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Source: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU

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  4.    <title>lipid</title>
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  12.    <pubDate>Sat, 04 May 2024 06:00:00 -0400</pubDate>
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  15.      <title>Concealing Organic Neuromorphic Devices with Neuronal-Inspired Supported Lipid Bilayers</title>
  16.      <link>https://pubmed.ncbi.nlm.nih.gov/38702931/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  17.      <description>Neurohybrid systems have gained large attention for their potential as in vitro and in vivo platform to interrogate and modulate the activity of cells and tissue within nervous system. In this scenario organic neuromorphic devices have been engineered as bioelectronic platforms to resemble characteristic neuronal functions. However, aiming to a functional communication with neuronal cells, material synthesis, and surface engineering can yet be exploited for optimizing bio-recognition processes...</description>
  18.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Adv Sci (Weinh). 2024 May 3:e2305860. doi: 10.1002/advs.202305860. 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">Neurohybrid systems have gained large attention for their potential as in vitro and in vivo platform to interrogate and modulate the activity of cells and tissue within nervous system. In this scenario organic neuromorphic devices have been engineered as bioelectronic platforms to resemble characteristic neuronal functions. However, aiming to a functional communication with neuronal cells, material synthesis, and surface engineering can yet be exploited for optimizing bio-recognition processes at the neuromorphic-neuronal hybrid interface. In this work, artificial neuronal-inspired lipid bilayers have been assembled on an electrochemical neuromorphic organic device (ENODe) to resemble post-synaptic structural and functional features of living synapses. Here, synaptic conditioning has been achieved by introducing two neurotransmitter-mediated biochemical signals, to induce an irreversible change in the device conductance thus achieving Pavlovian associative learning. This new class of in vitro devices can be further exploited for assembling hybrid neuronal networks and potentially for in vivo integration within living neuronal tissues.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702931/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702931</a> | DOI:<a href=https://doi.org/10.1002/advs.202305860>10.1002/advs.202305860</a></p></div>]]></content:encoded>
  19.      <guid isPermaLink="false">pubmed:38702931</guid>
  20.      <pubDate>Sat, 04 May 2024 06:00:00 -0400</pubDate>
  21.      <dc:creator>Chiara Ausilio</dc:creator>
  22.      <dc:creator>Claudia Lubrano</dc:creator>
  23.      <dc:creator>Daniela Rana</dc:creator>
  24.      <dc:creator>Giovanni Maria Matrone</dc:creator>
  25.      <dc:creator>Ugo Bruno</dc:creator>
  26.      <dc:creator>Francesca Santoro</dc:creator>
  27.      <dc:date>2024-05-04</dc:date>
  28.      <dc:source>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</dc:source>
  29.      <dc:title>Concealing Organic Neuromorphic Devices with Neuronal-Inspired Supported Lipid Bilayers</dc:title>
  30.      <dc:identifier>pmid:38702931</dc:identifier>
  31.      <dc:identifier>doi:10.1002/advs.202305860</dc:identifier>
  32.    </item>
  33.    <item>
  34.      <title>The effect of the apolipoprotein E ε4 allele and olfactory function on odor identification networks</title>
  35.      <link>https://pubmed.ncbi.nlm.nih.gov/38702902/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  36.      <description>CONCLUSIONS: The results contribute to the clarification of the neurocognitive structure of odor identification processing and suggest that poorer odor familiarity and identification in ε4 carriers may signal multi-network dysfunction. Odor familiarity and identification assessment in ε4 carriers may contribute to the predictive value of risk for MCI and AD due to the breakdown of sensory-cognitive network integration. Additional research on olfactory processing in those at risk for AD is...</description>
  37.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Brain Behav. 2024 May;14(5):e3524. doi: 10.1002/brb3.3524.</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: The combination of apolipoprotein E ε4 (ApoE ε4) status, odor identification, and odor familiarity predicts conversion to mild cognitive impairment (MCI) and Alzheimer's disease (AD).</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: To further understand olfactory disturbances and AD risk, ApoE ε4 carrier (mean age 76.38 ± 5.21) and ε4 non-carrier (mean age 76.8 ± 3.35) adults were given odor familiarity and identification tests and performed an odor identification task during fMRI scanning. Five task-related functional networks were detected using independent components analysis. Main and interaction effects of mean odor familiarity ratings, odor identification scores, and ε4 status on network activation and task-modulation of network functional connectivity (FC) during correct and incorrect odor identification (hits and misses), controlling for age and sex, were explored using multiple linear regression.</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: Findings suggested that sensory-olfactory network activation was positively associated with odor identification scores in ε4 carriers with intact odor familiarity. The FC of sensory-olfactory, multisensory-semantic integration, and occipitoparietal networks was altered in ε4 carriers with poorer odor familiarity and identification. In ε4 carriers with poorer familiarity, connectivity between superior frontal areas and the sensory-olfactory network was negatively associated with odor identification scores.</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 results contribute to the clarification of the neurocognitive structure of odor identification processing and suggest that poorer odor familiarity and identification in ε4 carriers may signal multi-network dysfunction. Odor familiarity and identification assessment in ε4 carriers may contribute to the predictive value of risk for MCI and AD due to the breakdown of sensory-cognitive network integration. Additional research on olfactory processing in those at risk for AD is warranted.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702902/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702902</a> | DOI:<a href=https://doi.org/10.1002/brb3.3524>10.1002/brb3.3524</a></p></div>]]></content:encoded>
  38.      <guid isPermaLink="false">pubmed:38702902</guid>
  39.      <pubDate>Sat, 04 May 2024 06:00:00 -0400</pubDate>
  40.      <dc:creator>Conner Frank</dc:creator>
  41.      <dc:creator>Abigail Albertazzi</dc:creator>
  42.      <dc:creator>Claire Murphy</dc:creator>
  43.      <dc:date>2024-05-04</dc:date>
  44.      <dc:source>Brain and behavior</dc:source>
  45.      <dc:title>The effect of the apolipoprotein E ε4 allele and olfactory function on odor identification networks</dc:title>
  46.      <dc:identifier>pmid:38702902</dc:identifier>
  47.      <dc:identifier>doi:10.1002/brb3.3524</dc:identifier>
  48.    </item>
  49.    <item>
  50.      <title>Parkinson's Disease-associated mutations in alpha-synuclein alters its lipid-bound state</title>
  51.      <link>https://pubmed.ncbi.nlm.nih.gov/38702883/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  52.      <description>Lipid binding properties of α-synuclein play a central role in protein aggregation and progression of Parkinson's Disease (PD). α-Synuclein, an intrinsically disordered protein, binds to lipid membranes through the formation of two amphipathic helices that insert into the lipid bilayer. All disease-associated single point mutations have been identified to be within these helical regions of α-synuclein: V15A, A30P, E46K, H50Q, G51D, A53T, and A53V. However, the effects of these mutations on the...</description>
  53.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Biophys J. 2024 May 2:S0006-3495(24)00316-3. doi: 10.1016/j.bpj.2024.05.002. 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">Lipid binding properties of α-synuclein play a central role in protein aggregation and progression of Parkinson's Disease (PD). α-Synuclein, an intrinsically disordered protein, binds to lipid membranes through the formation of two amphipathic helices that insert into the lipid bilayer. All disease-associated single point mutations have been identified to be within these helical regions of α-synuclein: V15A, A30P, E46K, H50Q, G51D, A53T, and A53V. However, the effects of these mutations on the bound states of the two α-helices of the protein have yet to be fully characterized. In this report, we use a tryptophan fluorescence assay to measure the binding of the α-helices of these PD-associated mutants to lipid membranes within the lipid depletion regime. We characterize the binding behavior of each helix, revealing that generally, the PD-associated mutants shift the equilibrium bound state away from the N-terminal helix of the protein toward Helix 2 at lower lipid concentrations. Altogether, our results indicate that disruption to the equilibrium binding of the two α-helices of α-synuclein could play a role in PD progression.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702883/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702883</a> | DOI:<a href=https://doi.org/10.1016/j.bpj.2024.05.002>10.1016/j.bpj.2024.05.002</a></p></div>]]></content:encoded>
  54.      <guid isPermaLink="false">pubmed:38702883</guid>
  55.      <pubDate>Sat, 04 May 2024 06:00:00 -0400</pubDate>
  56.      <dc:creator>Sofiya Maltseva</dc:creator>
  57.      <dc:creator>Daniel Kerr</dc:creator>
  58.      <dc:creator>Miah Turke</dc:creator>
  59.      <dc:creator>Erin J Adams</dc:creator>
  60.      <dc:creator>Ka Yee C Lee</dc:creator>
  61.      <dc:date>2024-05-04</dc:date>
  62.      <dc:source>Biophysical journal</dc:source>
  63.      <dc:title>Parkinson's Disease-associated mutations in alpha-synuclein alters its lipid-bound state</dc:title>
  64.      <dc:identifier>pmid:38702883</dc:identifier>
  65.      <dc:identifier>doi:10.1016/j.bpj.2024.05.002</dc:identifier>
  66.    </item>
  67.    <item>
  68.      <title>Association of non-insulin-based insulin resistance indices with disease severity and adverse outcome in idiopathic pulmonary arterial hypertension: a multi-center cohort study</title>
  69.      <link>https://pubmed.ncbi.nlm.nih.gov/38702735/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  70.      <description>CONCLUSIONS: IR is associated with the severity and long-term prognosis of IPAH. TyG-BMI and METS-IR can independently predict clinical worsening events, while METS-IR also provide incremental predictive performance beyond the ESC risk stratification.</description>
  71.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cardiovasc Diabetol. 2024 May 3;23(1):154. doi: 10.1186/s12933-024-02236-9.</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: Insulin resistance (IR) plays an important role in the pathophysiology of cardiovascular disease. Recent studies have shown that diabetes mellitus and impaired lipid metabolism are associated with the severity and prognosis of idiopathic pulmonary arterial hypertension (IPAH). However, the relationship between IR and pulmonary hypertension is poorly understood. This study explored the association between four IR indices and IPAH using data from a multicenter 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: A total of 602 consecutive participants with IPAH were included in this study between January 2015 and December 2022. The metabolic score for IR (METS-IR), triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio, triglyceride and glucose (TyG) index, and triglyceride-glucose-body mass index (TyG-BMI) were used to quantify IR levels in patients with IPAH. The correlation between non-insulin-based IR indices and long-term adverse outcomes was determined using multivariate Cox regression models and restricted cubic splines.</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 mean of 3.6 years' follow-up, 214 participants experienced all-cause death or worsening condition. Compared with in low to intermediate-low risk patients, the TG/HDL-C ratio (2.9 ± 1.7 vs. 3.3 ± 2.1, P = 0.003) and METS-IR (34.5 ± 6.7 vs. 36.4 ± 7.5, P &lt; 0.001) were significantly increased in high to intermediate-high risk patients. IR indices correlated with well-validated variables that reflected the severity of IPAH, such as the cardiac index and stroke volume index. Multivariate Cox regression analyses indicated that the TyG-BMI index (hazard ratio [HR] 1.179, 95% confidence interval [CI] 1.020, 1.363 per 1.0-standard deviation [SD] increment, P = 0.026) and METS-IR (HR 1.169, 95% CI 1.016, 1.345 per 1.0-SD increment, P = 0.030) independently predicted adverse outcomes. Addition of the TG/HDL-C ratio and METS-IR significantly improved the reclassification and discrimination ability beyond the European Society of Cardiology (ESC) risk score.</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: IR is associated with the severity and long-term prognosis of IPAH. TyG-BMI and METS-IR can independently predict clinical worsening events, while METS-IR also provide incremental predictive performance beyond the ESC risk stratification.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702735/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702735</a> | DOI:<a href=https://doi.org/10.1186/s12933-024-02236-9>10.1186/s12933-024-02236-9</a></p></div>]]></content:encoded>
  72.      <guid isPermaLink="false">pubmed:38702735</guid>
  73.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  74.      <dc:creator>Sicheng Zhang</dc:creator>
  75.      <dc:creator>Luyang Gao</dc:creator>
  76.      <dc:creator>Sicong Li</dc:creator>
  77.      <dc:creator>Manqing Luo</dc:creator>
  78.      <dc:creator>Lichuan Chen</dc:creator>
  79.      <dc:creator>Qunying Xi</dc:creator>
  80.      <dc:creator>Zhihui Zhao</dc:creator>
  81.      <dc:creator>Qing Zhao</dc:creator>
  82.      <dc:creator>Tao Yang</dc:creator>
  83.      <dc:creator>Qixian Zeng</dc:creator>
  84.      <dc:creator>Xin Li</dc:creator>
  85.      <dc:creator>Zhihua Huang</dc:creator>
  86.      <dc:creator>Anqi Duan</dc:creator>
  87.      <dc:creator>Yijia Wang</dc:creator>
  88.      <dc:creator>Qin Luo</dc:creator>
  89.      <dc:creator>Yansong Guo</dc:creator>
  90.      <dc:creator>Zhihong Liu</dc:creator>
  91.      <dc:date>2024-05-03</dc:date>
  92.      <dc:source>Cardiovascular diabetology</dc:source>
  93.      <dc:title>Association of non-insulin-based insulin resistance indices with disease severity and adverse outcome in idiopathic pulmonary arterial hypertension: a multi-center cohort study</dc:title>
  94.      <dc:identifier>pmid:38702735</dc:identifier>
  95.      <dc:identifier>doi:10.1186/s12933-024-02236-9</dc:identifier>
  96.    </item>
  97.    <item>
  98.      <title>Ferroptotic therapy in cancer: benefits, side effects, and risks</title>
  99.      <link>https://pubmed.ncbi.nlm.nih.gov/38702722/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  100.      <description>Ferroptosis is a type of regulated cell death characterized by iron accumulation and uncontrolled lipid peroxidation, leading to plasma membrane rupture and intracellular content release. Originally investigated as a targeted therapy for cancer cells carrying oncogenic RAS mutations, ferroptosis induction now exhibits potential to complement chemotherapy, immunotherapy, and radiotherapy in various cancer types. However, it can lead to side effects, including immune cell death, bone marrow...</description>
  101.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Mol Cancer. 2024 May 3;23(1):89. doi: 10.1186/s12943-024-01999-9.</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">Ferroptosis is a type of regulated cell death characterized by iron accumulation and uncontrolled lipid peroxidation, leading to plasma membrane rupture and intracellular content release. Originally investigated as a targeted therapy for cancer cells carrying oncogenic RAS mutations, ferroptosis induction now exhibits potential to complement chemotherapy, immunotherapy, and radiotherapy in various cancer types. However, it can lead to side effects, including immune cell death, bone marrow impairment, liver and kidney damage, cachexia (severe weight loss and muscle wasting), and secondary tumorigenesis. In this review, we discuss the advantages and offer an overview of the diverse range of documented side effects. Furthermore, we examine the underlying mechanisms and explore potential strategies for side effect mitigation.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702722/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702722</a> | DOI:<a href=https://doi.org/10.1186/s12943-024-01999-9>10.1186/s12943-024-01999-9</a></p></div>]]></content:encoded>
  102.      <guid isPermaLink="false">pubmed:38702722</guid>
  103.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  104.      <dc:creator>Jiandong Diao</dc:creator>
  105.      <dc:creator>Yuanyuan Jia</dc:creator>
  106.      <dc:creator>Enyong Dai</dc:creator>
  107.      <dc:creator>Jiao Liu</dc:creator>
  108.      <dc:creator>Rui Kang</dc:creator>
  109.      <dc:creator>Daolin Tang</dc:creator>
  110.      <dc:creator>Leng Han</dc:creator>
  111.      <dc:creator>Yingjie Zhong</dc:creator>
  112.      <dc:creator>Lingjun Meng</dc:creator>
  113.      <dc:date>2024-05-03</dc:date>
  114.      <dc:source>Molecular cancer</dc:source>
  115.      <dc:title>Ferroptotic therapy in cancer: benefits, side effects, and risks</dc:title>
  116.      <dc:identifier>pmid:38702722</dc:identifier>
  117.      <dc:identifier>doi:10.1186/s12943-024-01999-9</dc:identifier>
  118.    </item>
  119.    <item>
  120.      <title>The association between triglyceride-glucose index and the likelihood of cardiovascular disease in the U.S. population of older adults aged ≥ 60 years: a population-based study</title>
  121.      <link>https://pubmed.ncbi.nlm.nih.gov/38702717/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  122.      <description>CONCLUSION: A higher TyG index is linked to an increased likelihood of CVD in US adults aged ≥ 60 years. TyG index is anticipated to emerge as a more effective metric for identifying populations at early likelihood of CVD.</description>
  123.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cardiovasc Diabetol. 2024 May 3;23(1):151. doi: 10.1186/s12933-024-02248-5.</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: The association between the triglyceride-glucose (TyG) index and the likelihood of developing cardiovascular disease (CVD) in the general elderly population in the United States aged 60 and above is not well understood. The objective of our study was to examine the relationship between the TyG index and CVD likelihood in the general elderly population over 60 years of age in the United States.</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: Data for this cross-sectional study were sourced from the 2003-2018 National Health and Nutrition Examination Survey. Weighted multivariable regression analysis and subgroup analysis were conducted to estimate the independent relationship between the TyG index and the likelihood of CVD. Non-linear correlations were explored using restricted cubic splines.</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 6502 participants were included, with a mean TyG index of 8.75 ± 0.01. The average prevalence of CVD was 24.31% overall. Participants in the higher TyG quartiles showed high rates of CVD (Quartile 1: 19.91%; Quartile 2: 21.65%; Quartile 3: 23.82%; Quartile 4: 32.43%). For CVD, a possible association between the TyG index and the odds of CVD was observed. Our findings suggest a nonlinear association between the TyG index and the odds of CVD. The threshold of 8.73 for the likelihood of CVD. Interaction terms were employed to assess heterogeneities among each subgroup, revealing a significant difference specifically in alcohol consumption. This suggests that the positive association between the TyG index and the likelihood of CVD is dependent on the drinking status of the participants.</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: A higher TyG index is linked to an increased likelihood of CVD in US adults aged ≥ 60 years. TyG index is anticipated to emerge as a more effective metric for identifying populations at early likelihood of CVD.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702717/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702717</a> | DOI:<a href=https://doi.org/10.1186/s12933-024-02248-5>10.1186/s12933-024-02248-5</a></p></div>]]></content:encoded>
  124.      <guid isPermaLink="false">pubmed:38702717</guid>
  125.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  126.      <dc:creator>Dan Liang</dc:creator>
  127.      <dc:creator>Chang Liu</dc:creator>
  128.      <dc:creator>Yan Wang</dc:creator>
  129.      <dc:date>2024-05-03</dc:date>
  130.      <dc:source>Cardiovascular diabetology</dc:source>
  131.      <dc:title>The association between triglyceride-glucose index and the likelihood of cardiovascular disease in the U.S. population of older adults aged ≥ 60 years: a population-based study</dc:title>
  132.      <dc:identifier>pmid:38702717</dc:identifier>
  133.      <dc:identifier>doi:10.1186/s12933-024-02248-5</dc:identifier>
  134.    </item>
  135.    <item>
  136.      <title>The chain-mediating effect of Crp, BMI on the relationship between dietary intake of live microbes and hyperlipidaemia</title>
  137.      <link>https://pubmed.ncbi.nlm.nih.gov/38702682/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  138.      <description>CONCLUSION: Dietary live microbes intake is related to a lower hyperlipidaemia risk. Crp, BMI and their chain effect make a mediating impact on the relationship.</description>
  139.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Lipids Health Dis. 2024 May 3;23(1):130. doi: 10.1186/s12944-024-02107-y.</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: Inflammation and obesity are the risk factors for hyperlipidaemia. Nonetheless, research regarding the association between dietary live microbes intake and hyperlipidaemia is lacking. Therefore, this study focused on revealing the relationship between them and mediating roles of inflammation and obesity.</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: Totally 16,677 subjects were enrolled from the National Health and Nutrition Examination Survey (NHANES) (1999-2010 and 2015-2020). To explore the correlation between live microbes and hyperlipidaemia as well as blood lipid levels, respectively, multiple logistic regression and linear regression were employed. Furthermore, the mediating roles of body mass index (BMI), C-reactive protein (Crp) and their chain effect were explored through mediating analysis.</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: High dietary live microbes intake was the protective factor for hyperlipidaemia. In addition, high dietary live microbes intake exhibited a positive relationship to the high-density lipoprotein cholesterol (HDL-C) among males (β = 2.52, 95% CI: 1.29, 3.76, P &lt; 0.0001) and females (β = 2.22, 95% CI: 1.05, 3.38, P &lt; 0.001), but exhibited a negative correlation with triglyceride (TG) levels in males (β = -7.37, 95% CI: -13.16, -1.59, P = 0.02) and low-density lipoprotein cholesterol (LDL-C) levels in females (β = -2.75, 95% CI: -5.28, -0.21, P = 0.02). Crp, BMI and their chain effect mediated the relationship between live microbes with HDL-C levels. Moreover, BMI and the chain effect mediated the relationship between live microbes with LDL-C 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">CONCLUSION: Dietary live microbes intake is related to a lower hyperlipidaemia risk. Crp, BMI and their chain effect make a mediating impact on the relationship.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702682/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702682</a> | DOI:<a href=https://doi.org/10.1186/s12944-024-02107-y>10.1186/s12944-024-02107-y</a></p></div>]]></content:encoded>
  140.      <guid isPermaLink="false">pubmed:38702682</guid>
  141.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  142.      <dc:creator>Jingyi Chen</dc:creator>
  143.      <dc:creator>Shuhua Fang</dc:creator>
  144.      <dc:creator>Jinlin Huo</dc:creator>
  145.      <dc:creator>Nian Yang</dc:creator>
  146.      <dc:date>2024-05-03</dc:date>
  147.      <dc:source>Lipids in health and disease</dc:source>
  148.      <dc:title>The chain-mediating effect of Crp, BMI on the relationship between dietary intake of live microbes and hyperlipidaemia</dc:title>
  149.      <dc:identifier>pmid:38702682</dc:identifier>
  150.      <dc:identifier>doi:10.1186/s12944-024-02107-y</dc:identifier>
  151.    </item>
  152.    <item>
  153.      <title>The effect of a fermented soy beverage among patients with localized prostate cancer prior to radical prostatectomy</title>
  154.      <link>https://pubmed.ncbi.nlm.nih.gov/38702664/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  155.      <description>CONCLUSIONS: Short exposure to Q-Can® among patients with localized PCa was not associated with changes in PSA levels, PCa characteristics including grade and stage or serum testosterone. Due to early termination from inability to recruit, study power, was not achieved.</description>
  156.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMC Urol. 2024 May 3;24(1):102. doi: 10.1186/s12894-024-01483-y.</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: Fermented soy products have shown to possess inhibitory effects on prostate cancer (PCa). We evaluated the effect of a fermented soy beverage (Q-Can®), containing medium-chain triglycerides, ketones and soy isoflavones, among men with localized PCa prior to radical prostatectomy.</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 a placebo-controlled, double-blind randomized trial of Q-Can®. Stratified randomization (Cancer of the Prostate Risk Assessment (CAPRA) score at diagnosis) was used to assign patients to receive Q-Can® or placebo for 2-5 weeks before RP. Primary endpoint was change in serum PSA from baseline to end-of-study. We assessed changes in other clinical and pathologic endpoints. The primary ITT analysis compared PSA at end-of-study between randomization arms using repeated measures linear mixed model incorporating baseline CAPRA risk strata.</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 randomized 19 patients, 16 were eligible for analysis of the primary outcome. Mean age at enrollment was 61, 9(56.2%) were classified as low and intermediate risk, and 7(43.8%) high CAPRA risk. Among patients who received Q-Can®, mean PSA at baseline and end-of-study was 8.98(standard deviation, SD 4.07) and 8.02ng/mL(SD 3.99) compared with 8.66(SD 2.71) to 9.53ng/mL(SD 3.03), respectively, (Difference baseline - end-of-study, p = 0.36). There were no significant differences in Gleason score, clinical stage, surgical margin status, or CAPRA score between treatment arms (p &gt; 0.05), and no significant differences between treatment arms in end-of-study or change in lipids, testosterone and FACT-P scores (p &gt; 0.05).</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: Short exposure to Q-Can® among patients with localized PCa was not associated with changes in PSA levels, PCa characteristics including grade and stage or serum testosterone. Due to early termination from inability to recruit, study power, was not achieved.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702664/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702664</a> | DOI:<a href=https://doi.org/10.1186/s12894-024-01483-y>10.1186/s12894-024-01483-y</a></p></div>]]></content:encoded>
  157.      <guid isPermaLink="false">pubmed:38702664</guid>
  158.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  159.      <dc:creator>Soum D Lokeshwar</dc:creator>
  160.      <dc:creator>Ather Ali</dc:creator>
  161.      <dc:creator>Theresa R Weiss</dc:creator>
  162.      <dc:creator>Jesse Reynolds</dc:creator>
  163.      <dc:creator>Brian M Shuch</dc:creator>
  164.      <dc:creator>Thomas Ferencz</dc:creator>
  165.      <dc:creator>Tassos C Kyriakides</dc:creator>
  166.      <dc:creator>Wajahat Z Mehal</dc:creator>
  167.      <dc:creator>Joseph Brito</dc:creator>
  168.      <dc:creator>Joseph Renzulli</dc:creator>
  169.      <dc:creator>Michael S Leapman</dc:creator>
  170.      <dc:date>2024-05-03</dc:date>
  171.      <dc:source>BMC urology</dc:source>
  172.      <dc:title>The effect of a fermented soy beverage among patients with localized prostate cancer prior to radical prostatectomy</dc:title>
  173.      <dc:identifier>pmid:38702664</dc:identifier>
  174.      <dc:identifier>doi:10.1186/s12894-024-01483-y</dc:identifier>
  175.    </item>
  176.    <item>
  177.      <title>Prevalence and molecular characterization of colistin resistance in Pseudomonas aeruginosa isolates: insights from a study in Ardabil hospitals</title>
  178.      <link>https://pubmed.ncbi.nlm.nih.gov/38702660/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  179.      <description>CONCLUSION: This study reports the emergence of colistin resistance with various mechanisms among P. aeruginosa strains in Ardabil hospitals. We recommend avoiding unnecessary use of colistin to prevent potential future increases in colistin resistance.</description>
  180.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMC Microbiol. 2024 May 3;24(1):152. doi: 10.1186/s12866-024-03309-1.</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: Pseudomonas aeruginosa is a common cause of nosocomial infections. However, the emergence of multidrug-resistant strains has complicated the treatment of P. aeruginosa infections. While polymyxins have been the mainstay for treatment, there is a global increase in resistance to these antibiotics. Therefore, our study aimed to determine the prevalence and molecular details of colistin resistance in P. aeruginosa clinical isolates collected between June 2019 and May 2023, as well as the genetic linkage of colistin-resistant P. aeruginosa isolates.</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 resistance rate to colistin was 9% (n = 18) among P. aeruginosa isolates. All 18 colistin-resistant isolates were biofilm producers and carried genes associated with biofilm formation. Furthermore, the presence of genes encoding efflux pumps, TCSs, and outer membrane porin was observed in all colistin-resistant P. aeruginosa strains, while the mcr-1 gene was not detected. Amino acid substitutions were identified only in the PmrB protein of multidrug- and colistin-resistant strains. The expression levels of mexA, mexC, mexE, mexY, phoP, and pmrA genes in the 18 colistin-resistant P. aeruginosa strains were as follows: 88.8%, 94.4%, 11.1%, 83.3%, 83.3%, and 38.8%, respectively. Additionally, down-regulation of the oprD gene was observed in 44.4% of colistin-resistant P. aeruginosa strains.</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: This study reports the emergence of colistin resistance with various mechanisms among P. aeruginosa strains in Ardabil hospitals. We recommend avoiding unnecessary use of colistin to prevent potential future increases in colistin resistance.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702660/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702660</a> | DOI:<a href=https://doi.org/10.1186/s12866-024-03309-1>10.1186/s12866-024-03309-1</a></p></div>]]></content:encoded>
  181.      <guid isPermaLink="false">pubmed:38702660</guid>
  182.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  183.      <dc:creator>Saghar Jafari-Ramedani</dc:creator>
  184.      <dc:creator>Maryam Nazari</dc:creator>
  185.      <dc:creator>Mohsen Arzanlou</dc:creator>
  186.      <dc:creator>Hadi Peeri-Dogaheh</dc:creator>
  187.      <dc:creator>Amirhossein Sahebkar</dc:creator>
  188.      <dc:creator>Farzad Khademi</dc:creator>
  189.      <dc:date>2024-05-03</dc:date>
  190.      <dc:source>BMC microbiology</dc:source>
  191.      <dc:title>Prevalence and molecular characterization of colistin resistance in Pseudomonas aeruginosa isolates: insights from a study in Ardabil hospitals</dc:title>
  192.      <dc:identifier>pmid:38702660</dc:identifier>
  193.      <dc:identifier>doi:10.1186/s12866-024-03309-1</dc:identifier>
  194.    </item>
  195.    <item>
  196.      <title>Predicting Alzheimer's progression in MCI: a DTI-based white matter network model</title>
  197.      <link>https://pubmed.ncbi.nlm.nih.gov/38702626/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  198.      <description>CONCLUSIONS: A comprehensive model constructed based on white matter network markers can identify MCI patients at high risk of progression to AD and provide an adjunct biomarker helpful in early AD detection.</description>
  199.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMC Med Imaging. 2024 May 3;24(1):103. doi: 10.1186/s12880-024-01284-7.</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 study aimed to identify features of white matter network attributes based on diffusion tensor imaging (DTI) that might lead to progression from mild cognitive impairment (MCI) and construct a comprehensive model based on these features for predicting the population at high risk of progression to Alzheimer's disease (AD) in MCI 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">METHODS: This study enrolled 121 MCI patients from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Among them, 36 progressed to AD after four years of follow-up. A brain network was constructed for each patient based on white matter fiber tracts, and network attribute features were extracted. White matter network features were downscaled, and white matter markers were constructed using an integrated downscaling approach, followed by forming an integrated model with clinical features and performance 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">RESULTS: APOE4 and ADAS scores were used as independent predictors and combined with white matter network markers to construct a comprehensive model. The diagnostic efficacy of the comprehensive model was 0.924 and 0.919, sensitivity was 0.864 and 0.900, and specificity was 0.871 and 0.815 in the training and test groups, respectively. The Delong test showed significant differences (P &lt; 0.05) in the diagnostic efficacy of the combined model and APOE4 and ADAS scores, while there was no significant difference (P &gt; 0.05) between the combined model and white matter network biomarkers.</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: A comprehensive model constructed based on white matter network markers can identify MCI patients at high risk of progression to AD and provide an adjunct biomarker helpful in early AD detection.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702626/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702626</a> | DOI:<a href=https://doi.org/10.1186/s12880-024-01284-7>10.1186/s12880-024-01284-7</a></p></div>]]></content:encoded>
  200.      <guid isPermaLink="false">pubmed:38702626</guid>
  201.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  202.      <dc:creator>Qiaowei Song</dc:creator>
  203.      <dc:creator>Jiaxuan Peng</dc:creator>
  204.      <dc:creator>Zhenyu Shu</dc:creator>
  205.      <dc:creator>Yuyun Xu</dc:creator>
  206.      <dc:creator>Yuan Shao</dc:creator>
  207.      <dc:creator>Wen Yu</dc:creator>
  208.      <dc:creator>Liang Yu</dc:creator>
  209.      <dc:date>2024-05-03</dc:date>
  210.      <dc:source>BMC medical imaging</dc:source>
  211.      <dc:title>Predicting Alzheimer's progression in MCI: a DTI-based white matter network model</dc:title>
  212.      <dc:identifier>pmid:38702626</dc:identifier>
  213.      <dc:identifier>doi:10.1186/s12880-024-01284-7</dc:identifier>
  214.    </item>
  215.    <item>
  216.      <title>The association between the triglyceride-glucose index and in-stent restenosis in patients undergoing percutaneous coronary intervention: a systematic review and meta-analysis</title>
  217.      <link>https://pubmed.ncbi.nlm.nih.gov/38702615/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  218.      <description>CONCLUSIONS: The TyG index, an economical and precise surrogate for IR, is significantly linked with ISR. Furthermore, this correlation is unaffected by the type of coronary heart disease.</description>
  219.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMC Cardiovasc Disord. 2024 May 3;24(1):234. doi: 10.1186/s12872-024-03903-1.</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: Insulin resistance (IR) can lead to cellular metabolic disorders, activation of oxidative stress, and endothelial dysfunction, contributing to in-stent restenosis (ISR). The triglyceride-glucose index (TyG index), a new indicator reflecting IR, is extensively researched in the cardiovascular field. This study, through a meta-analysis, aimed to utilize a larger combined sample size and thereby enhance the overall test efficacy to explore the TyG index-ISR relationship.</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 thorough search was conducted in the PubMed, EMBASE, Web of Science, and Cochrane Library databases to find original papers and their references published between 1990 and January 2024. This search included both prospective and retrospective studies detailing the correlation between the TyG index and ISR in individuals with coronary heart disease (CHD).</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">OUTCOMES: The five included articles comprised 3,912 participants, and the odds ratio (OR) extracted from each study was combined using the Inverse Variance method. Results showed that, in the context of CHD patients, each incremental unit in the TyG index, when treated as a continuous variable, corresponded to a 42% elevation in ISR risk (95% CI 1.26-1.59, I²=13%, p &lt; 0.005). When analyzing the TyG index categorically, the results revealed a higher ISR risk in the highest TyG index group compared to the lowest group (OR: 1.69, 95% CI 1.32-2.17, I²=0). Additionally, in patients with chronic coronary syndrome (CCS), each unit increase in the TyG index, the risk of ISR in patients increased by 37% (95% CI 1.19-1.57, I²=0%, p &lt; 0.005). This correlation was also observable in acute coronary syndrome (ACS) patients (OR:1.48, 95% CI 1.19-1.85, I²=0, p &lt; 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">CONCLUSIONS: The TyG index, an economical and precise surrogate for IR, is significantly linked with ISR. Furthermore, this correlation is unaffected by the type of coronary heart disease.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702615/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702615</a> | DOI:<a href=https://doi.org/10.1186/s12872-024-03903-1>10.1186/s12872-024-03903-1</a></p></div>]]></content:encoded>
  220.      <guid isPermaLink="false">pubmed:38702615</guid>
  221.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  222.      <dc:creator>Haodong Jiang</dc:creator>
  223.      <dc:creator>Yuntong Liu</dc:creator>
  224.      <dc:creator>Haoyu Guo</dc:creator>
  225.      <dc:creator>Zhihao Liu</dc:creator>
  226.      <dc:creator>Zhibo Li</dc:creator>
  227.      <dc:date>2024-05-03</dc:date>
  228.      <dc:source>BMC cardiovascular disorders</dc:source>
  229.      <dc:title>The association between the triglyceride-glucose index and in-stent restenosis in patients undergoing percutaneous coronary intervention: a systematic review and meta-analysis</dc:title>
  230.      <dc:identifier>pmid:38702615</dc:identifier>
  231.      <dc:identifier>doi:10.1186/s12872-024-03903-1</dc:identifier>
  232.    </item>
  233.    <item>
  234.      <title>H&lt;sub&gt;2&lt;/sub&gt;S is involved in drought-mediated stomatal closure through PLDα1 in Arabidopsis</title>
  235.      <link>https://pubmed.ncbi.nlm.nih.gov/38702456/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  236.      <description>PLDα1 promoted H(2)S production by positively regulating the expression of LCD. Stomatal closure promoted by PLDα1 required the accumulation of H(2)S under drought stress. Phospholipase Dα1 (PLDα1) acting as one of the signal enzymes can respond to drought stress. It is well known that hydrogen sulfide (H(2)S) plays an important role in plant responding to biotic or abiotic stress. In this study, the functions and relationship between PLDα1 and H(2)S in drought stress resistance in Arabidopsis...</description>
  237.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Planta. 2024 May 4;259(6):142. doi: 10.1007/s00425-024-04421-2.</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">PLDα1 promoted H<sub>2</sub>S production by positively regulating the expression of LCD. Stomatal closure promoted by PLDα1 required the accumulation of H<sub>2</sub>S under drought stress. Phospholipase Dα1 (PLDα1) acting as one of the signal enzymes can respond to drought stress. It is well known that hydrogen sulfide (H<sub>2</sub>S) plays an important role in plant responding to biotic or abiotic stress. In this study, the functions and relationship between PLDα1 and H<sub>2</sub>S in drought stress resistance in Arabidopsis were explored. Our results indicated that drought stress promotes PLDα1 and H<sub>2</sub>S production by inducing the expression of PLDα1 and LCD genes. PLDα1 and LCD enhanced plant tolerance to drought by regulating membrane lipid peroxidation, proline accumulation, H<sub>2</sub>O<sub>2</sub> content and stomatal closure. Under drought stress, the H<sub>2</sub>O<sub>2</sub> content of PLDα1-deficient mutant (pldα1), L-cysteine desulfhydrase (LCD)-deficient mutant (lcd) was higher than that of ecotype (WT), the stomatal aperture of pldα1 and lcd was larger than that of WT. The transcriptional and translational levels of LCD were lower in pldα1 than that in WT. Exogenous application of the H<sub>2</sub>S donor NaHS or GYY reduced the stomatal aperture of WT, pldα1, PLDα1-CO, and PLDα1-OE lines, while exogenous application of the H<sub>2</sub>S scavenger hypotaurine (HT) increased the stomatal aperture. qRT-PCR analysis of stomatal movement-related genes showed that the expression of CAX1, ABCG5, SCAB1, and SLAC1 genes in pldα1 and lcd were down-regulated, while ACA1 and OST1 gene expression was significantly up-regulated. Thus, PLDα1 and LCD are required for stomatal closure to improve drought stress tolerance.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702456/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702456</a> | DOI:<a href=https://doi.org/10.1007/s00425-024-04421-2>10.1007/s00425-024-04421-2</a></p></div>]]></content:encoded>
  238.      <guid isPermaLink="false">pubmed:38702456</guid>
  239.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  240.      <dc:creator>Simin Wang</dc:creator>
  241.      <dc:creator>Cuixia Zhang</dc:creator>
  242.      <dc:creator>Rongshan Chen</dc:creator>
  243.      <dc:creator>Kailin Cheng</dc:creator>
  244.      <dc:creator>Liai Ma</dc:creator>
  245.      <dc:creator>Wei Wang</dc:creator>
  246.      <dc:creator>Ning Yang</dc:creator>
  247.      <dc:date>2024-05-03</dc:date>
  248.      <dc:source>Planta</dc:source>
  249.      <dc:title>H&lt;sub&gt;2&lt;/sub&gt;S is involved in drought-mediated stomatal closure through PLDα1 in Arabidopsis</dc:title>
  250.      <dc:identifier>pmid:38702456</dc:identifier>
  251.      <dc:identifier>doi:10.1007/s00425-024-04421-2</dc:identifier>
  252.    </item>
  253.    <item>
  254.      <title>The proteomic profile is altered but not repaired after bariatric surgery in type 2 diabetes pigs</title>
  255.      <link>https://pubmed.ncbi.nlm.nih.gov/38702370/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  256.      <description>To reveal the sources of obesity and type 2 diabetes (T2D) in humans, animal models, mainly rodents, have been used. Here, we propose a pig model of T2D. Weaned piglets were fed high fat/high sugar diet suppling 150% of metabolizable energy. Measurements of weight gain, blood morphology, glucose plasma levels, cholesterol, and triglycerides, as well as glucose tolerance (oral glucose tolerance test, OGTT) were employed to observe T2D development. The histology and mass spectrometry analyses were...</description>
  257.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Sci Rep. 2024 May 3;14(1):10235. doi: 10.1038/s41598-024-60022-9.</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">To reveal the sources of obesity and type 2 diabetes (T2D) in humans, animal models, mainly rodents, have been used. Here, we propose a pig model of T2D. Weaned piglets were fed high fat/high sugar diet suppling 150% of metabolizable energy. Measurements of weight gain, blood morphology, glucose plasma levels, cholesterol, and triglycerides, as well as glucose tolerance (oral glucose tolerance test, OGTT) were employed to observe T2D development. The histology and mass spectrometry analyses were made post mortem. Within 6 months, the high fat-high sugar (HFHS) fed pigs showed gradual and significant increase in plasma triglycerides and glucose levels in comparison to the controls. Using OGTT test, we found stable glucose intolerance in 10 out of 14 HFHS pigs. Mass spectrometry analysis indicated significant changes in 330 proteins in the intestine, liver, and pancreas of the HFHS pigs. These pigs showed also an increase in DNA base modifications and elevated level of the ALKBH proteins in the tissues. Six diabetic HFHS pigs underwent Scopinaro bariatric surgery restoring glycaemia one month after surgery. In conclusion, a high energy diet applied to piglets resulted in the development of hyperlipidaemia, hyperglycaemia, and type 2 diabetes being reversed by a bariatric procedure, excluding the proteomic profile utill one month after the surgery.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702370/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702370</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-60022-9>10.1038/s41598-024-60022-9</a></p></div>]]></content:encoded>
  258.      <guid isPermaLink="false">pubmed:38702370</guid>
  259.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  260.      <dc:creator>Karolina Ferenc</dc:creator>
  261.      <dc:creator>Michał Marcinkowski</dc:creator>
  262.      <dc:creator>Jarosław Olszewski</dc:creator>
  263.      <dc:creator>Paweł Kowalczyk</dc:creator>
  264.      <dc:creator>Tomaš Pilžys</dc:creator>
  265.      <dc:creator>Damian Garbicz</dc:creator>
  266.      <dc:creator>Naser Dib</dc:creator>
  267.      <dc:creator>Bianka Świderska</dc:creator>
  268.      <dc:creator>Piotr Matyba</dc:creator>
  269.      <dc:creator>Zdzisław Gajewski</dc:creator>
  270.      <dc:creator>Elżbieta Grzesiuk</dc:creator>
  271.      <dc:creator>Romuald Zabielski</dc:creator>
  272.      <dc:date>2024-05-03</dc:date>
  273.      <dc:source>Scientific reports</dc:source>
  274.      <dc:title>The proteomic profile is altered but not repaired after bariatric surgery in type 2 diabetes pigs</dc:title>
  275.      <dc:identifier>pmid:38702370</dc:identifier>
  276.      <dc:identifier>doi:10.1038/s41598-024-60022-9</dc:identifier>
  277.    </item>
  278.    <item>
  279.      <title>The severity of COVID-19 upon hospital admission is associated with plasma omega-3 fatty acids</title>
  280.      <link>https://pubmed.ncbi.nlm.nih.gov/38702342/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  281.      <description>Fatty acids are precursors of inflammatory oxylipins. In the context of COVID-19, an excessive production of pro-inflammatory cytokines is associated with disease severity. The objective was to investigate whether the baseline omega 3/omega 6 fatty acids ratio and the oxylipins were associated with inflammation and oxidative stress in unvaccinated patients with COVID-19, classified according to the severity of the disease during hospitalization. This Prospective population-based cohort study...</description>
  282.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Sci Rep. 2024 May 3;14(1):10238. doi: 10.1038/s41598-024-60815-y.</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">Fatty acids are precursors of inflammatory oxylipins. In the context of COVID-19, an excessive production of pro-inflammatory cytokines is associated with disease severity. The objective was to investigate whether the baseline omega 3/omega 6 fatty acids ratio and the oxylipins were associated with inflammation and oxidative stress in unvaccinated patients with COVID-19, classified according to the severity of the disease during hospitalization. This Prospective population-based cohort study included 180 hospitalized patients with COVID-19. The patients were classified into five groups according to the severity of their disease. Group 1 was the least severe and Group 5 was the most severe. Three specific types of fatty acids-eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA)-as well as their enzymatic and non-enzymatic oxylipins were determined using chromatography coupled mass spectrometry. There was no difference in the ratio of omega-3 to omega-6 fatty acids between the groups (p = 0.276). However, the EPA/AA ratio was lower in Group 4 compared to Group 1 (p = 0.015). This finding was associated with an increase in both C-Reactive Protein (p &lt; 0.001) and Interleukin-6 (p = 0.002). Furthermore, the concentration of F<sub>2</sub>-Isoprostanes was higher in Group 4 than in Group 1 (p = 0.009), while no significant changes were observed for other oxylipins among groups. Multivariate analysis did not present any standard of biomarkers, suggesting the high complexity of factors involved in the disease severity. Our hypothesis was confirmed in terms of EPA/AA ratio. A higher EPA/AA ratio upon hospital admission was found to be associated with lower concentration of C-Reactive Protein and Interleukin-6, leading to a better prognosis of hospitalized SARS-CoV-2 patients. Importantly, this beneficial outcome was achieved without any form of supplementation. The trial also provides important information that can be further applied to reduce the severity of infections associated with an uncontrolled synthesis of pro-inflammatory cytokines.Trial registration: https://clinicaltrials.gov/study/NCT04449718 -01/06/2020. ClinicalTrials.gov Identifier: NCT04449718.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702342/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702342</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-60815-y>10.1038/s41598-024-60815-y</a></p></div>]]></content:encoded>
  283.      <guid isPermaLink="false">pubmed:38702342</guid>
  284.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  285.      <dc:creator>Ligia P Fernandes</dc:creator>
  286.      <dc:creator>Igor H Murai</dc:creator>
  287.      <dc:creator>Alan L Fernandes</dc:creator>
  288.      <dc:creator>Lucas P Sales</dc:creator>
  289.      <dc:creator>Marcelo M Rogero</dc:creator>
  290.      <dc:creator>Bruno Gualano</dc:creator>
  291.      <dc:creator>Lúcia P Barroso</dc:creator>
  292.      <dc:creator>Ginger L Milne</dc:creator>
  293.      <dc:creator>Rosa M R Pereira</dc:creator>
  294.      <dc:creator>Inar A Castro</dc:creator>
  295.      <dc:date>2024-05-03</dc:date>
  296.      <dc:source>Scientific reports</dc:source>
  297.      <dc:title>The severity of COVID-19 upon hospital admission is associated with plasma omega-3 fatty acids</dc:title>
  298.      <dc:identifier>pmid:38702342</dc:identifier>
  299.      <dc:identifier>doi:10.1038/s41598-024-60815-y</dc:identifier>
  300.    </item>
  301.    <item>
  302.      <title>Synthetic BZLF1-targeted transcriptional activator for efficient lytic induction therapy against EBV-associated epithelial cancers</title>
  303.      <link>https://pubmed.ncbi.nlm.nih.gov/38702330/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  304.      <description>The unique virus-cell interaction in Epstein-Barr virus (EBV)-associated malignancies implies targeting the viral latent-lytic switch is a promising therapeutic strategy. However, the lack of specific and efficient therapeutic agents to induce lytic cycle in these cancers is a major challenge facing clinical implementation. We develop a synthetic transcriptional activator that specifically activates endogenous BZLF1 and efficiently induces lytic reactivation in EBV-positive cancer cells. A lipid...</description>
  305.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Nat Commun. 2024 May 3;15(1):3729. doi: 10.1038/s41467-024-48031-8.</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 unique virus-cell interaction in Epstein-Barr virus (EBV)-associated malignancies implies targeting the viral latent-lytic switch is a promising therapeutic strategy. However, the lack of specific and efficient therapeutic agents to induce lytic cycle in these cancers is a major challenge facing clinical implementation. We develop a synthetic transcriptional activator that specifically activates endogenous BZLF1 and efficiently induces lytic reactivation in EBV-positive cancer cells. A lipid nanoparticle encapsulating nucleoside-modified mRNA which encodes a BZLF1-specific transcriptional activator (mTZ3-LNP) is synthesized for EBV-targeted therapy. Compared with conventional chemical inducers, mTZ3-LNP more efficiently activates EBV lytic gene expression in EBV-associated epithelial cancers. Here we show the potency and safety of treatment with mTZ3-LNP to suppress tumor growth in EBV-positive cancer models. The combination of mTZ3-LNP and ganciclovir yields highly selective cytotoxic effects of mRNA-based lytic induction therapy against EBV-positive tumor cells, indicating the potential of mRNA nanomedicine in the treatment of EBV-associated epithelial cancers.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702330/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702330</a> | DOI:<a href=https://doi.org/10.1038/s41467-024-48031-8>10.1038/s41467-024-48031-8</a></p></div>]]></content:encoded>
  306.      <guid isPermaLink="false">pubmed:38702330</guid>
  307.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  308.      <dc:creator>Man Wu</dc:creator>
  309.      <dc:creator>Pok Man Hau</dc:creator>
  310.      <dc:creator>Linxian Li</dc:creator>
  311.      <dc:creator>Chi Man Tsang</dc:creator>
  312.      <dc:creator>Yike Yang</dc:creator>
  313.      <dc:creator>Aziz Taghbalout</dc:creator>
  314.      <dc:creator>Grace Tin-Yun Chung</dc:creator>
  315.      <dc:creator>Shin Yee Hui</dc:creator>
  316.      <dc:creator>Wing Chung Tang</dc:creator>
  317.      <dc:creator>Nathaniel Jillette</dc:creator>
  318.      <dc:creator>Jacqueline Jufen Zhu</dc:creator>
  319.      <dc:creator>Horace Hok Yeung Lee</dc:creator>
  320.      <dc:creator>Ee Ling Kong</dc:creator>
  321.      <dc:creator>Melissa Sue Ann Chan</dc:creator>
  322.      <dc:creator>Jason Ying Kuen Chan</dc:creator>
  323.      <dc:creator>Brigette Buig Yue Ma</dc:creator>
  324.      <dc:creator>Mei-Ru Chen</dc:creator>
  325.      <dc:creator>Charles Lee</dc:creator>
  326.      <dc:creator>Ka Fai To</dc:creator>
  327.      <dc:creator>Albert Wu Cheng</dc:creator>
  328.      <dc:creator>Kwok-Wai Lo</dc:creator>
  329.      <dc:date>2024-05-03</dc:date>
  330.      <dc:source>Nature communications</dc:source>
  331.      <dc:title>Synthetic BZLF1-targeted transcriptional activator for efficient lytic induction therapy against EBV-associated epithelial cancers</dc:title>
  332.      <dc:identifier>pmid:38702330</dc:identifier>
  333.      <dc:identifier>doi:10.1038/s41467-024-48031-8</dc:identifier>
  334.    </item>
  335.    <item>
  336.      <title>Designing function-specific minimal microbiomes from large microbial communities</title>
  337.      <link>https://pubmed.ncbi.nlm.nih.gov/38702322/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  338.      <description>Microorganisms exist in large communities of diverse species, exhibiting various functionalities. The mammalian gut microbiome, for instance, has the functionality of digesting dietary fibre and producing different short-chain fatty acids. Not all microbes present in a community contribute to a given functionality; it is possible to find a minimal microbiome, which is a subset of the large microbiome, that is capable of performing the functionality while maintaining other community properties...</description>
  339.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">NPJ Syst Biol Appl. 2024 May 3;10(1):46. doi: 10.1038/s41540-024-00373-1.</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">Microorganisms exist in large communities of diverse species, exhibiting various functionalities. The mammalian gut microbiome, for instance, has the functionality of digesting dietary fibre and producing different short-chain fatty acids. Not all microbes present in a community contribute to a given functionality; it is possible to find a minimal microbiome, which is a subset of the large microbiome, that is capable of performing the functionality while maintaining other community properties such as growth rate and metabolite production. Such a minimal microbiome will also contain keystone species for SCFA production in that community. In this work, we present a systematic constraint-based approach to identify a minimal microbiome from a large community for a user-proposed function. We employ a top-down approach with sequential deletion followed by solving a mixed-integer linear programming problem with the objective of minimising the L<sub>1</sub>-norm of the membership vector. Notably, we consider quantitative measures of community growth rate and metabolite production rates. We demonstrate the utility of our algorithm by identifying the minimal microbiomes corresponding to three model communities of the gut, and discuss their validity based on the presence of the keystone species in the community. Our approach is generic, flexible and finds application in studying a variety of microbial communities. The algorithm is available from https://github.com/RamanLab/minMicrobiome .</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702322/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702322</a> | DOI:<a href=https://doi.org/10.1038/s41540-024-00373-1>10.1038/s41540-024-00373-1</a></p></div>]]></content:encoded>
  340.      <guid isPermaLink="false">pubmed:38702322</guid>
  341.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  342.      <dc:creator>Aswathy K Raghu</dc:creator>
  343.      <dc:creator>Indumathi Palanikumar</dc:creator>
  344.      <dc:creator>Karthik Raman</dc:creator>
  345.      <dc:date>2024-05-03</dc:date>
  346.      <dc:source>NPJ systems biology and applications</dc:source>
  347.      <dc:title>Designing function-specific minimal microbiomes from large microbial communities</dc:title>
  348.      <dc:identifier>pmid:38702322</dc:identifier>
  349.      <dc:identifier>doi:10.1038/s41540-024-00373-1</dc:identifier>
  350.    </item>
  351.    <item>
  352.      <title>Development and in vitro antiviral activity of ivermectin liposomes as a potential drug carrier system</title>
  353.      <link>https://pubmed.ncbi.nlm.nih.gov/38702288/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  354.      <description>This study aimed to assess and compare diverse formulations of ivermectin-loaded liposomes, employing lipid film hydration and ethanol injection methods. Three lipids (DOPC, SPC, and DSPC) were used in predetermined molar ratios. A total of 18 formulations were created, and a factorial design determined the optimal formulation based on particle size, polydispersity index (PDI), zeta potential, and encapsulation efficiency. The average mean particle size, PDI and zeta potential of the selected...</description>
  355.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Arch Pharm (Weinheim). 2024 May 3:e2300708. doi: 10.1002/ardp.202300708. 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">This study aimed to assess and compare diverse formulations of ivermectin-loaded liposomes, employing lipid film hydration and ethanol injection methods. Three lipids (DOPC, SPC, and DSPC) were used in predetermined molar ratios. A total of 18 formulations were created, and a factorial design determined the optimal formulation based on particle size, polydispersity index (PDI), zeta potential, and encapsulation efficiency. The average mean particle size, PDI and zeta potential of the selected formulations (F1, F2, F7, F9, and F11) was, respectively, 196.40 ± 44.60 nm, 0.39 ± 0.09, and -40.24 ± 9.17. The encapsulation efficiency exceeded 80%, with a mean loading capacity of 4.00 ± 1.70%. In vitro studies included transmission electron microscopy, Fourier transform infrared spectroscopy, drug release, and antiviral activity assessments against SARS-CoV-2. The liposomal formulations demonstrated superior antiviral activity compared to free ivermectin, as indicated by lower IC<sub>50</sub> values. The results of this study emphasize the effectiveness of ivermectin-loaded liposomes in inhibiting viral activity, highlighting their potential as promising candidates for antiviral therapy. The findings suggest that the strategic use of liposomes as drug carriers can significantly modulate and improve the antiviral properties of ivermectin, offering a novel approach to harnessing its full therapeutic potential. Collectively, these results provide a robust foundation for further exploration of ivermectin as a viral protection tool and optimization of its delivery mechanisms.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702288/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702288</a> | DOI:<a href=https://doi.org/10.1002/ardp.202300708>10.1002/ardp.202300708</a></p></div>]]></content:encoded>
  356.      <guid isPermaLink="false">pubmed:38702288</guid>
  357.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  358.      <dc:creator>Meryem Kocas</dc:creator>
  359.      <dc:creator>Tansel Comoglu</dc:creator>
  360.      <dc:creator>Aykut Ozkul</dc:creator>
  361.      <dc:date>2024-05-03</dc:date>
  362.      <dc:source>Archiv der Pharmazie</dc:source>
  363.      <dc:title>Development and in vitro antiviral activity of ivermectin liposomes as a potential drug carrier system</dc:title>
  364.      <dc:identifier>pmid:38702288</dc:identifier>
  365.      <dc:identifier>doi:10.1002/ardp.202300708</dc:identifier>
  366.    </item>
  367.    <item>
  368.      <title>Early detection of severe hypertriglyceridemia using teleconsultation in a clinical laboratory setting</title>
  369.      <link>https://pubmed.ncbi.nlm.nih.gov/38702205/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  370.      <description>CONCLUSION: This extensive study has identified a family at high risk of cardiovascular disease and acute pancreatitis. These findings can help maximize lifestyle changes and improve the clinical management of their dyslipidemia.</description>
  371.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Clin Investig Arterioscler. 2024 May 2:S0214-9168(24)00036-6. doi: 10.1016/j.arteri.2024.03.004. 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: Teleconsultation in the context of clinical laboratories is a valuable tool for the early detection of dyslipidemia and prevention of cardiovascular risk. Here, we describe a patient who was referred to the Lipid Unit of the Virgen Macarena Hospital due to an alert for severe hypertriglyceridemia through its teleconsultation program.</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">CASE PRESENTATION: A comprehensive clinical and biochemical study of the patient was carried out, and genetic testing was performed on the patient and his family. The proband and his family showed mild to severe hypertriglyceridemia and various secondary factors, together with a genetic background associated with a triglyceride-raising effect.</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: This extensive study has identified a family at high risk of cardiovascular disease and acute pancreatitis. These findings can help maximize lifestyle changes and improve the clinical management of their dyslipidemia.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702205/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702205</a> | DOI:<a href=https://doi.org/10.1016/j.arteri.2024.03.004>10.1016/j.arteri.2024.03.004</a></p></div>]]></content:encoded>
  372.      <guid isPermaLink="false">pubmed:38702205</guid>
  373.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  374.      <dc:creator>Teresa Arrobas-Velilla</dc:creator>
  375.      <dc:creator>María José Ariza</dc:creator>
  376.      <dc:creator>Miguel Ángel Rico-Corral</dc:creator>
  377.      <dc:creator>Pedro Valdivielso</dc:creator>
  378.      <dc:date>2024-05-03</dc:date>
  379.      <dc:source>Clinica e investigacion en arteriosclerosis : publicacion oficial de la Sociedad Espanola de Arteriosclerosis</dc:source>
  380.      <dc:title>Early detection of severe hypertriglyceridemia using teleconsultation in a clinical laboratory setting</dc:title>
  381.      <dc:identifier>pmid:38702205</dc:identifier>
  382.      <dc:identifier>doi:10.1016/j.arteri.2024.03.004</dc:identifier>
  383.    </item>
  384.    <item>
  385.      <title>Effects of Qiye Shen'an Pian Combined with Glutamate and Vitamin B1 on Fatigue State, Immune Function and Quality of Life in Patients with Chronic Fatigue Syndrome</title>
  386.      <link>https://pubmed.ncbi.nlm.nih.gov/38702173/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  387.      <description>CONCLUSION: In this study, we observed that Qiye Shen'an Pian combined with glutathione and vitamin B1, produced significant improvements in immune function and antioxidant capacity in patients with chronic fatigue syndrome (CFS). Specifically, patients' CD4+, CD8+ levels, and superoxide dismutase (SOD) activity all showed positive changes after treatment. These changes are crucial for enhancing patients' disease resistance and reducing fatigue symptoms. Qiye Shen'an Pian combined with glutamine...</description>
  388.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Altern Ther Health Med. 2024 May 3:AT10308. 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: To observe the effects of Qiye Shen'an Pian combined with ghrelin and vitamin B1 on the fatigue status, immune function, and quality of life of patients with chronic fatigue syndrome (CFS), focusing specifically on the efficacy of this combination 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">METHODS: In this prospective study, 106 CFS patients admitted from June 2021 to June 2023 were selected. Using a simple randomisation method, patients were divided into two groups. The conventional group received glutathione and vitamin B1 treatment, while the Qiye Shen'an group received an additional treatment with Qiye Shen'an Pian on top of the standard glutathione and vitamin B1, for a continuous period of 8 weeks. To assess treatment efficacy, we compared immune function-related indexes (such as CD4+, CD8+, CD4+/CD8+ ratio, NK cell ratio), free radical metabolism indexes (like lipid peroxide, catalytic enzyme, and superoxide dismutase levels), TCM symptom scores, FS-14 scores, and SPHERE scores between the two groups. Adverse reactions were also recorded and statistically analyzed.</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: Notable improvements were observed in both groups, with the Qiye Shen'an group showing particularly significant enhancements. Post-treatment immune function indicators revealed a greater decrease in CD8+ levels in the Qiye Shen'an group (P &lt; .05), along with marked increases in CD4+, CD4+/CD8+ ratio, and NK cell ratio in both groups, more so in the Qiye Shen'an group (P &lt; .05). Free radical metabolism indicators, including lipid peroxide levels, decreased in both groups, with a more significant reduction observed in the Qiye Shen'an group (P &lt; .05). The levels of catalytic enzyme and superoxide dismutase increased in both groups, with a notably higher improvement in the Qiye Shen'an group (P &lt; .05). In terms of TCM symptom scores, FS-14 scores, and SPHERE scores, both groups showed a reduction after treatment, with a more substantial decrease in the Qiye Shen'an group (P &lt; .05).</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: In this study, we observed that Qiye Shen'an Pian combined with glutathione and vitamin B1, produced significant improvements in immune function and antioxidant capacity in patients with chronic fatigue syndrome (CFS). Specifically, patients' CD4+, CD8+ levels, and superoxide dismutase (SOD) activity all showed positive changes after treatment. These changes are crucial for enhancing patients' disease resistance and reducing fatigue symptoms. Qiye Shen'an Pian combined with glutamine and vitamin B1 in the treatment of CFS can alleviate the fatigue state of patients, improve the immune function, enhance the antioxidant capacity of the body, and improve somatic and psychological health. These findings underscore the potential of this combination therapy in effectively managing chronic fatigue syndrome, offering a promising direction for future treatment strategies.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702173/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702173</a></p></div>]]></content:encoded>
  389.      <guid isPermaLink="false">pubmed:38702173</guid>
  390.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  391.      <dc:creator>Jun Liu</dc:creator>
  392.      <dc:creator>Junfeng Liao</dc:creator>
  393.      <dc:creator>Fan Lin</dc:creator>
  394.      <dc:creator>Chenyang Nie</dc:creator>
  395.      <dc:date>2024-05-03</dc:date>
  396.      <dc:source>Alternative therapies in health and medicine</dc:source>
  397.      <dc:title>Effects of Qiye Shen'an Pian Combined with Glutamate and Vitamin B1 on Fatigue State, Immune Function and Quality of Life in Patients with Chronic Fatigue Syndrome</dc:title>
  398.      <dc:identifier>pmid:38702173</dc:identifier>
  399.    </item>
  400.    <item>
  401.      <title>From the Editors: Familial hypercholesterolemia: Still underdiagnosed and undertreated</title>
  402.      <link>https://pubmed.ncbi.nlm.nih.gov/38702142/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  403.      <description>No abstract</description>
  404.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Clin Lipidol. 2024 Mar-Apr;18(2):e130-e131. doi: 10.1016/j.jacl.2024.03.005.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702142/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702142</a> | DOI:<a href=https://doi.org/10.1016/j.jacl.2024.03.005>10.1016/j.jacl.2024.03.005</a></p></div>]]></content:encoded>
  405.      <guid isPermaLink="false">pubmed:38702142</guid>
  406.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  407.      <dc:creator>P Barton Duell</dc:creator>
  408.      <dc:creator>Kevin C Maki</dc:creator>
  409.      <dc:date>2024-05-03</dc:date>
  410.      <dc:source>Journal of clinical lipidology</dc:source>
  411.      <dc:title>From the Editors: Familial hypercholesterolemia: Still underdiagnosed and undertreated</dc:title>
  412.      <dc:identifier>pmid:38702142</dc:identifier>
  413.      <dc:identifier>doi:10.1016/j.jacl.2024.03.005</dc:identifier>
  414.    </item>
  415.    <item>
  416.      <title>Factors influencing optimal diabetes care and clinical outcomes in Thai patients with type 2 diabetes mellitus: a multilevel modelling analysis</title>
  417.      <link>https://pubmed.ncbi.nlm.nih.gov/38702083/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  418.      <description>CONCLUSION: This highlights the necessity for targeted interventions to bridge urban-suburban care gaps, optimise drug prescriptions and implement comprehensive care strategies for improved glycaemic control, DR prevention and CKD progression mitigation among in Thai patients with T2DM. The value of the clinical target aggregate (ABC) and the process of care aggregate (FAACE) was also conclusively demonstrated.</description>
  419.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMJ Open. 2024 May 3;14(5):e079415. doi: 10.1136/bmjopen-2023-079415.</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: Increasing levels of poor glycaemic control among Thai patients with type 2 diabetes mellitus (T2DM) motivated us to compare T2DM care between urban and suburban primary care units (PCUs), to identify gaps in care, and to identify significant factors that may influence strategies to enhance the quality of care and clinical outcomes in this population.</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 a cross-sectional study involving 2160 patients with T2DM treated at four Thai PCUs from 2019 to 2021, comprising one urban and three suburban facilities. Using mixed effects logistic regression, we compared care factors between urban and suburban PCUs.</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 attending suburban PCUs were significantly more likely to undergo eye (adjusted OR (AOR): 1.83, 95% CI 1.35 to 1.72), foot (AOR: 1.61, 95% CI 0.65 to 4.59) and HbA<sub>1c</sub> (AOR: 1.66, 95% CI 1.09 to 2.30) exams and achieved all ABC (HbA<sub>1c</sub>, blood pressure (BP) and low-density lipoprotein cholesterol (LDL-C)) goals (AOR: 2.23, 95% CI 1.30 to 3.83). Conversely, those at an urban PCU were more likely to undergo albuminuria exams. Variables significantly associated with good glycaemic control included age (AOR: 1.51, 95% CI 1.31 to 1.79), T2DM duration (AOR: 0.59, 95% CI 0.41 to 0.88), FAACE (foot, HbA<sub>1c</sub>, albuminuria, LDL-C and eye) goals (AOR: 1.23, 95% CI 1.12 to 1.36) and All8Q (AOR: 1.20, 95% CI 1.05 to 1.41). Chronic kidney disease (CKD) was significantly linked with high triglyceride and HbA<sub>1c</sub> levels (AOR: 5.23, 95% CI 1.21 to 7.61). Elevated HbA<sub>1c</sub> levels, longer T2DM duration, insulin use, high systolic BP and high lipid profile levels correlated strongly with diabetic retinopathy (DR) and CKD progression.</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: This highlights the necessity for targeted interventions to bridge urban-suburban care gaps, optimise drug prescriptions and implement comprehensive care strategies for improved glycaemic control, DR prevention and CKD progression mitigation among in Thai patients with T2DM. The value of the clinical target aggregate (ABC) and the process of care aggregate (FAACE) was also conclusively demonstrated.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702083/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702083</a> | DOI:<a href=https://doi.org/10.1136/bmjopen-2023-079415>10.1136/bmjopen-2023-079415</a></p></div>]]></content:encoded>
  420.      <guid isPermaLink="false">pubmed:38702083</guid>
  421.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  422.      <dc:creator>Apinya Surawit</dc:creator>
  423.      <dc:creator>Tanyaporn Pongkunakorn</dc:creator>
  424.      <dc:creator>Thamonwan Manosan</dc:creator>
  425.      <dc:creator>Pichanun Mongkolsucharitkul</dc:creator>
  426.      <dc:creator>Parinya Chamnan</dc:creator>
  427.      <dc:creator>Krishna Suvarnabhumi</dc:creator>
  428.      <dc:creator>Thanapat Puangpet</dc:creator>
  429.      <dc:creator>Sophida Suta</dc:creator>
  430.      <dc:creator>Sureeporn Pumeiam</dc:creator>
  431.      <dc:creator>Bonggochpass Pinsawas</dc:creator>
  432.      <dc:creator>Suphawan Ophakas</dc:creator>
  433.      <dc:creator>Sananon Pisitpornsuk</dc:creator>
  434.      <dc:creator>Chalita Utchin</dc:creator>
  435.      <dc:creator>Korapat Mayurasakorn</dc:creator>
  436.      <dc:date>2024-05-03</dc:date>
  437.      <dc:source>BMJ open</dc:source>
  438.      <dc:title>Factors influencing optimal diabetes care and clinical outcomes in Thai patients with type 2 diabetes mellitus: a multilevel modelling analysis</dc:title>
  439.      <dc:identifier>pmid:38702083</dc:identifier>
  440.      <dc:identifier>doi:10.1136/bmjopen-2023-079415</dc:identifier>
  441.    </item>
  442.    <item>
  443.      <title>Polymyxin B-induced Bartter syndrome</title>
  444.      <link>https://pubmed.ncbi.nlm.nih.gov/38702070/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  445.      <description>Bartter syndrome is a genetic disorder characterised by chloride-unresponsive metabolic alkalosis, hypokalaemia, hypomagnesaemia and hypercalciuria. While it commonly presents antenatally or in early infancy, sometimes, drugs can induce a state similar to Bartter syndrome in any age group, called acquired Bartter syndrome. Polymyxins and aminoglycosides are the most commonly implicated drugs. Polymyxin B and polymyxin E (popularly known as colistin) are the two chemically similar polymyxins that...</description>
  446.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMJ Case Rep. 2024 May 3;17(5):e255242. doi: 10.1136/bcr-2023-255242.</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">Bartter syndrome is a genetic disorder characterised by chloride-unresponsive metabolic alkalosis, hypokalaemia, hypomagnesaemia and hypercalciuria. While it commonly presents antenatally or in early infancy, sometimes, drugs can induce a state similar to Bartter syndrome in any age group, called acquired Bartter syndrome. Polymyxins and aminoglycosides are the most commonly implicated drugs. Polymyxin B and polymyxin E (popularly known as colistin) are the two chemically similar polymyxins that are commonly used clinically. While colistin is frequently associated with nephrotoxicity, polymyxin B is generally considered less nephrotoxic. This difference is due to the way these two drugs are handled by the kidneys. In this case report, we discuss a middle-aged male who developed Bartter syndrome due to polymyxin B, which resolved on discontinuation of the drug, and re-appeared after its re-introduction later. This case exemplifies the nephrotoxicity caused by polymyxin B and the need for vigilance when using this drug.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702070/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702070</a> | DOI:<a href=https://doi.org/10.1136/bcr-2023-255242>10.1136/bcr-2023-255242</a></p></div>]]></content:encoded>
  447.      <guid isPermaLink="false">pubmed:38702070</guid>
  448.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  449.      <dc:creator>Bhavesh Mohan Lal</dc:creator>
  450.      <dc:creator>Nimisha Musthafa Hafeesa</dc:creator>
  451.      <dc:creator>Naval Kishore Vikram</dc:creator>
  452.      <dc:creator>Animesh Ray</dc:creator>
  453.      <dc:date>2024-05-03</dc:date>
  454.      <dc:source>BMJ case reports</dc:source>
  455.      <dc:title>Polymyxin B-induced Bartter syndrome</dc:title>
  456.      <dc:identifier>pmid:38702070</dc:identifier>
  457.      <dc:identifier>doi:10.1136/bcr-2023-255242</dc:identifier>
  458.    </item>
  459.    <item>
  460.      <title>Association between gamma glutamyl transpeptidase to HDL-Cholesterol (GGT/HDL-C) ratio and metabolic syndrome resolution after sleeve gastrectomy</title>
  461.      <link>https://pubmed.ncbi.nlm.nih.gov/38702054/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  462.      <description>CONCLUSION: Eight out of 10 patients undergoing SG experience resolution of MetS within 6 months after surgery. Patients in the middle and lower tertiles of the GGT/HDL-C were more likely to achieve this outcome. Therefore, the GGT/HDL-C ratio should be considered a valuable and efficient biomarker for preoperative assessment of bariatric surgery candidates.</description>
  463.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Diab Vasc Dis Res. 2024 May-Jun;21(3):14791641241252553. doi: 10.1177/14791641241252553.</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: To evaluate the association between GGT/HDL-C ratio and resolution of MetS in adults after sleeve gastrectomy (SG).</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 a retrospective cohort study using secondary data from a Peruvian bariatric center. The study population consisted of adults aged 18 and above who underwent laparoscopic SG and were diagnosed with MetS prior to the surgery. The main outcome measured was MetS resolution 6 months post-surgery and the exposure variable was the GGT/HDL-C ratio.</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 137 patients with a mean age of 38.9 ± 10.9 years; 64.2% were females. The median GGT/HDL-C ratio was 1.1 [0.7 - 1.5], and 83.9% of patients experienced resolution of MetS. Furthermore, both the middle tertile of GGT/HDL-C (aRR: 1.28; 95% CI: 1.04 - 1.58; <i>p</i> = .019) and the lowest tertile (aRR: 1.27; 95% CI: 1.01 - 1.60; <i>p</i> = .038) showed a significant association with the resolution of MetS.</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: Eight out of 10 patients undergoing SG experience resolution of MetS within 6 months after surgery. Patients in the middle and lower tertiles of the GGT/HDL-C were more likely to achieve this outcome. Therefore, the GGT/HDL-C ratio should be considered a valuable and efficient biomarker for preoperative assessment of bariatric surgery candidates.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702054/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702054</a> | DOI:<a href=https://doi.org/10.1177/14791641241252553>10.1177/14791641241252553</a></p></div>]]></content:encoded>
  464.      <guid isPermaLink="false">pubmed:38702054</guid>
  465.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  466.      <dc:creator>Melanni L Lizarbe-Lezama</dc:creator>
  467.      <dc:creator>Jhoel E Rodriguez-Macedo</dc:creator>
  468.      <dc:creator>Daniel Fernandez-Guzman</dc:creator>
  469.      <dc:creator>Ana L Alcantara-Diaz</dc:creator>
  470.      <dc:creator>Gustavo Salinas-Sedo</dc:creator>
  471.      <dc:creator>Carlos J Toro-Huamanchumo</dc:creator>
  472.      <dc:date>2024-05-03</dc:date>
  473.      <dc:source>Diabetes &amp; vascular disease research</dc:source>
  474.      <dc:title>Association between gamma glutamyl transpeptidase to HDL-Cholesterol (GGT/HDL-C) ratio and metabolic syndrome resolution after sleeve gastrectomy</dc:title>
  475.      <dc:identifier>pmid:38702054</dc:identifier>
  476.      <dc:identifier>doi:10.1177/14791641241252553</dc:identifier>
  477.    </item>
  478.    <item>
  479.      <title>Impact of Annexin A2 on virus life cycles</title>
  480.      <link>https://pubmed.ncbi.nlm.nih.gov/38702018/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  481.      <description>Due to the limited size of viral genomes, hijacking host machinery by the viruses taking place throughout the virus life cycle is inevitable for the survival and proliferation of the virus in the infected hosts. Recent reports indicated that Annexin A2 (AnxA2), a calcium- and lipid-binding cellular protein, plays an important role as a critical regulator in various steps of the virus life cycle. The multifarious AnxA2 functions in cells, such as adhesion, adsorption, endocytosis, exocytosis,...</description>
  482.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Virus Res. 2024 May 1:199384. doi: 10.1016/j.virusres.2024.199384. 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">Due to the limited size of viral genomes, hijacking host machinery by the viruses taking place throughout the virus life cycle is inevitable for the survival and proliferation of the virus in the infected hosts. Recent reports indicated that Annexin A2 (AnxA2), a calcium- and lipid-binding cellular protein, plays an important role as a critical regulator in various steps of the virus life cycle. The multifarious AnxA2 functions in cells, such as adhesion, adsorption, endocytosis, exocytosis, cell proliferation and division, inflammation, cancer metastasis, angiogenesis, etc., are intimately related to the various clinical courses of viral infection. Ubiquitous expression of AnxA2 across multiple cell types indicates the broad range of susceptibility of diverse species of the virus to induce disparate viral disease in various tissues, and intracellular expression of AnxA2 in the cytoplasmic membrane, cytosol, and nucleus suggests the involvement of AnxA2 in the regulation of the different stages of various virus life cycles within host cells. However, it is yet unclear as to the molecular processes on how AnxA2 and the infected virus interplay to regulate virus life cycles and thereby the virus-associated disease courses, and hence elucidation of the molecular mechanisms on AnxA2-mediated virus life cycle will provide essential clues to develop therapeutics deterring viral disease.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702018/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702018</a> | DOI:<a href=https://doi.org/10.1016/j.virusres.2024.199384>10.1016/j.virusres.2024.199384</a></p></div>]]></content:encoded>
  483.      <guid isPermaLink="false">pubmed:38702018</guid>
  484.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  485.      <dc:creator>In-Woo Park</dc:creator>
  486.      <dc:creator>Hope K Fiadjoe</dc:creator>
  487.      <dc:creator>Pankaj Chaudhary</dc:creator>
  488.      <dc:date>2024-05-03</dc:date>
  489.      <dc:source>Virus research</dc:source>
  490.      <dc:title>Impact of Annexin A2 on virus life cycles</dc:title>
  491.      <dc:identifier>pmid:38702018</dc:identifier>
  492.      <dc:identifier>doi:10.1016/j.virusres.2024.199384</dc:identifier>
  493.    </item>
  494.    <item>
  495.      <title>DDX39B protects against sorafenib-induced ferroptosis by facilitating the splicing and cytoplasmic export of GPX4 pre-mRNA in hepatocellular carcinoma</title>
  496.      <link>https://pubmed.ncbi.nlm.nih.gov/38701867/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  497.      <description>Hepatocellular carcinoma (HCC) is the main histological subtype of primary liver cancer and remains one of the most common solid malignancies globally. Ferroptosis was recently defined as an iron-catalyzed form of regulated necrosis. Because cancer cells exhibit higher iron requirements than noncancer cells, treatment with ferroptosis-inducing compounds may be a feasible strategy for cancer therapy. However, cancer cells develop acquired resistance to evade ferroptosis, and the mechanisms...</description>
  498.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Biochem Pharmacol. 2024 May 1:116251. doi: 10.1016/j.bcp.2024.116251. 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">Hepatocellular carcinoma (HCC) is the main histological subtype of primary liver cancer and remains one of the most common solid malignancies globally. Ferroptosis was recently defined as an iron-catalyzed form of regulated necrosis. Because cancer cells exhibit higher iron requirements than noncancer cells, treatment with ferroptosis-inducing compounds may be a feasible strategy for cancer therapy. However, cancer cells develop acquired resistance to evade ferroptosis, and the mechanisms responsible for ferroptosis resistance are not fully clarified. In the current study, we reported that DDX39B was downregulated during sorafenib-induced ferroptosis in a dose- and time-dependent manner. Exogenous introduction of DDX39B ensured the survival of HCC cells upon exposure to sorafenib, while the opposite phenomenon was observed in DDX39B-silenced HCC cells. Mechanistically, we demonstrated that DDX39B increased GPX4 levels by promoting the splicing and cytoplasmic translocation of GPX4 pre-mRNA, which was sufficient to detoxify sorafenib-triggered excess lipid ROS production, lipid peroxidation accumulation, ferrous iron levels, and mitochondrial damage. Inhibition of DDX39B ATPase activity by CCT018159 repressed the splicing and cytoplasmic export of GPX4 pre-mRNA and synergistically assisted sorafenib-induced ferroptotic cell death in HCC cells. Taken together, our data uncover a novel role for DDX39B in ferroptosis resistance by modulating the maturation of GPX4 mRNA via a posttranscriptional approach and suggest that DDX39B inhibition may be a promising therapeutic strategy to enhance the sensitivity and vulnerability of HCC cells to sorafenib.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701867/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701867</a> | DOI:<a href=https://doi.org/10.1016/j.bcp.2024.116251>10.1016/j.bcp.2024.116251</a></p></div>]]></content:encoded>
  499.      <guid isPermaLink="false">pubmed:38701867</guid>
  500.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  501.      <dc:creator>Qin Li</dc:creator>
  502.      <dc:creator>Hang Yuan</dc:creator>
  503.      <dc:creator>Gang Zhao</dc:creator>
  504.      <dc:creator>Deqiong Ou</dc:creator>
  505.      <dc:creator>Jie Zhang</dc:creator>
  506.      <dc:creator>Liang Li</dc:creator>
  507.      <dc:creator>Siqi Li</dc:creator>
  508.      <dc:creator>Tianyu Feng</dc:creator>
  509.      <dc:creator>Rui Gu</dc:creator>
  510.      <dc:creator>Qiming Kou</dc:creator>
  511.      <dc:creator>Qijing Wang</dc:creator>
  512.      <dc:creator>Shan Li</dc:creator>
  513.      <dc:creator>Guanru Wang</dc:creator>
  514.      <dc:creator>Minghui Zhao</dc:creator>
  515.      <dc:creator>Huayang Yu</dc:creator>
  516.      <dc:creator>Jie Qu</dc:creator>
  517.      <dc:creator>Ping Lin</dc:creator>
  518.      <dc:creator>Kai Li</dc:creator>
  519.      <dc:date>2024-05-03</dc:date>
  520.      <dc:source>Biochemical pharmacology</dc:source>
  521.      <dc:title>DDX39B protects against sorafenib-induced ferroptosis by facilitating the splicing and cytoplasmic export of GPX4 pre-mRNA in hepatocellular carcinoma</dc:title>
  522.      <dc:identifier>pmid:38701867</dc:identifier>
  523.      <dc:identifier>doi:10.1016/j.bcp.2024.116251</dc:identifier>
  524.    </item>
  525.    <item>
  526.      <title>Statins in chronic liver disease: review of literature and future role</title>
  527.      <link>https://pubmed.ncbi.nlm.nih.gov/38701856/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  528.      <description>Chronic liver disease (CLD) is a major contributor to global mortality, morbidity, and healthcare burden. Progress in pharmacotherapeutic for CLD management is lagging given its impact on the global population. While statins are indicated for the management of dyslipidemia and cardiovascular disease, their role in CLD prevention and treatment is emerging. Beyond their lipid lowering effects, their liver-related mechanisms of action are multifactorial and include anti-inflammatory,...</description>
  529.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Semin Liver Dis. 2024 May 3. doi: 10.1055/a-2319-0694. 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">Chronic liver disease (CLD) is a major contributor to global mortality, morbidity, and healthcare burden. Progress in pharmacotherapeutic for CLD management is lagging given its impact on the global population. While statins are indicated for the management of dyslipidemia and cardiovascular disease, their role in CLD prevention and treatment is emerging. Beyond their lipid lowering effects, their liver-related mechanisms of action are multifactorial and include anti-inflammatory, anti-proliferative, and immune-protective effects. In this review, we highlight what is known about the clinical benefits of statins in viral and non-viral etiologies of CLD and HCC, and explore key mechanisms and pathways targeted by statins. While their benefits may span the spectrum of CLD and potentially HCC treatment, their role in CLD chemoprevention is likely to have the largest impact. As emerging data suggest that genetic variants may impact their benefits, the role of statins in precision hepatology will need to be further explored.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701856/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701856</a> | DOI:<a href=https://doi.org/10.1055/a-2319-0694>10.1055/a-2319-0694</a></p></div>]]></content:encoded>
  530.      <guid isPermaLink="false">pubmed:38701856</guid>
  531.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  532.      <dc:creator>Nguyen Pham</dc:creator>
  533.      <dc:creator>Jihane N Benhammou</dc:creator>
  534.      <dc:date>2024-05-03</dc:date>
  535.      <dc:source>Seminars in liver disease</dc:source>
  536.      <dc:title>Statins in chronic liver disease: review of literature and future role</dc:title>
  537.      <dc:identifier>pmid:38701856</dc:identifier>
  538.      <dc:identifier>doi:10.1055/a-2319-0694</dc:identifier>
  539.    </item>
  540.    <item>
  541.      <title>The mitochondrial multi-omic response to exercise training across rat tissues</title>
  542.      <link>https://pubmed.ncbi.nlm.nih.gov/38701776/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  543.      <description>Mitochondria have diverse functions critical to whole-body metabolic homeostasis. Endurance training alters mitochondrial activity, but systematic characterization of these adaptations is lacking. Here, the Molecular Transducers of Physical Activity Consortium mapped the temporal, multi-omic changes in mitochondrial analytes across 19 tissues in male and female rats trained for 1, 2, 4, or 8 weeks. Training elicited substantial changes in the adrenal gland, brown adipose, colon, heart, and...</description>
  544.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Metab. 2024 Apr 15:S1550-4131(23)00472-2. doi: 10.1016/j.cmet.2023.12.021. 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">Mitochondria have diverse functions critical to whole-body metabolic homeostasis. Endurance training alters mitochondrial activity, but systematic characterization of these adaptations is lacking. Here, the Molecular Transducers of Physical Activity Consortium mapped the temporal, multi-omic changes in mitochondrial analytes across 19 tissues in male and female rats trained for 1, 2, 4, or 8 weeks. Training elicited substantial changes in the adrenal gland, brown adipose, colon, heart, and skeletal muscle. The colon showed non-linear response dynamics, whereas mitochondrial pathways were downregulated in brown adipose and adrenal tissues. Protein acetylation increased in the liver, with a shift in lipid metabolism, whereas oxidative proteins increased in striated muscles. Exercise-upregulated networks were downregulated in human diabetes and cirrhosis. Knockdown of the central network protein 17-beta-hydroxysteroid dehydrogenase 10 (HSD17B10) elevated oxygen consumption, indicative of metabolic stress. We provide a multi-omic, multi-tissue, temporal atlas of the mitochondrial response to exercise training and identify candidates linked to mitochondrial dysfunction.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701776/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701776</a> | DOI:<a href=https://doi.org/10.1016/j.cmet.2023.12.021>10.1016/j.cmet.2023.12.021</a></p></div>]]></content:encoded>
  545.      <guid isPermaLink="false">pubmed:38701776</guid>
  546.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  547.      <dc:creator>David Amar</dc:creator>
  548.      <dc:creator>Nicole R Gay</dc:creator>
  549.      <dc:creator>David Jimenez-Morales</dc:creator>
  550.      <dc:creator>Pierre M Jean Beltran</dc:creator>
  551.      <dc:creator>Megan E Ramaker</dc:creator>
  552.      <dc:creator>Archana Natarajan Raja</dc:creator>
  553.      <dc:creator>Bingqing Zhao</dc:creator>
  554.      <dc:creator>Yifei Sun</dc:creator>
  555.      <dc:creator>Shruti Marwaha</dc:creator>
  556.      <dc:creator>David A Gaul</dc:creator>
  557.      <dc:creator>Steven G Hershman</dc:creator>
  558.      <dc:creator>Alexis Ferrasse</dc:creator>
  559.      <dc:creator>Ashley Xia</dc:creator>
  560.      <dc:creator>Ian Lanza</dc:creator>
  561.      <dc:creator>Facundo M Fernández</dc:creator>
  562.      <dc:creator>Stephen B Montgomery</dc:creator>
  563.      <dc:creator>Andrea L Hevener</dc:creator>
  564.      <dc:creator>Euan A Ashley</dc:creator>
  565.      <dc:creator>Martin J Walsh</dc:creator>
  566.      <dc:creator>Lauren M Sparks</dc:creator>
  567.      <dc:creator>Charles F Burant</dc:creator>
  568.      <dc:creator>R Scott Rector</dc:creator>
  569.      <dc:creator>John Thyfault</dc:creator>
  570.      <dc:creator>Matthew T Wheeler</dc:creator>
  571.      <dc:creator>Bret H Goodpaster</dc:creator>
  572.      <dc:creator>Paul M Coen</dc:creator>
  573.      <dc:creator>Simon Schenk</dc:creator>
  574.      <dc:creator>Sue C Bodine</dc:creator>
  575.      <dc:creator>Malene E Lindholm</dc:creator>
  576.      <dc:creator>MoTrPAC Study Group</dc:creator>
  577.      <dc:date>2024-05-03</dc:date>
  578.      <dc:source>Cell metabolism</dc:source>
  579.      <dc:title>The mitochondrial multi-omic response to exercise training across rat tissues</dc:title>
  580.      <dc:identifier>pmid:38701776</dc:identifier>
  581.      <dc:identifier>doi:10.1016/j.cmet.2023.12.021</dc:identifier>
  582.    </item>
  583.    <item>
  584.      <title>The tether function of the anoctamins</title>
  585.      <link>https://pubmed.ncbi.nlm.nih.gov/38701708/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  586.      <description>The core functions of the anoctamins are Cl^(-) channel activity and phosphatidylserine (and perhaps other lipids) scrambling. These functions have been extensively studied in various tissues and cells. However, another function of the anoctamins that is less recognized and minimally explored is as tethers at membrane contact sites. This short review aims to examine evidence supporting the localization of the anoctamins at membrane contact sites, their tether properties, and their functions as...</description>
  587.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Calcium. 2024 Apr 20;121:102875. doi: 10.1016/j.ceca.2024.102875. 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">The core functions of the anoctamins are Cl<sup>-</sup> channel activity and phosphatidylserine (and perhaps other lipids) scrambling. These functions have been extensively studied in various tissues and cells. However, another function of the anoctamins that is less recognized and minimally explored is as tethers at membrane contact sites. This short review aims to examine evidence supporting the localization of the anoctamins at membrane contact sites, their tether properties, and their functions as tethers.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701708/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701708</a> | DOI:<a href=https://doi.org/10.1016/j.ceca.2024.102875>10.1016/j.ceca.2024.102875</a></p></div>]]></content:encoded>
  588.      <guid isPermaLink="false">pubmed:38701708</guid>
  589.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  590.      <dc:creator>Wei-Yin Lin</dc:creator>
  591.      <dc:creator>Woo Young Chung</dc:creator>
  592.      <dc:creator>Shmuel Muallem</dc:creator>
  593.      <dc:date>2024-05-03</dc:date>
  594.      <dc:source>Cell calcium</dc:source>
  595.      <dc:title>The tether function of the anoctamins</dc:title>
  596.      <dc:identifier>pmid:38701708</dc:identifier>
  597.      <dc:identifier>doi:10.1016/j.ceca.2024.102875</dc:identifier>
  598.    </item>
  599.    <item>
  600.      <title>Enhancing high-density microalgae cultivation via exogenous supplementation of biostimulant derived from onion peel waste for sustainable biodiesel production</title>
  601.      <link>https://pubmed.ncbi.nlm.nih.gov/38701587/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  602.      <description>Microalgae demonstrate significant potential as a source of liquid-based biofuels. However, increasing biomass productivity in existing cultivation systems is a critical prerequisite for their successful integration into large-scale operations. Thus, the current work aimed to accelerate the growth of C. vulgaris via exogenous supplementation of biostimulant derived from onion peel waste. Under the optimal growth conditions, which entailed a biostimulant dosage of 37.5% v/v, a pH of 3, an air...</description>
  603.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Environ Manage. 2024 May 2;359:120988. doi: 10.1016/j.jenvman.2024.120988. 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">Microalgae demonstrate significant potential as a source of liquid-based biofuels. However, increasing biomass productivity in existing cultivation systems is a critical prerequisite for their successful integration into large-scale operations. Thus, the current work aimed to accelerate the growth of C. vulgaris via exogenous supplementation of biostimulant derived from onion peel waste. Under the optimal growth conditions, which entailed a biostimulant dosage of 37.5% v/v, a pH of 3, an air flow rate of 0.4 L/min, and a 2% v/v inoculum harvested during the mid-log phase, yielded a maximum biomass concentration of 1.865 g/L. Under the arbitrarily optimized parameters, a comparable growth pattern was evident in the upscaled cultivation of C. vulgaris, underscoring the potential commercial viability of the biostimulant. The biostimulant, characterized through gas chromatography-mass spectrometry (GC-MS) analysis, revealed a composition rich in polyphenolic and organo-sulphur compounds, notably including allyl trisulfide (28.13%), methyl allyl trisulfide (23.04%), and allyl disulfide (20.78%), showcasing potent antioxidant properties. Additionally, microalgae treated with the biostimulant consistently retained their lipid content at 18.44% without any significant reduction. Furthermore, a significant rise in saturated fatty acid (SFA) content was observed, with C16:0 and C18:1 dominating both bench-scale (44.08% and 14.01%) and upscaled (51.12% and 13.07%) microalgae cultures, in contrast to the control group where C18:2 was prevalent. Consequently, SFA contents reached 54.35% and 65.43% in bench-scale and upscaled samples respectively, compared to 33.73% in the control culture. These compositional characteristics align well with the requirements for producing high-quality crude biodiesel.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701587/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701587</a> | DOI:<a href=https://doi.org/10.1016/j.jenvman.2024.120988>10.1016/j.jenvman.2024.120988</a></p></div>]]></content:encoded>
  604.      <guid isPermaLink="false">pubmed:38701587</guid>
  605.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  606.      <dc:creator>Uganeeswary Suparmaniam</dc:creator>
  607.      <dc:creator>Man Kee Lam</dc:creator>
  608.      <dc:creator>Jun Wei Lim</dc:creator>
  609.      <dc:creator>Hemamalini Rawindran</dc:creator>
  610.      <dc:creator>Yeek Chia Ho</dc:creator>
  611.      <dc:creator>Inn Shi Tan</dc:creator>
  612.      <dc:creator>Jibrail Kansedo</dc:creator>
  613.      <dc:creator>Steven Lim</dc:creator>
  614.      <dc:creator>Yoke Wang Cheng</dc:creator>
  615.      <dc:creator>Salman Raza Naqvi</dc:creator>
  616.      <dc:date>2024-05-03</dc:date>
  617.      <dc:source>Journal of environmental management</dc:source>
  618.      <dc:title>Enhancing high-density microalgae cultivation via exogenous supplementation of biostimulant derived from onion peel waste for sustainable biodiesel production</dc:title>
  619.      <dc:identifier>pmid:38701587</dc:identifier>
  620.      <dc:identifier>doi:10.1016/j.jenvman.2024.120988</dc:identifier>
  621.    </item>
  622.    <item>
  623.      <title>A comparative study on the protective effects of cuminaldehyde, thymoquinone, and gallic acid against carbon tetrachloride-induced pulmonary and renal toxicity in rats by affecting ROS and NF-κB signaling</title>
  624.      <link>https://pubmed.ncbi.nlm.nih.gov/38701569/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  625.      <description>CCl(4) toxicity is a fatal condition that can cause numerous organ dysfunctions. We evaluated and compared the protective effects of cuminaldehyde (CuA), thymoquinone (TQ), and gallic acid (GA) on CCl(4)-induced pulmonary and renal toxicity in rats. The impacts of these compounds on CCl(4)-induced oxidative stress, inflammation, and morphological alterations were examined. The results showed that the compounds under investigation prevented CCl(4) from significantly increasing pulmonary and renal...</description>
  626.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Biomed Pharmacother. 2024 May 2;175:116692. doi: 10.1016/j.biopha.2024.116692. 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">CCl<sub>4</sub> toxicity is a fatal condition that can cause numerous organ dysfunctions. We evaluated and compared the protective effects of cuminaldehyde (CuA), thymoquinone (TQ), and gallic acid (GA) on CCl<sub>4</sub>-induced pulmonary and renal toxicity in rats. The impacts of these compounds on CCl<sub>4</sub>-induced oxidative stress, inflammation, and morphological alterations were examined. The results showed that the compounds under investigation prevented CCl<sub>4</sub> from significantly increasing pulmonary and renal lipid peroxidation and NO levels, as well as massively depleting GSH levels and GPX and SOD activities. Moreover, they suppressed the CCl<sub>4</sub>-induced increase in mucus secretion in the lung and upregulated the gene expression of pulmonary and renal NF-ҡB, iNOS, TNF-α, and COX-2. The heatmap cluster plots showed that GA and TQ had better protective potencies than CuA. The external organ morphology, histopathological results, and chest X-ray analysis confirmed the toxicity of CCl<sub>4</sub> and the protective influences of the tested compounds in both the lungs and kidneys of rats. These compounds displayed predicted competitive inhibitory effects on iNOS activity and may block the IL-13α2 receptor, as revealed by molecular docking analysis. Thus, CuA, TQ, and GA, particularly the latter two, are prospective protective compounds against the pulmonary and renal toxicity caused by CCl<sub>4</sub>.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701569/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701569</a> | DOI:<a href=https://doi.org/10.1016/j.biopha.2024.116692>10.1016/j.biopha.2024.116692</a></p></div>]]></content:encoded>
  627.      <guid isPermaLink="false">pubmed:38701569</guid>
  628.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  629.      <dc:creator>Nadia Z Shaban</dc:creator>
  630.      <dc:creator>Lamiaa A El Swify</dc:creator>
  631.      <dc:creator>Marwa M Abu-Serie</dc:creator>
  632.      <dc:creator>Adham M Maher</dc:creator>
  633.      <dc:creator>Noha H Habashy</dc:creator>
  634.      <dc:date>2024-05-03</dc:date>
  635.      <dc:source>Biomedicine &amp; pharmacotherapy = Biomedecine &amp; pharmacotherapie</dc:source>
  636.      <dc:title>A comparative study on the protective effects of cuminaldehyde, thymoquinone, and gallic acid against carbon tetrachloride-induced pulmonary and renal toxicity in rats by affecting ROS and NF-κB signaling</dc:title>
  637.      <dc:identifier>pmid:38701569</dc:identifier>
  638.      <dc:identifier>doi:10.1016/j.biopha.2024.116692</dc:identifier>
  639.    </item>
  640.    <item>
  641.      <title>Exploring in vivo combinatorial chemo-immunotherapy: Addressing p97 suppression and immune reinvigoration in pancreatic cancer with tumor microenvironment-responsive nanoformulation</title>
  642.      <link>https://pubmed.ncbi.nlm.nih.gov/38701563/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  643.      <description>Pancreatic ductal adenocarcinoma (PDAC) has an extremely devastating nature with poor prognosis and increasing incidence, making it a formidable challenge in the global fight against cancer-related mortality. In this innovative preclinical investigation, the VCP/p97 inhibitor CB-5083 (CB), miR-142, a PD-L1 inhibitor, and immunoadjuvant resiquimod (R848; R) were synergistically encapsulated in solid lipid nanoparticles (SLNs). These SLNs demonstrated features of peptides targeting PD-L1, EGFR,...</description>
  644.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Biomed Pharmacother. 2024 May 2;175:116660. doi: 10.1016/j.biopha.2024.116660. 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">Pancreatic ductal adenocarcinoma (PDAC) has an extremely devastating nature with poor prognosis and increasing incidence, making it a formidable challenge in the global fight against cancer-related mortality. In this innovative preclinical investigation, the VCP/p97 inhibitor CB-5083 (CB), miR-142, a PD-L1 inhibitor, and immunoadjuvant resiquimod (R848; R) were synergistically encapsulated in solid lipid nanoparticles (SLNs). These SLNs demonstrated features of peptides targeting PD-L1, EGFR, and the endoplasmic reticulum, enclosed in a pH-responsive polyglutamic (PGA)-polyethylene glycol (PEG) shell. The homogeneous size and zeta potential of the nanoparticles were stable for 28 days at 4°C. The study substantiated the concurrent modulation of key pathways by the CB, miR, and R-loaded nanoformulation, prominently affecting VCP/Bip/ATF6, PD-L1/TGF-β/IL-4, -8, -10, and TNF-α/IFN-γ/IL-1, -12/GM-CSF/CCL4 pathways. This adaptable nanoformulation induced durable antitumor immune responses and inhibited Panc-02 tumor growth by enhancing T cell infiltration, dendritic cell maturation, and suppressing Tregs and TAMs in mice bearing Panc-02 tumors. Furthermore, tissue distribution studies, biochemical assays, and histological examinations highlighted enhanced safety with PGA and peptide-modified nanoformulations for CB, miR, and/or R in Panc-02-bearing mice. This versatile nanoformulation allows tailored adjustment of the tumor microenvironment, thereby optimizing the localized delivery of combined therapy. These compelling findings advocate the potential development of a pH-sensitive, three-in-one PGA-PEG nanoformulation that combines a VCP inhibitor, a PD-L1 inhibitor, and an immunoadjuvant for cancer treatment via combinatorial chemo-immunotherapy.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701563/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701563</a> | DOI:<a href=https://doi.org/10.1016/j.biopha.2024.116660>10.1016/j.biopha.2024.116660</a></p></div>]]></content:encoded>
  645.      <guid isPermaLink="false">pubmed:38701563</guid>
  646.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  647.      <dc:creator>Yu-Li Lo</dc:creator>
  648.      <dc:creator>Ching-Yao Li</dc:creator>
  649.      <dc:creator>Tsui-Fen Chou</dc:creator>
  650.      <dc:creator>Ching-Ping Yang</dc:creator>
  651.      <dc:creator>Li-Ling Wu</dc:creator>
  652.      <dc:creator>Chun-Jung Chen</dc:creator>
  653.      <dc:creator>Yih-Hsin Chang</dc:creator>
  654.      <dc:date>2024-05-03</dc:date>
  655.      <dc:source>Biomedicine &amp; pharmacotherapy = Biomedecine &amp; pharmacotherapie</dc:source>
  656.      <dc:title>Exploring in vivo combinatorial chemo-immunotherapy: Addressing p97 suppression and immune reinvigoration in pancreatic cancer with tumor microenvironment-responsive nanoformulation</dc:title>
  657.      <dc:identifier>pmid:38701563</dc:identifier>
  658.      <dc:identifier>doi:10.1016/j.biopha.2024.116660</dc:identifier>
  659.    </item>
  660.    <item>
  661.      <title>Fatty acid composition and biophysical characteristics of the cell membrane of feline spermatozoa</title>
  662.      <link>https://pubmed.ncbi.nlm.nih.gov/38702489/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  663.      <description>Sperm membrane composition and biophysical characteristics play a pivotal role in many physiological processes (i.e. sperm motility, capacitation, acrosome reaction and fusion with the oocyte) as well as in semen processing (e.g. cryopreservation). The aim of this study was to characterize the fatty acid content and biophysical characteristics (anisotropy, generalized polarization) of the cell membrane of domestic cat spermatozoa. Semen was collected from 34 adult male cats by urethral...</description>
  664.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Sci Rep. 2024 May 3;14(1):10214. doi: 10.1038/s41598-024-61006-5.</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">Sperm membrane composition and biophysical characteristics play a pivotal role in many physiological processes (i.e. sperm motility, capacitation, acrosome reaction and fusion with the oocyte) as well as in semen processing (e.g. cryopreservation). The aim of this study was to characterize the fatty acid content and biophysical characteristics (anisotropy, generalized polarization) of the cell membrane of domestic cat spermatozoa. Semen was collected from 34 adult male cats by urethral catheterization. After a basic semen evaluation, the fatty acid content of some of the samples (n = 11) was evaluated by gas chromatography. Samples from other individuals (n = 23) were subjected to biophysical analysis: membrane anisotropy (which is inversely proportional to membrane fluidity) and generalized polarization (describing lipid order); both measured by fluorimetry at three temperature points: 38 °C, 25 °C and 5 °C. Spermatozoa from some samples (n = 10) were cryopreserved in TRIS egg yolk-glycerol extender and underwent the same biophysical analysis after thawing. Most fatty acids in feline spermatozoa were saturated (69.76 ± 24.45%), whereas the polyunsaturated fatty acid (PUFA) content was relatively low (6.12 ± 5.80%). Lowering the temperature caused a significant decrease in membrane fluidity and an increase in generalized polarization in fresh spermatozoa, and these effects were even more pronounced following cryopreservation. Anisotropy at 38 °C in fresh samples showed strong positive correlations with viability and motility parameters after thawing. In summary, feline spermatozoa are characterized by a very low PUFA content and a low ratio of unsaturated:saturated fatty acids, which may contribute to low oxidative stress. Cryopreservation alters the structure of the sperm membrane, increasing the fluidity of the hydrophobic portion of the bilayer and the lipid order in the hydrophilic portion. Because lower membrane fluidity in fresh semen was linked with better viability and motility after cryopreservation, this parameter may be considered an important factor in determination of sperm cryoresistance.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702489/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702489</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-61006-5>10.1038/s41598-024-61006-5</a></p></div>]]></content:encoded>
  665.      <guid isPermaLink="false">pubmed:38702489</guid>
  666.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  667.      <dc:creator>Sylwia Prochowska</dc:creator>
  668.      <dc:creator>Dorota Bonarska-Kujawa</dc:creator>
  669.      <dc:creator>Łukasz Bobak</dc:creator>
  670.      <dc:creator>Maria Eberhardt</dc:creator>
  671.      <dc:creator>Wojciech Niżański</dc:creator>
  672.      <dc:date>2024-05-03</dc:date>
  673.      <dc:source>Scientific reports</dc:source>
  674.      <dc:title>Fatty acid composition and biophysical characteristics of the cell membrane of feline spermatozoa</dc:title>
  675.      <dc:identifier>pmid:38702489</dc:identifier>
  676.      <dc:identifier>doi:10.1038/s41598-024-61006-5</dc:identifier>
  677.    </item>
  678.    <item>
  679.      <title>Evaluation of lipid nanoparticles for safe and efficient RNA delivery during pregnancy</title>
  680.      <link>https://pubmed.ncbi.nlm.nih.gov/38702459/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  681.      <description>No abstract</description>
  682.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Lab Anim (NY). 2024 May;53(5):112. doi: 10.1038/s41684-024-01374-7.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702459/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702459</a> | DOI:<a href=https://doi.org/10.1038/s41684-024-01374-7>10.1038/s41684-024-01374-7</a></p></div>]]></content:encoded>
  683.      <guid isPermaLink="false">pubmed:38702459</guid>
  684.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  685.      <dc:creator>Alexandra Le Bras</dc:creator>
  686.      <dc:date>2024-05-03</dc:date>
  687.      <dc:source>Lab animal</dc:source>
  688.      <dc:title>Evaluation of lipid nanoparticles for safe and efficient RNA delivery during pregnancy</dc:title>
  689.      <dc:identifier>pmid:38702459</dc:identifier>
  690.      <dc:identifier>doi:10.1038/s41684-024-01374-7</dc:identifier>
  691.    </item>
  692.    <item>
  693.      <title>Acetate reprogrammes tumour metabolism and promotes PD-L1 expression and immune evasion by upregulating c-Myc</title>
  694.      <link>https://pubmed.ncbi.nlm.nih.gov/38702440/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  695.      <description>Acetate, a precursor of acetyl-CoA, is instrumental in energy production, lipid synthesis and protein acetylation. However, whether acetate reprogrammes tumour metabolism and plays a role in tumour immune evasion remains unclear. Here, we show that acetate is the most abundant short-chain fatty acid in human non-small cell lung cancer tissues, with increased tumour-enriched acetate uptake. Acetate-derived acetyl-CoA induces c-Myc acetylation, which is mediated by the moonlighting function of the...</description>
  696.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Nat Metab. 2024 May 3. doi: 10.1038/s42255-024-01037-4. 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">Acetate, a precursor of acetyl-CoA, is instrumental in energy production, lipid synthesis and protein acetylation. However, whether acetate reprogrammes tumour metabolism and plays a role in tumour immune evasion remains unclear. Here, we show that acetate is the most abundant short-chain fatty acid in human non-small cell lung cancer tissues, with increased tumour-enriched acetate uptake. Acetate-derived acetyl-CoA induces c-Myc acetylation, which is mediated by the moonlighting function of the metabolic enzyme dihydrolipoamide S-acetyltransferase. Acetylated c-Myc increases its stability and subsequent transcription of the genes encoding programmed death-ligand 1, glycolytic enzymes, monocarboxylate transporter 1 and cell cycle accelerators. Dietary acetate supplementation promotes tumour growth and inhibits CD8<sup>+</sup> T cell infiltration, whereas disruption of acetate uptake inhibits immune evasion, which increases the efficacy of anti-PD-1-based therapy. These findings highlight a critical role of acetate promoting tumour growth beyond its metabolic role as a carbon source by reprogramming tumour metabolism and immune evasion, and underscore the potential of controlling acetate metabolism to curb tumour growth and improve the response to immune checkpoint blockade therapy.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702440/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702440</a> | DOI:<a href=https://doi.org/10.1038/s42255-024-01037-4>10.1038/s42255-024-01037-4</a></p></div>]]></content:encoded>
  697.      <guid isPermaLink="false">pubmed:38702440</guid>
  698.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  699.      <dc:creator>Juhong Wang</dc:creator>
  700.      <dc:creator>Yannan Yang</dc:creator>
  701.      <dc:creator>Fei Shao</dc:creator>
  702.      <dc:creator>Ying Meng</dc:creator>
  703.      <dc:creator>Dong Guo</dc:creator>
  704.      <dc:creator>Jie He</dc:creator>
  705.      <dc:creator>Zhimin Lu</dc:creator>
  706.      <dc:date>2024-05-03</dc:date>
  707.      <dc:source>Nature metabolism</dc:source>
  708.      <dc:title>Acetate reprogrammes tumour metabolism and promotes PD-L1 expression and immune evasion by upregulating c-Myc</dc:title>
  709.      <dc:identifier>pmid:38702440</dc:identifier>
  710.      <dc:identifier>doi:10.1038/s42255-024-01037-4</dc:identifier>
  711.    </item>
  712.    <item>
  713.      <title>Multiwaves, breathers, lump and other solutions for the Heimburg model in biomembranes and nerves</title>
  714.      <link>https://pubmed.ncbi.nlm.nih.gov/38702384/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  715.      <description>In this manuscript, a mathematical model known as the Heimburg model is investigated analytically to get the soliton solutions. Both biomembranes and nerves can be studied using this model. The cell membrane's lipid bilayer is regarded by the model as a substance that experiences phase transitions. It implies that the membrane responds to electrical disruptions in a nonlinear way. The importance of ionic conductance in nerve impulse propagation is shown by Heimburg's model. The dynamics of the...</description>
  716.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Sci Rep. 2024 May 3;14(1):10180. doi: 10.1038/s41598-024-60689-0.</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">In this manuscript, a mathematical model known as the Heimburg model is investigated analytically to get the soliton solutions. Both biomembranes and nerves can be studied using this model. The cell membrane's lipid bilayer is regarded by the model as a substance that experiences phase transitions. It implies that the membrane responds to electrical disruptions in a nonlinear way. The importance of ionic conductance in nerve impulse propagation is shown by Heimburg's model. The dynamics of the electromechanical pulse in a nerve are analytically investigated using the Hirota Bilinear method. The various types of solitons are investigates, such as homoclinic breather waves, interaction via double exponents, lump waves, multi-wave, mixed type solutions, and periodic cross kink solutions. The electromechanical pulse's ensuing three-dimensional and contour shapes offer crucial insight into how nerves function and may one day be used in medicine and the biological sciences. Our grasp of soliton dynamics is improved by this research, which also opens up new directions for biomedical investigation and medical developments. A few 3D and contour profiles have also been created for new solutions, and interaction behaviors have also been shown.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702384/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702384</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-60689-0>10.1038/s41598-024-60689-0</a></p></div>]]></content:encoded>
  717.      <guid isPermaLink="false">pubmed:38702384</guid>
  718.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  719.      <dc:creator>Dilber Uzun Ozsahin</dc:creator>
  720.      <dc:creator>Baboucarr Ceesay</dc:creator>
  721.      <dc:creator>Muhammad Zafarullah Baber</dc:creator>
  722.      <dc:creator>Nauman Ahmed</dc:creator>
  723.      <dc:creator>Ali Raza</dc:creator>
  724.      <dc:creator>Muhammad Rafiq</dc:creator>
  725.      <dc:creator>Hijaz Ahmad</dc:creator>
  726.      <dc:creator>Fuad A Awwad</dc:creator>
  727.      <dc:creator>Emad A A Ismail</dc:creator>
  728.      <dc:date>2024-05-03</dc:date>
  729.      <dc:source>Scientific reports</dc:source>
  730.      <dc:title>Multiwaves, breathers, lump and other solutions for the Heimburg model in biomembranes and nerves</dc:title>
  731.      <dc:identifier>pmid:38702384</dc:identifier>
  732.      <dc:identifier>doi:10.1038/s41598-024-60689-0</dc:identifier>
  733.    </item>
  734.    <item>
  735.      <title>Decellularised plant scaffolds facilitate porcine skeletal muscle tissue engineering for cultivated meat biomanufacturing</title>
  736.      <link>https://pubmed.ncbi.nlm.nih.gov/38702314/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  737.      <description>Cultivated meat (CM) offers a sustainable and ethical alternative to conventional animal agriculture, involving cell maturation in a controlled environment. To emulate the structural complexity of traditional meat, the development of animal-free and edible scaffolds is crucial, providing vital physical and biological support during tissue development. The aligned vascular bundles of the decellularised asparagus scaffold were selected to facilitate the attachment and alignment of murine myoblasts...</description>
  738.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">NPJ Sci Food. 2024 May 3;8(1):25. doi: 10.1038/s41538-024-00262-1.</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">Cultivated meat (CM) offers a sustainable and ethical alternative to conventional animal agriculture, involving cell maturation in a controlled environment. To emulate the structural complexity of traditional meat, the development of animal-free and edible scaffolds is crucial, providing vital physical and biological support during tissue development. The aligned vascular bundles of the decellularised asparagus scaffold were selected to facilitate the attachment and alignment of murine myoblasts (C2C12) and porcine adipose-derived mesenchymal stem cells (pADMSCs). Muscle differentiation was assessed through immunofluorescence staining with muscle markers, including Myosin heavy chain (MHC), Myogenin (MYOG), and Desmin. The metabolic activity of Creatine Kinase in C2C12 differentiated cells significantly increased compared to proliferated cells. Quantitative PCR analysis revealed a significant increase in Myosin Heavy Polypeptide 1 (MYH1) and MYOG expression compared to Day 0. These results highlight the application of decellularised plant scaffold (DPS) as a promising, edible material conducive to cell attachment, proliferation, and differentiation into muscle tissue. To create a CM prototype with biological mimicry, pADMSC-derived muscle and fat cells were also co-cultured on the same scaffold. The co-culture was confirmed through immunofluorescence staining of muscle markers and LipidTOX staining, revealing distinct muscle fibres and adipocytes containing lipid droplets respectively. Texture profile analysis conducted on uncooked CM prototypes and pork loin showed no significant differences in textural values. However, the pan-fried CM prototype differed significantly in hardness and chewiness compared to pork loin. Understanding the scaffolds' textural profile enhances our insight into the potential sensory attributes of CM products. DPS shows potential for advancing CM biomanufacturing.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702314/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702314</a> | DOI:<a href=https://doi.org/10.1038/s41538-024-00262-1>10.1038/s41538-024-00262-1</a></p></div>]]></content:encoded>
  739.      <guid isPermaLink="false">pubmed:38702314</guid>
  740.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  741.      <dc:creator>Priyatharshini Murugan</dc:creator>
  742.      <dc:creator>Wee Swan Yap</dc:creator>
  743.      <dc:creator>Hariharan Ezhilarasu</dc:creator>
  744.      <dc:creator>Ratima Suntornnond</dc:creator>
  745.      <dc:creator>Quang Bach Le</dc:creator>
  746.      <dc:creator>Satnam Singh</dc:creator>
  747.      <dc:creator>Jasmine Si Han Seah</dc:creator>
  748.      <dc:creator>Pei Leng Tan</dc:creator>
  749.      <dc:creator>Weibiao Zhou</dc:creator>
  750.      <dc:creator>Lay Poh Tan</dc:creator>
  751.      <dc:creator>Deepak Choudhury</dc:creator>
  752.      <dc:date>2024-05-03</dc:date>
  753.      <dc:source>NPJ science of food</dc:source>
  754.      <dc:title>Decellularised plant scaffolds facilitate porcine skeletal muscle tissue engineering for cultivated meat biomanufacturing</dc:title>
  755.      <dc:identifier>pmid:38702314</dc:identifier>
  756.      <dc:identifier>doi:10.1038/s41538-024-00262-1</dc:identifier>
  757.    </item>
  758.    <item>
  759.      <title>MIER2/PGC1A elicits sunitinib resistance via lipid metabolism in renal cell carcinoma</title>
  760.      <link>https://pubmed.ncbi.nlm.nih.gov/38702028/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  761.      <description>CONCLUSION: Our findings highlight MIER2 as a key player in anchoring HDAC1 and inhibiting PGC1A expression through the deacetylation of P53, thereby inducing lipid accumulation in RCC and promoting drug resistance. Lipid-rich RCC cells compensate for energy production and sustain their own growth in a glycolysis-independent manner, evading the cytotoxic effects of targeted drugs and ultimately culminating in the development of drug resistance.</description>
  762.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Adv Res. 2024 May 1:S2090-1232(24)00177-2. doi: 10.1016/j.jare.2024.04.032. 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: Renal cell carcinoma (RCC) is one of the most common malignant tumors of the urinary system and accounts for more than 90 % of all renal tumors. Resistance to targeted therapy has emerged as a pivotal factor that contributes to the progressive deterioration of patients with advanced RCC. Metabolic reprogramming is a hallmark of tumorigenesis and progression, with an increasing body of evidence indicating that abnormal lipid metabolism plays a crucial role in the advancement of renal clear cell carcinoma.</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: Clarify the precise mechanisms underlying abnormal lipid metabolism and drug resistance.</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: Bioinformatics screening and analyses were performed to identify hub gene. qRT-PCR, western blot, chromatin immunoprecipitation (ChIP) assays, and other biological methods were used to explore and verify related pathways. Various cell line models and animal models were used to perform biological functional experiments.</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, we identified Mesoderm induction early response 2 (MIER2) as a novel biomarker for RCC, demonstrating its role in promoting malignancy and sunitinib resistance by influencing lipid metabolism in RCC. Mechanistically, MIER2 facilitated P53 deacetylation by binding to HDAC1. Acetylation modification augmented the stability and transcriptional function of P53, while deacetylation of P53 hindered the transcriptional process of PGC1A, leading to intracellular lipid accumulation in RCC. Furthermore, Trichostatin A (TSA), an inhibitor of HDAC1, was found to impede the MIER2/HDAC1/P53/PGC1A pathway, offering potential benefits for patients with sunitinib-resistant renal cell cancer.</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 findings highlight MIER2 as a key player in anchoring HDAC1 and inhibiting PGC1A expression through the deacetylation of P53, thereby inducing lipid accumulation in RCC and promoting drug resistance. Lipid-rich RCC cells compensate for energy production and sustain their own growth in a glycolysis-independent manner, evading the cytotoxic effects of targeted drugs and ultimately culminating in the development of drug resistance.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702028/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702028</a> | DOI:<a href=https://doi.org/10.1016/j.jare.2024.04.032>10.1016/j.jare.2024.04.032</a></p></div>]]></content:encoded>
  763.      <guid isPermaLink="false">pubmed:38702028</guid>
  764.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  765.      <dc:creator>Zhihao Wei</dc:creator>
  766.      <dc:creator>Yuzhong Ye</dc:creator>
  767.      <dc:creator>Chenchen Liu</dc:creator>
  768.      <dc:creator>Qi Wang</dc:creator>
  769.      <dc:creator>Yunxuan Zhang</dc:creator>
  770.      <dc:creator>Kailei Chen</dc:creator>
  771.      <dc:creator>Gong Cheng</dc:creator>
  772.      <dc:creator>Xiaoping Zhang</dc:creator>
  773.      <dc:date>2024-05-03</dc:date>
  774.      <dc:source>Journal of advanced research</dc:source>
  775.      <dc:title>MIER2/PGC1A elicits sunitinib resistance via lipid metabolism in renal cell carcinoma</dc:title>
  776.      <dc:identifier>pmid:38702028</dc:identifier>
  777.      <dc:identifier>doi:10.1016/j.jare.2024.04.032</dc:identifier>
  778.    </item>
  779.    <item>
  780.      <title>Cetyltrimethylammonium-chloride assisted in situ metabolic incorporation of nano-sized ROS-generating cascade-reaction containers in Gram-positive and Gram-negative peptidoglycan layers for the control of bacterially-induced sepsis</title>
  781.      <link>https://pubmed.ncbi.nlm.nih.gov/38702010/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  782.      <description>Cascade-reaction containers generating reactive oxygen species (ROS) as an alternative for antibiotic-based strategies for bacterial infection control, require endogenous oxygen-sources and ROS-generation close to or preferably inside target bacteria. Here, this is achieved by cetyltrimethylammonium-chloride (CTAC) assisted in situ metabolic labeling and incorporation of mesoporous SiO(2)-nanoparticles, dual-loaded with glucose-oxidase and Fe(3)O(4)-nanoparticles as cascade-reaction containers,...</description>
  783.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Acta Biomater. 2024 May 1:S1742-7061(24)00228-9. doi: 10.1016/j.actbio.2024.04.045. 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">Cascade-reaction containers generating reactive oxygen species (ROS) as an alternative for antibiotic-based strategies for bacterial infection control, require endogenous oxygen-sources and ROS-generation close to or preferably inside target bacteria. Here, this is achieved by cetyltrimethylammonium-chloride (CTAC) assisted in situ metabolic labeling and incorporation of mesoporous SiO<sub>2</sub>-nanoparticles, dual-loaded with glucose-oxidase and Fe<sub>3</sub>O<sub>4</sub>-nanoparticles as cascade-reaction containers, inside bacterial cell walls. First, azide-functionalized D-alanine (D-Ala-N<sub>3</sub>) was inserted in cell wall peptidoglycan layers of growing Gram-positive pathogens. In Gram-negatives, this could only be achieved after outer lipid-membrane permeabilization, using a low concentration of CTAC. Low concentrations of CTAC had no adverse effect on in vitro blood clotting or hemolysis nor on the health of mice when blood-injected. Next, dibenzocyclooctyne-polyethylene-glycol modified, SiO<sub>2</sub>-nanoparticles were in situ click-reacted with D-Ala-N<sub>3</sub> in bacterial cell wall peptidoglycan layers. Herewith, a two-step cascade-reaction is facilitated inside bacteria, in which glucose-oxidase generates H<sub>2</sub>O<sub>2</sub> at endogenously-available glucose concentrations, while subsequently Fe<sub>3</sub>O<sub>4</sub>-nanoparticles catalyze generation of •OH from the H<sub>2</sub>O<sub>2</sub> generated. Generation of •OH inside bacterial cell walls by dual-loaded mesoporous SiO<sub>2</sub>-nanoparticles yielded more effective in vitro killing of both planktonic Gram-positive and Gram-negative bacteria suspended in 10% plasma than SiO<sub>2</sub>-nanoparticles solely loaded with glucose-oxidase. Gram-positive or Gram-negative bacterially induced sepsis in mice could be effectively treated by in situ pre-treatment with tail-vein injected CTAC and D-Ala-N<sub>3</sub>, followed by injection of dual-loaded cascade-reaction containers without using antibiotics. This makes in situ metabolic incorporation of cascade-reaction containers as described attractive for further investigation with respect to the control of other types of infections comprising planktonic bacteria. STATEMENT OF SIGNIFICANCE: In situ metabolic-incorporation of cascade-reaction-containers loaded with glucose-oxidase and Fe<sub>3</sub>O<sub>4</sub> nanoparticles into bacterial cell-wall peptidoglycan is described, yielding ROS-generation from endogenous glucose, non-antibiotically killing bacteria before ROS inactivates. Hitherto, only Gram-positives could be metabolically-labeled, because Gram-negatives possess two lipid-membranes. The outer membrane impedes direct access to the peptidoglycan. This problem was solved by outer-membrane permeabilization using a quaternary-ammonium compound. Several studies on metabolic-labeling perform crucial labeling steps during bacterial-culturing that in real-life should be part of a treatment. In situ metabolic-incorporation as described, can be applied in well-plates during in vitro experiments or in the body as during in vivo animal experiments. Surprisingly, metabolic-incorporation proceeded unhampered in blood and a murine, bacterially-induced sepsis could be well treated.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702010/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702010</a> | DOI:<a href=https://doi.org/10.1016/j.actbio.2024.04.045>10.1016/j.actbio.2024.04.045</a></p></div>]]></content:encoded>
  784.      <guid isPermaLink="false">pubmed:38702010</guid>
  785.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  786.      <dc:creator>Guang Yang</dc:creator>
  787.      <dc:creator>Da-Yuan Wang</dc:creator>
  788.      <dc:creator>Jianwen Song</dc:creator>
  789.      <dc:creator>Yijin Ren</dc:creator>
  790.      <dc:creator>Yingli An</dc:creator>
  791.      <dc:creator>Henk J Busscher</dc:creator>
  792.      <dc:creator>Henny C van der Mei</dc:creator>
  793.      <dc:creator>Linqi Shi</dc:creator>
  794.      <dc:date>2024-05-03</dc:date>
  795.      <dc:source>Acta biomaterialia</dc:source>
  796.      <dc:title>Cetyltrimethylammonium-chloride assisted in situ metabolic incorporation of nano-sized ROS-generating cascade-reaction containers in Gram-positive and Gram-negative peptidoglycan layers for the control of bacterially-induced sepsis</dc:title>
  797.      <dc:identifier>pmid:38702010</dc:identifier>
  798.      <dc:identifier>doi:10.1016/j.actbio.2024.04.045</dc:identifier>
  799.    </item>
  800.    <item>
  801.      <title>Macromolecules with predominant β-pleated sheet proteins in extracellular vesicles released from Raphanus sativus L. var. caudatus Alef microgreens induce DNA damage-mediated apoptosis in HCT116 colon cancer cells</title>
  802.      <link>https://pubmed.ncbi.nlm.nih.gov/38702007/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  803.      <description>Plant-derived bioactive macromolecules (i.e., proteins, lipids, and nucleic acids) were prepared as extracellular vesicles (EVs). Plant-derived EVs are gaining pharmaceutical research interest because of their bioactive components and delivery properties. The spherical nanosized EVs derived from Raphanus sativus L. var. caudatus Alef microgreens previously showed antiproliferative activity in HCT116 colon cancer cells from macromolecular compositions (predominantly proteins). To understand the...</description>
  804.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Int J Biol Macromol. 2024 May 1:132001. doi: 10.1016/j.ijbiomac.2024.132001. 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">Plant-derived bioactive macromolecules (i.e., proteins, lipids, and nucleic acids) were prepared as extracellular vesicles (EVs). Plant-derived EVs are gaining pharmaceutical research interest because of their bioactive components and delivery properties. The spherical nanosized EVs derived from Raphanus sativus L. var. caudatus Alef microgreens previously showed antiproliferative activity in HCT116 colon cancer cells from macromolecular compositions (predominantly proteins). To understand the mechanism of action, the biological activity studies, i.e., antiproliferation, cellular biochemical changes, DNA conformational changes, DNA damage, apoptotic nuclear morphological changes, apoptosis induction, and apoptotic pathways, were determined by neutral red uptake assay, synchrotron radiation-based Fourier transform infrared microspectroscopy, circular dichroism spectroscopy, comet assay, 4',6-diamidino-2-phenylindole (DAPI) staining, flow cytometry, and caspase activity assay, respectively. EVs inhibited HCT116 cell growth in concentration- and time-dependent manners, with a half-maximal inhibitory concentration of 675.4 ± 33.8 μg/ml at 48 h and a selectivity index of 1.5 ± 0.076. HCT116 treated with EVs mainly changed the cellular biochemical compositions in the nucleic acids and carbohydrates region. The DNA damage caused no changes in DNA conformation. The apoptotic nuclear morphological changes were associated with the increased apoptotic cell population. The apoptotic cell death was induced by both extrinsic and intrinsic pathways. EVs have potential as antiproliferative bioparticles.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702007/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702007</a> | DOI:<a href=https://doi.org/10.1016/j.ijbiomac.2024.132001>10.1016/j.ijbiomac.2024.132001</a></p></div>]]></content:encoded>
  805.      <guid isPermaLink="false">pubmed:38702007</guid>
  806.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  807.      <dc:creator>Karnchanok Kaimuangpak</dc:creator>
  808.      <dc:creator>Reny Rosalina</dc:creator>
  809.      <dc:creator>Kanjana Thumanu</dc:creator>
  810.      <dc:creator>Natthida Weerapreeyakul</dc:creator>
  811.      <dc:date>2024-05-03</dc:date>
  812.      <dc:source>International journal of biological macromolecules</dc:source>
  813.      <dc:title>Macromolecules with predominant β-pleated sheet proteins in extracellular vesicles released from Raphanus sativus L. var. caudatus Alef microgreens induce DNA damage-mediated apoptosis in HCT116 colon cancer cells</dc:title>
  814.      <dc:identifier>pmid:38702007</dc:identifier>
  815.      <dc:identifier>doi:10.1016/j.ijbiomac.2024.132001</dc:identifier>
  816.    </item>
  817.    <item>
  818.      <title>Anhydroparthenin as a dual-target inhibitor against Sterol C-24 methyltransferase and Sterol 14-α demethylase of Leishmania donovani: A comprehensive in vitro and in silico study</title>
  819.      <link>https://pubmed.ncbi.nlm.nih.gov/38702006/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  820.      <description>Parthenium hysterophorus plant has a diverse chemical profile and immense bioactive potential. It exhibits excellent pharmacological properties such as anti-cancer, anti-inflammatory, anti-malarial, microbicidal, and anti-trypanosomal. The present study aims to evaluate the anti-leishmanial potential and toxicological safety of anhydroparthenin isolated from P. hysterophorus. Anydroparthenin was extracted from the leaves of P. hysterophorus and characterized through detailed analysis of ¹H,...</description>
  821.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Int J Biol Macromol. 2024 May 1:132034. doi: 10.1016/j.ijbiomac.2024.132034. 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">Parthenium hysterophorus plant has a diverse chemical profile and immense bioactive potential. It exhibits excellent pharmacological properties such as anti-cancer, anti-inflammatory, anti-malarial, microbicidal, and anti-trypanosomal. The present study aims to evaluate the anti-leishmanial potential and toxicological safety of anhydroparthenin isolated from P. hysterophorus. Anydroparthenin was extracted from the leaves of P. hysterophorus and characterized through detailed analysis of <sup>1</sup>H, <sup>13</sup>C NMR, and HRMS. Dye-based in vitro and ex vivo assays confirmed that anhydroparthenin significantly inhibited both promastigote and amastigote forms of the Leishmania donovani parasites. Both the cytotoxicity experiment and hemolytic assay revealed its non-toxic nature and safety index in the range of 10 to 15. Further, various mechanistic assays suggested that anhydroparthenin led to the generation of oxidative stress, intracellular ATP depletion, alterations in morphology and mitochondrial membrane potential, formation of intracellular lipid bodies, and acidic vesicles, ultimately leading to parasite death. As a dual targeting approach, computational studies and sterol quantification assays confirmed that anhydroparthenin inhibits the Sterol C-24 methyl transferase and Sterol 14-α demethylase proteins involved in the ergosterol biosynthesis in Leishmania parasites. These results suggest that anhydroparthenin could be a promising anti-leishmanial molecule and can be developed as a novel therapeutic stratagem against leishmaniasis.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38702006/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38702006</a> | DOI:<a href=https://doi.org/10.1016/j.ijbiomac.2024.132034>10.1016/j.ijbiomac.2024.132034</a></p></div>]]></content:encoded>
  822.      <guid isPermaLink="false">pubmed:38702006</guid>
  823.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  824.      <dc:creator>Diksha Kumari</dc:creator>
  825.      <dc:creator>Parampreet Kour</dc:creator>
  826.      <dc:creator>Chetan Paul Singh</dc:creator>
  827.      <dc:creator>Rinku Choudhary</dc:creator>
  828.      <dc:creator>Syed Mudassir Ali</dc:creator>
  829.      <dc:creator>Sagar Bhayye</dc:creator>
  830.      <dc:creator>Yogesh P Bharitkar</dc:creator>
  831.      <dc:creator>Kuljit Singh</dc:creator>
  832.      <dc:date>2024-05-03</dc:date>
  833.      <dc:source>International journal of biological macromolecules</dc:source>
  834.      <dc:title>Anhydroparthenin as a dual-target inhibitor against Sterol C-24 methyltransferase and Sterol 14-α demethylase of Leishmania donovani: A comprehensive in vitro and in silico study</dc:title>
  835.      <dc:identifier>pmid:38702006</dc:identifier>
  836.      <dc:identifier>doi:10.1016/j.ijbiomac.2024.132034</dc:identifier>
  837.    </item>
  838.    <item>
  839.      <title>Predicting PFAS fate in fish: Assessing the roles of dietary, respiratory, and dermal uptake in bioaccumulation modeling</title>
  840.      <link>https://pubmed.ncbi.nlm.nih.gov/38701889/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  841.      <description>An increasing number of per- and polyfluoroalkyl substances (PFAS) exposed to the environment may pose a threat to organisms and human beings. However, there is a lack of simulations comprehensively addressing and comparing the bioaccumulation of PFAS across all three major exposure routes (oral, inhalation, and dermal), especially for dermal uptake. In this study, we proposed a physiologically based kinetic (PBK) model for PFAS, aiming to predict bioaccumulation factors (BAF) in fish by...</description>
  842.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Environ Res. 2024 May 1:119036. doi: 10.1016/j.envres.2024.119036. 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">An increasing number of per- and polyfluoroalkyl substances (PFAS) exposed to the environment may pose a threat to organisms and human beings. However, there is a lack of simulations comprehensively addressing and comparing the bioaccumulation of PFAS across all three major exposure routes (oral, inhalation, and dermal), especially for dermal uptake. In this study, we proposed a physiologically based kinetic (PBK) model for PFAS, aiming to predict bioaccumulation factors (BAF) in fish by considering these diverse exposure routes. 15 PFAS were used for model validation, and 11 PFAS from Taihu Lake were used for exposure contribution modeling. Approximately 64% of estimations fell within 10-fold model bias from measurements in Taihu Lake, underscoring the potential efficacy of the developed PBK model in predicting BAFs for fish. The dermal route emerges as a contributor to short-chain PFAS exposure. For example, it ranged widely from 46% to 75% (mean) for all modeling short-chain PFAS (C6-C7) in Taihu Lake. It indicated the criticality of considering dermal exposure for PFAS in fish, highlighting a gap in field studies to unravel cutaneous intake mechanisms and contributions. For longer carbon chains of PFAS (C8-C12), dermal exposure accounted for 2%-27% for all species of aquatic organisms. The fish's lipid fraction and water content played a significant role in the contribution of PFAS intake through cutaneous exposure and inhalation. had a significant positive correlation with skin intake rate (p&lt;0.05) and gill intake rate (p&lt;0.001), while having a significant negative correlation with skin intake (p&lt;0.05) and skin intake contribution (p&lt;0.001). Based on the proposed modeling approach, we have introduced a simulation spreadsheet for projecting PFAS BAFs in fish tissues, hopefully broadening the predictive operational tool for a variety of chemical species.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701889/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701889</a> | DOI:<a href=https://doi.org/10.1016/j.envres.2024.119036>10.1016/j.envres.2024.119036</a></p></div>]]></content:encoded>
  843.      <guid isPermaLink="false">pubmed:38701889</guid>
  844.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  845.      <dc:creator>Jie Xiong</dc:creator>
  846.      <dc:creator>Zijian Li</dc:creator>
  847.      <dc:date>2024-05-03</dc:date>
  848.      <dc:source>Environmental research</dc:source>
  849.      <dc:title>Predicting PFAS fate in fish: Assessing the roles of dietary, respiratory, and dermal uptake in bioaccumulation modeling</dc:title>
  850.      <dc:identifier>pmid:38701889</dc:identifier>
  851.      <dc:identifier>doi:10.1016/j.envres.2024.119036</dc:identifier>
  852.    </item>
  853.    <item>
  854.      <title>Cell selective BCL-2 inhibition enabled by lipid nanoparticles alleviates lung fibrosis</title>
  855.      <link>https://pubmed.ncbi.nlm.nih.gov/38701884/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  856.      <description>Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease with a high mortality rate due to limited treatment options. Current therapies cannot effectively reverse the damage caused by IPF. Research suggests that promoting programmed cell death (apoptosis) in myofibroblasts, the key cells driving fibrosis, could be a promising strategy. However, inducing apoptosis in healthy cells like epithelial and endothelial cells can cause unwanted side effects. This project addresses this challenge...</description>
  857.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Control Release. 2024 May 1:S0168-3659(24)00284-0. doi: 10.1016/j.jconrel.2024.04.055. 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">Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease with a high mortality rate due to limited treatment options. Current therapies cannot effectively reverse the damage caused by IPF. Research suggests that promoting programmed cell death (apoptosis) in myofibroblasts, the key cells driving fibrosis, could be a promising strategy. However, inducing apoptosis in healthy cells like epithelial and endothelial cells can cause unwanted side effects. This project addresses this challenge by developing a targeted approach to induce apoptosis specifically in myofibroblasts. We designed liposomes (LPS) decorated with peptides that recognize VCAM-1, a protein highly expressed on myofibroblasts in fibrotic lungs. These VCAM1-targeted LPS encapsulate Venetoclax (VNT), a small molecule drug that inhibits BCL-2, an anti-apoptotic protein. By delivering VNT directly to myofibroblasts, we hypothesize that VCAM1-VNT-LPS can selectively induce apoptosis in these cells, leading to reduced fibrosis and improved lung function. We successfully characterized VCAM1-VNT-LPS for size, surface charge, and drug loading efficiency. Additionally, we evaluated their stability over three months at different temperatures. In vitro and in vivo studies using a bleomycin-induced mouse model of lung fibrosis demonstrated the therapeutic potential of VCAM1-VNT-LPS. These studies showed a reduction in fibrosis-associated proteins (collagen, α-SMA, VCAM1) and BCL-2, while simultaneously increasing apoptosis in myofibroblasts. These findings suggest that VCAM1-targeted delivery of BCL-2 inhibitors using liposomes presents a promising and potentially selective therapeutic approach for IPF.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701884/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701884</a> | DOI:<a href=https://doi.org/10.1016/j.jconrel.2024.04.055>10.1016/j.jconrel.2024.04.055</a></p></div>]]></content:encoded>
  858.      <guid isPermaLink="false">pubmed:38701884</guid>
  859.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  860.      <dc:creator>Rimpy Diwan</dc:creator>
  861.      <dc:creator>Himanshu N Bhatt</dc:creator>
  862.      <dc:creator>Rui Dong</dc:creator>
  863.      <dc:creator>Igor L Estevao</dc:creator>
  864.      <dc:creator>Armando Varela-Ramirez</dc:creator>
  865.      <dc:creator>Md Nurunnabi</dc:creator>
  866.      <dc:date>2024-05-03</dc:date>
  867.      <dc:source>Journal of controlled release : official journal of the Controlled Release Society</dc:source>
  868.      <dc:title>Cell selective BCL-2 inhibition enabled by lipid nanoparticles alleviates lung fibrosis</dc:title>
  869.      <dc:identifier>pmid:38701884</dc:identifier>
  870.      <dc:identifier>doi:10.1016/j.jconrel.2024.04.055</dc:identifier>
  871.    </item>
  872.    <item>
  873.      <title>Small-molecule-induced epigenetic rejuvenation promotes SREBP condensation and overcomes barriers to CNS myelin regeneration</title>
  874.      <link>https://pubmed.ncbi.nlm.nih.gov/38701782/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  875.      <description>Remyelination failure in diseases like multiple sclerosis (MS) was thought to involve suppressed maturation of oligodendrocyte precursors; however, oligodendrocytes are present in MS lesions yet lack myelin production. We found that oligodendrocytes in the lesions are epigenetically silenced. Developing a transgenic reporter labeling differentiated oligodendrocytes for phenotypic screening, we identified a small-molecule epigenetic-silencing-inhibitor (ESI1) that enhances myelin production and...</description>
  876.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell. 2024 Apr 25:S0092-8674(24)00400-8. doi: 10.1016/j.cell.2024.04.005. 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">Remyelination failure in diseases like multiple sclerosis (MS) was thought to involve suppressed maturation of oligodendrocyte precursors; however, oligodendrocytes are present in MS lesions yet lack myelin production. We found that oligodendrocytes in the lesions are epigenetically silenced. Developing a transgenic reporter labeling differentiated oligodendrocytes for phenotypic screening, we identified a small-molecule epigenetic-silencing-inhibitor (ESI1) that enhances myelin production and ensheathment. ESI1 promotes remyelination in animal models of demyelination and enables de novo myelinogenesis on regenerated CNS axons. ESI1 treatment lengthened myelin sheaths in human iPSC-derived organoids and augmented (re)myelination in aged mice while reversing age-related cognitive decline. Multi-omics revealed that ESI1 induces an active chromatin landscape that activates myelinogenic pathways and reprograms metabolism. Notably, ESI1 triggered nuclear condensate formation of master lipid-metabolic regulators SREBP1/2, concentrating transcriptional co-activators to drive lipid/cholesterol biosynthesis. Our study highlights the potential of targeting epigenetic silencing to enable CNS myelin regeneration in demyelinating diseases and aging.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701782/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701782</a> | DOI:<a href=https://doi.org/10.1016/j.cell.2024.04.005>10.1016/j.cell.2024.04.005</a></p></div>]]></content:encoded>
  877.      <guid isPermaLink="false">pubmed:38701782</guid>
  878.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  879.      <dc:creator>Xuezhao Liu</dc:creator>
  880.      <dc:creator>Dazhuan Eric Xin</dc:creator>
  881.      <dc:creator>Xiaowen Zhong</dc:creator>
  882.      <dc:creator>Chuntao Zhao</dc:creator>
  883.      <dc:creator>Zhidan Li</dc:creator>
  884.      <dc:creator>Liguo Zhang</dc:creator>
  885.      <dc:creator>Adam J Dourson</dc:creator>
  886.      <dc:creator>Lindsay Lee</dc:creator>
  887.      <dc:creator>Shreya Mishra</dc:creator>
  888.      <dc:creator>Arman E Bayat</dc:creator>
  889.      <dc:creator>Eva Nicholson</dc:creator>
  890.      <dc:creator>William L Seibel</dc:creator>
  891.      <dc:creator>Bingfang Yan</dc:creator>
  892.      <dc:creator>Joel Mason</dc:creator>
  893.      <dc:creator>Bradley J Turner</dc:creator>
  894.      <dc:creator>David G Gonsalvez</dc:creator>
  895.      <dc:creator>William Ong</dc:creator>
  896.      <dc:creator>Sing Yian Chew</dc:creator>
  897.      <dc:creator>Balaram Ghosh</dc:creator>
  898.      <dc:creator>Sung Ok Yoon</dc:creator>
  899.      <dc:creator>Mei Xin</dc:creator>
  900.      <dc:creator>Zhigang He</dc:creator>
  901.      <dc:creator>Jason Tchieu</dc:creator>
  902.      <dc:creator>Michael Wegner</dc:creator>
  903.      <dc:creator>Klaus-Armin Nave</dc:creator>
  904.      <dc:creator>Robin J M Franklin</dc:creator>
  905.      <dc:creator>Ranjan Dutta</dc:creator>
  906.      <dc:creator>Bruce D Trapp</dc:creator>
  907.      <dc:creator>Ming Hu</dc:creator>
  908.      <dc:creator>Matthew A Smith</dc:creator>
  909.      <dc:creator>Michael P Jankowski</dc:creator>
  910.      <dc:creator>Samantha K Barton</dc:creator>
  911.      <dc:creator>Xuelian He</dc:creator>
  912.      <dc:creator>Q Richard Lu</dc:creator>
  913.      <dc:date>2024-05-03</dc:date>
  914.      <dc:source>Cell</dc:source>
  915.      <dc:title>Small-molecule-induced epigenetic rejuvenation promotes SREBP condensation and overcomes barriers to CNS myelin regeneration</dc:title>
  916.      <dc:identifier>pmid:38701782</dc:identifier>
  917.      <dc:identifier>doi:10.1016/j.cell.2024.04.005</dc:identifier>
  918.    </item>
  919.    <item>
  920.      <title>Emerging ferroptosis inhibitors as a novel therapeutic strategy for the treatment of neonatal hypoxic-ischemic encephalopathy</title>
  921.      <link>https://pubmed.ncbi.nlm.nih.gov/38701713/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  922.      <description>Neonatal hypoxia-ischemia encephalopathy (NHIE), an oxygen deprivation-mediated brain injury due to birth asphyxia or reduced cerebral blood perfusion, often leads to lifelong sequelae, including seizures, cerebral palsy, and mental retardation. NHIE poses a significant health challenge, as one of the leading causes of neonatal morbidity and mortality globally. Despite this, available therapies are limited. Numerous studies have recently demonstrated that ferroptosis, an iron-dependent...</description>
  923.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Eur J Med Chem. 2024 Apr 26;271:116453. doi: 10.1016/j.ejmech.2024.116453. 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">Neonatal hypoxia-ischemia encephalopathy (NHIE), an oxygen deprivation-mediated brain injury due to birth asphyxia or reduced cerebral blood perfusion, often leads to lifelong sequelae, including seizures, cerebral palsy, and mental retardation. NHIE poses a significant health challenge, as one of the leading causes of neonatal morbidity and mortality globally. Despite this, available therapies are limited. Numerous studies have recently demonstrated that ferroptosis, an iron-dependent non-apoptotic regulated form of cell death characterized by lipid peroxidation (LPO) and iron dyshomeostasis, plays a role in the genesis of NHIE. Moreover, recently discovered compounds have been shown to exert potential therapeutic effects on NHIE by inhibiting ferroptosis. This comprehensive review summarizes the fundamental mechanisms of ferroptosis contributing to NHIE. We focus on various emerging therapeutic compounds exhibiting characteristics of ferroptosis inhibition and delineate their pharmacological benefits for the treatment of NHIE. This review suggests that pharmacological inhibition of ferroptosis may be a potential therapeutic strategy for NHIE.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701713/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701713</a> | DOI:<a href=https://doi.org/10.1016/j.ejmech.2024.116453>10.1016/j.ejmech.2024.116453</a></p></div>]]></content:encoded>
  924.      <guid isPermaLink="false">pubmed:38701713</guid>
  925.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  926.      <dc:creator>Liang Huo</dc:creator>
  927.      <dc:creator>Jianhua Fu</dc:creator>
  928.      <dc:creator>Shimeng Wang</dc:creator>
  929.      <dc:creator>Hua Wang</dc:creator>
  930.      <dc:creator>Xueyan Liu</dc:creator>
  931.      <dc:date>2024-05-03</dc:date>
  932.      <dc:source>European journal of medicinal chemistry</dc:source>
  933.      <dc:title>Emerging ferroptosis inhibitors as a novel therapeutic strategy for the treatment of neonatal hypoxic-ischemic encephalopathy</dc:title>
  934.      <dc:identifier>pmid:38701713</dc:identifier>
  935.      <dc:identifier>doi:10.1016/j.ejmech.2024.116453</dc:identifier>
  936.    </item>
  937.    <item>
  938.      <title>Cadmium phytoremediation potential of Houttuynia cordata: Insights from growth, uptake, and rhizosphere mechanisms</title>
  939.      <link>https://pubmed.ncbi.nlm.nih.gov/38701655/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  940.      <description>Cadmium (Cd) pollutes 7.0 % of China's land area. This study examined the potential of Houttuynia cordata for Cd phytoremediation because of its ability to accumulate Cd in its growth matrix. H. cordata were planted in plastic pots filled with paddy field soils having low (LCd), medium (MCd), and high (HCd) Cd levels of 0.19, 0.69, and 2.91 mg/kg, respectively. After six months of growth, harvested plant parts were evaluated for Cd uptake and tolerance mechanisms. Metabolomics and metagenomics...</description>
  941.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Ecotoxicol Environ Saf. 2024 May 2;278:116417. doi: 10.1016/j.ecoenv.2024.116417. 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">Cadmium (Cd) pollutes 7.0 % of China's land area. This study examined the potential of Houttuynia cordata for Cd phytoremediation because of its ability to accumulate Cd in its growth matrix. H. cordata were planted in plastic pots filled with paddy field soils having low (LCd), medium (MCd), and high (HCd) Cd levels of 0.19, 0.69, and 2.91 mg/kg, respectively. After six months of growth, harvested plant parts were evaluated for Cd uptake and tolerance mechanisms. Metabolomics and metagenomics approaches were employed to investigate the soil rhizosphere mechanism. Results showed that the average plant biomass increased as soil Cd increased. The biomass Cd contents surpassed the allowable Cd limits for food (≤ 0.2 mg/kg) and medicinal uses (≤ 0.3 mg/kg). Cd contents were higher in H. cordata roots (30.59-86.27 mg/kg) than in other plant parts (0.63-2.90 mg/kg), with significantly increasing values as Cd soil level increased. Phenolic acids, lipids, amino acids and derivatives, organic acids, and alkaloids comprised the majority (69 in MCd vs HCd and 73 % in LCd vs HCd) of the shared upregulated metabolites. In addition, 13 metabolites specific to H. cordata root exudates were significantly increased. The top two principal metabolic pathways were arginine and proline metabolism, and beta-alanine metabolism. H. cordata increased the abundance of Firmicutes and Glomeromycota across all three Cd levels, and also stimulated the growth of Patescibacteria, Rozellomycota, and Claroideoglomus in HCd. Accordingly, H. cordata demonstrated potential for remediation of Cd-contaminated soils, and safety measures for its production and food use must be highly considered.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701655/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701655</a> | DOI:<a href=https://doi.org/10.1016/j.ecoenv.2024.116417>10.1016/j.ecoenv.2024.116417</a></p></div>]]></content:encoded>
  942.      <guid isPermaLink="false">pubmed:38701655</guid>
  943.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  944.      <dc:creator>QingQing Zhang</dc:creator>
  945.      <dc:creator>Cheng'Ai Jiang</dc:creator>
  946.      <dc:creator>LuoYan Jiang</dc:creator>
  947.      <dc:creator>RongLiang Qiu</dc:creator>
  948.      <dc:creator>ZeBin Wei</dc:creator>
  949.      <dc:creator>QiTang Wu</dc:creator>
  950.      <dc:date>2024-05-03</dc:date>
  951.      <dc:source>Ecotoxicology and environmental safety</dc:source>
  952.      <dc:title>Cadmium phytoremediation potential of Houttuynia cordata: Insights from growth, uptake, and rhizosphere mechanisms</dc:title>
  953.      <dc:identifier>pmid:38701655</dc:identifier>
  954.      <dc:identifier>doi:10.1016/j.ecoenv.2024.116417</dc:identifier>
  955.    </item>
  956.    <item>
  957.      <title>A Current Understanding of FXR in NAFLD: The multifaceted regulatory role of FXR and novel lead discovery for drug development</title>
  958.      <link>https://pubmed.ncbi.nlm.nih.gov/38701562/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  959.      <description>The global prevalence of nonalcoholic fatty liver disease (NAFLD) has reached 30 %, with an annual increase. The incidence of NAFLD-induced cirrhosis is rapidly rising and has become the leading indicator for liver transplantation in the US. However, there are currently no US Food and Drug Administration-approved drugs for NAFLD. Increasing evidence underscores the close association between NAFLD and bile acid metabolism disorder, highlighting the feasibility of targeting the bile acid signaling...</description>
  960.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Biomed Pharmacother. 2024 May 2;175:116658. doi: 10.1016/j.biopha.2024.116658. 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">The global prevalence of nonalcoholic fatty liver disease (NAFLD) has reached 30 %, with an annual increase. The incidence of NAFLD-induced cirrhosis is rapidly rising and has become the leading indicator for liver transplantation in the US. However, there are currently no US Food and Drug Administration-approved drugs for NAFLD. Increasing evidence underscores the close association between NAFLD and bile acid metabolism disorder, highlighting the feasibility of targeting the bile acid signaling pathway for NAFLD treatment. The farnesoid X receptor (FXR) is an endogenous receptor for bile acids that exhibits favorable effects in ameliorating the metabolic imbalance of bile acids, lipid disorders, and disruption of intestinal homeostasis, all of which are key characteristics of NAFLD, making FXR a promising therapeutic target for NAFLD. The present review provides a comprehensive overview of the diverse mechanisms through which FXR improves NAFLD, with particular emphasis on its involvement in regulating bile acid homeostasis and the recent advancements in drug development targeting FXR for NAFLD treatment.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701562/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701562</a> | DOI:<a href=https://doi.org/10.1016/j.biopha.2024.116658>10.1016/j.biopha.2024.116658</a></p></div>]]></content:encoded>
  961.      <guid isPermaLink="false">pubmed:38701562</guid>
  962.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  963.      <dc:creator>Yuhong Tang</dc:creator>
  964.      <dc:creator>Yujuan Fan</dc:creator>
  965.      <dc:creator>Yiming Wang</dc:creator>
  966.      <dc:creator>Dong Wang</dc:creator>
  967.      <dc:creator>Qingyu Huang</dc:creator>
  968.      <dc:creator>Tongqing Chen</dc:creator>
  969.      <dc:creator>Xinyue Cao</dc:creator>
  970.      <dc:creator>Cailing Wen</dc:creator>
  971.      <dc:creator>Xiaoyan Shen</dc:creator>
  972.      <dc:creator>Jian Li</dc:creator>
  973.      <dc:creator>Yan You</dc:creator>
  974.      <dc:date>2024-05-03</dc:date>
  975.      <dc:source>Biomedicine &amp; pharmacotherapy = Biomedecine &amp; pharmacotherapie</dc:source>
  976.      <dc:title>A Current Understanding of FXR in NAFLD: The multifaceted regulatory role of FXR and novel lead discovery for drug development</dc:title>
  977.      <dc:identifier>pmid:38701562</dc:identifier>
  978.      <dc:identifier>doi:10.1016/j.biopha.2024.116658</dc:identifier>
  979.    </item>
  980.    <item>
  981.      <title>GPR30 selective agonist G-1 induced insulin resistance in ovariectomized mice on high fat diet and its mechanism</title>
  982.      <link>https://pubmed.ncbi.nlm.nih.gov/38701557/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  983.      <description>CONCLUSION: Despite G-1's the potential efficacy in weight reduction, the concomitant induction of insulin resistance and cardiac impairment in conjunction with an HFD raises significant concerns. Therefore, comprehensive studies of its safety profile and effects under specific conditions are essential prior to clinical use.</description>
  984.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Biochem Biophys Res Commun. 2024 Apr 27;716:150026. doi: 10.1016/j.bbrc.2024.150026. 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: Previous in vivo and in vitro studies have demonstrated that estrogen receptor agonist G-1 regulates glucose and lipid metabolism. This study focused on the effects of G-1 on cardiometabolic syndrome and anti-obesity under a high fat diet (HFD).</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: Bilateral ovariectomized female mice were fed an HFD for 6 weeks, and treated them with G-1. A cardiomyocyte insulin resistance model was used to simulate the in vivo environment. The main outcome measures were blood glucose, body weight, and serum insulin levels to assess insulin resistance, while cardiac function and degree of fibrosis were assessed by cardiac ultrasound and pathological observations. We also examined the expression of p-AMPK, p-AKT, and GLUT4 in mice hearts and in vitro models to explore the mechanism by which G-1 regulates insulin signaling.</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: G-1 reduced body weight in mice on an HFD, but simultaneously increased blood glucose and promoted insulin resistance, resulting in myocardial damage. This damage included disordered cardiomyocytes, massive accumulation of glycogen, extensive fibrosis of the heart, and thickening of the front and rear walls of the left ventricle. At the molecular level, G-1 enhances gluconeogenesis and promotes glucose production by increasing the activity of pyruvate carboxylase (PC) while inhibiting GLUT4 translocation via the AMPK/TBC1D1 pathway, thereby limiting glucose uptake.</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: Despite G-1's the potential efficacy in weight reduction, the concomitant induction of insulin resistance and cardiac impairment in conjunction with an HFD raises significant concerns. Therefore, comprehensive studies of its safety profile and effects under specific conditions are essential prior to clinical use.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701557/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701557</a> | DOI:<a href=https://doi.org/10.1016/j.bbrc.2024.150026>10.1016/j.bbrc.2024.150026</a></p></div>]]></content:encoded>
  985.      <guid isPermaLink="false">pubmed:38701557</guid>
  986.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  987.      <dc:creator>Congcong Lu</dc:creator>
  988.      <dc:creator>Da Liu</dc:creator>
  989.      <dc:creator>Min Li</dc:creator>
  990.      <dc:creator>Xiaocui Shi</dc:creator>
  991.      <dc:creator>Jingyue Guan</dc:creator>
  992.      <dc:creator>Guoyuan Song</dc:creator>
  993.      <dc:creator>Yajuan Yin</dc:creator>
  994.      <dc:creator>Mingqi Zheng</dc:creator>
  995.      <dc:creator>Fangfang Ma</dc:creator>
  996.      <dc:creator>Gang Liu</dc:creator>
  997.      <dc:date>2024-05-03</dc:date>
  998.      <dc:source>Biochemical and biophysical research communications</dc:source>
  999.      <dc:title>GPR30 selective agonist G-1 induced insulin resistance in ovariectomized mice on high fat diet and its mechanism</dc:title>
  1000.      <dc:identifier>pmid:38701557</dc:identifier>
  1001.      <dc:identifier>doi:10.1016/j.bbrc.2024.150026</dc:identifier>
  1002.    </item>
  1003.    <item>
  1004.      <title>Ultrasonication followed by aqueous two-phase system for extraction, on-site modification and isolation of microalgal starch with reduced digestibility</title>
  1005.      <link>https://pubmed.ncbi.nlm.nih.gov/38701549/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  1006.      <description>Microalgae are new and sustainable sources of starch with higher productivity and flexible production modes than conventional terrestrial crops, but the downstream processes need further development. Here, ultrasonication (with power of 200 W or 300 W and duration of 10, 15, 20, or 25 min) was applied to simultaneously extract and modify starch from a marine microalga Tetraselmis subcordiformis for reducing the digestibility, and an aqueous two-phase system (ATPS) of ethanol/NaH(2)PO(4) was then...</description>
  1007.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Ultrason Sonochem. 2024 Apr 29;106:106891. doi: 10.1016/j.ultsonch.2024.106891. 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">Microalgae are new and sustainable sources of starch with higher productivity and flexible production modes than conventional terrestrial crops, but the downstream processes need further development. Here, ultrasonication (with power of 200 W or 300 W and duration of 10, 15, 20, or 25 min) was applied to simultaneously extract and modify starch from a marine microalga Tetraselmis subcordiformis for reducing the digestibility, and an aqueous two-phase system (ATPS) of ethanol/NaH<sub>2</sub>PO<sub>4</sub> was then used to isolate the starches with varied properties. Increasing ultrasonic duration facilitated the partition of starch into the bottom pellet, while enhancing the ultrasonic power was conducive to the allocation in the interphase of the ATPS. The overall starch recovery yield reached 73 ∼ 87 % and showed no significant difference among the ultrasonic conditions tested. The sequential ultrasonication-ATPS process successfully enriched the starch with purities up to 65 % ∼ 88 %, which was among the top levels reported in microalgal starch isolated. Ultrasonication produced more amylose which was mainly fractionated into the interface of the ATPS. The digestibility of the starch was altered under different ultrasonic conditions and varied from different ATPS phases as well, with the one under the ultrasonic power of 200 W for 15 min at the bottom pellet having the highest resistant starch content (RS, 39.7 %). The structural and compositional analysis evidenced that the ultrasonication-ATPS process could exert impacts on the digestibility through altering the surface roughness and fissures of the starch granules, modulating the impurity compositions (protein and lipid) that could interact with starch, and modifying the long- and short-range ordered structures. The developed ultrasonication-ATPS process provided novel insights into the mechanism and strategy for efficient production of functional starch from microalgae with a potential in industrial application.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701549/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701549</a> | DOI:<a href=https://doi.org/10.1016/j.ultsonch.2024.106891>10.1016/j.ultsonch.2024.106891</a></p></div>]]></content:encoded>
  1008.      <guid isPermaLink="false">pubmed:38701549</guid>
  1009.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  1010.      <dc:creator>Longren Liao</dc:creator>
  1011.      <dc:creator>Yuhan Shen</dc:creator>
  1012.      <dc:creator>Chenglin Xie</dc:creator>
  1013.      <dc:creator>Yongkui Zhang</dc:creator>
  1014.      <dc:creator>Changhong Yao</dc:creator>
  1015.      <dc:date>2024-05-03</dc:date>
  1016.      <dc:source>Ultrasonics sonochemistry</dc:source>
  1017.      <dc:title>Ultrasonication followed by aqueous two-phase system for extraction, on-site modification and isolation of microalgal starch with reduced digestibility</dc:title>
  1018.      <dc:identifier>pmid:38701549</dc:identifier>
  1019.      <dc:identifier>doi:10.1016/j.ultsonch.2024.106891</dc:identifier>
  1020.    </item>
  1021.    <item>
  1022.      <title>Excess Intramyocellular Lipid Does Not Affect Muscle Fiber Biophysical Properties in Mice or People with Metabolically Abnormal Obesity</title>
  1023.      <link>https://pubmed.ncbi.nlm.nih.gov/38701374/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  1024.      <description>Observational studies show correlations between intramyocellular lipid (IMCL) content and muscle strength and contractile function in people with "metabolically abnormal" obesity. However, a clear physiologic mechanism for this association is lacking and causation is debated. We combined immunofluorescent confocal imaging with force measurements on permeabilized muscle fibers from metabolically normal and metabolically abnormal mice and metabolically normal (defined as normal fasting plasma...</description>
  1025.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Diabetes. 2024 May 3:db230991. doi: 10.2337/db23-0991. 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">Observational studies show correlations between intramyocellular lipid (IMCL) content and muscle strength and contractile function in people with "metabolically abnormal" obesity. However, a clear physiologic mechanism for this association is lacking and causation is debated. We combined immunofluorescent confocal imaging with force measurements on permeabilized muscle fibers from metabolically normal and metabolically abnormal mice and metabolically normal (defined as normal fasting plasma glucose and glucose tolerance) and metabolically abnormal (defined as pre-diabetes and type 2 diabetes) people with overweight/obesity to evaluate relationships among myocellular lipid droplet characteristics (droplet size and density) and biophysical (active contractile and passive viscoelastic) properties. The fiber type specificity of lipid droplet parameters varied between metabolically abnormal and normal mice and among metabolically normal and metabolically abnormal people. However, despite considerable quantities of IMCL in the metabolically abnormal groups, there were no significant differences in peak active tension or passive viscoelasticity between the metabolically abnormal groups and the control group in mice or people. Additionally, there were no significant relationships among IMCL parameters and biophysical variables. Thus, we conclude that IMCL accumulation per se does not impact muscle fiber biophysical properties or physically impede contraction.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701374/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701374</a> | DOI:<a href=https://doi.org/10.2337/db23-0991>10.2337/db23-0991</a></p></div>]]></content:encoded>
  1026.      <guid isPermaLink="false">pubmed:38701374</guid>
  1027.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  1028.      <dc:creator>Karen C Shen</dc:creator>
  1029.      <dc:creator>Kelsey H Collins</dc:creator>
  1030.      <dc:creator>Jeremie L A Ferey</dc:creator>
  1031.      <dc:creator>Alan Fappi</dc:creator>
  1032.      <dc:creator>Jeremy J McCormick</dc:creator>
  1033.      <dc:creator>Bettina Mittendorfer</dc:creator>
  1034.      <dc:creator>Farshid Guilak</dc:creator>
  1035.      <dc:creator>Gretchen A Meyer</dc:creator>
  1036.      <dc:date>2024-05-03</dc:date>
  1037.      <dc:source>Diabetes</dc:source>
  1038.      <dc:title>Excess Intramyocellular Lipid Does Not Affect Muscle Fiber Biophysical Properties in Mice or People with Metabolically Abnormal Obesity</dc:title>
  1039.      <dc:identifier>pmid:38701374</dc:identifier>
  1040.      <dc:identifier>doi:10.2337/db23-0991</dc:identifier>
  1041.    </item>
  1042.    <item>
  1043.      <title>Comprehensive clinical and genetic analyses of circulating bile acids and their associations with diabetes and its indices</title>
  1044.      <link>https://pubmed.ncbi.nlm.nih.gov/38701355/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&amp;fc=None&amp;ff=20240504180251&amp;v=2.18.0.post9+e462414</link>
  1045.      <description>Bile acids (BAs) are cholesterol-derived compounds that regulate glucose, lipid, and energy metabolism. Despite their significance in glucose homeostasis, the association between specific BA molecular species and their synthetic pathways with diabetes mellitus (DM) is unclear. Here, we used a recently validated stable-isotope dilution highperformance liquid chromatography with tandem mass spectrometry (LC-MS/MS) method to quantify a panel of BAs in fasting plasma from subjects (n=2,145) and...</description>
  1046.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Diabetes. 2024 May 3:db230676. doi: 10.2337/db23-0676. 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">Bile acids (BAs) are cholesterol-derived compounds that regulate glucose, lipid, and energy metabolism. Despite their significance in glucose homeostasis, the association between specific BA molecular species and their synthetic pathways with diabetes mellitus (DM) is unclear. Here, we used a recently validated stable-isotope dilution highperformance liquid chromatography with tandem mass spectrometry (LC-MS/MS) method to quantify a panel of BAs in fasting plasma from subjects (n=2,145) and explored structural and genetic determinants of BAs linked to DM, insulin resistance and obesity. Multiple 12α-hydroxylated BAs were associated with DM [adjusted odds ratios (aORs):1.3-1.9 (all P&lt;0.05)] and insulin resistance [aORs:1.3-2.2 (all P&lt;0.05)]. Conversely, multiple 6a-hydroxylated BAs and isolithocholic acid (Iso-LCA) were inversely associated with DM and obesity [aORs:0.3-0.9 (all P&lt;0.05)]. Genome-wide association studies (GWAS) revealed multiple genome-wide significant loci linked with nine of the 14 DM-associated BAs, including a locus for Iso-LCA (rs11866815). Mendelian randomization analyses showed genetically elevated DCA levels were causally associated with higher BMI, and Iso-LCA levels were causally associated with reduced BMI and DM risk. In conclusion, comprehensive large-scale quantitative mass spectrometry and genetics analyses show circulating levels of multiple structurally specific BAs, especially DCA and Iso-LCA, are clinically associated with and genetically linked to obesity and DM.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38701355/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240504180251&v=2.18.0.post9+e462414">38701355</a> | DOI:<a href=https://doi.org/10.2337/db23-0676>10.2337/db23-0676</a></p></div>]]></content:encoded>
  1047.      <guid isPermaLink="false">pubmed:38701355</guid>
  1048.      <pubDate>Fri, 03 May 2024 06:00:00 -0400</pubDate>
  1049.      <dc:creator>Ibrahim Choucair</dc:creator>
  1050.      <dc:creator>Deepthi P Mallela</dc:creator>
  1051.      <dc:creator>James R Hilser</dc:creator>
  1052.      <dc:creator>Jaana A Hartiala</dc:creator>
  1053.      <dc:creator>Ina Nemet</dc:creator>
  1054.      <dc:creator>Valentin Gogonea</dc:creator>
  1055.      <dc:creator>Lin Li</dc:creator>
  1056.      <dc:creator>Aldons J Lusis</dc:creator>
  1057.      <dc:creator>Michael A Fischbach</dc:creator>
  1058.      <dc:creator>W H Wilson Tang</dc:creator>
  1059.      <dc:creator>Hooman Allayee</dc:creator>
  1060.      <dc:creator>Stanley L Hazen</dc:creator>
  1061.      <dc:date>2024-05-03</dc:date>
  1062.      <dc:source>Diabetes</dc:source>
  1063.      <dc:title>Comprehensive clinical and genetic analyses of circulating bile acids and their associations with diabetes and its indices</dc:title>
  1064.      <dc:identifier>pmid:38701355</dc:identifier>
  1065.      <dc:identifier>doi:10.2337/db23-0676</dc:identifier>
  1066.    </item>
  1067.  </channel>
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  1069.  

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