creator>Gisele Abissegue</dc:creator>
864.      <dc:creator>Seidina Iliasu Yakubu</dc:creator>
865.      <dc:creator>Aiswarya Seema Ajay</dc:creator>
866.      <dc:creator>Faatihah Niyi-Odumosu</dc:creator>
867.      <dc:date>2024-04-25</dc:date>
868.      <dc:source>Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association</dc:source>
869.      <dc:title>A Systematic Review of the Epidemiology and The Public Health Implications of Stroke in Sub-Saharan Africa</dc:title>
870.      <dc:identifier>pmid:38663647</dc:identifier>
871.      <dc:identifier>doi:10.1016/j.jstrokecerebrovasdis.2024.107733</dc:identifier>
872.    </item>
873.    <item>
874.      <title>Blocking cGAS-STING pathway promotes post-stroke functional recovery in an extended treatment window via facilitating remyelination</title>
875.      <link>https://pubmed.ncbi.nlm.nih.gov/38663402/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
876.      <description>CONCLUSIONS: Manipulating the cGAS-STING pathway has an extended treatment window in promoting long-term post-stroke functional recovery via facilitating remyelination in a mouse stroke model. Our results highlight the roles of the cGAS-STING pathway in aggregating stroke pathology and propose a new way for improving functional recovery after ischemic stroke.</description>
877.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Med. 2024 Apr 16:S2666-6340(24)00130-2. doi: 10.1016/j.medj.2024.03.018. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Ischemic stroke is a major cause of worldwide death and disability, with recombinant tissue plasminogen activator being the sole effective treatment, albeit with a limited treatment window. The cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING) pathway is emerging as the major DNA-sensing pathway to invoke immune responses in neuroinflammatory disorders.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: By performing a series of neurobehavioral assessments, electrophysiological analysis, high-throughput sequencing, and cell-based assays based on the transient middle cerebral artery occlusion (tMCAO) mouse stroke model, we examined the effects and underlying mechanisms of genetic and pharmacological inhibition of the cGAS-STING pathway on long-term post-stroke neurological functional outcomes.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">FINDINGS: Blocking the cGAS-STING pathway, even 3 days after tMCAO, significantly promoted functional recovery in terms of white matter structural and functional integrity as well as sensorimotor and cognitive functions. Mechanistically, the neuroprotective effects via inhibiting the cGAS-STING pathway were contributed not only by inflammation repression at the early stage of tMCAO but also by modifying the cell state of phagocytes to facilitate remyelination at the sub-acute phase. The activation of the cGAS-STING pathway significantly impeded post-stroke remyelination through restraining myelin debris uptake and degradation and hindering oligodendrocyte differentiation and maturation.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Manipulating the cGAS-STING pathway has an extended treatment window in promoting long-term post-stroke functional recovery via facilitating remyelination in a mouse stroke model. Our results highlight the roles of the cGAS-STING pathway in aggregating stroke pathology and propose a new way for improving functional recovery after ischemic stroke.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">FUNDING: This work was primarily funded by the National Key R&amp;D Program of China.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38663402/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38663402</a> | DOI:<a href=https://doi.org/10.1016/j.medj.2024.03.018>10.1016/j.medj.2024.03.018</a></p></div>]]></content:encoded>
878.      <guid isPermaLink="false">pubmed:38663402</guid>
879.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
880.      <dc:creator>Munire Maimaiti</dc:creator>
881.      <dc:creator>Chenhui Li</dc:creator>
882.      <dc:creator>Mingxing Cheng</dc:creator>
883.      <dc:creator>Ziwei Zhong</dc:creator>
884.      <dc:creator>Jiameng Hu</dc:creator>
885.      <dc:creator>Lei Yang</dc:creator>
886.      <dc:creator>Lele Zhang</dc:creator>
887.      <dc:creator>Ze Hong</dc:creator>
888.      <dc:creator>Jinyi Song</dc:creator>
889.      <dc:creator>Mingyu Pan</dc:creator>
890.      <dc:creator>Xiaonan Ma</dc:creator>
891.      <dc:creator>Shufang Cui</dc:creator>
892.      <dc:creator>Peng Zhang</dc:creator>
893.      <dc:creator>Haiping Hao</dc:creator>
894.      <dc:creator>Chen Wang</dc:creator>
895.      <dc:creator>Haiyang Hu</dc:creator>
896.      <dc:date>2024-04-25</dc:date>
897.      <dc:source>Med (New York, N.Y.)</dc:source>
898.      <dc:title>Blocking cGAS-STING pathway promotes post-stroke functional recovery in an extended treatment window via facilitating remyelination</dc:title>
899.      <dc:identifier>pmid:38663402</dc:identifier>
900.      <dc:identifier>doi:10.1016/j.medj.2024.03.018</dc:identifier>
901.    </item>
902.    <item>
903.      <title>The enhanced reliability of higher national institute of health stroke scale thresholds over the conventional 6-point scale</title>
904.      <link>https://pubmed.ncbi.nlm.nih.gov/38663199/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
905.      <description>CONCLUSION: Higher thresholds can better differentiate small and medium infarcts as true-negatives and substantially reduce false-positive referrals for mechanical thrombectomy.</description>
906.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Clin Neurol Neurosurg. 2024 Apr 12;241:108284. doi: 10.1016/j.clineuro.2024.108284. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">INTRODUCTION: It is still uncertain if higher thresholds on National Institute of Health Stroke Scale (NIHSS) are better predictors of large infarctions than the conventional 6-point cutoff.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We used 6-point and higher NIHSS thresholds including 8, 9, and 10-point to predict relative infarct areas, expressed as percentage of the affected hemisphere on axial brain computed tomography images, beginning at 5% with 5% increments each time until reaching the 40% cutoff for large infarctions, or achieving 100% sensitivity. Results were compared using area under the receiver operating characteristic curves (AUROC).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: We enrolled 151 patients of acute ischemic stroke (Mean age: 62.88 years ± 12.71; Female: 48.34%). 77 patients (50.99%) exhibited left hemisphere strokes, while 74 (49%) had right hemisphere involvement. Sensitivity values of the 6-point for infarcts measuring 5%, 10%, 20%, 30%, and 40% were 62%, 64%, 77%, 82%, and 100%, respectively. At 40% infarct-size, 8-point achieved comparable results (52%, 55%, 69%, 76%, 100%), closely aligning with the 9-point (50%, 53%, 69%, 76%, 100%). The10-point was slightly trailing behind in sensitivity at 40% infarct-core (96%). Moreover, higher thresholds exhibited improved false-positive rates (FPR). At 40% infarct size, the FPRs of 6, 8, 9, and 10 points were 39%, 27%, 27%, and 21% respectively. Higher thresholds had augmented AUROC values (0.86, 0.86, 0.89) as compared to the 6-point (0.80). Logistic regression identified 14-point as definitive cutoff for large infarctions.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Higher thresholds can better differentiate small and medium infarcts as true-negatives and substantially reduce false-positive referrals for mechanical thrombectomy.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38663199/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38663199</a> | DOI:<a href=https://doi.org/10.1016/j.clineuro.2024.108284>10.1016/j.clineuro.2024.108284</a></p></div>]]></content:encoded>
907.      <guid isPermaLink="false">pubmed:38663199</guid>
908.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
909.      <dc:creator>Sohail Adnan</dc:creator>
910.      <dc:creator>Sadaf Nawab</dc:creator>
911.      <dc:creator>Shafi Ullah Khan</dc:creator>
912.      <dc:creator>Farid Hussain</dc:creator>
913.      <dc:date>2024-04-25</dc:date>
914.      <dc:source>Clinical neurology and neurosurgery</dc:source>
915.      <dc:title>The enhanced reliability of higher national institute of health stroke scale thresholds over the conventional 6-point scale</dc:title>
916.      <dc:identifier>pmid:38663199</dc:identifier>
917.      <dc:identifier>doi:10.1016/j.clineuro.2024.108284</dc:identifier>
918.    </item>
919.    <item>
920.      <title>Transportation Noise Pollution and Cardiovascular Health</title>
921.      <link>https://pubmed.ncbi.nlm.nih.gov/38662856/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
922.      <description>Epidemiological studies have found that transportation noise increases the risk for cardiovascular morbidity and mortality, with solid evidence for ischemic heart disease, heart failure, and stroke. According to the World Health Organization, at least 1.6 million healthy life years are lost annually from traffic-related noise in Western Europe. Traffic noise at night causes fragmentation and shortening of sleep, elevation of stress hormone levels, and increased oxidative stress in the...</description>
923.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Circ Res. 2024 Apr 26;134(9):1113-1135. doi: 10.1161/CIRCRESAHA.123.323584. Epub 2024 Apr 25.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Epidemiological studies have found that transportation noise increases the risk for cardiovascular morbidity and mortality, with solid evidence for ischemic heart disease, heart failure, and stroke. According to the World Health Organization, at least 1.6 million healthy life years are lost annually from traffic-related noise in Western Europe. Traffic noise at night causes fragmentation and shortening of sleep, elevation of stress hormone levels, and increased oxidative stress in the vasculature and the brain. These factors can promote vascular (endothelial) dysfunction, inflammation, and arterial hypertension, thus elevating cardiovascular risk. The present review focusses on the indirect, nonauditory cardiovascular health effects of noise. We provide an updated overview of epidemiological research on the effects of transportation noise on cardiovascular risk factors and disease, and mechanistic insights based on the latest clinical and experimental studies and propose new risk markers to address noise-induced cardiovascular effects in the general population. We will discuss the potential effects of noise on vascular dysfunction, oxidative stress, and inflammation in humans and animals. We will elaborately explain the underlying pathomechanisms by alterations of gene networks, epigenetic pathways, circadian rhythm, signal transduction along the neuronal-cardiovascular axis, and metabolism. We will describe current and future noise mitigation strategies. Finally, we will conduct an overall evaluation of the status of the current evidence of noise as a significant cardiovascular risk factor.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662856/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662856</a> | DOI:<a href=https://doi.org/10.1161/CIRCRESAHA.123.323584>10.1161/CIRCRESAHA.123.323584</a></p></div>]]></content:encoded>
924.      <guid isPermaLink="false">pubmed:38662856</guid>
925.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
926.      <dc:creator>Thomas Münzel</dc:creator>
927.      <dc:creator>Michael Molitor</dc:creator>
928.      <dc:creator>Marin Kuntic</dc:creator>
929.      <dc:creator>Omar Hahad</dc:creator>
930.      <dc:creator>Martin Röösli</dc:creator>
931.      <dc:creator>Nicole Engelmann</dc:creator>
932.      <dc:creator>Mathias Basner</dc:creator>
933.      <dc:creator>Andreas Daiber</dc:creator>
934.      <dc:creator>Mette Sørensen</dc:creator>
935.      <dc:date>2024-04-25</dc:date>
936.      <dc:source>Circulation research</dc:source>
937.      <dc:title>Transportation Noise Pollution and Cardiovascular Health</dc:title>
938.      <dc:identifier>pmid:38662856</dc:identifier>
939.      <dc:identifier>doi:10.1161/CIRCRESAHA.123.323584</dc:identifier>
940.    </item>
941.    <item>
942.      <title>Relationship between electronically monitored adherence to direct oral anticoagulants and ischemic or hemorrhagic events after an initial ischemic stroke-A case control study</title>
943.      <link>https://pubmed.ncbi.nlm.nih.gov/38662779/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
944.      <description>CONCLUSION: Because recurrent ischemic events after an AF-related stroke were associated with low adherence to DOAC &lt;76%, adherence enhancing interventions seem crucial in anticoagulated AF-patients. However, AF-patients with high adherence might benefit from a regular re-assessment of the bleeding risk as hemorrhagic complications were associated with adherence to DOAC &gt;96%.</description>
945.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">PLoS One. 2024 Apr 25;19(4):e0301421. doi: 10.1371/journal.pone.0301421. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Patients with atrial fibrillation (AF) have a high risk for recurrent clinical events after an ischemic stroke. Direct oral anticoagulants (DOAC) are prescribed for secondary prevention. Adherence to DOAC is crucial mainly because of their short elimination half-life. Non-adherence to DOAC can negatively impact patients' outcomes. The relationship between (non-)adherence and recurrent clinical events is unknown in AF patients after initial stroke. We investigated adherence to DOAC in stroke survivors with AF who were included in the MAAESTRO study at the University Hospital Basel, Switzerland, between 2008 and 2022.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: This study is a secondary analysis of data from MAAESTRO with a matched nested case-control design and 1:2 ratio. DOAC intake was measured with a small electronic device (Time4MedTM). We defined two arbitrary intervals of 17 days and 95 days as the longest time spans with electronic monitoring data per patient to maximize the number of participants with adequate amount of observation time available for analysis. Taking and timing adherence were calculated retrospectively i.e., prior to the recurrent event for cases. Trendline analysis of adherence over 95 days was calculated. Linear regression analysis was performed after adjusting for the co-variables age and daily pill burden. Sensitivity analysis was performed with controls for intervals in the reverse direction (prospectively).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: We analyzed 11 cases and 22 matched controls (mean age: 75.9 ± 9.2 years vs. 73.1 ± 8.4 years; n.s.) with similar stroke characteristics (NIHSS, mRS, MoCA) and 36.4% women in each group. Mean adherence values were high and similar between cases and controls (95 days taking: 87.0 ± 18.9% (cases) vs. 90.8 ± 9.8% (controls), n.s.; similar values for timing adherence). Six hemorrhagic and five ischemic events had occurred. Compared to controls, a significantly higher 95 days taking adherence was observed for hemorrhagic events (96.0 ± 5.0% (cases) vs. 88.1 ± 11.5% (controls); p&lt;0.01) and a significantly lower 95 days taking adherence was observed for ischemic events (75.7 ± 24.8% (cases) vs. 94.2 ± 6.2% (controls), p = 0.024). Values for timing adherence were similar. A non-significant downward linear trend of adherence was observed over 95 days independently of the clinical events. The sensitivity analysis showed that the direction of the interval had negligible impact on the 95 days adherence.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Because recurrent ischemic events after an AF-related stroke were associated with low adherence to DOAC &lt;76%, adherence enhancing interventions seem crucial in anticoagulated AF-patients. However, AF-patients with high adherence might benefit from a regular re-assessment of the bleeding risk as hemorrhagic complications were associated with adherence to DOAC &gt;96%.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">TRIAL REGISTRATION: ClinicalTrials.gov NCT03344146.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662779/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662779</a> | DOI:<a href=https://doi.org/10.1371/journal.pone.0301421>10.1371/journal.pone.0301421</a></p></div>]]></content:encoded>
946.      <guid isPermaLink="false">pubmed:38662779</guid>
947.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
948.      <dc:creator>Katharina Rekk</dc:creator>
949.      <dc:creator>Isabelle Arnet</dc:creator>
950.      <dc:creator>Fine Dietrich</dc:creator>
951.      <dc:creator>Alexandros A Polymeris</dc:creator>
952.      <dc:creator>Philippe A Lyrer</dc:creator>
953.      <dc:creator>Stefan T Engelter</dc:creator>
954.      <dc:creator>Sabine Schaedelin</dc:creator>
955.      <dc:creator>Samuel S Allemann</dc:creator>
956.      <dc:date>2024-04-25</dc:date>
957.      <dc:source>PloS one</dc:source>
958.      <dc:title>Relationship between electronically monitored adherence to direct oral anticoagulants and ischemic or hemorrhagic events after an initial ischemic stroke-A case control study</dc:title>
959.      <dc:identifier>pmid:38662779</dc:identifier>
960.      <dc:identifier>doi:10.1371/journal.pone.0301421</dc:identifier>
961.    </item>
962.    <item>
963.      <title>Type 2 diabetes mellitus in patients with ischemic stroke - A nationwide study</title>
964.      <link>https://pubmed.ncbi.nlm.nih.gov/38662635/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
965.      <description>CONCLUSIONS: The prevalence of T2D in IS increased over time. The 30- and 365-day mortality rates decreased over the time-period but were consistently higher in IS with co-morbid T2D. Readmissions were also higher in IS with T2D. This highlights an urgent need for strategies to further improve the prognosis in IS patients with co-morbid T2D.</description>
966.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Diabet Med. 2024 Apr 25:e15337. doi: 10.1111/dme.15337. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">AIMS: Type 2 diabetes (T2D) is a risk factor for ischemic stroke (IS) and associated with an adverse prognosis. Both stroke and diabetes care has evolved substantially during the last decade. This study aimed to determine the prevalence of T2D among IS patients along with time trends in the risk profile, use of glucose-lowering medications, quality-of-care and clinical outcomes, including stroke severity; length-of-stay; mortality, readmission and recurrent stroke in a large national cohort.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Registry-based cohort study including all IS events in Denmark from 2004 to 2020. IS with co-morbid T2D were compared to IS without diabetes while adjusting for age, sex, stroke severity, co-morbidity and socio-economic factors.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: The study included 169,262 IS events; 24,479 with co-morbid T2D. The prevalence of T2D in IS increased from 12.0% (2004-2006) to 17.0% (2019-2020). The adjusted absolute 30-day mortality risk in IS with T2D decreased from 9.9% (2004-2006) to 7.8% (2019-2020). The corresponding adjusted risk ratios (aRR) were 1.22 95% confidence interval (1.09-1.37) and 1.29 (1.11-1.50), respectively. The aRR of 365-day mortality was in 2004-2006: 1.20 (1.12-1.29) and in 2019-2020: 1.34 (1.22-1.47). The 30- and 365-day readmissions rates were also consistently higher in IS with T2D.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: The prevalence of T2D in IS increased over time. The 30- and 365-day mortality rates decreased over the time-period but were consistently higher in IS with co-morbid T2D. Readmissions were also higher in IS with T2D. This highlights an urgent need for strategies to further improve the prognosis in IS patients with co-morbid T2D.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662635/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662635</a> | DOI:<a href=https://doi.org/10.1111/dme.15337>10.1111/dme.15337</a></p></div>]]></content:encoded>
967.      <guid isPermaLink="false">pubmed:38662635</guid>
968.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
969.      <dc:creator>Sidsel Hastrup</dc:creator>
970.      <dc:creator>Jakob Nebeling Hedegaard</dc:creator>
971.      <dc:creator>Grethe Andersen</dc:creator>
972.      <dc:creator>Jorgen Rungby</dc:creator>
973.      <dc:creator>Soren Paaske Johnsen</dc:creator>
974.      <dc:date>2024-04-25</dc:date>
975.      <dc:source>Diabetic medicine : a journal of the British Diabetic Association</dc:source>
976.      <dc:title>Type 2 diabetes mellitus in patients with ischemic stroke - A nationwide study</dc:title>
977.      <dc:identifier>pmid:38662635</dc:identifier>
978.      <dc:identifier>doi:10.1111/dme.15337</dc:identifier>
979.    </item>
980.    <item>
981.      <title>Deployment to Military Bases With Open Burn Pits and Respiratory and Cardiovascular Disease</title>
982.      <link>https://pubmed.ncbi.nlm.nih.gov/38662371/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
983.      <description>CONCLUSIONS AND RELEVANCE: In this cohort study, prolonged deployment to military bases with open burn pits was associated with increased risk of developing asthma, COPD, and hypertension. The results also point to a possible increased risk in ischemic stroke. The novel ability to use integrated data on deployment and health outcomes provides a model for additional studies of the health impact of environmental exposures during military service.</description>
984.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">JAMA Netw Open. 2024 Apr 1;7(4):e247629. doi: 10.1001/jamanetworkopen.2024.7629.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">IMPORTANCE: Many veterans who served in Afghanistan and Iraq during Operations Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) were deployed to military bases with open burn pits and exposed to their emissions, with limited understanding of the long-term health consequences.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVE: To determine the association between deployment to military bases where open burn pits were used for waste disposal and the subsequent risk of developing respiratory and cardiovascular diseases.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">DESIGN, SETTING, AND PARTICIPANTS: This retrospective observational cohort study used Veterans Health Administration medical records and declassified deployment records from the Department of Defense to assess Army and Air Force veterans who were deployed between 2001 and 2011 and subsequently received health care from the Veterans Health Administration, with follow-up through December 2020. Data were analyzed from January 2023 through February 2024.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">EXPOSURE: Duration of deployment to military bases with open burn pits.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">MAIN OUTCOMES AND MEASURES: Diagnosis of asthma, chronic obstructive pulmonary disease, interstitial lung disease, hypertension, myocardial infarction, congestive heart failure, ischemic stroke, and hemorrhagic stroke.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: The study population included 459 381 OEF and OIF veterans (mean [SD] age, 31.6 [8.7] years; 399 754 [87.0%] male). Median (IQR) follow-up from end of deployment was 10.9 (9.4-12.7) years. For every 100 days of deployment to bases with burn pits, veterans experienced increased adjusted odds for asthma (adjusted odds ratio [aOR], 1.01; 95% CI, 1.01-1.02), chronic obstructive pulmonary disease (aOR, 1.04; 95% CI, 1.02-1.07), hypertension (aOR, 1.02; 95% CI, 1.02-1.03), and ischemic stroke (aOR, 1.06; 95% CI, 0.97-1.14). Odds of interstitial lung disease, myocardial infarction, congestive heart failure, or hemorrhagic stroke were not increased. Results based on tertiles of duration of burn pit exposures were consistent with those from the continuous exposure measures.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS AND RELEVANCE: In this cohort study, prolonged deployment to military bases with open burn pits was associated with increased risk of developing asthma, COPD, and hypertension. The results also point to a possible increased risk in ischemic stroke. The novel ability to use integrated data on deployment and health outcomes provides a model for additional studies of the health impact of environmental exposures during military service.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662371/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662371</a> | DOI:<a href=https://doi.org/10.1001/jamanetworkopen.2024.7629>10.1001/jamanetworkopen.2024.7629</a></p></div>]]></content:encoded>
985.      <guid isPermaLink="false">pubmed:38662371</guid>
986.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
987.      <dc:creator>David A Savitz</dc:creator>
988.      <dc:creator>Susan R Woskie</dc:creator>
989.      <dc:creator>Anila Bello</dc:creator>
990.      <dc:creator>Rachel Gaither</dc:creator>
991.      <dc:creator>Joseph Gasper</dc:creator>
992.      <dc:creator>Lan Jiang</dc:creator>
993.      <dc:creator>Christopher Rennix</dc:creator>
994.      <dc:creator>Gregory A Wellenius</dc:creator>
995.      <dc:creator>Amal N Trivedi</dc:creator>
996.      <dc:date>2024-04-25</dc:date>
997.      <dc:source>JAMA network open</dc:source>
998.      <dc:title>Deployment to Military Bases With Open Burn Pits and Respiratory and Cardiovascular Disease</dc:title>
999.      <dc:identifier>pmid:38662371</dc:identifier>
1000.      <dc:identifier>doi:10.1001/jamanetworkopen.2024.7629</dc:identifier>
1001.    </item>
1002.    <item>
1003.      <title>Excitotoxic Storms of Ischemic Stroke: A Non-neuronal Perspective</title>
1004.      <link>https://pubmed.ncbi.nlm.nih.gov/38662299/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1005.      <description>Numerous neurological disorders share a fatal pathologic process known as glutamate excitotoxicity. Among which, ischemic stroke is the major cause of mortality and disability worldwide. For a long time, the main idea of developing anti-excitotoxic neuroprotective agents was to block glutamate receptors. Despite this, there has been little successful clinical translation to date. After decades of "neuron-centered" views, a growing number of studies have recently revealed the importance of...</description>
1006.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Mol Neurobiol. 2024 Apr 25. doi: 10.1007/s12035-024-04184-7. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Numerous neurological disorders share a fatal pathologic process known as glutamate excitotoxicity. Among which, ischemic stroke is the major cause of mortality and disability worldwide. For a long time, the main idea of developing anti-excitotoxic neuroprotective agents was to block glutamate receptors. Despite this, there has been little successful clinical translation to date. After decades of "neuron-centered" views, a growing number of studies have recently revealed the importance of non-neuronal cells. Glial cells, cerebral microvascular endothelial cells, blood cells, and so forth are extensively engaged in glutamate synthesis, release, reuptake, and metabolism. They also express functional glutamate receptors and can listen and respond for fast synaptic transmission. This broadens the thoughts of developing excitotoxicity antagonists. In this review, the critical contribution of non-neuronal cells in glutamate excitotoxicity during ischemic stroke will be emphasized in detail, and the latest research progress as well as corresponding therapeutic strategies will be updated at length, aiming to reconceptualize glutamate excitotoxicity in a non-neuronal perspective.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662299/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662299</a> | DOI:<a href=https://doi.org/10.1007/s12035-024-04184-7>10.1007/s12035-024-04184-7</a></p></div>]]></content:encoded>
1007.      <guid isPermaLink="false">pubmed:38662299</guid>
1008.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1009.      <dc:creator>Xiao-Man Yang</dc:creator>
1010.      <dc:creator>Hao Yu</dc:creator>
1011.      <dc:creator>Jia-Xin Li</dc:creator>
1012.      <dc:creator>Na Li</dc:creator>
1013.      <dc:creator>Chong Li</dc:creator>
1014.      <dc:creator>Dong-Han Xu</dc:creator>
1015.      <dc:creator>Hao Zhang</dc:creator>
1016.      <dc:creator>Tian-He Fang</dc:creator>
1017.      <dc:creator>Shi-Jun Wang</dc:creator>
1018.      <dc:creator>Pei-Yu Yan</dc:creator>
1019.      <dc:creator>Bing-Bing Han</dc:creator>
1020.      <dc:date>2024-04-25</dc:date>
1021.      <dc:source>Molecular neurobiology</dc:source>
1022.      <dc:title>Excitotoxic Storms of Ischemic Stroke: A Non-neuronal Perspective</dc:title>
1023.      <dc:identifier>pmid:38662299</dc:identifier>
1024.      <dc:identifier>doi:10.1007/s12035-024-04184-7</dc:identifier>
1025.    </item>
1026.    <item>
1027.      <title>The Impact of Metabolic Bariatric Surgery on Cardiovascular Diseases in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease</title>
1028.      <link>https://pubmed.ncbi.nlm.nih.gov/38662250/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1029.      <description>CONCLUSION: The current study showed that MBS is significantly associated with a reduced risk of hospitalization for CVD in patients with MASLD.</description>
1030.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Obes Surg. 2024 Apr 25. doi: 10.1007/s11695-024-07238-w. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">PURPOSE: There is a strong association between metabolic dysfunction-associated steatotic liver disease (MASLD) and obesity which are both important risk factors for cardiovascular diseases (CVDs). The current study aimed to assess the association of MBS with different CVDs in patients with MASLD.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">MATERIALS AND METHODS: The National Inpatient Sample (NIS) database from 2016 to 2020 were analyzed by using ICD-10 codes. A propensity score matching in a 1:1 ratio was done to match the MBS and non-MBS groups.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: After weighted analysis, 1,124,155 and 68,215 patients were included in non-MBS and MBS groups, respectively. MBS was associated with significantly lower risk of hospitalization for coronary artery disease (OR 0.633 (0.569-0.703), p value &lt; 0.001), acute myocardial infarction (OR 0.606 (0.523-0.701), p value &lt; 0.001), percutaneous coronary intervention (OR 0.578 (0.489-0.682), p value &lt; 0.001), and thrombolysis (OR 0.765 (0.589-0.993), p value = 0.044) compared to the non-MBS group in patients with MASLD. Furthermore, MBS was associated with 52% reduced risk of hospitalization for hemorrhagic stroke in patients with MASLD (OR 0.481, 95% CI 0.337-0.686, p value &lt; 0.001). However, ischemic stroke was not significant between the two groups (OR 1.108 (0.905-1.356), p value = 0.322). In addition, MBS was associated with 63% and 60% reduced risk of hospitalization for heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF) in patients with MASLD (OR 0.373, 95% CI 0.300-0.465 and OR 0.405, 95% CI 0.325-0.504, p value &lt; 0.001 for both), respectively.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: The current study showed that MBS is significantly associated with a reduced risk of hospitalization for CVD in patients with MASLD.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662250/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662250</a> | DOI:<a href=https://doi.org/10.1007/s11695-024-07238-w>10.1007/s11695-024-07238-w</a></p></div>]]></content:encoded>
1031.      <guid isPermaLink="false">pubmed:38662250</guid>
1032.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1033.      <dc:creator>Ali Esparham</dc:creator>
1034.      <dc:creator>Saeed Shoar</dc:creator>
1035.      <dc:creator>Ali Mehri</dc:creator>
1036.      <dc:creator>Zhamak Khorgami</dc:creator>
1037.      <dc:creator>Venkat R Modukuru</dc:creator>
1038.      <dc:date>2024-04-25</dc:date>
1039.      <dc:source>Obesity surgery</dc:source>
1040.      <dc:title>The Impact of Metabolic Bariatric Surgery on Cardiovascular Diseases in Patients with Metabolic Dysfunction-Associated Steatotic Liver Disease</dc:title>
1041.      <dc:identifier>pmid:38662250</dc:identifier>
1042.      <dc:identifier>doi:10.1007/s11695-024-07238-w</dc:identifier>
1043.    </item>
1044.    <item>
1045.      <title>Endovascular thrombectomy in wake-up stroke guided by arterial spin-labeling and fluid-attenuated inversion recovery versus diffusion-weighted imaging mismatch on MRI</title>
1046.      <link>https://pubmed.ncbi.nlm.nih.gov/38662115/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1047.      <description>CONCLUSION: Guided by the ASL-DWI and FLAIR-DWI double mismatch, endovascular thrombectomy combined with standard medical treatment appears to yield superior functional outcomes in patients with WUS and large vessel occlusion compared to standard medical treatment alone.</description>
1048.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Thromb Thrombolysis. 2024 Apr 25. doi: 10.1007/s11239-024-02973-4. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVE: This purpose of this study is to investigate the effectiveness and safety of utilizing the arterial spin-labeling (ASL) combined with diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) combined with DWI double mismatch in the endovascular treatment of patients diagnosed with wake-up stroke (WUS).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: In this single-center trial, patients diagnosed with WUS underwent thrombectomy if acute ischemic lesions were observed on DWI indicating large precerebral circulation occlusion. Patients with no significant parenchymal hypersignal on FLAIR and ASL imaging showing a hypoperfusion tissue to infarct core volume ratio of at least 1.2 were included. The participants were divided into groups receiving endovascular thrombectomy plus medical therapy or medical therapy alone, based on their subjective preference. Functional outcomes were assessed using the ordinal score on the modified Rankin scale (mRs) at 90 days, along with the rate of functional independence.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: In this study, a total of 77 patients were included, comprising 38 patients in the endovascular therapy group and 39 patients in the medical therapy group. The endovascular therapy group exhibited more favorable changes in the distribution of functional prognosis measured by mRs at 90 days, compared to the medical therapy group (adjusted common odds ratio, 3.25; 95% CI, 1.03 to 10.26; P &lt; 0.01). Additionally, the endovascular therapy group had a higher proportion of patients achieving functional independence (odds ratio, 4.0; 95% CI, 1.36 to 11.81; P &lt; 0.01). Importantly, there were no significant differences observed in the incidence of intracranial hemorrhage or mortality rates between the two groups.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Guided by the ASL-DWI and FLAIR-DWI double mismatch, endovascular thrombectomy combined with standard medical treatment appears to yield superior functional outcomes in patients with WUS and large vessel occlusion compared to standard medical treatment alone.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662115/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662115</a> | DOI:<a href=https://doi.org/10.1007/s11239-024-02973-4>10.1007/s11239-024-02973-4</a></p></div>]]></content:encoded>
1049.      <guid isPermaLink="false">pubmed:38662115</guid>
1050.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1051.      <dc:creator>Hong-Feng Wen</dc:creator>
1052.      <dc:creator>Qin Li</dc:creator>
1053.      <dc:creator>Pei-Fu Wang</dc:creator>
1054.      <dc:creator>Ji-Lai Li</dc:creator>
1055.      <dc:creator>Ji-Chen Du</dc:creator>
1056.      <dc:date>2024-04-25</dc:date>
1057.      <dc:source>Journal of thrombosis and thrombolysis</dc:source>
1058.      <dc:title>Endovascular thrombectomy in wake-up stroke guided by arterial spin-labeling and fluid-attenuated inversion recovery versus diffusion-weighted imaging mismatch on MRI</dc:title>
1059.      <dc:identifier>pmid:38662115</dc:identifier>
1060.      <dc:identifier>doi:10.1007/s11239-024-02973-4</dc:identifier>
1061.    </item>
1062.    <item>
1063.      <title>The foundation for investigating factor XI as a target for inhibition in human cardiovascular disease</title>
1064.      <link>https://pubmed.ncbi.nlm.nih.gov/38662114/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1065.      <description>Anticoagulant therapy is a mainstay in the management of patients with cardiovascular disease and related conditions characterized by a heightened risk for thrombosis. Acute coronary syndrome, chronic coronary syndrome, ischemic stroke, and atrial fibrillation are the most common. In addition to their proclivity for thrombosis, each of these four conditions is also characterized by local and systemic inflammation, endothelial/endocardial injury and dysfunction, oxidative stress, impaired...</description>
1066.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Thromb Thrombolysis. 2024 Apr 25. doi: 10.1007/s11239-024-02985-0. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Anticoagulant therapy is a mainstay in the management of patients with cardiovascular disease and related conditions characterized by a heightened risk for thrombosis. Acute coronary syndrome, chronic coronary syndrome, ischemic stroke, and atrial fibrillation are the most common. In addition to their proclivity for thrombosis, each of these four conditions is also characterized by local and systemic inflammation, endothelial/endocardial injury and dysfunction, oxidative stress, impaired tissue-level reparative capabilities, and immune dysregulation that plays a critical role in linking molecular events, environmental triggers, and phenotypic expressions. Knowing that cardiovascular disease and thrombosis are complex and dynamic, can the scientific community identify a common pathway or specific point of interface susceptible to pharmacological inhibition or alteration that is likely to be safe and effective? The contact factors of coagulation may represent the proverbial "sweet spot" and are worthy of investigation. The following review provides a summary of the fundamental biochemistry of factor XI, its biological activity in thrombosis, inflammation, and angiogenesis, new targeting drugs, and a pragmatic approach to managing hemostatic requirements in clinical trials and possibly day-to-day patient care in the future.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662114/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662114</a> | DOI:<a href=https://doi.org/10.1007/s11239-024-02985-0>10.1007/s11239-024-02985-0</a></p></div>]]></content:encoded>
1067.      <guid isPermaLink="false">pubmed:38662114</guid>
1068.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1069.      <dc:creator>Ahmed E Ali</dc:creator>
1070.      <dc:creator>Richard C Becker</dc:creator>
1071.      <dc:date>2024-04-25</dc:date>
1072.      <dc:source>Journal of thrombosis and thrombolysis</dc:source>
1073.      <dc:title>The foundation for investigating factor XI as a target for inhibition in human cardiovascular disease</dc:title>
1074.      <dc:identifier>pmid:38662114</dc:identifier>
1075.      <dc:identifier>doi:10.1007/s11239-024-02985-0</dc:identifier>
1076.    </item>
1077.    <item>
1078.      <title>Impact of ischemic stroke topography on early clinical outcome of basilar artery occlusion: a retrospective study</title>
1079.      <link>https://pubmed.ncbi.nlm.nih.gov/38662099/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1080.      <description>CONCLUSION: Unfavorable early outcomes in patients with BAOS may be explained by a higher likelihood of inferior brain stem infarcts and lower rates of reperfusion success.</description>
1081.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Eur Radiol. 2024 Apr 25. doi: 10.1007/s00330-024-10755-y. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVES: Basilar artery occlusion (BAO) may be etiologically attributed to embolism or in situ thrombosis due to basilar stenosis (BS). Patients with BAO due to BS (BAOS) are known to have worse outcomes than patients with embolic occlusions (BAOE). BAOS occurs more proximally in the basilar artery (BA) than BAOE. We hypothesize that differing brain stem infarct patterns contribute to outcome differences between these stroke etiologies.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: This retrospective study includes 199 consecutive patients with BAO who received endovascular treatment at a single center. Final infarction in brain parenchyma dependent on the posterior circulation was graded semiquantitatively on magnetic resonance imaging (MRI). Associations to underlying stenosis and angiographic and clinical outcome variables were tested. The primary endpoint was early good clinical outcome (EGCO, mRS score ≤ 3 at discharge).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Infarct extension of the medulla oblongata (OR = 0.25; 95% CI = 0.07-0.86; p = 0.03), the inferior pons (OR = 0.328; 95% CI = 0.17-0.63; p = 0.001), the superior pons (OR = 0.57; 95% CI = 0.33-0.99; p = 0.046), and the occipital lobes (OR = 0.46; 95% CI = 0.26-0.80; p = 0.006) negatively predicted EGCO. Infarct extension for other posterior-circulation-dependent brain regions was not independently associated with unfavorable early outcomes. Patients with BAOS had more proximal occlusions and greater infarct volumes in the inferior brain stem. Successful reperfusion (mTICI 2b-3) occurred more often in patients with BAOE than in BAOS (BAOE: 131 (96.3%); BAOS: 47 (83.9%), p = 0.005).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Unfavorable early outcomes in patients with BAOS may be explained by a higher likelihood of inferior brain stem infarcts and lower rates of reperfusion success.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CLINICAL RELEVANCE STATEMENT: Basilar artery occlusion due to underlying stenosis is associated with a poorer prognosis than that caused by embolism; these results suggest that aggressive endovascular therapy, usually involving the placement of a permanent stent, may be warranted in these patients.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">KEY POINTS: Inferior brain stem and occipital infarcts are prognostically unfavorable in basilar artery occlusion. Basilar artery occlusion due to stenosis occurs more proximally and is associated with worse outcomes. Differentiating etiologies of basilar artery occlusion may influence how aggressively treated the occlusion is.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38662099/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38662099</a> | DOI:<a href=https://doi.org/10.1007/s00330-024-10755-y>10.1007/s00330-024-10755-y</a></p></div>]]></content:encoded>
1082.      <guid isPermaLink="false">pubmed:38662099</guid>
1083.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1084.      <dc:creator>Moritz R Hernandez Petzsche</dc:creator>
1085.      <dc:creator>Christian Maegerlein</dc:creator>
1086.      <dc:creator>Silke Wunderlich</dc:creator>
1087.      <dc:creator>Benno Ikenberg</dc:creator>
1088.      <dc:creator>Claus Zimmer</dc:creator>
1089.      <dc:creator>Jan S Kirschke</dc:creator>
1090.      <dc:creator>Tobias Boeckh-Behrens</dc:creator>
1091.      <dc:creator>Maria Berndt</dc:creator>
1092.      <dc:date>2024-04-25</dc:date>
1093.      <dc:source>European radiology</dc:source>
1094.      <dc:title>Impact of ischemic stroke topography on early clinical outcome of basilar artery occlusion: a retrospective study</dc:title>
1095.      <dc:identifier>pmid:38662099</dc:identifier>
1096.      <dc:identifier>doi:10.1007/s00330-024-10755-y</dc:identifier>
1097.    </item>
1098.    <item>
1099.      <title>Risk factors of neonatal stroke from different origins: a systematic review and meta-analysis</title>
1100.      <link>https://pubmed.ncbi.nlm.nih.gov/38661815/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1101.      <description>CONCLUSIONS: This study provides a succinct overview and comparative analysis of maternal, perinatal, and additional risk factors associated with neonatal cerebral artery ischemic stroke and neonatal hemorrhagic stroke, furnishing critical insights for healthcare practitioners involved in the diagnosis and prevention of neonatal stroke. This research also broadens the conceptual framework for future investigations.</description>
1102.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Eur J Pediatr. 2024 Apr 25. doi: 10.1007/s00431-024-05531-5. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Given the persistent ambiguity regarding the etiology of neonatal stroke across diverse origins, our objective was to conduct a comprehensive evaluation of both qualitative and quantitative risk factors. An exhaustive search of eight databases was executed to amass all pertinent observational studies concerning risk factors for neonatal stroke from various origins. Subsequent to independent screening, data extraction, and bias assessment by two researchers, a meta-analysis was conducted utilizing RevMan and Stata software. Nineteen studies, encompassing a total of 30 factors, were incorporated into this analysis. Beyond established risk factors, our investigation unveiled gestational diabetes (OR, 5.51; P &lt; 0.00001), a history of infertility (OR, 2.44; P &lt; 0.05), placenta previa (OR, 3.92; P = 0.02), postdates (OR, 2.07; P = 0.01), preterm labor (OR, 2.32; P &lt; 0.00001), premature rupture of membranes (OR, 3.02; P = 0.007), a prolonged second stage of labor (OR, 3.94; P &lt; 0.00001), and chorioamnionitis (OR, 4.35; P &lt; 0.00001) as potential risk factors for neonatal cerebral arterial ischemic stroke. Additionally, postdates (OR, 4.31; P = 0.003), preterm labor (OR, 1.60; P &lt; 0.00001), an abnormal CTG tracing (OR, 9.32; P &lt; 0.0001), cesarean section (OR, 4.29; P = 0.0004), male gender (OR, 1.73; P = 0.02), and vaginal delivery (OR, 1.39; P &lt; 0.00001) were associated with an elevated risk for neonatal hemorrhagic stroke.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: This study provides a succinct overview and comparative analysis of maternal, perinatal, and additional risk factors associated with neonatal cerebral artery ischemic stroke and neonatal hemorrhagic stroke, furnishing critical insights for healthcare practitioners involved in the diagnosis and prevention of neonatal stroke. This research also broadens the conceptual framework for future investigations.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">WHAT IS KNOWN: • Research indicates that prenatal, perinatal, and neonatal risk factors can elevate the risk of neonatal arterial ischemic stroke (NAIS). However, the risk factors for neonatal cerebral arterial ischemic stroke remain contentious, and those for neonatal hemorrhagic stroke (NHS) and neonatal cerebral venous sinus thrombosis (CVST) are still not well-defined.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">WHAT IS NEW: • This study is the inaugural comprehensive review and meta-analysis encompassing 19 studies that explore maternal, perinatal, and various risk factors linked to neonatal stroke of differing etiologies. Notably, our analysis elucidates eight risk factors associated with NAIS: gestational diabetes mellitus, a history of infertility, placenta previa, postdates, preterm birth, premature rupture of membranes, a prolonged second stage of labor, and chorioamnionitis. Furthermore, we identify six risk factors correlated with NHS: postdates, preterm birth, an abnormal CTG, the method of delivery, male gender, and vaginal delivery. Additionally, our systematic review delineates risk factors associated with CVST.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38661815/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38661815</a> | DOI:<a href=https://doi.org/10.1007/s00431-024-05531-5>10.1007/s00431-024-05531-5</a></p></div>]]></content:encoded>
1103.      <guid isPermaLink="false">pubmed:38661815</guid>
1104.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1105.      <dc:creator>Yankun Song</dc:creator>
1106.      <dc:creator>Shangbin Li</dc:creator>
1107.      <dc:creator>Ling Hao</dc:creator>
1108.      <dc:creator>Yiwei Han</dc:creator>
1109.      <dc:creator>Wenhui Wu</dc:creator>
1110.      <dc:creator>Yuqing Fan</dc:creator>
1111.      <dc:creator>Xiong Gao</dc:creator>
1112.      <dc:creator>Xueying Li</dc:creator>
1113.      <dc:creator>Changjun Ren</dc:creator>
1114.      <dc:creator>Yuan Chen</dc:creator>
1115.      <dc:date>2024-04-25</dc:date>
1116.      <dc:source>European journal of pediatrics</dc:source>
1117.      <dc:title>Risk factors of neonatal stroke from different origins: a systematic review and meta-analysis</dc:title>
1118.      <dc:identifier>pmid:38661815</dc:identifier>
1119.      <dc:identifier>doi:10.1007/s00431-024-05531-5</dc:identifier>
1120.    </item>
1121.    <item>
1122.      <title>Curcumin nanogel and its efficacy against oxidative stress and inflammation in rat models of ischemic stroke</title>
1123.      <link>https://pubmed.ncbi.nlm.nih.gov/38661738/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1124.      <description>Aim: The study was designed to develop and analyze curcumin nanoparticles. Methods: Curcumin nanoparticles were formulated and evaluated. Their efficacy in protecting against brain damage was investigated in a rat model of ischemic stroke, considering motor function, muscle strength and antioxidant enzyme activity. Results: Curcumin nanoparticles displayed a zeta potential of -55 ± 13.5 mV and an average particle size of 51.40 ± 21.70 nm. In ischemic stroke rat models, curcumin nanoparticle...</description>
1125.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Nanomedicine (Lond). 2024 Apr 25. doi: 10.2217/nnm-2024-0008. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one"><b>Aim:</b> The study was designed to develop and analyze curcumin nanoparticles. <b>Methods:</b> Curcumin nanoparticles were formulated and evaluated. Their efficacy in protecting against brain damage was investigated in a rat model of ischemic stroke, considering motor function, muscle strength and antioxidant enzyme activity. <b>Results:</b> Curcumin nanoparticles displayed a zeta potential of -55 ± 13.5 mV and an average particle size of 51.40 ± 21.70 nm. In ischemic stroke rat models, curcumin nanoparticle treatment significantly improved motor functions, and muscle strength and increased the activities of antioxidant enzymes like glutathione peroxidase, glutathione, glutathione S-transferase, superoxide dismutase and catalase, reducing oxidative stress and inflammation. <b>Conclusion:</b> Curcumin nanoparticles showed significant neuroprotective effects in ischemic stroke models.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38661738/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38661738</a> | DOI:<a href=https://doi.org/10.2217/nnm-2024-0008>10.2217/nnm-2024-0008</a></p></div>]]></content:encoded>
1126.      <guid isPermaLink="false">pubmed:38661738</guid>
1127.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1128.      <dc:creator>Gulrana Khuwaja</dc:creator>
1129.      <dc:creator>Sivakumar S Moni</dc:creator>
1130.      <dc:creator>Mohammad Firoz Alam</dc:creator>
1131.      <dc:creator>Hafiz A Makeen</dc:creator>
1132.      <dc:creator>Sarvat Zafar</dc:creator>
1133.      <dc:creator>Mohammad Ashafaq</dc:creator>
1134.      <dc:creator>Hasan Alhazmi</dc:creator>
1135.      <dc:creator>Asim Najmi</dc:creator>
1136.      <dc:creator>Shabihul Fatma Sayed</dc:creator>
1137.      <dc:creator>Syed Mohammad Shakeel Iqubal</dc:creator>
1138.      <dc:date>2024-04-25</dc:date>
1139.      <dc:source>Nanomedicine (London, England)</dc:source>
1140.      <dc:title>Curcumin nanogel and its efficacy against oxidative stress and inflammation in rat models of ischemic stroke</dc:title>
1141.      <dc:identifier>pmid:38661738</dc:identifier>
1142.      <dc:identifier>doi:10.2217/nnm-2024-0008</dc:identifier>
1143.    </item>
1144.    <item>
1145.      <title>Clinical Impact of Early Rhythm Control and Healthy Lifestyles in Patients With Atrial Fibrillation</title>
1146.      <link>https://pubmed.ncbi.nlm.nih.gov/38661604/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1147.      <description>CONCLUSIONS: Each of ERC and HLS might reduce the risk of ischemic stroke in patients with new-onset AF. The presence of both ERC and HLS is associated with an enhanced benefit for stroke prevention in this population.</description>
1148.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">JACC Clin Electrophysiol. 2024 Apr 4:S2405-500X(24)00159-2. doi: 10.1016/j.jacep.2024.02.016. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: There are limited data regarding the combined effect of early rhythm control (ERC) and healthy lifestyle (HLS) behaviors on the risk of ischemic stroke in patients with atrial fibrillation (AF).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVES: This study sought to evaluate how the combination of ERC and HLS behaviors affects the risk of ischemic stroke in patients with AF.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Using the Korean National Health Insurance database, we included patients with new-onset AF between 2009 and 2016 (n = 208,662). Patients who received rhythm control therapy within 2 years after AF diagnosis were defined as the ERC group. Patients with ≥2 HLS behaviors were defined as the HLS group. Patients were categorized into 4 groups: group 1, without ERC and without HLS (n = 46,972); group 2, with HLS alone (n = 110,479); group 3, with ERC alone (n = 15,133); and group 4, with both ERC and HLS (n = 36,078). The primary outcome was ischemic stroke.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Compared to group 1, group 2 and group 3 were associated with a lower risk of stroke (HR: 0.769 [95% CI: 0.728-0.881] and HR: 0.774 [95% CI: 0.703-0.852], respectively). Group 4 showed the lowest risk of stroke (HR: 0.575; 95% CI: 0.536-0.617). After propensity score weighting, the incorporation of additional ERC alongside HLS was associated with a relative risk reduction of 22% for stroke, and additional HLS alongside ERC were associated with a relative risk reduction of 27% for stroke.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Each of ERC and HLS might reduce the risk of ischemic stroke in patients with new-onset AF. The presence of both ERC and HLS is associated with an enhanced benefit for stroke prevention in this population.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38661604/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38661604</a> | DOI:<a href=https://doi.org/10.1016/j.jacep.2024.02.016>10.1016/j.jacep.2024.02.016</a></p></div>]]></content:encoded>
1149.      <guid isPermaLink="false">pubmed:38661604</guid>
1150.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1151.      <dc:creator>So-Ryoung Lee</dc:creator>
1152.      <dc:creator>Eue-Keun Choi</dc:creator>
1153.      <dc:creator>Seung-Woo Lee</dc:creator>
1154.      <dc:creator>Kyung-Do Han</dc:creator>
1155.      <dc:creator>Seil Oh</dc:creator>
1156.      <dc:creator>Gregory Y H Lip</dc:creator>
1157.      <dc:date>2024-04-25</dc:date>
1158.      <dc:source>JACC. Clinical electrophysiology</dc:source>
1159.      <dc:title>Clinical Impact of Early Rhythm Control and Healthy Lifestyles in Patients With Atrial Fibrillation</dc:title>
1160.      <dc:identifier>pmid:38661604</dc:identifier>
1161.      <dc:identifier>doi:10.1016/j.jacep.2024.02.016</dc:identifier>
1162.    </item>
1163.    <item>
1164.      <title>Endothelial lincRNA-p21 alleviates cerebral ischemia/reperfusion injury by maintaining blood-brain barrier integrity</title>
1165.      <link>https://pubmed.ncbi.nlm.nih.gov/38661094/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&amp;fc=None&amp;ff=20240426165415&amp;v=2.18.0.post9+e462414</link>
1166.      <description>Blood-brain barrier (BBB) disruption is increasingly recognized as an early contributor to the pathophysiology of cerebral ischemia/reperfusion (I/R) injury, and is also a key event in triggering secondary damage to the central nervous system. Recently, long non-coding RNA (lncRNA) have been found to be associated with ischemic stroke. However, the roles of lncRNA in BBB homeostasis remain largely unknown. Here, we report that long intergenic non-coding RNA-p21 (lincRNA-p21) was the most...</description>
1167.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Cereb Blood Flow Metab. 2024 Apr 25:271678X241248907. doi: 10.1177/0271678X241248907. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Blood-brain barrier (BBB) disruption is increasingly recognized as an early contributor to the pathophysiology of cerebral ischemia/reperfusion (I/R) injury, and is also a key event in triggering secondary damage to the central nervous system. Recently, long non-coding RNA (lncRNA) have been found to be associated with ischemic stroke. However, the roles of lncRNA in BBB homeostasis remain largely unknown. Here, we report that long intergenic non-coding RNA-p21 (lincRNA-p21) was the most significantly down-regulated lncRNA in human brain microvascular endothelial cells (HBMECs) after oxygen and glucose deprivation/reoxygenation (OGD/R) treatment among candidate lncRNA, which were both sensitive to hypoxia and involved in atherosclerosis. Exogenous brain-endothelium-specific overexpression of lincRNA-p21 could alleviate BBB disruption, diminish infarction volume and attenuate motor function deficits in middle cerebral artery occlusion/reperfusion (MCAO/R) mice. Further results showed that lincRNA-p21 was critical to maintain BBB integrity by inhibiting the degradation of junction proteins under MCAO/R and OGD/R conditions. Specifically, lincRNA-p21 could inhibit autophagy-dependent degradation of occludin by activating PI3K/AKT/mTOR signaling pathway. Besides, lincRNA-p21 could inhibit VE-cadherin degradation by binding with miR-101-3p. Together, we identify that lincRNA-p21 is critical for BBB integrity maintenance, and endothelial lincRNA-p21 overexpression could alleviate cerebral I/R injury in mice, pointing to a potential strategy to treat cerebral I/R injury.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38661094/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib&ff=20240426165415&v=2.18.0.post9+e462414">38661094</a> | DOI:<a href=https://doi.org/10.1177/0271678X241248907>10.1177/0271678X241248907</a></p></div>]]></content:encoded>
1168.      <guid isPermaLink="false">pubmed:38661094</guid>
1169.      <pubDate>Thu, 25 Apr 2024 06:00:00 -0400</pubDate>
1170.      <dc:creator>Yun-Hua Zhao</dc:creator>
1171.      <dc:creator>Yu Liang</dc:creator>
1172.      <dc:creator>Kang-Ji Wang</dc:creator>
1173.      <dc:creator>Sheng-Nan Jin</dc:creator>
1174.      <dc:creator>Xiao-Meng Yu</dc:creator>
1175.      <dc:creator>Qian Zhang</dc:creator>
1176.      <dc:creator>Jia-Yi Wei</dc:creator>
1177.      <dc:creator>Hui Liu</dc:creator>
1178.      <dc:creator>Wen-Gang Fang</dc:creator>
1179.      <dc:creator>Wei-Dong Zhao</dc:creator>
1180.      <dc:creator>Yuan Li</dc:creator>
1181.      <dc:creator>Yu-Hua Chen</dc:creator>
1182.      <dc:date>2024-04-25</dc:date>
1183.      <dc:source>Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism</dc:source>
1184.      <dc:title>Endothelial lincRNA-p21 alleviates cerebral ischemia/reperfusion injury by maintaining blood-brain barrier integrity</dc:title>
1185.      <dc:identifier>pmid:38661094</dc:identifier>
1186.      <dc:identifier>doi:10.1177/0271678X241248907</dc:identifier>
1187.    </item>
1188.  </channel>
1189. </rss>
1190.  

If you would like to create a banner that links to this page (i.e. this validation result), do the following:

1. Download the "valid RSS" banner.

2. Upload the image to your own server. (This step is important. Please do not link directly to the image on this server.)

3. Add this HTML to your page (change the image src attribute if necessary):

   <a href="http://www.feedvalidator.org/check.cgi?url=http%3A//www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi%3Frss_guid%3D1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib"><img src="valid-rss-rogers.png" alt="[Valid RSS]" title="Validate my RSS feed" /></a>

If you would like to create a text link instead, here is the URL you can use:

http://www.feedvalidator.org/check.cgi?url=http%3A//www.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi%3Frss_guid%3D1vGIiL00qKeT4_BrQf0tnV0RbCw41XEP22XBMPcA09_yeH4Yib

Home · About · News · Docs · Terms