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  4.    <title>riordan, neil[author]</title>
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  12.    <pubDate>Sat, 26 Aug 2023 06:00:00 -0400</pubDate>
  13.    <ttl>120</ttl>
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  15.      <title>Comparison of Cost and Potency of Human Mesenchymal Stromal Cell Conditioned Medium Derived from 2- and 3-Dimensional Cultures</title>
  16.      <link>https://pubmed.ncbi.nlm.nih.gov/37627815/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  17.      <description>Mesenchymal stromal cell (MSC)-derived products, such as trophic factors (MTFs), have anti-inflammatory properties that make them attractive for cell-free treatment. Three-dimensional (3D) culture can enhance these properties, and large-scale expansion using a bioreactor can reduce manufacturing costs. Three lots of MTFs were obtained from umbilical cord MSCs produced by either monolayer culture (Monol MTF) or using a 3D microcarrier in a spinner flask dynamic system (Bioreactor MTF). The...</description>
  18.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Bioengineering (Basel). 2023 Aug 4;10(8):930. doi: 10.3390/bioengineering10080930.</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">Mesenchymal stromal cell (MSC)-derived products, such as trophic factors (MTFs), have anti-inflammatory properties that make them attractive for cell-free treatment. Three-dimensional (3D) culture can enhance these properties, and large-scale expansion using a bioreactor can reduce manufacturing costs. Three lots of MTFs were obtained from umbilical cord MSCs produced by either monolayer culture (Monol MTF) or using a 3D microcarrier in a spinner flask dynamic system (Bioreactor MTF). The resulting MTFs were tested and compared using anti-inflammatory potency assays in two different systems: (1) a phytohemagglutinin-activated peripheral blood mononuclear cell (PBMNC) system and (2) a lipopolysaccharide (LPS)-activated macrophage system. Cytokine expression by macrophages was measured via RT-PCR. The production costs of hypothetical units of anti-inflammatory effects were calculated using the percentage of TNF-α inhibition by MTF exposure. Bioreactor MTFs had a higher inhibitory effect on TNF (<i>p</i> &lt; 0.01) than monolayer MTFs (<i>p</i> &lt; 0.05). The anti-inflammatory effect of Bioreactor MTFs on IL-1β, TNF-α, IL-8, IL-6, and MIP-1 was significantly higher than that of monolayer MTFs. The production cost of 1% inhibition of TNF-α was 11-40% higher using monolayer culture compared to bioreactor-derived MTFs. A 3D dynamic culture was, therefore, able to produce high-quality MTFs, with robust anti-inflammatory properties, more efficiently than monolayer static systems.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/37627815/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">37627815</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC10451979/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC10451979</a> | DOI:<a href=https://doi.org/10.3390/bioengineering10080930>10.3390/bioengineering10080930</a></p></div>]]></content:encoded>
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  20.      <pubDate>Sat, 26 Aug 2023 06:00:00 -0400</pubDate>
  21.      <dc:creator>Marialaura Madrigal</dc:creator>
  22.      <dc:creator>Patricia L Fernández</dc:creator>
  23.      <dc:creator>Ricardo Lleonart</dc:creator>
  24.      <dc:creator>Lizmar Carreño</dc:creator>
  25.      <dc:creator>Kaiser Alejandro Villalobos Gorday</dc:creator>
  26.      <dc:creator>Ellís Rodríguez</dc:creator>
  27.      <dc:creator>Kathya de Cupeiro</dc:creator>
  28.      <dc:creator>Carlos M Restrepo</dc:creator>
  29.      <dc:creator>K S Jagannatha Rao</dc:creator>
  30.      <dc:creator>Neil H Riordan</dc:creator>
  31.      <dc:date>2023-08-26</dc:date>
  32.      <dc:source>Bioengineering (Basel, Switzerland)</dc:source>
  33.      <dc:title>Comparison of Cost and Potency of Human Mesenchymal Stromal Cell Conditioned Medium Derived from 2- and 3-Dimensional Cultures</dc:title>
  34.      <dc:identifier>pmid:37627815</dc:identifier>
  35.      <dc:identifier>pmc:PMC10451979</dc:identifier>
  36.      <dc:identifier>doi:10.3390/bioengineering10080930</dc:identifier>
  37.    </item>
  38.    <item>
  39.      <title>Case report: effect of umbilical cord mesenchymal stem cells on immunoglobulin A nephropathy after acute renal failure</title>
  40.      <link>https://pubmed.ncbi.nlm.nih.gov/35958462/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  41.      <description>Immunoglobulin A nephropathy is an inflammatory, autoimmune condition that may lead to renal impairment in its most aggressive forms. In this case report, a 50-year-old male with acute renal failure was diagnosed with IgA nephropathy, having elevated creatinine levels (3.0 mg/dL) and hypertension. He received intravenous infusions of a total of 120 million umbilical cord-derived mesenchymal stem cells (UC-MSCs) and was followed-up for 6 months. No adverse events were reported during or after...</description>
  42.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Am J Transl Res. 2022 Jul 15;14(7):4855-4859. eCollection 2022.</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">Immunoglobulin A nephropathy is an inflammatory, autoimmune condition that may lead to renal impairment in its most aggressive forms. In this case report, a 50-year-old male with acute renal failure was diagnosed with IgA nephropathy, having elevated creatinine levels (3.0 mg/dL) and hypertension. He received intravenous infusions of a total of 120 million umbilical cord-derived mesenchymal stem cells (UC-MSCs) and was followed-up for 6 months. No adverse events were reported during or after administration or any of the follow-up visits. Creatinine levels decreased to and remained normal (1.0 mg/dL) in the 6 months following treatment. Anti-hypertensive medications were no longer needed. UC-MSC administration was safe, well-tolerated, and beneficial for this patient with IgA nephropathy.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/35958462/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">35958462</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC9360881/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC9360881</a></p></div>]]></content:encoded>
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  44.      <pubDate>Fri, 12 Aug 2022 06:00:00 -0400</pubDate>
  45.      <dc:creator>Neil H Riordan</dc:creator>
  46.      <dc:creator>Richard A Ambrozic</dc:creator>
  47.      <dc:creator>Jorge Paz-Rodríguez</dc:creator>
  48.      <dc:date>2022-08-12</dc:date>
  49.      <dc:source>American journal of translational research</dc:source>
  50.      <dc:title>Case report: effect of umbilical cord mesenchymal stem cells on immunoglobulin A nephropathy after acute renal failure</dc:title>
  51.      <dc:identifier>pmid:35958462</dc:identifier>
  52.      <dc:identifier>pmc:PMC9360881</dc:identifier>
  53.    </item>
  54.    <item>
  55.      <title>The Effects of Vitamin C on the Multiple Pathophysiological Stages of COVID-19</title>
  56.      <link>https://pubmed.ncbi.nlm.nih.gov/34947872/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  57.      <description>Currently available anti-viral drugs may be useful in reducing the viral load but are not providing the necessary physiological effects to reduce the SARS-CoV-2 complications efficiently. Treatments that provide better clinical outcomes are urgently needed. Vitamin C (ascorbic acid, AA) is an essential nutrient with many biological roles that have been proven to play an important part in immune function; it serves as an antioxidant, an anti-viral, and exerts anti-thrombotic effects among many...</description>
  58.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Life (Basel). 2021 Dec 3;11(12):1341. doi: 10.3390/life11121341.</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">Currently available anti-viral drugs may be useful in reducing the viral load but are not providing the necessary physiological effects to reduce the SARS-CoV-2 complications efficiently. Treatments that provide better clinical outcomes are urgently needed. Vitamin C (ascorbic acid, AA) is an essential nutrient with many biological roles that have been proven to play an important part in immune function; it serves as an antioxidant, an anti-viral, and exerts anti-thrombotic effects among many other physiological benefits. Research has proven that AA at pharmacological doses can be beneficial to patients with acute respiratory distress syndrome (ARDS) and other respiratory illnesses, including sepsis. In addition, High-Dose Intravenous Vitamin C (HDIVC) has proven to be effective in patients with different viral diseases, such as influenza, chikungunya, Zika, and dengue. Moreover, HDIVC has been demonstrated to be very safe. Regarding COVID-19, vitamin C can suppress the cytokine storm, reduce thrombotic complications, and diminish alveolar and vascular damage, among other benefits. Due to these reasons, the use of HDIVC should be seriously considered in complicated COVID-19 patients. In this article, we will emphasize vitamin C's multiple roles in the most prominent pathophysiological processes presented by the COVID-19 disease.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/34947872/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">34947872</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC8708699/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC8708699</a> | DOI:<a href=https://doi.org/10.3390/life11121341>10.3390/life11121341</a></p></div>]]></content:encoded>
  59.      <guid isPermaLink="false">pubmed:34947872</guid>
  60.      <pubDate>Fri, 24 Dec 2021 06:00:00 -0500</pubDate>
  61.      <dc:creator>Jorge R Miranda-Massari</dc:creator>
  62.      <dc:creator>Alondra P Toro</dc:creator>
  63.      <dc:creator>Doris Loh</dc:creator>
  64.      <dc:creator>Jose R Rodriguez</dc:creator>
  65.      <dc:creator>Raul Morales Borges</dc:creator>
  66.      <dc:creator>Victor Marcial-Vega</dc:creator>
  67.      <dc:creator>Jose Olalde</dc:creator>
  68.      <dc:creator>Miguel J Berdiel</dc:creator>
  69.      <dc:creator>Neil H Riordan</dc:creator>
  70.      <dc:creator>Juan Manuel Martinez</dc:creator>
  71.      <dc:creator>Armando Gil</dc:creator>
  72.      <dc:creator>Michael J Gonzalez</dc:creator>
  73.      <dc:date>2021-12-24</dc:date>
  74.      <dc:source>Life (Basel, Switzerland)</dc:source>
  75.      <dc:title>The Effects of Vitamin C on the Multiple Pathophysiological Stages of COVID-19</dc:title>
  76.      <dc:identifier>pmid:34947872</dc:identifier>
  77.      <dc:identifier>pmc:PMC8708699</dc:identifier>
  78.      <dc:identifier>doi:10.3390/life11121341</dc:identifier>
  79.    </item>
  80.    <item>
  81.      <title>Addressing concerns regarding associated costs, transparency, and integrity of research in recent stem cell trial</title>
  82.      <link>https://pubmed.ncbi.nlm.nih.gov/34453783/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  83.      <description>No abstract</description>
  84.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Stem Cells Transl Med. 2021 Dec;10(12):1715-1716. doi: 10.1002/sctm.21-0234. Epub 2021 Aug 28.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/34453783/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">34453783</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC8641074/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC8641074</a> | DOI:<a href=https://doi.org/10.1002/sctm.21-0234>10.1002/sctm.21-0234</a></p></div>]]></content:encoded>
  85.      <guid isPermaLink="false">pubmed:34453783</guid>
  86.      <pubDate>Sat, 28 Aug 2021 06:00:00 -0400</pubDate>
  87.      <dc:creator>Neil H Riordan</dc:creator>
  88.      <dc:creator>Jorge Paz Rodríguez</dc:creator>
  89.      <dc:date>2021-08-28</dc:date>
  90.      <dc:source>Stem cells translational medicine</dc:source>
  91.      <dc:title>Addressing concerns regarding associated costs, transparency, and integrity of research in recent stem cell trial</dc:title>
  92.      <dc:identifier>pmid:34453783</dc:identifier>
  93.      <dc:identifier>pmc:PMC8641074</dc:identifier>
  94.      <dc:identifier>doi:10.1002/sctm.21-0234</dc:identifier>
  95.    </item>
  96.    <item>
  97.      <title>Correction to: Clinical feasibility of umbilical cord tissue-derived mesenchymal stem cells in the treatment of multiple sclerosis</title>
  98.      <link>https://pubmed.ncbi.nlm.nih.gov/33971900/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  99.      <description>No abstract</description>
  100.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2021 May 10;19(1):197. doi: 10.1186/s12967-021-02869-4.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/33971900/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">33971900</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC8108340/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC8108340</a> | DOI:<a href=https://doi.org/10.1186/s12967-021-02869-4>10.1186/s12967-021-02869-4</a></p></div>]]></content:encoded>
  101.      <guid isPermaLink="false">pubmed:33971900</guid>
  102.      <pubDate>Tue, 11 May 2021 06:00:00 -0400</pubDate>
  103.      <dc:creator>Neil H Riordan</dc:creator>
  104.      <dc:creator>Isabela Morales</dc:creator>
  105.      <dc:creator>Giselle Fernández</dc:creator>
  106.      <dc:creator>Nicole Allen</dc:creator>
  107.      <dc:creator>Neal E Fearnot</dc:creator>
  108.      <dc:creator>Michael E Leckrone</dc:creator>
  109.      <dc:creator>Dedra Jones Markovich</dc:creator>
  110.      <dc:creator>Darla Mansfield</dc:creator>
  111.      <dc:creator>Dorita Avila</dc:creator>
  112.      <dc:creator>Amit N Patel</dc:creator>
  113.      <dc:creator>Santosh Kesari</dc:creator>
  114.      <dc:creator>Jorge Paz Rodriguez</dc:creator>
  115.      <dc:date>2021-05-11</dc:date>
  116.      <dc:source>Journal of translational medicine</dc:source>
  117.      <dc:title>Correction to: Clinical feasibility of umbilical cord tissue-derived mesenchymal stem cells in the treatment of multiple sclerosis</dc:title>
  118.      <dc:identifier>pmid:33971900</dc:identifier>
  119.      <dc:identifier>pmc:PMC8108340</dc:identifier>
  120.      <dc:identifier>doi:10.1186/s12967-021-02869-4</dc:identifier>
  121.    </item>
  122.    <item>
  123.      <title>Dodging COVID-19 infection: low expression and localization of ACE2 and TMPRSS2 in multiple donor-derived lines of human umbilical cord-derived mesenchymal stem cells</title>
  124.      <link>https://pubmed.ncbi.nlm.nih.gov/33853637/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  125.      <description>CONCLUSIONS: We have demonstrated negative expression of ACE2 and low expression of TMPRSS2 in 24 lots of hUC-MSCs. This has crucial implications for the design of future therapeutic options for COVID-19, since hUC-MSCs would have the ability to "dodge" viral infection to exert their immunomodulatory effects.</description>
  126.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2021 Apr 14;19(1):149. doi: 10.1186/s12967-021-02813-6.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Mesenchymal stem cells derived from human umbilical cord (hUC-MSCs) have immunomodulatory properties that are of interest to treat novel coronavirus disease 2019 (COVID-19). Leng et al. recently reported that hUC-MSCs derived from one donor negatively expressed Angiotensin-Converting Enzyme 2 (ACE2), a key protein for viral infection along with Transmembrane Serine Protease 2 (TMPRSS2). The purpose of this study was to quantify the expression of ACE2 and TMPRSS2 in hUC-MSCs lots derived from multiple donors using molecular-based techniques in order to demonstrate their inability to be a host to SARS-CoV-2.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Expression of ACE2 and TMPRSS2 was analyzed in 24 lots of hUC-MSCs derived from Wharton's jelly via quantitative polymerase chain reaction (qPCR), Western Blot, immunofluorescence and flow cytometry using 24 different donors.</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: hUC-MSCs had significantly lower ACE2 (p = 0.002) and TMPRSS2 (p = 0.008) expression compared with human lung tissue homogenates in Western blot analyses. Little to no expression of ACE2 was observed in hUC-MSC by qPCR, and they were not observable with immunofluorescence in hUC-MSCs cell membranes. A negative ACE2 and TMPRSS2 population percentage of 95.3% ± 15.55 was obtained for hUC-MSCs via flow cytometry, with only 4.6% ACE2 and 29.5% TMPRSS2 observable positive populations.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: We have demonstrated negative expression of ACE2 and low expression of TMPRSS2 in 24 lots of hUC-MSCs. This has crucial implications for the design of future therapeutic options for COVID-19, since hUC-MSCs would have the ability to "dodge" viral infection to exert their immunomodulatory effects.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/33853637/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">33853637</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC8045575/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC8045575</a> | DOI:<a href=https://doi.org/10.1186/s12967-021-02813-6>10.1186/s12967-021-02813-6</a></p></div>]]></content:encoded>
  127.      <guid isPermaLink="false">pubmed:33853637</guid>
  128.      <pubDate>Thu, 15 Apr 2021 06:00:00 -0400</pubDate>
  129.      <dc:creator>Jonathan J Hernandez</dc:creator>
  130.      <dc:creator>Doyle E Beaty</dc:creator>
  131.      <dc:creator>Logan L Fruhwirth</dc:creator>
  132.      <dc:creator>Ana P Lopes Chaves</dc:creator>
  133.      <dc:creator>Neil H Riordan</dc:creator>
  134.      <dc:date>2021-04-15</dc:date>
  135.      <dc:source>Journal of translational medicine</dc:source>
  136.      <dc:title>Dodging COVID-19 infection: low expression and localization of ACE2 and TMPRSS2 in multiple donor-derived lines of human umbilical cord-derived mesenchymal stem cells</dc:title>
  137.      <dc:identifier>pmid:33853637</dc:identifier>
  138.      <dc:identifier>pmc:PMC8045575</dc:identifier>
  139.      <dc:identifier>doi:10.1186/s12967-021-02813-6</dc:identifier>
  140.    </item>
  141.    <item>
  142.      <title>Allogeneic Human Umbilical Cord Mesenchymal Stem Cells for the Treatment of Autism Spectrum Disorder in Children: Safety Profile and Effect on Cytokine Levels</title>
  143.      <link>https://pubmed.ncbi.nlm.nih.gov/31187597/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  144.      <description>Individuals with autism spectrum disorder (ASD) suffer from developmental disabilities that impact communication, behavior, and social interaction. Immune dysregulation and inflammation have been linked to children with ASD, the latter manifesting in serum levels of macrophage-derived chemokine (MDC) and thymus, and activation-regulated chemokine (TARC). Mesenchymal stem cells derived from umbilical cord tissue (UC-MSCs) have immune-modulatory and anti-inflammatory properties, and have been...</description>
  145.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Stem Cells Transl Med. 2019 Oct;8(10):1008-1016. doi: 10.1002/sctm.19-0010. Epub 2019 Jun 11.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Individuals with autism spectrum disorder (ASD) suffer from developmental disabilities that impact communication, behavior, and social interaction. Immune dysregulation and inflammation have been linked to children with ASD, the latter manifesting in serum levels of macrophage-derived chemokine (MDC) and thymus, and activation-regulated chemokine (TARC). Mesenchymal stem cells derived from umbilical cord tissue (UC-MSCs) have immune-modulatory and anti-inflammatory properties, and have been safely used to treat a variety of conditions. This study investigated the safety and efficacy of UC-MSCs administered to children diagnosed with ASD. Efficacy was evaluated with the Autism Treatment Evaluation Checklist (ATEC) and the Childhood Autism Rating Scale (CARS), and with measurements of MDC and TARC serum levels. Twenty subjects received a dose of 36 million intravenous UC-MSCs every 12 weeks (four times over a 9-month period), and were followed up at 3 and 12 months after treatment completion. Adverse events related to treatment were mild or moderate and short in duration. The CARS and ATEC scores of eight subjects decreased over the course of treatment, placing them in a lower ASD symptom category when compared with baseline. MDC and TARC inflammatory cytokine levels also decreased for five of these eight subjects. The mean MDC, TARC, ATEC, and CARS values attained their lowest levels 3 months after the last administration. UC-MSC administration in children with ASD was therefore determined to be safe. Although some signals of efficacy were observed in a small group of children, possible links between inflammation levels and ASD symptoms should be further investigated. Stem Cells Translational Medicine 2019;8:1008-1016.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/31187597/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">31187597</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC6766688/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC6766688</a> | DOI:<a href=https://doi.org/10.1002/sctm.19-0010>10.1002/sctm.19-0010</a></p></div>]]></content:encoded>
  146.      <guid isPermaLink="false">pubmed:31187597</guid>
  147.      <pubDate>Thu, 13 Jun 2019 06:00:00 -0400</pubDate>
  148.      <dc:creator>Neil H Riordan</dc:creator>
  149.      <dc:creator>Maria Luisa Hincapié</dc:creator>
  150.      <dc:creator>Isabela Morales</dc:creator>
  151.      <dc:creator>Giselle Fernández</dc:creator>
  152.      <dc:creator>Nicole Allen</dc:creator>
  153.      <dc:creator>Cindy Leu</dc:creator>
  154.      <dc:creator>Marialaura Madrigal</dc:creator>
  155.      <dc:creator>Jorge Paz Rodríguez</dc:creator>
  156.      <dc:creator>Nelson Novarro</dc:creator>
  157.      <dc:date>2019-06-13</dc:date>
  158.      <dc:source>Stem cells translational medicine</dc:source>
  159.      <dc:title>Allogeneic Human Umbilical Cord Mesenchymal Stem Cells for the Treatment of Autism Spectrum Disorder in Children: Safety Profile and Effect on Cytokine Levels</dc:title>
  160.      <dc:identifier>pmid:31187597</dc:identifier>
  161.      <dc:identifier>pmc:PMC6766688</dc:identifier>
  162.      <dc:identifier>doi:10.1002/sctm.19-0010</dc:identifier>
  163.    </item>
  164.    <item>
  165.      <title>Clinical feasibility of umbilical cord tissue-derived mesenchymal stem cells in the treatment of multiple sclerosis</title>
  166.      <link>https://pubmed.ncbi.nlm.nih.gov/29523171/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  167.      <description>CONCLUSIONS: Treatment with UCMSC intravenous infusions for subjects with MS is safe, and potential therapeutic benefits should be further investigated. Trial registration ClinicalTrials.gov NCT02034188. Registered Jan 13, 2014. https://clinicaltrials.gov/ct2/show/NCT02034188.</description>
  168.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2018 Mar 9;16(1):57. doi: 10.1186/s12967-018-1433-7.</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">BACKGROUND: Multiple sclerosis (MS) is a progressively debilitating neurological condition in which the immune system abnormally erodes the myelin sheath insulating the nerves. Mesenchymal stem cells (MSC) have been used in the last decade to safely treat certain immune and inflammatory conditions.</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 safety and feasibility study was completed on the use of umbilical cord MSC (UCMSC) as a treatment for MS. In this 1-year study, consenting subjects received seven intravenous infusions of 20 × 10<sup>6</sup> UCMSC over 7 days. Efficacy was assessed at baseline, 1 month and 1 year after treatment, including magnetic resonance imaging (MRI) scans, Kurtzke Expanded Disability Status Scale (EDSS), Scripps Neurological Rating Scale, Nine-Hole Peg Test, 25-Foot Walk Test, and RAND Short Form-36 quality of life questionnaire.</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: Twenty subjects were enrolled in this study. No serious adverse events were reported. Of the mild AEs denoted as possibly related to treatment, most were headache or fatigue. Symptom improvements were most notable 1 month after treatment. Improvements were seen in EDSS scores (p &lt; 0.03), as well as in bladder, bowel, and sexual dysfunction (p &lt; 0.01), in non-dominant hand average scores (p &lt; 0.01), in walk times (p &lt; 0.02) and general perspective of a positive health change and improved quality of life. MRI scans of the brain and the cervical spinal cord showed inactive lesions in 15/18 (83.3%) subjects after 1 year.</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: Treatment with UCMSC intravenous infusions for subjects with MS is safe, and potential therapeutic benefits should be further investigated. Trial registration ClinicalTrials.gov NCT02034188. Registered Jan 13, 2014. https://clinicaltrials.gov/ct2/show/NCT02034188.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/29523171/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">29523171</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC5845260/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC5845260</a> | DOI:<a href=https://doi.org/10.1186/s12967-018-1433-7>10.1186/s12967-018-1433-7</a></p></div>]]></content:encoded>
  169.      <guid isPermaLink="false">pubmed:29523171</guid>
  170.      <pubDate>Sun, 11 Mar 2018 06:00:00 -0400</pubDate>
  171.      <dc:creator>Neil H Riordan</dc:creator>
  172.      <dc:creator>Isabela Morales</dc:creator>
  173.      <dc:creator>Giselle Fernández</dc:creator>
  174.      <dc:creator>Nicole Allen</dc:creator>
  175.      <dc:creator>Neal E Fearnot</dc:creator>
  176.      <dc:creator>Michael E Leckrone</dc:creator>
  177.      <dc:creator>Dedra Jones Markovich</dc:creator>
  178.      <dc:creator>Darla Mansfield</dc:creator>
  179.      <dc:creator>Dorita Avila</dc:creator>
  180.      <dc:creator>Amit N Patel</dc:creator>
  181.      <dc:creator>Santosh Kesari</dc:creator>
  182.      <dc:creator>Jorge Paz Rodriguez</dc:creator>
  183.      <dc:date>2018-03-11</dc:date>
  184.      <dc:source>Journal of translational medicine</dc:source>
  185.      <dc:title>Clinical feasibility of umbilical cord tissue-derived mesenchymal stem cells in the treatment of multiple sclerosis</dc:title>
  186.      <dc:identifier>pmid:29523171</dc:identifier>
  187.      <dc:identifier>pmc:PMC5845260</dc:identifier>
  188.      <dc:identifier>doi:10.1186/s12967-018-1433-7</dc:identifier>
  189.    </item>
  190.    <item>
  191.      <title>Effect of Infla-Kine supplementation on the gene expression of inflammatory markers in peripheral mononuclear cells and on C-reactive protein in blood</title>
  192.      <link>https://pubmed.ncbi.nlm.nih.gov/29058588/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  193.      <description>CONCLUSIONS: Overall, our data demonstrate that twice daily administration of Infla-Kine for 4 weeks reduces inflammatory markers and quality of life in healthy volunteers.</description>
  194.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2017 Oct 20;15(1):213. doi: 10.1186/s12967-017-1315-4.</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: Chronic inflammation is a predisposing factor to numerous degenerative diseases including cancer, heart failure and Alzheimer's disease. Infla-Kine is a natural supplement comprised of a proprietary blend of Lactobacillus fermentum extract, burdock seed (arctigenin), zinc, alpha lipoic acid, papaya enzyme and an enhanced absorption bio-curcumin complex (BCM-95<sup>®</sup>).</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: Infla-Kine was administered twice daily to 24 health volunteers for 4 weeks. Quantitative RT-PCR was used to assess mRNA transcripts of IL-1b, IL8, IL-6, NF-κB, and TNF-α from peripheral blood mononuclear cells (PBMC). C reactive protein (CRP) was measured from serum. Additionally, quality of life questionnaires were employed to assess general feeling of well-being. Assessments were made before treatment and at conclusion of treatment (4 weeks).</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: As compared to pre-treatment, after 4 weeks, a statistically significant reduction of IL8, IL-6, NF-κB, and TNF-α transcripts was observed in PBMC. Furthermore, reduction of IL-1b transcript and serum CRP was observed but did not reach statistical significance. Quality of life improvements were most prevalent in muscle and joint pains.</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: Overall, our data demonstrate that twice daily administration of Infla-Kine for 4 weeks reduces inflammatory markers and quality of life in healthy volunteers.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/29058588/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">29058588</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC5651612/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC5651612</a> | DOI:<a href=https://doi.org/10.1186/s12967-017-1315-4>10.1186/s12967-017-1315-4</a></p></div>]]></content:encoded>
  195.      <guid isPermaLink="false">pubmed:29058588</guid>
  196.      <pubDate>Tue, 24 Oct 2017 06:00:00 -0400</pubDate>
  197.      <dc:creator>Nina A Mikirova</dc:creator>
  198.      <dc:creator>Santosh Kesari</dc:creator>
  199.      <dc:creator>Thomas E Ichim</dc:creator>
  200.      <dc:creator>Neil H Riordan</dc:creator>
  201.      <dc:date>2017-10-24</dc:date>
  202.      <dc:source>Journal of translational medicine</dc:source>
  203.      <dc:title>Effect of Infla-Kine supplementation on the gene expression of inflammatory markers in peripheral mononuclear cells and on C-reactive protein in blood</dc:title>
  204.      <dc:identifier>pmid:29058588</dc:identifier>
  205.      <dc:identifier>pmc:PMC5651612</dc:identifier>
  206.      <dc:identifier>doi:10.1186/s12967-017-1315-4</dc:identifier>
  207.    </item>
  208.    <item>
  209.      <title>Cellular immunotherapy of cancer: an overview and future directions</title>
  210.      <link>https://pubmed.ncbi.nlm.nih.gov/28595516/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  211.      <description>The clinical success of checkpoint inhibitors has led to a renaissance of interest in cancer immunotherapies. In particular, the possibility of ex vivo expanding autologous lymphocytes that specifically recognize tumor cells has attracted much research and clinical trial interest. In this review, we discuss the historical background of tumor immunotherapy using cell-based approaches, and provide some rationale for overcoming current barriers to success of autologous immunotherapy. An overview of...</description>
  212.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Immunotherapy. 2017 Jun;9(7):589-606. doi: 10.2217/imt-2016-0086.</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 clinical success of checkpoint inhibitors has led to a renaissance of interest in cancer immunotherapies. In particular, the possibility of ex vivo expanding autologous lymphocytes that specifically recognize tumor cells has attracted much research and clinical trial interest. In this review, we discuss the historical background of tumor immunotherapy using cell-based approaches, and provide some rationale for overcoming current barriers to success of autologous immunotherapy. An overview of adoptive transfer of lymphocytes, tumor infiltrating lymphocytes and dendritic cell therapies is provided. We conclude with discussing the possibility of gene-manipulating immune cells in order to augment therapeutic activity, including silencing of the immune-suppressive zinc finger orphan nuclear receptor, NR2F6, as an attractive means of overcoming tumor-associated immune suppression.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/28595516/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">28595516</a> | DOI:<a href=https://doi.org/10.2217/imt-2016-0086>10.2217/imt-2016-0086</a></p></div>]]></content:encoded>
  213.      <guid isPermaLink="false">pubmed:28595516</guid>
  214.      <pubDate>Sat, 10 Jun 2017 06:00:00 -0400</pubDate>
  215.      <dc:creator>Ziqi Tao</dc:creator>
  216.      <dc:creator>Shuang Li</dc:creator>
  217.      <dc:creator>Thomas E Ichim</dc:creator>
  218.      <dc:creator>Junbao Yang</dc:creator>
  219.      <dc:creator>Neil Riordan</dc:creator>
  220.      <dc:creator>Venkata Yenugonda</dc:creator>
  221.      <dc:creator>Ivan Babic</dc:creator>
  222.      <dc:creator>Santosh Kesari</dc:creator>
  223.      <dc:date>2017-06-10</dc:date>
  224.      <dc:source>Immunotherapy</dc:source>
  225.      <dc:title>Cellular immunotherapy of cancer: an overview and future directions</dc:title>
  226.      <dc:identifier>pmid:28595516</dc:identifier>
  227.      <dc:identifier>doi:10.2217/imt-2016-0086</dc:identifier>
  228.    </item>
  229.    <item>
  230.      <title>High-Dose Intravenous Vitamin C Treatment of a Child with Neurofibromatosis Type 1 and Optic Pathway Glioma: A Case Report</title>
  231.      <link>https://pubmed.ncbi.nlm.nih.gov/27773919/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  232.      <description>BACKGROUND In neurofibromatosis type 1 (NF1) disease, the loss of the tumor suppressor function of the neurofibromin gene leads to proliferation of neural tumors. In children, the most frequently identified tumor is the optic pathway glioma. CASE REPORT We describe the case of a 5-year-old child who was diagnosed with NF1 and optic pathway tumor onset at the age of 14 months. Because of the tumor progression, chemotherapy with carboplatin and vincristine was prescribed at this early age and...</description>
  233.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Am J Case Rep. 2016 Oct 24;17:774-781. doi: 10.12659/ajcr.899754.</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 In neurofibromatosis type 1 (NF1) disease, the loss of the tumor suppressor function of the neurofibromin gene leads to proliferation of neural tumors. In children, the most frequently identified tumor is the optic pathway glioma. CASE REPORT We describe the case of a 5-year-old child who was diagnosed with NF1 and optic pathway tumor onset at the age of 14 months. Because of the tumor progression, chemotherapy with carboplatin and vincristine was prescribed at this early age and continued for one year. As the progression of disease continued after chemotherapy, the child, at the age of 2.8 years, was started on high-dose intravenous vitamin C (IVC) treatment (7-15 grams per week) for 30 months. After 30 months, the results of IVC treatments demonstrated reduction and stabilization of the tumors in the optic chiasm, hypothalamus, and left optic nerve according to radiographic imaging. The right-sided optic nerve mass seen before IVC treatment disappeared by the end of the treatment. CONCLUSIONS This case highlights the positive effects of treating NF1 glioma with IVC. Additional studies are necessary to evaluate the role of high-dose IVC in glioma treatment.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/27773919/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">27773919</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC5081233/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC5081233</a> | DOI:<a href=https://doi.org/10.12659/ajcr.899754>10.12659/ajcr.899754</a></p></div>]]></content:encoded>
  234.      <guid isPermaLink="false">pubmed:27773919</guid>
  235.      <pubDate>Tue, 25 Oct 2016 06:00:00 -0400</pubDate>
  236.      <dc:creator>Nina Mikirova</dc:creator>
  237.      <dc:creator>Ronald Hunnunghake</dc:creator>
  238.      <dc:creator>Ruth C Scimeca</dc:creator>
  239.      <dc:creator>Charles Chinshaw</dc:creator>
  240.      <dc:creator>Faryal Ali</dc:creator>
  241.      <dc:creator>Chris Brannon</dc:creator>
  242.      <dc:creator>Neil Riordan</dc:creator>
  243.      <dc:date>2016-10-25</dc:date>
  244.      <dc:source>The American journal of case reports</dc:source>
  245.      <dc:title>High-Dose Intravenous Vitamin C Treatment of a Child with Neurofibromatosis Type 1 and Optic Pathway Glioma: A Case Report</dc:title>
  246.      <dc:identifier>pmid:27773919</dc:identifier>
  247.      <dc:identifier>pmc:PMC5081233</dc:identifier>
  248.      <dc:identifier>doi:10.12659/ajcr.899754</dc:identifier>
  249.    </item>
  250.    <item>
  251.      <title>Safety of targeting tumor endothelial cell antigens</title>
  252.      <link>https://pubmed.ncbi.nlm.nih.gov/27071457/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  253.      <description>The mechanisms underlying discrimination between "self" and "non-self", a central immunological principle, require careful consideration in immune oncology therapeutics where eliciting anti-cancer immunity must be weighed against the risk of autoimmunity due to the self origin of tumors. Whole cell vaccines are one promising immunotherapeutic avenue whereby a myriad of tumor antigens are introduced in an immunogenic context with the aim of eliciting tumor rejection. Despite the possibility...</description>
  254.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2016 Apr 12;14:90. doi: 10.1186/s12967-016-0842-8.</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 mechanisms underlying discrimination between "self" and "non-self", a central immunological principle, require careful consideration in immune oncology therapeutics where eliciting anti-cancer immunity must be weighed against the risk of autoimmunity due to the self origin of tumors. Whole cell vaccines are one promising immunotherapeutic avenue whereby a myriad of tumor antigens are introduced in an immunogenic context with the aim of eliciting tumor rejection. Despite the possibility collateral damage to healthy tissues, cancer immunotherapy can be designed such that off target autoimmunity remains limited in scope and severity or completely non-existent. Here we provide an immunological basis for reconciling the safety of cancer vaccines, focusing on tumor endothelial cell vaccines, by discussing the following topics: (a) Antigenic differences between neoplastic and healthy tissues that can be leveraged in cancer vaccine design; (b) The layers of tolerance that control T cell responses directed against antigens expressed in healthy tissues and tumors; and, (c) The hierarchy of antigenic epitope selection and display in response to whole cell vaccines, and how antigen processing and presentation can afford a degree of selectivity against tumors. We conclude with an example of early clinical data utilizing ValloVax™, an immunogenic placental endothelial cell vaccine that is being advanced to target the tumor endothelium of diverse cancers, and we report on the safety and efficacy of ValloVax™ for inducing immunity against tumor endothelial antigens. </p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/27071457/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">27071457</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC4830034/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC4830034</a> | DOI:<a href=https://doi.org/10.1186/s12967-016-0842-8>10.1186/s12967-016-0842-8</a></p></div>]]></content:encoded>
  255.      <guid isPermaLink="false">pubmed:27071457</guid>
  256.      <pubDate>Thu, 14 Apr 2016 06:00:00 -0400</pubDate>
  257.      <dc:creator>Samuel C Wagner</dc:creator>
  258.      <dc:creator>Neil H Riordan</dc:creator>
  259.      <dc:creator>Thomas E Ichim</dc:creator>
  260.      <dc:creator>Julia Szymanski</dc:creator>
  261.      <dc:creator>Hong Ma</dc:creator>
  262.      <dc:creator>Jesus A Perez</dc:creator>
  263.      <dc:creator>Javier Lopez</dc:creator>
  264.      <dc:creator>Juan J Plata-Munoz</dc:creator>
  265.      <dc:creator>Francisco Silva</dc:creator>
  266.      <dc:creator>Amit N Patel</dc:creator>
  267.      <dc:creator>Santosh Kesari</dc:creator>
  268.      <dc:date>2016-04-14</dc:date>
  269.      <dc:source>Journal of translational medicine</dc:source>
  270.      <dc:title>Safety of targeting tumor endothelial cell antigens</dc:title>
  271.      <dc:identifier>pmid:27071457</dc:identifier>
  272.      <dc:identifier>pmc:PMC4830034</dc:identifier>
  273.      <dc:identifier>doi:10.1186/s12967-016-0842-8</dc:identifier>
  274.    </item>
  275.    <item>
  276.      <title>Modulation of Cytokines in Cancer Patients by Intravenous Ascorbate Therapy</title>
  277.      <link>https://pubmed.ncbi.nlm.nih.gov/26724916/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  278.      <description>CONCLUSIONS: We are able to show that average z-scores for several inflammatory and angiogenesis promoting cytokines are positive, indicating that they are higher than averages for healthy controls, and that their levels decreased over the course of treatment. In addition, serum concentrations of tumor markers decreased during the time period of IVC treatment and there were reductions in cMyc and Ras, 2 proteins implicated in being upregulated in cancer.</description>
  279.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Med Sci Monit. 2016 Jan 3;22:14-25. doi: 10.12659/msm.895368.</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: Cytokines play an important role in tumor angiogenesis and inflammation. There is evidence in the literature that high doses of ascorbate can reduce inflammatory cytokine levels in cancer patients. The objective of this study was to investigate the effect of treatment by intravenous vitamin C (IVC) on cytokines and tumor markers.</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">MATERIAL/METHODS: With the availability of protein array kits allowing assessment of many cytokines in a single sample, we measured 174 cytokines and additional 54 proteins and tumor markers in 12 cancer patients before and after a series of IVC treatments.</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: Presented results show for our 12 patients the effect of treatment resulted in normalization of many cytokine levels. Cytokines that were most consistently elevated prior to treatments included M-CSF-R, Leptin, EGF, FGF-6, TNF-α, β, TARC, MCP-1,4, MIP, IL-4, 10, IL-4, and TGF-β. Cytokine levels tended to decrease during the course of treatment. These include mitogens (EGF, Fit-3 ligand, HGF, IGF-1, IL-21R) and chemo-attractants (CTAC, Eotaxin, E-selectin, Lymphotactin, MIP-1, MCP-1, TARC, SDF-1), as well as inflammation and angiogenesis factors (FGF-6, IL-1β, TGF-1).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: We are able to show that average z-scores for several inflammatory and angiogenesis promoting cytokines are positive, indicating that they are higher than averages for healthy controls, and that their levels decreased over the course of treatment. In addition, serum concentrations of tumor markers decreased during the time period of IVC treatment and there were reductions in cMyc and Ras, 2 proteins implicated in being upregulated in cancer.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/26724916/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">26724916</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC4756791/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC4756791</a> | DOI:<a href=https://doi.org/10.12659/msm.895368>10.12659/msm.895368</a></p></div>]]></content:encoded>
  280.      <guid isPermaLink="false">pubmed:26724916</guid>
  281.      <pubDate>Mon, 04 Jan 2016 06:00:00 -0500</pubDate>
  282.      <dc:creator>Nina Mikirova</dc:creator>
  283.      <dc:creator>Neil Riordan</dc:creator>
  284.      <dc:creator>Joseph Casciari</dc:creator>
  285.      <dc:date>2016-01-04</dc:date>
  286.      <dc:source>Medical science monitor : international medical journal of experimental and clinical research</dc:source>
  287.      <dc:title>Modulation of Cytokines in Cancer Patients by Intravenous Ascorbate Therapy</dc:title>
  288.      <dc:identifier>pmid:26724916</dc:identifier>
  289.      <dc:identifier>pmc:PMC4756791</dc:identifier>
  290.      <dc:identifier>doi:10.12659/msm.895368</dc:identifier>
  291.    </item>
  292.    <item>
  293.      <title>Case report of non-healing surgical wound treated with dehydrated human amniotic membrane</title>
  294.      <link>https://pubmed.ncbi.nlm.nih.gov/26205894/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  295.      <description>INTRODUCTION: Non-healing wounds can pose a medical challenge as in the case of vasculopathic venostasis resulting in a surgical ulcer. When traditional approaches to wound care fail, an amniotic patch (a dehydrated tissue allograft derived from human amnion) can function as a biologic scaffold to facilitate and enhance tissue regeneration and rehabilitation.</description>
  296.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2015 Jul 24;13:242. doi: 10.1186/s12967-015-0608-8.</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">INTRODUCTION: Non-healing wounds can pose a medical challenge as in the case of vasculopathic venostasis resulting in a surgical ulcer. When traditional approaches to wound care fail, an amniotic patch (a dehydrated tissue allograft derived from human amnion) can function as a biologic scaffold to facilitate and enhance tissue regeneration and rehabilitation.</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: Amniotic AlphaPatches contain concentrated molecules of PGE2, WNT4, and GDF-11 which have angiogenic, trophic, and anti-inflammatory effects on tissues that may be useful in enhancing wound healing.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">AIM-CASE REPORT: We present a case of a severe non-healing surgical wound in a 78-year-old male 17 days post right total knee arthroplasty. The full-thickness wound exhibited a mobile flap, measured 4 cm long × 3 cm wide, and showed undermining down to patellar tissue. We treated the wound conservatively for 6 weeks with no evidence of wound healing. Upon failure of the conservative treatment, two amniotic AlphaPatch (Amniotic Therapies, Dallas, TX, USA) were applied to the wound, and the wound healed completely in 10 weeks.</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 the OR, the wound was irrigated with three liters of double antibiotic solution under pulse lavage. Two dry amniotic AlphaPatch (4 cm × 4 cm) were placed over the wound with Acticoat applied on top.</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: At the two-week follow-up visit (following the incision and drainage of the wound dehiscence and application of the amniotic AlphaPatch), a central scab had formed centrally in the wound dehiscence area. At the four-week follow-up visit, the wound dehiscence area had completely scabbed over with no open areas left. At the eight-week follow-up visit, the scab had just fallen off, and the wound was healing well with immature skin representing the size of a penny. At the ten-week follow-up visit, the wound was completely healed.</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">DISCUSSION/CONCLUSION: Sterile, dehydrated amniotic tissue AlphaPatches (containing trophic factors known to enhance wound healing) have proven effective in completely healing an otherwise non-healing wound in a 78-year-old male who failed six weeks of conservative wound care treatment.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/26205894/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">26205894</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC4513638/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC4513638</a> | DOI:<a href=https://doi.org/10.1186/s12967-015-0608-8>10.1186/s12967-015-0608-8</a></p></div>]]></content:encoded>
  297.      <guid isPermaLink="false">pubmed:26205894</guid>
  298.      <pubDate>Sat, 25 Jul 2015 06:00:00 -0400</pubDate>
  299.      <dc:creator>Neil H Riordan</dc:creator>
  300.      <dc:creator>Ben A George</dc:creator>
  301.      <dc:creator>Troy B Chandler</dc:creator>
  302.      <dc:creator>Randall W McKenna</dc:creator>
  303.      <dc:date>2015-07-25</dc:date>
  304.      <dc:source>Journal of translational medicine</dc:source>
  305.      <dc:title>Case report of non-healing surgical wound treated with dehydrated human amniotic membrane</dc:title>
  306.      <dc:identifier>pmid:26205894</dc:identifier>
  307.      <dc:identifier>pmc:PMC4513638</dc:identifier>
  308.      <dc:identifier>doi:10.1186/s12967-015-0608-8</dc:identifier>
  309.    </item>
  310.    <item>
  311.      <title>Scalable efficient expansion of mesenchymal stem cells in xeno free media using commercially available reagents</title>
  312.      <link>https://pubmed.ncbi.nlm.nih.gov/26183703/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  313.      <description>CONCLUSIONS: These data support the implementation of human platelet lysate supplemented media as an alternative to xenogeneic containing preparations which may lead to safer MSC products with therapeutic uses.</description>
  314.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2015 Jul 17;13:232. doi: 10.1186/s12967-015-0561-6.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: The rapid clinical translation of mesenchymal stem cells (MSC) has resulted in the development of cell-based strategies for multiple indications. Unfortunately one major barrier to widespread implementation of MSC-based therapies is the limited supply of fetal calf serum (FCS) used to expand cells to therapeutic numbers. Additionally, the xenogeneic element of fetal calf serum has been previously demonstrated to stimulate antibody mediated reactions and in some cases sensitization leading to anaphylaxis.</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">METHOD: XcytePLUS™ media, a human platelet lysate based product, was used to supplement the culture medium at 5, 7.5 and 10% and compared to fetal calf serum at 10%, for human umbilical cord MSC expansion. Properties of the expanded cells were investigated.</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: This study demonstrated equivalent or superior effects of human platelet lysate compared to standard FCS supplemented media, based on doubling rate, without loss of identity or function, as demonstrated with flow cytometry characterization. Differentiation into osteocytes, adipocytes and chondrocytes was comparable from cells expanded in either media supplement.</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: These data support the implementation of human platelet lysate supplemented media as an alternative to xenogeneic containing preparations which may lead to safer MSC products with therapeutic uses.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/26183703/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">26183703</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC4504159/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC4504159</a> | DOI:<a href=https://doi.org/10.1186/s12967-015-0561-6>10.1186/s12967-015-0561-6</a></p></div>]]></content:encoded>
  315.      <guid isPermaLink="false">pubmed:26183703</guid>
  316.      <pubDate>Sat, 18 Jul 2015 06:00:00 -0400</pubDate>
  317.      <dc:creator>Neil H Riordan</dc:creator>
  318.      <dc:creator>Marialaura Madrigal</dc:creator>
  319.      <dc:creator>Jason Reneau</dc:creator>
  320.      <dc:creator>Kathya de Cupeiro</dc:creator>
  321.      <dc:creator>Natalia Jiménez</dc:creator>
  322.      <dc:creator>Sergio Ruiz</dc:creator>
  323.      <dc:creator>Nelsy Sanchez</dc:creator>
  324.      <dc:creator>Thomas E Ichim</dc:creator>
  325.      <dc:creator>Francisco Silva</dc:creator>
  326.      <dc:creator>Amit N Patel</dc:creator>
  327.      <dc:date>2015-07-18</dc:date>
  328.      <dc:source>Journal of translational medicine</dc:source>
  329.      <dc:title>Scalable efficient expansion of mesenchymal stem cells in xeno free media using commercially available reagents</dc:title>
  330.      <dc:identifier>pmid:26183703</dc:identifier>
  331.      <dc:identifier>pmc:PMC4504159</dc:identifier>
  332.      <dc:identifier>doi:10.1186/s12967-015-0561-6</dc:identifier>
  333.    </item>
  334.    <item>
  335.      <title>Metabolic correction: a functional biochemical mechanism against disease--Part 1: concept and historical background</title>
  336.      <link>https://pubmed.ncbi.nlm.nih.gov/25856870/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  337.      <description>Human physiology depends on countless biochemical reactions, numerous of which are co-dependent and interrelated. The speed and level of completion of reactions usually depend on the availability of precursors and enzymes. The enzymatic activity depends on the bioavailability of micronutrient cofactors such as vitamins and minerals. In order to achieve a healthy physiological state, the organism requires that biochemical reactions occur at a controlled rate. To achieve this state it is required...</description>
  338.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">P R Health Sci J. 2015 Mar;34(1):3-8.</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">Human physiology depends on countless biochemical reactions, numerous of which are co-dependent and interrelated. The speed and level of completion of reactions usually depend on the availability of precursors and enzymes. The enzymatic activity depends on the bioavailability of micronutrient cofactors such as vitamins and minerals. In order to achieve a healthy physiological state, the organism requires that biochemical reactions occur at a controlled rate. To achieve this state it is required that metabolic reactions reach what can be considered an optimal metabolic equilibrium. A combination of genetic makeup, dietary patterns, trauma, disease, toxins, medications, and environmental stressors can elevate the demand for the nutrients needed to reach this optimal metabolic equilibrium. In this, part 1, the general concept of metabolic correction is presented with an elaboration explaining how this concept is increasing in importance as we become aware of the presence of genetic variants that affect enzymatic reactions causing metabolic disturbances that themselves favor or promote the disease state. In addition, part 1 reviews how prominent scientists have contributed in fundamental ways to our understanding of the importance of micronutrients in health and disease and in the development of the metabolic correction concept.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/25856870/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">25856870</a></p></div>]]></content:encoded>
  339.      <guid isPermaLink="false">pubmed:25856870</guid>
  340.      <pubDate>Sat, 11 Apr 2015 06:00:00 -0400</pubDate>
  341.      <dc:creator>Michael J González</dc:creator>
  342.      <dc:creator>Jorge R Miranda-Massari</dc:creator>
  343.      <dc:creator>Jorge Duconge</dc:creator>
  344.      <dc:creator>Myriam Z Allende-Vigo</dc:creator>
  345.      <dc:creator>Francisco J Jiménez-Ramírez</dc:creator>
  346.      <dc:creator>Kenneth Cintrón</dc:creator>
  347.      <dc:creator>Jose R Rodríguez-Gómez</dc:creator>
  348.      <dc:creator>Glorivee Rosario</dc:creator>
  349.      <dc:creator>Carlos Ricart</dc:creator>
  350.      <dc:creator>Juan A Santiago-Cornier</dc:creator>
  351.      <dc:creator>Rafael Zaragoza-Urdaz</dc:creator>
  352.      <dc:creator>Alex Vázquez</dc:creator>
  353.      <dc:creator>Steve Hickey</dc:creator>
  354.      <dc:creator>Miguel Jabbar-Berdiel</dc:creator>
  355.      <dc:creator>Neil Riordan</dc:creator>
  356.      <dc:creator>Thomas Ichim</dc:creator>
  357.      <dc:creator>Oscar Santiago</dc:creator>
  358.      <dc:creator>Gilberto Alvarado</dc:creator>
  359.      <dc:creator>Pramod Vora</dc:creator>
  360.      <dc:date>2015-04-11</dc:date>
  361.      <dc:source>Puerto Rico health sciences journal</dc:source>
  362.      <dc:title>Metabolic correction: a functional biochemical mechanism against disease--Part 1: concept and historical background</dc:title>
  363.      <dc:identifier>pmid:25856870</dc:identifier>
  364.    </item>
  365.    <item>
  366.      <title>A review of therapeutic effects of mesenchymal stem cell secretions and induction of secretory modification by different culture methods</title>
  367.      <link>https://pubmed.ncbi.nlm.nih.gov/25304688/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  368.      <description>The mesenchymal stem cell (MSC) is being broadly studied in clinical trials. Contrary to the early paradigm of cell replacement and differentiation as a therapeutic mechanism of action, evidence is mounting that the secretions of the cells are responsible for their therapeutic effects. These secretions include molecules and extracellular vesicles that have both local and distant effects. This review summarizes the up- and down-regulation of MSC anti-inflammatory, immune modulating, anti-tumor,...</description>
  369.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2014 Oct 11;12:260. doi: 10.1186/s12967-014-0260-8.</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 mesenchymal stem cell (MSC) is being broadly studied in clinical trials. Contrary to the early paradigm of cell replacement and differentiation as a therapeutic mechanism of action, evidence is mounting that the secretions of the cells are responsible for their therapeutic effects. These secretions include molecules and extracellular vesicles that have both local and distant effects. This review summarizes the up- and down-regulation of MSC anti-inflammatory, immune modulating, anti-tumor, and regenerative secretions resulting from different stimuli including: a) hypoxia, which increases the production of growth factors and anti-inflammatory molecules; b) pro-inflammatory stimuli that induce the secretion of immune modulating and anti-inflammatory factors; and c) 3 dimensional growth which up regulates the production of anti-cancer factors and anti-inflammatory molecules compared to monolayer culture. Finally we review in detail the most important factors present in conditioned medium of MSC that can be considered protagonists of MSC physiological effects including HGF, TGF-b, VEGF, TSG-6, PGE2 and galectins 1, and 9. We conclude that there is potential for the development of acellular therapeutic interventions for autoimmune, inflammatory, and malignant diseases and tissue regeneration from cellular secretions derived from MSCs cultured under the appropriate conditions. </p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/25304688/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">25304688</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC4197270/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC4197270</a> | DOI:<a href=https://doi.org/10.1186/s12967-014-0260-8>10.1186/s12967-014-0260-8</a></p></div>]]></content:encoded>
  370.      <guid isPermaLink="false">pubmed:25304688</guid>
  371.      <pubDate>Sun, 12 Oct 2014 06:00:00 -0400</pubDate>
  372.      <dc:creator>Marialaura Madrigal</dc:creator>
  373.      <dc:creator>Kosagisharaf S Rao</dc:creator>
  374.      <dc:creator>Neil H Riordan</dc:creator>
  375.      <dc:date>2014-10-12</dc:date>
  376.      <dc:source>Journal of translational medicine</dc:source>
  377.      <dc:title>A review of therapeutic effects of mesenchymal stem cell secretions and induction of secretory modification by different culture methods</dc:title>
  378.      <dc:identifier>pmid:25304688</dc:identifier>
  379.      <dc:identifier>pmc:PMC4197270</dc:identifier>
  380.      <dc:identifier>doi:10.1186/s12967-014-0260-8</dc:identifier>
  381.    </item>
  382.    <item>
  383.      <title>Intravenous ascorbic acid as an adjuvant to interleukin-2 immunotherapy</title>
  384.      <link>https://pubmed.ncbi.nlm.nih.gov/24884532/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  385.      <description>Interleukin-2 (IL-2) therapy has been demonstrated to induce responses in 10-20% of advanced melanoma and renal cell carcinoma patients, which translates into durable remissions in up to half of the responsers. Unfortunately the use of IL-2 has been associated with severe toxicity and death. It has been previously observed and reported that IL-2 therapy causes a major drop in circulating levels of ascorbic acid (AA). The IL-2 induced toxicity shares many features with sepsis such as capillary...</description>
  386.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2014 May 13;12:127. doi: 10.1186/1479-5876-12-127.</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">Interleukin-2 (IL-2) therapy has been demonstrated to induce responses in 10-20% of advanced melanoma and renal cell carcinoma patients, which translates into durable remissions in up to half of the responsers. Unfortunately the use of IL-2 has been associated with severe toxicity and death. It has been previously observed and reported that IL-2 therapy causes a major drop in circulating levels of ascorbic acid (AA). The IL-2 induced toxicity shares many features with sepsis such as capillary leakage, systemic complement activation, and a relatively non-specific rise in inflammatory mediators such as TNF-alpha, C-reactive protein, and in advanced cases organ failure. Animal models and clinical studies have shown rapid depletion of AA in conditions of sepsis and amelioration associated with administration of AA (JTM 9:1-7, 2011). In contrast to other approaches to dealing with IL-2 toxicity, which may also interfere with therapeutic effects, AA possesses the added advantage of having direct antitumor activity through cytotoxic mechanisms and suppression of angiogenesis. Here we present a scientific rationale to support the assessment of intravenous AA as an adjuvant to decrease IL-2 mediated toxicity and possibly increase treatment efficacy. </p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/24884532/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">24884532</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC4028098/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC4028098</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-12-127>10.1186/1479-5876-12-127</a></p></div>]]></content:encoded>
  387.      <guid isPermaLink="false">pubmed:24884532</guid>
  388.      <pubDate>Tue, 03 Jun 2014 06:00:00 -0400</pubDate>
  389.      <dc:creator>Samuel C Wagner</dc:creator>
  390.      <dc:creator>Boris Markosian</dc:creator>
  391.      <dc:creator>Naseem Ajili</dc:creator>
  392.      <dc:creator>Brandon R Dolan</dc:creator>
  393.      <dc:creator>Andy J Kim</dc:creator>
  394.      <dc:creator>Doru T Alexandrescu</dc:creator>
  395.      <dc:creator>Constantin A Dasanu</dc:creator>
  396.      <dc:creator>Boris Minev</dc:creator>
  397.      <dc:creator>James Koropatnick</dc:creator>
  398.      <dc:creator>Francesco M Marincola</dc:creator>
  399.      <dc:creator>Neil H Riordan</dc:creator>
  400.      <dc:date>2014-06-03</dc:date>
  401.      <dc:source>Journal of translational medicine</dc:source>
  402.      <dc:title>Intravenous ascorbic acid as an adjuvant to interleukin-2 immunotherapy</dc:title>
  403.      <dc:identifier>pmid:24884532</dc:identifier>
  404.      <dc:identifier>pmc:PMC4028098</dc:identifier>
  405.      <dc:identifier>doi:10.1186/1479-5876-12-127</dc:identifier>
  406.    </item>
  407.    <item>
  408.      <title>Schedule Dependence in Cancer Therapy: Intravenous Vitamin C and the Systemic Saturation Hypothesis</title>
  409.      <link>https://pubmed.ncbi.nlm.nih.gov/24860238/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  410.      <description>Despite the significant number of in vitro and in vivo studies to assess vitamin C effects on cancer following the application of large doses and its extensive use by alternative medicine practitioners in the USA; the precise schedule for successful cancer therapy is still unknown. Based on interpretation of the available data, we postulate that the relationship between Vitamin C doses and plasma concentration x time, the capability of tissue stores upon distribution, and the saturable mechanism...</description>
  411.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Orthomol Med. 2012 Jan 1;27(1):9-12.</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">Despite the significant number of in vitro and in vivo studies to assess vitamin C effects on cancer following the application of large doses and its extensive use by alternative medicine practitioners in the USA; the precise schedule for successful cancer therapy is still unknown. Based on interpretation of the available data, we postulate that the relationship between Vitamin C doses and plasma concentration x time, the capability of tissue stores upon distribution, and the saturable mechanism of urinary excretion are all important determinants to understand the physiology of high intravenous vitamin C dose administration and its effect on cancer. Practitioners should pay more attention to the cumulative vitamin C effect instead of the vitamin C concentrations to account for observed discrepancy in antitumor response. We suggest that multiple, intermittent, short-term intravenous infusions of vitamin C over a longer time period will correlate with greater antitumor effects than do single continuous IV doses of the same total exposure. This approach would be expected to minimize saturation of renal reabsorption, providing a continuous "dynamic flow" of vitamin C in the body for optimal systemic exposure and clinical outcomes. This prevents the "systemic saturation" phenomena, which may recycle vitamin C and render it less effective as an anticancer agent. Nonetheless, more pharmacokinetic and pharmacodynamic studies are needed to fully understand this schedule-dependence phenomenon.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/24860238/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">24860238</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC4031610/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC4031610</a></p></div>]]></content:encoded>
  412.      <guid isPermaLink="false">pubmed:24860238</guid>
  413.      <pubDate>Tue, 27 May 2014 06:00:00 -0400</pubDate>
  414.      <dc:creator>Michael J Gonzalez</dc:creator>
  415.      <dc:creator>Jorge R Miranda Massari</dc:creator>
  416.      <dc:creator>Jorge Duconge</dc:creator>
  417.      <dc:creator>Neil H Riordan</dc:creator>
  418.      <dc:creator>Thomas Ichim</dc:creator>
  419.      <dc:date>2014-05-27</dc:date>
  420.      <dc:source>Journal of orthomolecular medicine : official journal of the Academy of Orthomolecular Medicine</dc:source>
  421.      <dc:title>Schedule Dependence in Cancer Therapy: Intravenous Vitamin C and the Systemic Saturation Hypothesis</dc:title>
  422.      <dc:identifier>pmid:24860238</dc:identifier>
  423.      <dc:identifier>pmc:PMC4031610</dc:identifier>
  424.    </item>
  425.    <item>
  426.      <title>Clinical experience with intravenous administration of ascorbic acid: achievable levels in blood for different states of inflammation and disease in cancer patients</title>
  427.      <link>https://pubmed.ncbi.nlm.nih.gov/23947403/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  428.      <description>CONCLUSIONS: The data indicate that, while potentially therapeutic plasma ascorbate concentrations can be achieved with IVC, levels attained will vary based on tumor burden and degree of inflammation (among other factors). Evidence suggests that IVC may be able to modulate inflammation, which in turn might improve outcomes for cancer patients. IVC may serve as a safe, adjunctive therapy in clinical cancer care.</description>
  429.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2013 Aug 15;11:191. doi: 10.1186/1479-5876-11-191.</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: Ascorbic acid (vitamin C, ascorbate) is a key water soluble antioxidant that, when administered in doses well above its recommended dietary allowance, may have preventative and therapeutic value against a number of pathologies. The intravenous administration of high dose ascorbate (IVC) has increased in popularity among complementary and alternative medicine practitioners: thousands of patients received IVC, at an average dose of 0.5 g/kg, without significant side effects. While IVC may have a variety of possible applications, it has generated the most interest for its potential use in treating 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">METHODS: Medical records of patients with cancer treated with IVC at the Riordan Clinic were retrospectively reviewed. Cancer patients, for whom plasma ascorbate concentration data before and after treatment were available, along with C-reactive protein (CRP) measurements, were chosen for 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: The results of the analysis can be summarized as follows. IVC produces peak plasma ascorbate concentrations on the order of ten millimolars with lower peak plasma concentrations obtained in cancer patients as compared to healthy subjects. Cancer patients who are deficient in vitamin C prior to therapy tend to achieve lower plasma levels post infusion. High inflammation or tumor burdens, as measured by CRP or tumor antigen levels, tend to lower peak plasma ascorbate levels after IVC. When compared to patients with localized tumors, patients with metastatic tumors tend to achieve lower post infusion plasma ascorbate concentrations.</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 data indicate that, while potentially therapeutic plasma ascorbate concentrations can be achieved with IVC, levels attained will vary based on tumor burden and degree of inflammation (among other factors). Evidence suggests that IVC may be able to modulate inflammation, which in turn might improve outcomes for cancer patients. IVC may serve as a safe, adjunctive therapy in clinical cancer care.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/23947403/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">23947403</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3751545/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3751545</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-11-191>10.1186/1479-5876-11-191</a></p></div>]]></content:encoded>
  430.      <guid isPermaLink="false">pubmed:23947403</guid>
  431.      <pubDate>Sat, 17 Aug 2013 06:00:00 -0400</pubDate>
  432.      <dc:creator>Nina Mikirova</dc:creator>
  433.      <dc:creator>Joseph Casciari</dc:creator>
  434.      <dc:creator>Neil Riordan</dc:creator>
  435.      <dc:creator>Ronald Hunninghake</dc:creator>
  436.      <dc:date>2013-08-17</dc:date>
  437.      <dc:source>Journal of translational medicine</dc:source>
  438.      <dc:title>Clinical experience with intravenous administration of ascorbic acid: achievable levels in blood for different states of inflammation and disease in cancer patients</dc:title>
  439.      <dc:identifier>pmid:23947403</dc:identifier>
  440.      <dc:identifier>pmc:PMC3751545</dc:identifier>
  441.      <dc:identifier>doi:10.1186/1479-5876-11-191</dc:identifier>
  442.    </item>
  443.    <item>
  444.      <title>Mitochondria, Energy and Cancer: The Relationship with Ascorbic Acid</title>
  445.      <link>https://pubmed.ncbi.nlm.nih.gov/23565030/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  446.      <description>Ascorbic Acid (AA) has been used in the prevention and treatment of cancer with reported effectiveness. Mitochondria may be one of the principal targets of ascorbate's cellular activity and it may play an important role in the development and progression of cancer. Mitochondria, besides generating adenosine triphosphate (ATP), has a role in apoptosis regulation and in the production of regulatory oxidative species that may be relevant in gene expression. At higher concentrations AA may increase...</description>
  447.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Orthomol Med. 2010;25(1):29-38.</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">Ascorbic Acid (AA) has been used in the prevention and treatment of cancer with reported effectiveness. Mitochondria may be one of the principal targets of ascorbate's cellular activity and it may play an important role in the development and progression of cancer. Mitochondria, besides generating adenosine triphosphate (ATP), has a role in apoptosis regulation and in the production of regulatory oxidative species that may be relevant in gene expression. At higher concentrations AA may increase ATP production by increasing mitochondrial electron flux, also may induce apoptotic cell death in tumor cell lines, probably via its pro-oxidant action In contrast, at lower concentrations AA displays antioxidant properties that may prevent the activation of oxidant-induced apoptosis. These concentration dependent activities of ascorbate may explain in part the seemingly contradictory results that have been reported previously.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/23565030/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">23565030</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3615720/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3615720</a></p></div>]]></content:encoded>
  448.      <guid isPermaLink="false">pubmed:23565030</guid>
  449.      <pubDate>Tue, 09 Apr 2013 06:00:00 -0400</pubDate>
  450.      <dc:creator>Michael J González</dc:creator>
  451.      <dc:creator>Glorivee Rosario-Pérez</dc:creator>
  452.      <dc:creator>Angélica M Guzmán</dc:creator>
  453.      <dc:creator>Jorge R Miranda-Massari</dc:creator>
  454.      <dc:creator>Jorge Duconge</dc:creator>
  455.      <dc:creator>Julio Lavergne</dc:creator>
  456.      <dc:creator>Nadia Fernandez</dc:creator>
  457.      <dc:creator>Norma Ortiz</dc:creator>
  458.      <dc:creator>Ana Quintero</dc:creator>
  459.      <dc:creator>Nina Mikirova</dc:creator>
  460.      <dc:creator>Neil H Riordan</dc:creator>
  461.      <dc:creator>Carlos M Ricart</dc:creator>
  462.      <dc:date>2013-04-09</dc:date>
  463.      <dc:source>Journal of orthomolecular medicine : official journal of the Academy of Orthomolecular Medicine</dc:source>
  464.      <dc:title>Mitochondria, Energy and Cancer: The Relationship with Ascorbic Acid</dc:title>
  465.      <dc:identifier>pmid:23565030</dc:identifier>
  466.      <dc:identifier>pmc:PMC3615720</dc:identifier>
  467.    </item>
  468.    <item>
  469.      <title>The bio-energetic theory of carcinogenesis</title>
  470.      <link>https://pubmed.ncbi.nlm.nih.gov/22809841/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  471.      <description>The altered energy metabolism of tumor cells provides a viable target for a non toxic chemotherapeutic approach. An increased glucose consumption rate has been observed in malignant cells. Warburg (Nobel Laureate in medicine) postulated that the respiratory process of malignant cells was impaired and that the transformation of a normal cell to malignant was due to defects in the aerobic respiratory pathways. Szent-Györgyi (Nobel Laureate in medicine) also viewed cancer as originating from...</description>
  472.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Med Hypotheses. 2012 Oct;79(4):433-9. doi: 10.1016/j.mehy.2012.06.015. Epub 2012 Jul 17.</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 altered energy metabolism of tumor cells provides a viable target for a non toxic chemotherapeutic approach. An increased glucose consumption rate has been observed in malignant cells. Warburg (Nobel Laureate in medicine) postulated that the respiratory process of malignant cells was impaired and that the transformation of a normal cell to malignant was due to defects in the aerobic respiratory pathways. Szent-Györgyi (Nobel Laureate in medicine) also viewed cancer as originating from insufficient availability of oxygen. Oxygen by itself has an inhibitory action on malignant cell proliferation by interfering with anaerobic respiration (fermentation and lactic acid production). Interestingly, during cell differentiation (where cell energy level is high) there is an increased cellular production of oxidants that appear to provide one type of physiological stimulation for changes in gene expression that may lead to a terminal differentiated state. The failure to maintain high ATP production (high cell energy levels) may be a consequence of inactivation of key enzymes, especially those related to the Krebs cycle and the electron transport system. A distorted mitochondrial function (transmembrane potential) may result. This aspect could be suggestive of an important mitochondrial involvement in the carcinogenic process in addition to presenting it as a possible therapeutic target for cancer. Intermediate metabolic correction of the mitochondria is postulated as a possible non-toxic therapeutic approach for cancer.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/22809841/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">22809841</a> | DOI:<a href=https://doi.org/10.1016/j.mehy.2012.06.015>10.1016/j.mehy.2012.06.015</a></p></div>]]></content:encoded>
  473.      <guid isPermaLink="false">pubmed:22809841</guid>
  474.      <pubDate>Fri, 20 Jul 2012 06:00:00 -0400</pubDate>
  475.      <dc:creator>Michael J Gonzalez</dc:creator>
  476.      <dc:creator>Jorge R Miranda Massari</dc:creator>
  477.      <dc:creator>Jorge Duconge</dc:creator>
  478.      <dc:creator>Neil H Riordan</dc:creator>
  479.      <dc:creator>Thomas Ichim</dc:creator>
  480.      <dc:creator>Ana I Quintero-Del-Rio</dc:creator>
  481.      <dc:creator>Norma Ortiz</dc:creator>
  482.      <dc:date>2012-07-20</dc:date>
  483.      <dc:source>Medical hypotheses</dc:source>
  484.      <dc:title>The bio-energetic theory of carcinogenesis</dc:title>
  485.      <dc:identifier>pmid:22809841</dc:identifier>
  486.      <dc:identifier>doi:10.1016/j.mehy.2012.06.015</dc:identifier>
  487.    </item>
  488.    <item>
  489.      <title>Autologous stromal vascular fraction therapy for rheumatoid arthritis: rationale and clinical safety</title>
  490.      <link>https://pubmed.ncbi.nlm.nih.gov/22313603/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  491.      <description> Advancements in rheumatoid arthritis (RA) treatment protocols and introduction of targeted biological therapies have markedly improved patient outcomes, despite this, up to 50% of patients still fail to achieve a significant clinical response. In veterinary medicine, stem cell therapy in the form of autologous stromal vascular fraction (SVF) is an accepted therapeutic modality for degenerative conditions with 80% improvement and no serious treatment associated adverse events reported. Clinical...</description>
  492.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Int Arch Med. 2012 Feb 8;5:5. doi: 10.1186/1755-7682-5-5.</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"> Advancements in rheumatoid arthritis (RA) treatment protocols and introduction of targeted biological therapies have markedly improved patient outcomes, despite this, up to 50% of patients still fail to achieve a significant clinical response. In veterinary medicine, stem cell therapy in the form of autologous stromal vascular fraction (SVF) is an accepted therapeutic modality for degenerative conditions with 80% improvement and no serious treatment associated adverse events reported. Clinical translation of SVF therapy relies on confirmation of veterinary findings in targeted patient populations. Here we describe the rationale and preclinical data supporting the use of autologous SVF in treatment of RA, as well as provide 1, 3, 6, and 13 month safety outcomes in 13 RA patients treated with this approach.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/22313603/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">22313603</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3296619/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3296619</a> | DOI:<a href=https://doi.org/10.1186/1755-7682-5-5>10.1186/1755-7682-5-5</a></p></div>]]></content:encoded>
  493.      <guid isPermaLink="false">pubmed:22313603</guid>
  494.      <pubDate>Thu, 09 Feb 2012 06:00:00 -0500</pubDate>
  495.      <dc:creator>Jorge Paz Rodriguez</dc:creator>
  496.      <dc:creator>Michael P Murphy</dc:creator>
  497.      <dc:creator>Soonjun Hong</dc:creator>
  498.      <dc:creator>Marialaura Madrigal</dc:creator>
  499.      <dc:creator>Keith L March</dc:creator>
  500.      <dc:creator>Boris Minev</dc:creator>
  501.      <dc:creator>Robert J Harman</dc:creator>
  502.      <dc:creator>Chien-Shing Chen</dc:creator>
  503.      <dc:creator>Ruben Berrocal Timmons</dc:creator>
  504.      <dc:creator>Annette M Marleau</dc:creator>
  505.      <dc:creator>Neil H Riordan</dc:creator>
  506.      <dc:date>2012-02-09</dc:date>
  507.      <dc:source>International archives of medicine</dc:source>
  508.      <dc:title>Autologous stromal vascular fraction therapy for rheumatoid arthritis: rationale and clinical safety</dc:title>
  509.      <dc:identifier>pmid:22313603</dc:identifier>
  510.      <dc:identifier>pmc:PMC3296619</dc:identifier>
  511.      <dc:identifier>doi:10.1186/1755-7682-5-5</dc:identifier>
  512.    </item>
  513.    <item>
  514.      <title>The king is dead, long live the king: entering a new era of stem cell research and clinical development</title>
  515.      <link>https://pubmed.ncbi.nlm.nih.gov/22185188/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  516.      <description>In mid November the biopharma industry was shocked by the announcement from Geron that they were ending work on embryonic stem cell research and therapy. For more than 10 years the public image of all stem cell research has been equated with embryonic stem cells. Unfortunately, a fundamentally important medical and financial fact was being ignored: embryonic stem cell therapy is extremely immature. In parallel to efforts in embryonic stem cell research and development, scientists and physicians...</description>
  517.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2011 Dec 20;9:218. doi: 10.1186/1479-5876-9-218.</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 mid November the biopharma industry was shocked by the announcement from Geron that they were ending work on embryonic stem cell research and therapy. For more than 10 years the public image of all stem cell research has been equated with embryonic stem cells. Unfortunately, a fundamentally important medical and financial fact was being ignored: embryonic stem cell therapy is extremely immature. In parallel to efforts in embryonic stem cell research and development, scientists and physicians in the field of adult stem cells realized that the natural role of adult stem cells in the body is to promote healing and to act like endogenous "repair cells" and, as a result, numerous companies have entered the field of adult stem cell therapy with the goal of expanding numbers of adult stem cells for administration to patients with various conditions. In contrast to embryonic stem cells, which are extremely expensive and potentially dangerous, adult cell cells are inexpensive and have an excellent safety record when used in humans. Many studies are now showing that adult stem cells are practical, patient-applicable, therapeutics that are very close to being available for incorporation into the practice of medicine. These events signal the entrance of the field of stem cells into a new era: an era where hype and misinformation no longer triumph over economic and medical realities.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/22185188/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">22185188</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3275507/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3275507</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-9-218>10.1186/1479-5876-9-218</a></p></div>]]></content:encoded>
  518.      <guid isPermaLink="false">pubmed:22185188</guid>
  519.      <pubDate>Thu, 22 Dec 2011 06:00:00 -0500</pubDate>
  520.      <dc:creator>Thomas Ichim</dc:creator>
  521.      <dc:creator>Neil H Riordan</dc:creator>
  522.      <dc:creator>David F Stroncek</dc:creator>
  523.      <dc:date>2011-12-22</dc:date>
  524.      <dc:source>Journal of translational medicine</dc:source>
  525.      <dc:title>The king is dead, long live the king: entering a new era of stem cell research and clinical development</dc:title>
  526.      <dc:identifier>pmid:22185188</dc:identifier>
  527.      <dc:identifier>pmc:PMC3275507</dc:identifier>
  528.      <dc:identifier>doi:10.1186/1479-5876-9-218</dc:identifier>
  529.    </item>
  530.    <item>
  531.      <title>IFN-conditioned dendritic cells for the therapy of melanoma: what is missing?</title>
  532.      <link>https://pubmed.ncbi.nlm.nih.gov/22025902/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  533.      <description>No abstract</description>
  534.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Immunother. 2011 Oct;34(8):607-609. doi: 10.1097/CJI.0b013e31822b9ffc.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/22025902/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">22025902</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3184394/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3184394</a> | DOI:<a href=https://doi.org/10.1097/CJI.0b013e31822b9ffc>10.1097/CJI.0b013e31822b9ffc</a></p></div>]]></content:encoded>
  535.      <guid isPermaLink="false">pubmed:22025902</guid>
  536.      <pubDate>Wed, 26 Oct 2011 06:00:00 -0400</pubDate>
  537.      <dc:creator>Doru T Alexandrescu</dc:creator>
  538.      <dc:creator>Thomas E Ichim</dc:creator>
  539.      <dc:creator>Neil H Riordan</dc:creator>
  540.      <dc:creator>Francesco M Marincola</dc:creator>
  541.      <dc:creator>Constantin A Dasanu</dc:creator>
  542.      <dc:date>2011-10-26</dc:date>
  543.      <dc:source>Journal of immunotherapy (Hagerstown, Md. : 1997)</dc:source>
  544.      <dc:title>IFN-conditioned dendritic cells for the therapy of melanoma: what is missing?</dc:title>
  545.      <dc:identifier>pmid:22025902</dc:identifier>
  546.      <dc:identifier>pmc:PMC3184394</dc:identifier>
  547.      <dc:identifier>doi:10.1097/CJI.0b013e31822b9ffc</dc:identifier>
  548.    </item>
  549.    <item>
  550.      <title>Could metabolic syndrome, lipodystrophy, and aging be mesenchymal stem cell exhaustion syndromes?</title>
  551.      <link>https://pubmed.ncbi.nlm.nih.gov/21716667/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  552.      <description>One of the most important and complex diseases of modern society is metabolic syndrome. This syndrome has not been completely understood, and therefore an effective treatment is not available yet. We propose a possible stem cell mechanism involved in the development of metabolic syndrome. This way of thinking lets us consider also other significant pathologies that could have similar etiopathogenic pathways, like lipodystrophic syndromes, progeria, and aging. All these clinical situations could...</description>
  553.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Stem Cells Int. 2011;2011:943216. doi: 10.4061/2011/943216. Epub 2011 Jun 13.</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">One of the most important and complex diseases of modern society is metabolic syndrome. This syndrome has not been completely understood, and therefore an effective treatment is not available yet. We propose a possible stem cell mechanism involved in the development of metabolic syndrome. This way of thinking lets us consider also other significant pathologies that could have similar etiopathogenic pathways, like lipodystrophic syndromes, progeria, and aging. All these clinical situations could be the consequence of a progressive and persistent stem cell exhaustion syndrome (SCES). The main outcome of this SCES would be an irreversible loss of the effective regenerative mesenchymal stem cells (MSCs) pools. In this way, the normal repairing capacities of the organism could become inefficient. Our point of view could open the possibility for a new strategy of treatment in metabolic syndrome, lipodystrophic syndromes, progeria, and even aging: stem cell therapies.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/21716667/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">21716667</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3118295/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3118295</a> | DOI:<a href=https://doi.org/10.4061/2011/943216>10.4061/2011/943216</a></p></div>]]></content:encoded>
  554.      <guid isPermaLink="false">pubmed:21716667</guid>
  555.      <pubDate>Fri, 01 Jul 2011 06:00:00 -0400</pubDate>
  556.      <dc:creator>Eduardo Mansilla</dc:creator>
  557.      <dc:creator>Vanina Díaz Aquino</dc:creator>
  558.      <dc:creator>Daniel Zambón</dc:creator>
  559.      <dc:creator>Gustavo Horacio Marin</dc:creator>
  560.      <dc:creator>Karina Mártire</dc:creator>
  561.      <dc:creator>Gustavo Roque</dc:creator>
  562.      <dc:creator>Thomas Ichim</dc:creator>
  563.      <dc:creator>Neil H Riordan</dc:creator>
  564.      <dc:creator>Amit Patel</dc:creator>
  565.      <dc:creator>Flavio Sturla</dc:creator>
  566.      <dc:creator>Gustavo Larsen</dc:creator>
  567.      <dc:creator>Rubén Spretz</dc:creator>
  568.      <dc:creator>Luis Núñez</dc:creator>
  569.      <dc:creator>Carlos Soratti</dc:creator>
  570.      <dc:creator>Ricardo Ibar</dc:creator>
  571.      <dc:creator>Michiel van Leeuwen</dc:creator>
  572.      <dc:creator>José María Tau</dc:creator>
  573.      <dc:creator>Hugo Drago</dc:creator>
  574.      <dc:creator>Alberto Maceira</dc:creator>
  575.      <dc:date>2011-07-01</dc:date>
  576.      <dc:source>Stem cells international</dc:source>
  577.      <dc:title>Could metabolic syndrome, lipodystrophy, and aging be mesenchymal stem cell exhaustion syndromes?</dc:title>
  578.      <dc:identifier>pmid:21716667</dc:identifier>
  579.      <dc:identifier>pmc:PMC3118295</dc:identifier>
  580.      <dc:identifier>doi:10.4061/2011/943216</dc:identifier>
  581.    </item>
  582.    <item>
  583.      <title>Intravenous ascorbic acid to prevent and treat cancer-associated sepsis?</title>
  584.      <link>https://pubmed.ncbi.nlm.nih.gov/21375761/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  585.      <description>The history of ascorbic acid (AA) and cancer has been marked with controversy. Clinical studies evaluating AA in cancer outcome continue to the present day. However, the wealth of data suggesting that AA may be highly beneficial in addressing cancer-associated inflammation, particularly progression to systemic inflammatory response syndrome (SIRS) and multi organ failure (MOF), has been largely overlooked. Patients with advanced cancer are generally deficient in AA. Once these patients develop...</description>
  586.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2011 Mar 4;9:25. doi: 10.1186/1479-5876-9-25.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">The history of ascorbic acid (AA) and cancer has been marked with controversy. Clinical studies evaluating AA in cancer outcome continue to the present day. However, the wealth of data suggesting that AA may be highly beneficial in addressing cancer-associated inflammation, particularly progression to systemic inflammatory response syndrome (SIRS) and multi organ failure (MOF), has been largely overlooked. Patients with advanced cancer are generally deficient in AA. Once these patients develop septic symptoms, a further decrease in ascorbic acid levels occurs. Given the known role of ascorbate in: a) maintaining endothelial and suppression of inflammatory markers; b) protection from sepsis in animal models; and c) direct antineoplastic effects, we propose the use of ascorbate as an adjuvant to existing modalities in the treatment and prevention of cancer-associated sepsis.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/21375761/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">21375761</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3061919/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3061919</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-9-25>10.1186/1479-5876-9-25</a></p></div>]]></content:encoded>
  587.      <guid isPermaLink="false">pubmed:21375761</guid>
  588.      <pubDate>Tue, 08 Mar 2011 06:00:00 -0500</pubDate>
  589.      <dc:creator>Thomas E Ichim</dc:creator>
  590.      <dc:creator>Boris Minev</dc:creator>
  591.      <dc:creator>Todd Braciak</dc:creator>
  592.      <dc:creator>Brandon Luna</dc:creator>
  593.      <dc:creator>Ron Hunninghake</dc:creator>
  594.      <dc:creator>Nina A Mikirova</dc:creator>
  595.      <dc:creator>James A Jackson</dc:creator>
  596.      <dc:creator>Michael J Gonzalez</dc:creator>
  597.      <dc:creator>Jorge R Miranda-Massari</dc:creator>
  598.      <dc:creator>Doru T Alexandrescu</dc:creator>
  599.      <dc:creator>Constantin A Dasanu</dc:creator>
  600.      <dc:creator>Vladimir Bogin</dc:creator>
  601.      <dc:creator>Janis Ancans</dc:creator>
  602.      <dc:creator>R Brian Stevens</dc:creator>
  603.      <dc:creator>Boris Markosian</dc:creator>
  604.      <dc:creator>James Koropatnick</dc:creator>
  605.      <dc:creator>Chien-Shing Chen</dc:creator>
  606.      <dc:creator>Neil H Riordan</dc:creator>
  607.      <dc:date>2011-03-08</dc:date>
  608.      <dc:source>Journal of translational medicine</dc:source>
  609.      <dc:title>Intravenous ascorbic acid to prevent and treat cancer-associated sepsis?</dc:title>
  610.      <dc:identifier>pmid:21375761</dc:identifier>
  611.      <dc:identifier>pmc:PMC3061919</dc:identifier>
  612.      <dc:identifier>doi:10.1186/1479-5876-9-25</dc:identifier>
  613.    </item>
  614.    <item>
  615.      <title>On the missing link between inflammation and cancer</title>
  616.      <link>https://pubmed.ncbi.nlm.nih.gov/21272501/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  617.      <description>A various array of cutaneous granulomatous disorders have been found to be associated with internal malignancy. Among them, sarcoidosis, granuloma anulare (GA), psoriasis, pyoderma gangrenosum (PG), or other neutrophilic dermatoses such as the Sweet syndrome and subcorneal pustular dermatosis may precede the development of a neoplastic process by months or years. Pathogenic links of inflammation with cancer are discussed, including inflammation, intrinsic immune dysfunction, cytokines and...</description>
  618.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Dermatol Online J. 2011 Jan 15;17(1):10.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">A various array of cutaneous granulomatous disorders have been found to be associated with internal malignancy. Among them, sarcoidosis, granuloma anulare (GA), psoriasis, pyoderma gangrenosum (PG), or other neutrophilic dermatoses such as the Sweet syndrome and subcorneal pustular dermatosis may precede the development of a neoplastic process by months or years. Pathogenic links of inflammation with cancer are discussed, including inflammation, intrinsic immune dysfunction, cytokines and interleukins, angiogenetic factors, and epigenetic changes.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/21272501/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">21272501</a></p></div>]]></content:encoded>
  619.      <guid isPermaLink="false">pubmed:21272501</guid>
  620.      <pubDate>Sat, 29 Jan 2011 06:00:00 -0500</pubDate>
  621.      <dc:creator>Doru T Alexandrescu</dc:creator>
  622.      <dc:creator>Neil H Riordan</dc:creator>
  623.      <dc:creator>Thomas E Ichim</dc:creator>
  624.      <dc:creator>C Lisa Kauffman</dc:creator>
  625.      <dc:creator>Filamer Kabigting</dc:creator>
  626.      <dc:creator>Constance T Dutton</dc:creator>
  627.      <dc:creator>Constantin A Dasanu</dc:creator>
  628.      <dc:date>2011-01-29</dc:date>
  629.      <dc:source>Dermatology online journal</dc:source>
  630.      <dc:title>On the missing link between inflammation and cancer</dc:title>
  631.      <dc:identifier>pmid:21272501</dc:identifier>
  632.    </item>
  633.    <item>
  634.      <title>Cutaneous sarcoidosis and malignancy: An association between sarcoidosis with skin manifestations and systemic neoplasia</title>
  635.      <link>https://pubmed.ncbi.nlm.nih.gov/21272493/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  636.      <description>CONCLUSIONS: Sarcoidosis with cutaneous manifestations appears to be associated with malignancy, possibly at a higher rate than other systemic forms of sarcoidosis. The predominant occurrence of sarcoidosis before the development of neoplasia may indicate that an immune dysregulation, such as impairment of cellular immunity mediated by sarcoidosis or the effects of treatment may contribute to an increased risk of malignancy in predisposed individuals. Physician recognition of this link between...</description>
  637.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Dermatol Online J. 2011 Jan 15;17(1):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">BACKGROUND: Whereas the association between multisystem and pulmonary sarcoidosis and malignancy has been documented, a relationship between cutaneous sarcoidosis and neoplasia has not yet been reported. Because cutaneous manifestations are seen in 20-25 percent of cases of sarcoidosis, this association deserves further investigation.</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 reviewed the relevant literature, in addition to our case series, for a total of 110 cases of cutaneous and non-cutaneous sarcoidosis associated with malignancy with the aim of analyzing possible associations between cutaneous sarcoidosis and malignancy and to enhance the dermatologist's understanding of their critical role in the management of this disease. A search for consecutive cases, which were encountered during the past 20 years, identified 10 cases of confirmed cutaneous sarcoidosis. A review of the relevant literature was also conducted to identify cases of malignancy associated with cutaneous and non-cutaneous sarcoidosis.</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: Cutaneous localization of sarcoidosis was identified in 58 of 100 patients with sarcoidosis and cancer found in the literature (58%) and in 4 of 10 patients in our series (40%). In our series, all cases manifested solid tumors, including breast (n=4 tumors), prostate cancer, colon cancer, kidney cancer, and squamous cell carcinoma of the skin (n=1 of each type). Among the 6 patients in our series with cancers and non-cutaneous sarcoidosis, the types of neoplasias encountered were renal cancer (n=1), mycosis fungoides (n=1), diffuse large B-cell lymphoma (n=1), colon cancer (n=1), and ADK of parotid (n=2). Neoplasias developed after an average of 7.14 years in the literature cases and eight years in our series, following the diagnosis of sarcoidosis. Among the 100 cases of cutaneous (n=58) and non-cutaneous (n=42) sarcoidosis associates with malignancy, which were extracted from the literature, hematologic malignancies accounted for 73 percent of cases and sarcoidosis preceded the detection of neoplasia in a majority (76%) of cases. Among 110 total cases analyzed in this paper, cutaneous sarcoidosis was confirmed in 56.4 percent of overall cases, a figure exceeding expected rates of cutaneous involvement (20-25%) in the general sarcoidosis 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">CONCLUSIONS: Sarcoidosis with cutaneous manifestations appears to be associated with malignancy, possibly at a higher rate than other systemic forms of sarcoidosis. The predominant occurrence of sarcoidosis before the development of neoplasia may indicate that an immune dysregulation, such as impairment of cellular immunity mediated by sarcoidosis or the effects of treatment may contribute to an increased risk of malignancy in predisposed individuals. Physician recognition of this link between sarcoidosis and malignancy is critical. Dermatologists, in particular, play an important role, given that many of these associated cases manifest initially, or even solely, with cutaneous findings.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/21272493/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">21272493</a></p></div>]]></content:encoded>
  638.      <guid isPermaLink="false">pubmed:21272493</guid>
  639.      <pubDate>Sat, 29 Jan 2011 06:00:00 -0500</pubDate>
  640.      <dc:creator>Doru T Alexandrescu</dc:creator>
  641.      <dc:creator>C Lisa Kauffman</dc:creator>
  642.      <dc:creator>Thomas E Ichim</dc:creator>
  643.      <dc:creator>Neil H Riordan</dc:creator>
  644.      <dc:creator>Filamer Kabigting</dc:creator>
  645.      <dc:creator>Constantin A Dasanu</dc:creator>
  646.      <dc:date>2011-01-29</dc:date>
  647.      <dc:source>Dermatology online journal</dc:source>
  648.      <dc:title>Cutaneous sarcoidosis and malignancy: An association between sarcoidosis with skin manifestations and systemic neoplasia</dc:title>
  649.      <dc:identifier>pmid:21272493</dc:identifier>
  650.    </item>
  651.    <item>
  652.      <title>Prevention of hyperglycemia-induced myocardial apoptosis by gene silencing of Toll-like receptor-4</title>
  653.      <link>https://pubmed.ncbi.nlm.nih.gov/21159162/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  654.      <description>CONCLUSIONS: In summary, we present novel evidence that TLR4 plays a critical role in cardiac apoptosis. This is the first demonstration of the prevention of cardiac apoptosis in diabetic mice through silencing of the TLR4 gene.</description>
  655.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2010 Dec 15;8:133. doi: 10.1186/1479-5876-8-133.</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: Apoptosis is an early event involved in cardiomyopathy associated with diabetes mellitus. Toll-like receptor (TLR) signaling triggers cell apoptosis through multiple mechanisms. Up-regulation of TLR4 expression has been shown in diabetic mice. This study aimed to delineate the role of TLR4 in myocardial apoptosis, and to block this process through gene silencing of TLR4 in the myocardia of diabetic mice.</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: Diabetes was induced in C57/BL6 mice by the injection of streptozotocin. Diabetic mice were treated with 50 μg of TLR4 siRNA or scrambled siRNA as control. Myocardial apoptosis was determined by TUNEL assay.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: After 7 days of hyperglycemia, the level of TLR4 mRNA in myocardial tissue was significantly elevated. Treatment of TLR4 siRNA knocked down gene expression as well as diminished its elevation in diabetic mice. Apoptosis was evident in cardiac tissues of diabetic mice as detected by a TUNEL assay. In contrast, treatment with TLR4 siRNA minimized apoptosis in myocardial tissues. Mechanistically, caspase-3 activation was significantly inhibited in mice that were treated with TLR4 siRNA, but not in mice treated with control siRNA. Additionally, gene silencing of TLR4 resulted in suppression of apoptotic cascades, such as Fas and caspase-3 gene expression. TLR4 deficiency resulted in inhibition of reactive oxygen species (ROS) production and NADPH oxidase activity, suggesting suppression of hyperglycemia-induced apoptosis by TLR4 is associated with attenuation of oxidative stress to the cardiomyocytes.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: In summary, we present novel evidence that TLR4 plays a critical role in cardiac apoptosis. This is the first demonstration of the prevention of cardiac apoptosis in diabetic mice through silencing of the TLR4 gene.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/21159162/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">21159162</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3020152/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3020152</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-8-133>10.1186/1479-5876-8-133</a></p></div>]]></content:encoded>
  656.      <guid isPermaLink="false">pubmed:21159162</guid>
  657.      <pubDate>Fri, 17 Dec 2010 06:00:00 -0500</pubDate>
  658.      <dc:creator>Yuwei Zhang</dc:creator>
  659.      <dc:creator>Tianqing Peng</dc:creator>
  660.      <dc:creator>Huaqing Zhu</dc:creator>
  661.      <dc:creator>Xiufen Zheng</dc:creator>
  662.      <dc:creator>Xusheng Zhang</dc:creator>
  663.      <dc:creator>Nan Jiang</dc:creator>
  664.      <dc:creator>Xiaoshu Cheng</dc:creator>
  665.      <dc:creator>Xiaoyan Lai</dc:creator>
  666.      <dc:creator>Aminah Shunnar</dc:creator>
  667.      <dc:creator>Manpreet Singh</dc:creator>
  668.      <dc:creator>Neil Riordan</dc:creator>
  669.      <dc:creator>Vladimir Bogin</dc:creator>
  670.      <dc:creator>Nanwei Tong</dc:creator>
  671.      <dc:creator>Wei-Ping Min</dc:creator>
  672.      <dc:date>2010-12-17</dc:date>
  673.      <dc:source>Journal of translational medicine</dc:source>
  674.      <dc:title>Prevention of hyperglycemia-induced myocardial apoptosis by gene silencing of Toll-like receptor-4</dc:title>
  675.      <dc:identifier>pmid:21159162</dc:identifier>
  676.      <dc:identifier>pmc:PMC3020152</dc:identifier>
  677.      <dc:identifier>doi:10.1186/1479-5876-8-133</dc:identifier>
  678.    </item>
  679.    <item>
  680.      <title>Feasibility of combination allogeneic stem cell therapy for spinal cord injury: a case report</title>
  681.      <link>https://pubmed.ncbi.nlm.nih.gov/21070647/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  682.      <description> Cellular therapy for spinal cord injury (SCI) is overviewed focusing on bone marrow mononuclear cells, olfactory ensheathing cells, and mesenchymal stem cells. A case is made for the possibility of combining cell types, as well as for allogeneic use. We report the case of 29 year old male who suffered a crush fracture of the L1 vertebral body, lacking lower sensorimotor function, being a score A on the ASIA scale. Stem cell therapy comprised of intrathecal administration of allogeneic umbilical...</description>
  683.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Int Arch Med. 2010 Nov 11;3:30. doi: 10.1186/1755-7682-3-30.</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"> Cellular therapy for spinal cord injury (SCI) is overviewed focusing on bone marrow mononuclear cells, olfactory ensheathing cells, and mesenchymal stem cells. A case is made for the possibility of combining cell types, as well as for allogeneic use. We report the case of 29 year old male who suffered a crush fracture of the L1 vertebral body, lacking lower sensorimotor function, being a score A on the ASIA scale. Stem cell therapy comprised of intrathecal administration of allogeneic umbilical cord blood ex-vivo expanded CD34 and umbilical cord matrix MSC was performed 5 months, 8 months, and 14 months after injury. Cell administration was well tolerated with no adverse effects observed. Neuropathic pain subsided from intermittent 10/10 to once a week 3/10 VAS. Recovery of muscle, bowel and sexual function was noted, along with a decrease in ASIA score to "D". This case supports further investigation into allogeneic-based stem cell therapies for SCI.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/21070647/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">21070647</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2989319/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2989319</a> | DOI:<a href=https://doi.org/10.1186/1755-7682-3-30>10.1186/1755-7682-3-30</a></p></div>]]></content:encoded>
  684.      <guid isPermaLink="false">pubmed:21070647</guid>
  685.      <pubDate>Sat, 13 Nov 2010 06:00:00 -0500</pubDate>
  686.      <dc:creator>Thomas E Ichim</dc:creator>
  687.      <dc:creator>Fabio Solano</dc:creator>
  688.      <dc:creator>Fabian Lara</dc:creator>
  689.      <dc:creator>Eugenia Paris</dc:creator>
  690.      <dc:creator>Federico Ugalde</dc:creator>
  691.      <dc:creator>Jorge Paz Rodriguez</dc:creator>
  692.      <dc:creator>Boris Minev</dc:creator>
  693.      <dc:creator>Vladimir Bogin</dc:creator>
  694.      <dc:creator>Famela Ramos</dc:creator>
  695.      <dc:creator>Erik J Woods</dc:creator>
  696.      <dc:creator>Michael P Murphy</dc:creator>
  697.      <dc:creator>Amit N Patel</dc:creator>
  698.      <dc:creator>Robert J Harman</dc:creator>
  699.      <dc:creator>Neil H Riordan</dc:creator>
  700.      <dc:date>2010-11-13</dc:date>
  701.      <dc:source>International archives of medicine</dc:source>
  702.      <dc:title>Feasibility of combination allogeneic stem cell therapy for spinal cord injury: a case report</dc:title>
  703.      <dc:identifier>pmid:21070647</dc:identifier>
  704.      <dc:identifier>pmc:PMC2989319</dc:identifier>
  705.      <dc:identifier>doi:10.1186/1755-7682-3-30</dc:identifier>
  706.    </item>
  707.    <item>
  708.      <title>Safety evaluation of allogeneic umbilical cord blood mononuclear cell therapy for degenerative conditions</title>
  709.      <link>https://pubmed.ncbi.nlm.nih.gov/20682053/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  710.      <description>CONCLUSION: The current hematology-based paradigm of need for matching and immune suppression needs to be revisited when cord blood is used for non-hematopoietic regenerative purposes in immune competent recipients.</description>
  711.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2010 Aug 3;8:75. doi: 10.1186/1479-5876-8-75.</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 current paradigm for cord blood transplantation is that HLA matching and immune suppression are strictly required to prevent graft versus host disease (GVHD). Immunological arguments and historical examples have been made that the use of cord blood for non-hematopoietic activities such as growth factor production, stimulation of angiogenesis, and immune modulation may not require matching or immune suppression.</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: 114 patients suffering from non-hematopoietic degenerative conditions were treated with non-matched, allogeneic cord blood. Doses of 1-3 x 10(7) cord blood mononuclear cells per treatment, with 4-5 treatments both intrathecal and intravenously were performed. Adverse events and hematological, immunological, and biochemical parameters were analyzed for safety 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: No serious adverse effects were reported. Hematological, immunological, and biochemical parameters did not deviate from normal ranges as a result of therapy.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: The current hematology-based paradigm of need for matching and immune suppression needs to be revisited when cord blood is used for non-hematopoietic regenerative purposes in immune competent recipients.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20682053/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20682053</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2922090/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2922090</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-8-75>10.1186/1479-5876-8-75</a></p></div>]]></content:encoded>
  712.      <guid isPermaLink="false">pubmed:20682053</guid>
  713.      <pubDate>Thu, 05 Aug 2010 06:00:00 -0400</pubDate>
  714.      <dc:creator>Wan-Zhang Yang</dc:creator>
  715.      <dc:creator>Yun Zhang</dc:creator>
  716.      <dc:creator>Fang Wu</dc:creator>
  717.      <dc:creator>Wei-Ping Min</dc:creator>
  718.      <dc:creator>Boris Minev</dc:creator>
  719.      <dc:creator>Min Zhang</dc:creator>
  720.      <dc:creator>Xiao-Ling Luo</dc:creator>
  721.      <dc:creator>Famela Ramos</dc:creator>
  722.      <dc:creator>Thomas E Ichim</dc:creator>
  723.      <dc:creator>Neil H Riordan</dc:creator>
  724.      <dc:creator>Xiang Hu</dc:creator>
  725.      <dc:date>2010-08-05</dc:date>
  726.      <dc:source>Journal of translational medicine</dc:source>
  727.      <dc:title>Safety evaluation of allogeneic umbilical cord blood mononuclear cell therapy for degenerative conditions</dc:title>
  728.      <dc:identifier>pmid:20682053</dc:identifier>
  729.      <dc:identifier>pmc:PMC2922090</dc:identifier>
  730.      <dc:identifier>doi:10.1186/1479-5876-8-75</dc:identifier>
  731.    </item>
  732.    <item>
  733.      <title>Immunotherapy for melanoma: current status and perspectives</title>
  734.      <link>https://pubmed.ncbi.nlm.nih.gov/20551839/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  735.      <description>Immunotherapy is an important modality in the therapy of patients with malignant melanoma. As our knowledge about this disease continues to expand, so does the immunotherapeutic armamentarium. Nevertheless, successful preclinical models do not always translate into clinically meaningful results. The authors give a comprehensive analysis of most recent advances in the immune anti-melanoma therapy, including interleukins, interferons, other cytokines, adoptive immunotherapy, biochemotherapy, as...</description>
  736.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Immunother. 2010 Jul-Aug;33(6):570-90. doi: 10.1097/CJI.0b013e3181e032e8.</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">Immunotherapy is an important modality in the therapy of patients with malignant melanoma. As our knowledge about this disease continues to expand, so does the immunotherapeutic armamentarium. Nevertheless, successful preclinical models do not always translate into clinically meaningful results. The authors give a comprehensive analysis of most recent advances in the immune anti-melanoma therapy, including interleukins, interferons, other cytokines, adoptive immunotherapy, biochemotherapy, as well as the use of different vaccines. We also present the fundamental concepts behind various immune enhancement strategies, passive immunotherapy, as well as the use of immune adjuvants. This review brings into discussion the results of newer and older clinical trials, as well as potential limitations and drawbacks seen with the utilization of various immune therapies in malignant melanoma. Development of novel therapeutic approaches, along with optimization of existing therapies, continues to hold a great promise in the field of melanoma therapy research. Use of anti-CTLA4 and anti-PD1 antibodies, realization of the importance of co-stimulatory signals, which translated into the use of agonist CD40 monoclonal antibodies, as well as activation of innate immunity through enhanced expression of co-stimulatory molecules on the surface of dendritic cells by TLR agonists are only a few items on the list of recent advances in the treatment of melanoma. The need to engineer better immune interactions and to boost positive feedback loops appear crucial for the future of melanoma therapy, which ultimately resides in our understanding of the complexity of immune responses in this disease.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20551839/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20551839</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3517185/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3517185</a> | DOI:<a href=https://doi.org/10.1097/CJI.0b013e3181e032e8>10.1097/CJI.0b013e3181e032e8</a></p></div>]]></content:encoded>
  737.      <guid isPermaLink="false">pubmed:20551839</guid>
  738.      <pubDate>Thu, 17 Jun 2010 06:00:00 -0400</pubDate>
  739.      <dc:creator>Doru T Alexandrescu</dc:creator>
  740.      <dc:creator>Thomas E Ichim</dc:creator>
  741.      <dc:creator>Neil H Riordan</dc:creator>
  742.      <dc:creator>Francesco M Marincola</dc:creator>
  743.      <dc:creator>Anna Di Nardo</dc:creator>
  744.      <dc:creator>Filamer D Kabigting</dc:creator>
  745.      <dc:creator>Constantin A Dasanu</dc:creator>
  746.      <dc:date>2010-06-17</dc:date>
  747.      <dc:source>Journal of immunotherapy (Hagerstown, Md. : 1997)</dc:source>
  748.      <dc:title>Immunotherapy for melanoma: current status and perspectives</dc:title>
  749.      <dc:identifier>pmid:20551839</dc:identifier>
  750.      <dc:identifier>pmc:PMC3517185</dc:identifier>
  751.      <dc:identifier>doi:10.1097/CJI.0b013e3181e032e8</dc:identifier>
  752.    </item>
  753.    <item>
  754.      <title>Autologous stromal vascular fraction cells: a tool for facilitating tolerance in rheumatic disease</title>
  755.      <link>https://pubmed.ncbi.nlm.nih.gov/20537320/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  756.      <description>Since the days of Medawar, the goal of therapeutic tolerogenesis has been a "Holy Grail" for immunologists. While knowledge of cellular and molecular mechanisms of this process has been increasing at an exponential rate, clinical progress has been minimal. To provide a mechanistic background of tolerogenesis, we overview common processes in the naturally occurring examples of: pregnancy, cancer, oral tolerance and anterior chamber associated immune deviation. The case is made that an easily...</description>
  757.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Immunol. 2010;264(1):7-17. doi: 10.1016/j.cellimm.2010.04.002. Epub 2010 Apr 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">Since the days of Medawar, the goal of therapeutic tolerogenesis has been a "Holy Grail" for immunologists. While knowledge of cellular and molecular mechanisms of this process has been increasing at an exponential rate, clinical progress has been minimal. To provide a mechanistic background of tolerogenesis, we overview common processes in the naturally occurring examples of: pregnancy, cancer, oral tolerance and anterior chamber associated immune deviation. The case is made that an easily accessible byproduct of plastic surgery, the adipose stromal vascular fraction, contains elements directly capable of promoting tolerogenesis such as T regulatory cells and inhibitory macrophages. The high content of mesenchymal and hematopoietic stem cells from this source provides the possibility of trophic/regenerative potential, which would augment tolerogenic processes by decreasing ongoing inflammation. We discuss the application of this autologous cell source in the context of rheumatoid arthritis, concluding with some practical examples of its applications.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20537320/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20537320</a> | DOI:<a href=https://doi.org/10.1016/j.cellimm.2010.04.002>10.1016/j.cellimm.2010.04.002</a></p></div>]]></content:encoded>
  758.      <guid isPermaLink="false">pubmed:20537320</guid>
  759.      <pubDate>Sat, 12 Jun 2010 06:00:00 -0400</pubDate>
  760.      <dc:creator>Thomas E Ichim</dc:creator>
  761.      <dc:creator>Robert J Harman</dc:creator>
  762.      <dc:creator>Wei-Ping Min</dc:creator>
  763.      <dc:creator>Boris Minev</dc:creator>
  764.      <dc:creator>Fabio Solano</dc:creator>
  765.      <dc:creator>Jorge Paz Rodriguez</dc:creator>
  766.      <dc:creator>Doru T Alexandrescu</dc:creator>
  767.      <dc:creator>Rosalia De Necochea-Campion</dc:creator>
  768.      <dc:creator>Xiang Hu</dc:creator>
  769.      <dc:creator>Annette M Marleau</dc:creator>
  770.      <dc:creator>Neil H Riordan</dc:creator>
  771.      <dc:date>2010-06-12</dc:date>
  772.      <dc:source>Cellular immunology</dc:source>
  773.      <dc:title>Autologous stromal vascular fraction cells: a tool for facilitating tolerance in rheumatic disease</dc:title>
  774.      <dc:identifier>pmid:20537320</dc:identifier>
  775.      <dc:identifier>doi:10.1016/j.cellimm.2010.04.002</dc:identifier>
  776.    </item>
  777.    <item>
  778.      <title>Tumor vaccines in 2010: need for integration</title>
  779.      <link>https://pubmed.ncbi.nlm.nih.gov/20434139/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  780.      <description>Induction of tumor-specific immunity is an attractive approach to cancer therapy, however to date every major pivotal trial has resulted in failure. While the phenomena of tumor-mediated immune suppression has been known for decades, only recently have specific molecular pathways been elucidated, and for the first time, rationale means of intervening and observing results of intervention have been developed. In this review we describe major advances in our understanding of tumor escape from...</description>
  781.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Immunol. 2010;263(2):138-47. doi: 10.1016/j.cellimm.2010.03.019. Epub 2010 Apr 3.</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">Induction of tumor-specific immunity is an attractive approach to cancer therapy, however to date every major pivotal trial has resulted in failure. While the phenomena of tumor-mediated immune suppression has been known for decades, only recently have specific molecular pathways been elucidated, and for the first time, rationale means of intervening and observing results of intervention have been developed. In this review we describe major advances in our understanding of tumor escape from immunological pressure and provide some possible therapeutic scenarios for enhancement of efficacy in future cancer vaccine trials.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20434139/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20434139</a> | DOI:<a href=https://doi.org/10.1016/j.cellimm.2010.03.019>10.1016/j.cellimm.2010.03.019</a></p></div>]]></content:encoded>
  782.      <guid isPermaLink="false">pubmed:20434139</guid>
  783.      <pubDate>Tue, 04 May 2010 06:00:00 -0400</pubDate>
  784.      <dc:creator>David Koos</dc:creator>
  785.      <dc:creator>Steven F Josephs</dc:creator>
  786.      <dc:creator>Doru T Alexandrescu</dc:creator>
  787.      <dc:creator>Ray Chun-Fai Chan</dc:creator>
  788.      <dc:creator>Famela Ramos</dc:creator>
  789.      <dc:creator>Vladimir Bogin</dc:creator>
  790.      <dc:creator>Vincent Gammill</dc:creator>
  791.      <dc:creator>Constantin A Dasanu</dc:creator>
  792.      <dc:creator>Rosalia De Necochea-Campion</dc:creator>
  793.      <dc:creator>Neil H Riordan</dc:creator>
  794.      <dc:creator>Ewa Carrier</dc:creator>
  795.      <dc:date>2010-05-04</dc:date>
  796.      <dc:source>Cellular immunology</dc:source>
  797.      <dc:title>Tumor vaccines in 2010: need for integration</dc:title>
  798.      <dc:identifier>pmid:20434139</dc:identifier>
  799.      <dc:identifier>doi:10.1016/j.cellimm.2010.03.019</dc:identifier>
  800.    </item>
  801.    <item>
  802.      <title>Combination stem cell therapy for heart failure</title>
  803.      <link>https://pubmed.ncbi.nlm.nih.gov/20398245/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  804.      <description>Patients with congestive heart failure (CHF) that are not eligible for transplantation have limited therapeutic options. Stem cell therapy such as autologous bone marrow, mobilized peripheral blood, or purified cells thereof has been used clinically since 2001. To date over 1000 patients have received cellular therapy as part of randomized trials, with the general consensus being that a moderate but statistically significant benefit occurs. Therefore, one of the important next steps in the field...</description>
  805.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Int Arch Med. 2010 Apr 14;3(1):5. doi: 10.1186/1755-7682-3-5.</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">Patients with congestive heart failure (CHF) that are not eligible for transplantation have limited therapeutic options. Stem cell therapy such as autologous bone marrow, mobilized peripheral blood, or purified cells thereof has been used clinically since 2001. To date over 1000 patients have received cellular therapy as part of randomized trials, with the general consensus being that a moderate but statistically significant benefit occurs. Therefore, one of the important next steps in the field is optimization. In this paper we discuss three ways to approach this issue: a) increasing stem cell migration to the heart; b) augmenting stem cell activity; and c) combining existing stem cell therapies to recapitulate a "therapeutic niche". We conclude by describing a case report of a heart failure patient treated with a combination stem cell protocol in an attempt to augment beneficial aspects of cord blood CD34 cells and mesenchymal-like stem cells.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20398245/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20398245</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC3003238/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC3003238</a> | DOI:<a href=https://doi.org/10.1186/1755-7682-3-5>10.1186/1755-7682-3-5</a></p></div>]]></content:encoded>
  806.      <guid isPermaLink="false">pubmed:20398245</guid>
  807.      <pubDate>Tue, 20 Apr 2010 06:00:00 -0400</pubDate>
  808.      <dc:creator>Thomas E Ichim</dc:creator>
  809.      <dc:creator>Fabio Solano</dc:creator>
  810.      <dc:creator>Fabian Lara</dc:creator>
  811.      <dc:creator>Jorge Paz Rodriguez</dc:creator>
  812.      <dc:creator>Octav Cristea</dc:creator>
  813.      <dc:creator>Boris Minev</dc:creator>
  814.      <dc:creator>Famela Ramos</dc:creator>
  815.      <dc:creator>Erik J Woods</dc:creator>
  816.      <dc:creator>Michael P Murphy</dc:creator>
  817.      <dc:creator>Doru T Alexandrescu</dc:creator>
  818.      <dc:creator>Amit N Patel</dc:creator>
  819.      <dc:creator>Neil H Riordan</dc:creator>
  820.      <dc:date>2010-04-20</dc:date>
  821.      <dc:source>International archives of medicine</dc:source>
  822.      <dc:title>Combination stem cell therapy for heart failure</dc:title>
  823.      <dc:identifier>pmid:20398245</dc:identifier>
  824.      <dc:identifier>pmc:PMC3003238</dc:identifier>
  825.      <dc:identifier>doi:10.1186/1755-7682-3-5</dc:identifier>
  826.    </item>
  827.    <item>
  828.      <title>Nutraceutical augmentation of circulating endothelial progenitor cells and hematopoietic stem cells in human subjects</title>
  829.      <link>https://pubmed.ncbi.nlm.nih.gov/20377846/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  830.      <description>The medical significance of circulating endothelial or hematopoietic progenitors is becoming increasing recognized. While therapeutic augmentation of circulating progenitor cells using G-CSF has resulted in promising preclinical and early clinical data for several degenerative conditions, this approach is limited by cost and inability to perform chronic administration. Stem-Kine is a food supplement that was previously reported to augment circulating EPC in a pilot study. Here we report a trial...</description>
  831.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2010 Apr 8;8:34. doi: 10.1186/1479-5876-8-34.</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 medical significance of circulating endothelial or hematopoietic progenitors is becoming increasing recognized. While therapeutic augmentation of circulating progenitor cells using G-CSF has resulted in promising preclinical and early clinical data for several degenerative conditions, this approach is limited by cost and inability to perform chronic administration. Stem-Kine is a food supplement that was previously reported to augment circulating EPC in a pilot study. Here we report a trial in 18 healthy volunteers administered Stem-Kine twice daily for a 2 week period. Significant increases in circulating CD133 and CD34 cells were observed at days 1, 2, 7, and 14 subsequent to initiation of administration, which correlated with increased hematopoietic progenitors as detected by the HALO assay. Augmentation of EPC numbers in circulation was detected by KDR-1/CD34 staining and colony forming assays. These data suggest Stem-Kine supplementation may be useful as a stimulator of reparative processes associated with mobilization of hematopoietic and endothelial progenitors.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20377846/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20377846</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2862021/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2862021</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-8-34>10.1186/1479-5876-8-34</a></p></div>]]></content:encoded>
  832.      <guid isPermaLink="false">pubmed:20377846</guid>
  833.      <pubDate>Sat, 10 Apr 2010 06:00:00 -0400</pubDate>
  834.      <dc:creator>Nina A Mikirova</dc:creator>
  835.      <dc:creator>James A Jackson</dc:creator>
  836.      <dc:creator>Ron Hunninghake</dc:creator>
  837.      <dc:creator>Julian Kenyon</dc:creator>
  838.      <dc:creator>Kyle W H Chan</dc:creator>
  839.      <dc:creator>Cathy A Swindlehurst</dc:creator>
  840.      <dc:creator>Boris Minev</dc:creator>
  841.      <dc:creator>Amit N Patel</dc:creator>
  842.      <dc:creator>Michael P Murphy</dc:creator>
  843.      <dc:creator>Leonard Smith</dc:creator>
  844.      <dc:creator>Famela Ramos</dc:creator>
  845.      <dc:creator>Thomas E Ichim</dc:creator>
  846.      <dc:creator>Neil H Riordan</dc:creator>
  847.      <dc:date>2010-04-10</dc:date>
  848.      <dc:source>Journal of translational medicine</dc:source>
  849.      <dc:title>Nutraceutical augmentation of circulating endothelial progenitor cells and hematopoietic stem cells in human subjects</dc:title>
  850.      <dc:identifier>pmid:20377846</dc:identifier>
  851.      <dc:identifier>pmc:PMC2862021</dc:identifier>
  852.      <dc:identifier>doi:10.1186/1479-5876-8-34</dc:identifier>
  853.    </item>
  854.    <item>
  855.      <title>The lysosomotropic agent, hydroxychloroquine, delivered in a biodegradable nanoparticle system, overcomes drug resistance of B-chronic lymphocytic leukemia cells in vitro</title>
  856.      <link>https://pubmed.ncbi.nlm.nih.gov/20187802/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  857.      <description>Nonviral delivery systems are relatively easy to produce in the large scale, are safe, and elicit a negligible immune response. Nanoparticles (NPs) offer promise as nonviral vectors as biocompatible and -degradable carriers of drugs with targeting to specific sites by surface receptors of monoclonal antibodies (mAbs). We investigated the effect of four PEG-PLGA (polyethylene glycol-polylactic-co-glycolic acid) NP systems on drug-resistant B-chronic lymphocytic leukemia (B-CLL) cells in vitro,...</description>
  858.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cancer Biother Radiopharm. 2010 Feb;25(1):97-103. doi: 10.1089/cbr.2009.0655.</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">Nonviral delivery systems are relatively easy to produce in the large scale, are safe, and elicit a negligible immune response. Nanoparticles (NPs) offer promise as nonviral vectors as biocompatible and -degradable carriers of drugs with targeting to specific sites by surface receptors of monoclonal antibodies (mAbs). We investigated the effect of four PEG-PLGA (polyethylene glycol-polylactic-co-glycolic acid) NP systems on drug-resistant B-chronic lymphocytic leukemia (B-CLL) cells in vitro, three of them encapsulating the drug, hydroxylchloroquine (HDQ), two with NP surface coatings of mAbs (NP1) CD20, (NP2) CD19, and CD20, and one (NP3) with no mAb, but tagged with the fluorescent marker, fluorescein isothiocyanate. The fourth NP system (NP4) was coated with anti-CD19/FITC and anti-CD20/Alexa-Fluor((R)) antibodies, but did not contain the active drug, HCQ. Our data indicate that PEG-PLGA nanoparticles with surface mAbs are suitable for selective drug delivery to B-CLL cells and produce a strong apoptotic effect when loaded with the lysosomotropic agent, HDQ.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20187802/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20187802</a> | DOI:<a href=https://doi.org/10.1089/cbr.2009.0655>10.1089/cbr.2009.0655</a></p></div>]]></content:encoded>
  859.      <guid isPermaLink="false">pubmed:20187802</guid>
  860.      <pubDate>Tue, 02 Mar 2010 06:00:00 -0500</pubDate>
  861.      <dc:creator>Eduardo Mansilla</dc:creator>
  862.      <dc:creator>Gustavo H Marin</dc:creator>
  863.      <dc:creator>Luis Nuñez</dc:creator>
  864.      <dc:creator>Hugo Drago</dc:creator>
  865.      <dc:creator>Flavio Sturla</dc:creator>
  866.      <dc:creator>Carol Mertz</dc:creator>
  867.      <dc:creator>Luis Rivera</dc:creator>
  868.      <dc:creator>Thomas Ichim</dc:creator>
  869.      <dc:creator>Neil Riordan</dc:creator>
  870.      <dc:creator>Clemente Raimondi</dc:creator>
  871.      <dc:date>2010-03-02</dc:date>
  872.      <dc:source>Cancer biotherapy &amp; radiopharmaceuticals</dc:source>
  873.      <dc:title>The lysosomotropic agent, hydroxychloroquine, delivered in a biodegradable nanoparticle system, overcomes drug resistance of B-chronic lymphocytic leukemia cells in vitro</dc:title>
  874.      <dc:identifier>pmid:20187802</dc:identifier>
  875.      <dc:identifier>doi:10.1089/cbr.2009.0655</dc:identifier>
  876.    </item>
  877.    <item>
  878.      <title>Ascorbate inhibition of angiogenesis in aortic rings ex vivo and subcutaneous Matrigel plugs in vivo</title>
  879.      <link>https://pubmed.ncbi.nlm.nih.gov/20150992/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  880.      <description>CONCLUSIONS: We conclude that the inhibition of angiogenesis by ascorbate suggested in vitro is confirmed in vivo, and that angiogenesis inhibition may be one mechanism by which intravenous ascorbate therapy shows efficacy in animal experiments and clinical case studies.</description>
  881.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Angiogenes Res. 2010 Jan 18;2:2. doi: 10.1186/2040-2384-2-2.</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">BACKGROUND: Angiogenesis is critical to tumor growth and is therefore a potential target for cancer therapy. As many current inhibitors of angiogenesis exhibit host toxicity, natural alternatives are needed. At millimolar concentrations, ascorbate (vitamin C) inhibits migration and tubule formation by mature endothelial cells and endothelial progenitors. In the present study, we examined the effects of ascorbate, at levels relevant during intravenous infusion therapy, on angiogenesis using an ex vivo an in vivo assay.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Two assays were used to evaluate effect of high-doses ascorbic acid on angiogenesis: ex vivo rat aortic ring explant assay in Matrigel matrices and in vivo Matrigel plug assay. In aortic rings, we quantified microvessel growth, branching and vessel regression under different treatment conditions. In murine angiogenesis assay, male C57 mice 6-8 weeks old were treated by high-dose ascorbic acid and the number of microvessels was analyzed by histological method. To characterize the population of cells that formed capillary network and microvessels, the sections were stained by CD34 and CD31 antibodies.</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: Results show that sprouting of endothelial tubules from aortic rings was reduced in a concentration-dependent fashion by ascorbate: while controls roughly tripled sprout densities during the study, ascorbate (1 mg/mL, 5.5 mM) actually reduced sprout density. In vivo, the ability of mice to vascularize subcutaneously implanted Matrigel plug was diminished if the mice were treated with 430 mg/kg vitamin C: numbers of vessels, and vessel densities, in plugs from treated mice were roughly 30% less than those in plugs from untreated mice.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: We conclude that the inhibition of angiogenesis by ascorbate suggested in vitro is confirmed in vivo, and that angiogenesis inhibition may be one mechanism by which intravenous ascorbate therapy shows efficacy in animal experiments and clinical case studies.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20150992/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20150992</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2820478/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2820478</a> | DOI:<a href=https://doi.org/10.1186/2040-2384-2-2>10.1186/2040-2384-2-2</a></p></div>]]></content:encoded>
  882.      <guid isPermaLink="false">pubmed:20150992</guid>
  883.      <pubDate>Sat, 13 Feb 2010 06:00:00 -0500</pubDate>
  884.      <dc:creator>Nina A Mikirova</dc:creator>
  885.      <dc:creator>Joseph J Casciari</dc:creator>
  886.      <dc:creator>Neil H Riordan</dc:creator>
  887.      <dc:date>2010-02-13</dc:date>
  888.      <dc:source>Journal of angiogenesis research</dc:source>
  889.      <dc:title>Ascorbate inhibition of angiogenesis in aortic rings ex vivo and subcutaneous Matrigel plugs in vivo</dc:title>
  890.      <dc:identifier>pmid:20150992</dc:identifier>
  891.      <dc:identifier>pmc:PMC2820478</dc:identifier>
  892.      <dc:identifier>doi:10.1186/2040-2384-2-2</dc:identifier>
  893.    </item>
  894.    <item>
  895.      <title>Circulating endothelial progenitor cells: a new approach to anti-aging medicine?</title>
  896.      <link>https://pubmed.ncbi.nlm.nih.gov/20003528/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  897.      <description>Endothelial dysfunction is associated with major causes of morbidity and mortality, as well as numerous age-related conditions. The possibility of preserving or even rejuvenating endothelial function offers a potent means of preventing/treating some of the most fearful aspects of aging such as loss of mental, cardiovascular, and sexual function.Endothelial precursor cells (EPC) provide a continual source of replenishment for damaged or senescent blood vessels. In this review we discuss the...</description>
  898.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2009 Dec 15;7:106. doi: 10.1186/1479-5876-7-106.</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">Endothelial dysfunction is associated with major causes of morbidity and mortality, as well as numerous age-related conditions. The possibility of preserving or even rejuvenating endothelial function offers a potent means of preventing/treating some of the most fearful aspects of aging such as loss of mental, cardiovascular, and sexual function.Endothelial precursor cells (EPC) provide a continual source of replenishment for damaged or senescent blood vessels. In this review we discuss the biological relevance of circulating EPC in a variety of pathologies in order to build the case that these cells act as an endogenous mechanism of regeneration. Factors controlling EPC mobilization, migration, and function, as well as therapeutic interventions based on mobilization of EPC will be reviewed. We conclude by discussing several clinically-relevant approaches to EPC mobilization and provide preliminary data on a food supplement, Stem-Kine, which enhanced EPC mobilization in human subjects.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/20003528/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">20003528</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2804590/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2804590</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-7-106>10.1186/1479-5876-7-106</a></p></div>]]></content:encoded>
  899.      <guid isPermaLink="false">pubmed:20003528</guid>
  900.      <pubDate>Thu, 17 Dec 2009 06:00:00 -0500</pubDate>
  901.      <dc:creator>Nina A Mikirova</dc:creator>
  902.      <dc:creator>James A Jackson</dc:creator>
  903.      <dc:creator>Ron Hunninghake</dc:creator>
  904.      <dc:creator>Julian Kenyon</dc:creator>
  905.      <dc:creator>Kyle W H Chan</dc:creator>
  906.      <dc:creator>Cathy A Swindlehurst</dc:creator>
  907.      <dc:creator>Boris Minev</dc:creator>
  908.      <dc:creator>Amit N Patel</dc:creator>
  909.      <dc:creator>Michael P Murphy</dc:creator>
  910.      <dc:creator>Leonard Smith</dc:creator>
  911.      <dc:creator>Doru T Alexandrescu</dc:creator>
  912.      <dc:creator>Thomas E Ichim</dc:creator>
  913.      <dc:creator>Neil H Riordan</dc:creator>
  914.      <dc:date>2009-12-17</dc:date>
  915.      <dc:source>Journal of translational medicine</dc:source>
  916.      <dc:title>Circulating endothelial progenitor cells: a new approach to anti-aging medicine?</dc:title>
  917.      <dc:identifier>pmid:20003528</dc:identifier>
  918.      <dc:identifier>pmc:PMC2804590</dc:identifier>
  919.      <dc:identifier>doi:10.1186/1479-5876-7-106</dc:identifier>
  920.    </item>
  921.    <item>
  922.      <title>Mesenchymal stem cells as anti-inflammatories: implications for treatment of Duchenne muscular dystrophy</title>
  923.      <link>https://pubmed.ncbi.nlm.nih.gov/19917503/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  924.      <description>Duchenne muscular dystrophy (DMD) is a lethal X-linked musculodegenerative condition consisting of an underlying genetic defect whose manifestation is augmented by inflammatory mechanisms. Previous treatment approaches using gene replacement, exon-skipping or allogeneic cell therapy have been relatively unsuccessful. The only intervention to mediate improvement in survival, albeit minor, is glucocorticoid treatment. Given this modality appears to function via suppression of underlying...</description>
  925.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Immunol. 2010;260(2):75-82. doi: 10.1016/j.cellimm.2009.10.006.</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">Duchenne muscular dystrophy (DMD) is a lethal X-linked musculodegenerative condition consisting of an underlying genetic defect whose manifestation is augmented by inflammatory mechanisms. Previous treatment approaches using gene replacement, exon-skipping or allogeneic cell therapy have been relatively unsuccessful. The only intervention to mediate improvement in survival, albeit minor, is glucocorticoid treatment. Given this modality appears to function via suppression of underlying inflammation; we focus this review on the inflammatory response as a target for mesenchymal stem cell (MSC) therapy. In contrast to other cell based therapies attempted in DMD, MSC have the advantages of (a) ability to fuse with and genetically complement dystrophic muscle; (b) possess anti-inflammatory activities; and (c) produce trophic factors that may augment activity of endogenous repair cells. We conclude by describing one practical scenario of stem cell therapy for DMD.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/19917503/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">19917503</a> | DOI:<a href=https://doi.org/10.1016/j.cellimm.2009.10.006>10.1016/j.cellimm.2009.10.006</a></p></div>]]></content:encoded>
  926.      <guid isPermaLink="false">pubmed:19917503</guid>
  927.      <pubDate>Wed, 18 Nov 2009 06:00:00 -0500</pubDate>
  928.      <dc:creator>Thomas E Ichim</dc:creator>
  929.      <dc:creator>Doru T Alexandrescu</dc:creator>
  930.      <dc:creator>Fabio Solano</dc:creator>
  931.      <dc:creator>Fabian Lara</dc:creator>
  932.      <dc:creator>Rosalia De Necochea Campion</dc:creator>
  933.      <dc:creator>Eugenia Paris</dc:creator>
  934.      <dc:creator>Erik J Woods</dc:creator>
  935.      <dc:creator>Michael P Murphy</dc:creator>
  936.      <dc:creator>Constantin A Dasanu</dc:creator>
  937.      <dc:creator>Amit N Patel</dc:creator>
  938.      <dc:creator>Annette M Marleau</dc:creator>
  939.      <dc:creator>Alejandro Leal</dc:creator>
  940.      <dc:creator>Neil H Riordan</dc:creator>
  941.      <dc:date>2009-11-18</dc:date>
  942.      <dc:source>Cellular immunology</dc:source>
  943.      <dc:title>Mesenchymal stem cells as anti-inflammatories: implications for treatment of Duchenne muscular dystrophy</dc:title>
  944.      <dc:identifier>pmid:19917503</dc:identifier>
  945.      <dc:identifier>doi:10.1016/j.cellimm.2009.10.006</dc:identifier>
  946.    </item>
  947.    <item>
  948.      <title>Non-expanded adipose stromal vascular fraction cell therapy for multiple sclerosis</title>
  949.      <link>https://pubmed.ncbi.nlm.nih.gov/19393041/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  950.      <description>The stromal vascular fraction (SVF) of adipose tissue is known to contain mesenchymal stem cells (MSC), T regulatory cells, endothelial precursor cells, preadipocytes, as well as anti-inflammatory M2 macrophages. Safety of autologous adipose tissue implantation is supported by extensive use of this procedure in cosmetic surgery, as well as by ongoing studies using in vitro expanded adipose derived MSC. Equine and canine studies demonstrating anti-inflammatory and regenerative effects of...</description>
  951.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2009 Apr 24;7:29. doi: 10.1186/1479-5876-7-29.</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 stromal vascular fraction (SVF) of adipose tissue is known to contain mesenchymal stem cells (MSC), T regulatory cells, endothelial precursor cells, preadipocytes, as well as anti-inflammatory M2 macrophages. Safety of autologous adipose tissue implantation is supported by extensive use of this procedure in cosmetic surgery, as well as by ongoing studies using in vitro expanded adipose derived MSC. Equine and canine studies demonstrating anti-inflammatory and regenerative effects of non-expanded SVF cells have yielded promising results. Although non-expanded SVF cells have been used successfully in accelerating healing of Crohn's fistulas, to our knowledge clinical use of these cells for systemic immune modulation has not been reported. In this communication we discuss the rationale for use of autologous SVF in treatment of multiple sclerosis and describe our experiences with three patients. Based on this rationale and initial experiences, we propose controlled trials of autologous SVF in various inflammatory conditions.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/19393041/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">19393041</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2679713/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2679713</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-7-29>10.1186/1479-5876-7-29</a></p></div>]]></content:encoded>
  952.      <guid isPermaLink="false">pubmed:19393041</guid>
  953.      <pubDate>Tue, 28 Apr 2009 06:00:00 -0400</pubDate>
  954.      <dc:creator>Neil H Riordan</dc:creator>
  955.      <dc:creator>Thomas E Ichim</dc:creator>
  956.      <dc:creator>Wei-Ping Min</dc:creator>
  957.      <dc:creator>Hao Wang</dc:creator>
  958.      <dc:creator>Fabio Solano</dc:creator>
  959.      <dc:creator>Fabian Lara</dc:creator>
  960.      <dc:creator>Miguel Alfaro</dc:creator>
  961.      <dc:creator>Jorge Paz Rodriguez</dc:creator>
  962.      <dc:creator>Robert J Harman</dc:creator>
  963.      <dc:creator>Amit N Patel</dc:creator>
  964.      <dc:creator>Michael P Murphy</dc:creator>
  965.      <dc:creator>Roland R Lee</dc:creator>
  966.      <dc:creator>Boris Minev</dc:creator>
  967.      <dc:date>2009-04-28</dc:date>
  968.      <dc:source>Journal of translational medicine</dc:source>
  969.      <dc:title>Non-expanded adipose stromal vascular fraction cell therapy for multiple sclerosis</dc:title>
  970.      <dc:identifier>pmid:19393041</dc:identifier>
  971.      <dc:identifier>pmc:PMC2679713</dc:identifier>
  972.      <dc:identifier>doi:10.1186/1479-5876-7-29</dc:identifier>
  973.    </item>
  974.    <item>
  975.      <title>Feasibility investigation of allogeneic endometrial regenerative cells</title>
  976.      <link>https://pubmed.ncbi.nlm.nih.gov/19232091/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  977.      <description>Endometrial Regenerative Cells (ERC) are a population of mesenchymal-like stem cells having pluripotent differentiation activity and ability to induce neoangiogenesis. In vitro and animal studies suggest ERC are immune privileged and in certain situations actively suppress ongoing immune responses. In this paper we describe the production of clinical grade ERC and initial safety experiences in 4 patients with multiple sclerosis treated intravenously and intrathecally. The case with the longest...</description>
  978.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2009 Feb 20;7:15. doi: 10.1186/1479-5876-7-15.</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">Endometrial Regenerative Cells (ERC) are a population of mesenchymal-like stem cells having pluripotent differentiation activity and ability to induce neoangiogenesis. In vitro and animal studies suggest ERC are immune privileged and in certain situations actively suppress ongoing immune responses. In this paper we describe the production of clinical grade ERC and initial safety experiences in 4 patients with multiple sclerosis treated intravenously and intrathecally. The case with the longest follow up, of more than one year, revealed no immunological reactions or treatment associated adverse effects. These preliminary data suggest feasibility of clinical ERC administration and support further studies with this novel stem cell type.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/19232091/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">19232091</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2649897/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2649897</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-7-15>10.1186/1479-5876-7-15</a></p></div>]]></content:encoded>
  979.      <guid isPermaLink="false">pubmed:19232091</guid>
  980.      <pubDate>Tue, 24 Feb 2009 06:00:00 -0500</pubDate>
  981.      <dc:creator>Zhaohui Zhong</dc:creator>
  982.      <dc:creator>Amit N Patel</dc:creator>
  983.      <dc:creator>Thomas E Ichim</dc:creator>
  984.      <dc:creator>Neil H Riordan</dc:creator>
  985.      <dc:creator>Hao Wang</dc:creator>
  986.      <dc:creator>Wei-Ping Min</dc:creator>
  987.      <dc:creator>Erik J Woods</dc:creator>
  988.      <dc:creator>Michael Reid</dc:creator>
  989.      <dc:creator>Eduardo Mansilla</dc:creator>
  990.      <dc:creator>Gustavo H Marin</dc:creator>
  991.      <dc:creator>Hugo Drago</dc:creator>
  992.      <dc:creator>Michael P Murphy</dc:creator>
  993.      <dc:creator>Boris Minev</dc:creator>
  994.      <dc:date>2009-02-24</dc:date>
  995.      <dc:source>Journal of translational medicine</dc:source>
  996.      <dc:title>Feasibility investigation of allogeneic endometrial regenerative cells</dc:title>
  997.      <dc:identifier>pmid:19232091</dc:identifier>
  998.      <dc:identifier>pmc:PMC2649897</dc:identifier>
  999.      <dc:identifier>doi:10.1186/1479-5876-7-15</dc:identifier>
  1000.    </item>
  1001.    <item>
  1002.      <title>Inhibition of intracranial glioma growth by endometrial regenerative cells</title>
  1003.      <link>https://pubmed.ncbi.nlm.nih.gov/19197154/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  1004.      <description>Animal studies have demonstrated that selective tropism of mesenchymal stem cells (MSC) for glioma may be used as a means of selective delivery of cytotoxic payloads. Endometrial Regenerative Cells (ERC) are a population of mesenchymal-like cells which possesse pluripotent differentiation capacity and is characterized by unique surface markers and growth factor production. In this study we sought to determine whether unmanipulated ERC would alter the growth of glioma using the aggressive...</description>
  1005.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Cycle. 2009 Feb 15;8(4):606-10. doi: 10.4161/cc.8.4.7731. Epub 2009 Mar 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">Animal studies have demonstrated that selective tropism of mesenchymal stem cells (MSC) for glioma may be used as a means of selective delivery of cytotoxic payloads. Endometrial Regenerative Cells (ERC) are a population of mesenchymal-like cells which possesse pluripotent differentiation capacity and is characterized by unique surface markers and growth factor production. In this study we sought to determine whether unmanipulated ERC would alter the growth of glioma using the aggressive C6/LacZ7 (C6) into Sprague Dawley rat model. ERC administration by intravenous (i.v.) or intratumoral (i.t.) showed significant inhibition of glioma: volume reduction of 49% after i.v. treatment (p &lt; 0.05), and about 46% i.t. treatment (p &lt; 0.05). Tumor reduction was associated with inhibition of angiogenesis and reduced numbers of CD133 positive cells in the incranial tumor. Despite the angiogenic potential of ERC in the hindlimb ischemia model, these data support a paradoxical tumor inhibitory activity of ERC. Further studies are needed to determine the qualitative differences between physiological angiogenesis, which seems to be supported by ERC and tumor angiogenesis which appeared to be inhibited.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/19197154/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">19197154</a> | DOI:<a href=https://doi.org/10.4161/cc.8.4.7731>10.4161/cc.8.4.7731</a></p></div>]]></content:encoded>
  1006.      <guid isPermaLink="false">pubmed:19197154</guid>
  1007.      <pubDate>Sat, 07 Feb 2009 06:00:00 -0500</pubDate>
  1008.      <dc:creator>Xiaodi Han</dc:creator>
  1009.      <dc:creator>Xiaolong Meng</dc:creator>
  1010.      <dc:creator>Zhenglian Yin</dc:creator>
  1011.      <dc:creator>Andrea Rogers</dc:creator>
  1012.      <dc:creator>Jie Zhong</dc:creator>
  1013.      <dc:creator>Paul Rillema</dc:creator>
  1014.      <dc:creator>James A Jackson</dc:creator>
  1015.      <dc:creator>Thomas E Ichim</dc:creator>
  1016.      <dc:creator>Boris Minev</dc:creator>
  1017.      <dc:creator>Ewa Carrier</dc:creator>
  1018.      <dc:creator>Amit N Patel</dc:creator>
  1019.      <dc:creator>Michael P Murphy</dc:creator>
  1020.      <dc:creator>Wei-Ping Min</dc:creator>
  1021.      <dc:creator>Neil H Riordan</dc:creator>
  1022.      <dc:date>2009-02-07</dc:date>
  1023.      <dc:source>Cell cycle (Georgetown, Tex.)</dc:source>
  1024.      <dc:title>Inhibition of intracranial glioma growth by endometrial regenerative cells</dc:title>
  1025.      <dc:identifier>pmid:19197154</dc:identifier>
  1026.      <dc:identifier>doi:10.4161/cc.8.4.7731</dc:identifier>
  1027.    </item>
  1028.    <item>
  1029.      <title>Anti-angiogenic effect of high doses of ascorbic acid</title>
  1030.      <link>https://pubmed.ncbi.nlm.nih.gov/18789157/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  1031.      <description>Pharmaceutical doses of ascorbic acid (AA, vitamin C, or its salts) have been reported to exert anticancer activity in vitro and in vivo. One proposed mechanism involves direct cytotoxicity mediated by accumulation of ascorbic acid radicals and hydrogen peroxide in the extracellular environment of tumor cells. However, therapeutic effects have been reported at concentrations insufficient to induce direct tumor cell death. We hypothesized that AA may exert anti-angiogenic effects. To test this,...</description>
  1032.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2008 Sep 12;6:50. doi: 10.1186/1479-5876-6-50.</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">Pharmaceutical doses of ascorbic acid (AA, vitamin C, or its salts) have been reported to exert anticancer activity in vitro and in vivo. One proposed mechanism involves direct cytotoxicity mediated by accumulation of ascorbic acid radicals and hydrogen peroxide in the extracellular environment of tumor cells. However, therapeutic effects have been reported at concentrations insufficient to induce direct tumor cell death. We hypothesized that AA may exert anti-angiogenic effects. To test this, we expanded endothelial progenitor cells (EPCs) from peripheral blood and assessed, whether or not high dose AA would inhibit EPC ability to migrate, change energy metabolism, and tube formation ability. We also evaluated the effects of high dose AA on angiogenic activities of HUVECs (human umbilical vein endothelial cells) and HUAECs (human umbilical arterial endothelial cells). According to our data, concentrations of AA higher than 100 mg/dl suppressed capillary-like tube formation on Matrigel for all cells tested and the effect was more pronounced for progenitor cells in comparison with mature cells. Co-culture of differentiated endothelial cells with progenitor cells showed that there was incorporation of EPCs in vessels formed by HUVECs and HUAECs. Cell migration was assessed using an in vitro wound healing model. The results of these experiments showed an inverse correlation between AA concentrations relative to both cell migration and gap filling capacity. Suppression of NO (nitric oxide) generation appeared to be one of the mechanisms by which AA mediated angiostatic effects. This study supports further investigation into non-cytotoxic antitumor activities of AA.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/18789157/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">18789157</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2562367/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2562367</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-6-50>10.1186/1479-5876-6-50</a></p></div>]]></content:encoded>
  1033.      <guid isPermaLink="false">pubmed:18789157</guid>
  1034.      <pubDate>Tue, 16 Sep 2008 06:00:00 -0400</pubDate>
  1035.      <dc:creator>Nina A Mikirova</dc:creator>
  1036.      <dc:creator>Thomas E Ichim</dc:creator>
  1037.      <dc:creator>Neil H Riordan</dc:creator>
  1038.      <dc:date>2008-09-16</dc:date>
  1039.      <dc:source>Journal of translational medicine</dc:source>
  1040.      <dc:title>Anti-angiogenic effect of high doses of ascorbic acid</dc:title>
  1041.      <dc:identifier>pmid:18789157</dc:identifier>
  1042.      <dc:identifier>pmc:PMC2562367</dc:identifier>
  1043.      <dc:identifier>doi:10.1186/1479-5876-6-50</dc:identifier>
  1044.    </item>
  1045.    <item>
  1046.      <title>Allogeneic endometrial regenerative cells: an "Off the shelf solution" for critical limb ischemia?</title>
  1047.      <link>https://pubmed.ncbi.nlm.nih.gov/18713449/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  1048.      <description>Critical limb ischemia (CLI) is an advanced form of peripheral artery disease which is responsible for approximately 100,000 amputations per year in the US. Trials to date have reported clinical improvement and reduced need for amputation in CLI patients receiving autologous bone marrow or mobilized peripheral blood stem cells for stimulation of angiogenesis. While such treatments are currently entering Phase III trials, practical and scientific pitfalls will limit widespread implementation if...</description>
  1049.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2008 Aug 19;6:45. doi: 10.1186/1479-5876-6-45.</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">Critical limb ischemia (CLI) is an advanced form of peripheral artery disease which is responsible for approximately 100,000 amputations per year in the US. Trials to date have reported clinical improvement and reduced need for amputation in CLI patients receiving autologous bone marrow or mobilized peripheral blood stem cells for stimulation of angiogenesis. While such treatments are currently entering Phase III trials, practical and scientific pitfalls will limit widespread implementation if efficacy is proven. Hurdles to be overcome include: a) reduced angiogenic potential of autologous cells in aged patients with cardiovascular risk factors; b) invasiveness/adverse effects of bone marrow extraction and G-CSF mobilization, respectively; and c) need for on-site cellular manipulation. The Endometrial Regenerative Cell (ERC) is a mesenchymal-like stem cell derived from the menstrual blood that is believed to be associated with endometrial angiogenesis. We discuss the possibility of using allogeneic ERCs as an "off the shelf" treatment for CLI based on the following properties: a) High levels of growth factors and matrix metalloprotease production; b) Ability to inhibits inflammatory responses and lack of immunogenicity; and c) Expandability to great quantities without loss of differentiation ability or karyotypic abnormalities.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/18713449/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">18713449</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2533293/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2533293</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-6-45>10.1186/1479-5876-6-45</a></p></div>]]></content:encoded>
  1050.      <guid isPermaLink="false">pubmed:18713449</guid>
  1051.      <pubDate>Thu, 21 Aug 2008 06:00:00 -0400</pubDate>
  1052.      <dc:creator>Michael P Murphy</dc:creator>
  1053.      <dc:creator>Hao Wang</dc:creator>
  1054.      <dc:creator>Amit N Patel</dc:creator>
  1055.      <dc:creator>Suman Kambhampati</dc:creator>
  1056.      <dc:creator>Niren Angle</dc:creator>
  1057.      <dc:creator>Kyle Chan</dc:creator>
  1058.      <dc:creator>Annette M Marleau</dc:creator>
  1059.      <dc:creator>Andrew Pyszniak</dc:creator>
  1060.      <dc:creator>Ewa Carrier</dc:creator>
  1061.      <dc:creator>Thomas E Ichim</dc:creator>
  1062.      <dc:creator>Neil H Riordan</dc:creator>
  1063.      <dc:date>2008-08-21</dc:date>
  1064.      <dc:source>Journal of translational medicine</dc:source>
  1065.      <dc:title>Allogeneic endometrial regenerative cells: an "Off the shelf solution" for critical limb ischemia?</dc:title>
  1066.      <dc:identifier>pmid:18713449</dc:identifier>
  1067.      <dc:identifier>pmc:PMC2533293</dc:identifier>
  1068.      <dc:identifier>doi:10.1186/1479-5876-6-45</dc:identifier>
  1069.    </item>
  1070.    <item>
  1071.      <title>Granulocyte activity in patients with cancer and healthy subjects</title>
  1072.      <link>https://pubmed.ncbi.nlm.nih.gov/18708759/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  1073.      <description>In our study, we investigated the intracellular killing ability of granulocytes for healthy and ill subjects by measuring NADH oxidase activity and release of hydrogen peroxide. The protocol methodology measured the hydrogen peroxide released after granulocytes activation by PMA (phorbol 12-myristate 13-acetate) by using the Amplex Red assay, which included counting granulocytes by flow cytometer and measurement of the kinetic curve of NADPH oxidase activity by fluorometer. Two parameters were...</description>
  1074.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cancer Biol Ther. 2008 Sep;7(9):1362-7. doi: 10.4161/cbt.7.9.6417. Epub 2008 Sep 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">In our study, we investigated the intracellular killing ability of granulocytes for healthy and ill subjects by measuring NADH oxidase activity and release of hydrogen peroxide. The protocol methodology measured the hydrogen peroxide released after granulocytes activation by PMA (phorbol 12-myristate 13-acetate) by using the Amplex Red assay, which included counting granulocytes by flow cytometer and measurement of the kinetic curve of NADPH oxidase activity by fluorometer. Two parameters were used to describe the level of granulocyte activity: the initial rate of NADPH-oxidase enzyme activity and the level of hydrogen peroxide released after 20 min of granulocyte activation. The method was applied to measure granulocyte activity in 55 healthy subjects and 30 patients with cancer. It was demonstrated that applied procedure is sensitive for estimation of the disease activity. The granulocyte activity in patients with cancer was compared with the granulocyte activity of healthy subjects and demonstrated the downregulation of NADPH oxidase activity. We showed that granulocytes of cancer patients had inhibited oxidative burst and less NADPH oxidase activity.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/18708759/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">18708759</a> | DOI:<a href=https://doi.org/10.4161/cbt.7.9.6417>10.4161/cbt.7.9.6417</a></p></div>]]></content:encoded>
  1075.      <guid isPermaLink="false">pubmed:18708759</guid>
  1076.      <pubDate>Tue, 19 Aug 2008 06:00:00 -0400</pubDate>
  1077.      <dc:creator>Nina A Mikirova</dc:creator>
  1078.      <dc:creator>Arkady A Klykov</dc:creator>
  1079.      <dc:creator>James A Jackson</dc:creator>
  1080.      <dc:creator>Neil H Riordan</dc:creator>
  1081.      <dc:date>2008-08-19</dc:date>
  1082.      <dc:source>Cancer biology &amp; therapy</dc:source>
  1083.      <dc:title>Granulocyte activity in patients with cancer and healthy subjects</dc:title>
  1084.      <dc:identifier>pmid:18708759</dc:identifier>
  1085.      <dc:identifier>doi:10.4161/cbt.7.9.6417</dc:identifier>
  1086.    </item>
  1087.    <item>
  1088.      <title>Exosomes as a tumor immune escape mechanism: possible therapeutic implications</title>
  1089.      <link>https://pubmed.ncbi.nlm.nih.gov/18644158/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  1090.      <description>Advances in cancer therapy have been substantial in terms of molecular understanding of disease mechanisms, however these advances have not translated into increased survival in the majority of cancer types. One unsolved problem in current cancer therapeutics is the substantial immune suppression seen in patients. Conventionally, investigations in this area have focused on antigen-nonspecific immune suppressive molecules such as cytokines and T cell apoptosis inducing molecules such as Fas...</description>
  1091.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Transl Med. 2008 Jul 22;6:37. doi: 10.1186/1479-5876-6-37.</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">Advances in cancer therapy have been substantial in terms of molecular understanding of disease mechanisms, however these advances have not translated into increased survival in the majority of cancer types. One unsolved problem in current cancer therapeutics is the substantial immune suppression seen in patients. Conventionally, investigations in this area have focused on antigen-nonspecific immune suppressive molecules such as cytokines and T cell apoptosis inducing molecules such as Fas ligand. More recently, studies have demonstrated nanovesicle particles termed exosomes are involved not only in stimulation but also inhibition of immunity in physiological conditions. Interestingly, exosomes secreted by cancer cells have been demonstrated to express tumor antigens, as well as immune suppressive molecules such as PD-1L and FasL. Concentrations of exosomes from plasma of cancer patients have been associated with spontaneous T cell apoptosis, which is associated in some situations with shortened survival. In this paper we place the "exosome-immune suppression" concept in perspective of other tumor immune evasion mechanisms. We conclude by discussing a novel therapeutic approach to cancer immune suppression by extracorporeal removal of exosomes using hollow fiber filtration technology.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/18644158/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">18644158</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC2504474/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">PMC2504474</a> | DOI:<a href=https://doi.org/10.1186/1479-5876-6-37>10.1186/1479-5876-6-37</a></p></div>]]></content:encoded>
  1092.      <guid isPermaLink="false">pubmed:18644158</guid>
  1093.      <pubDate>Wed, 23 Jul 2008 06:00:00 -0400</pubDate>
  1094.      <dc:creator>Thomas E Ichim</dc:creator>
  1095.      <dc:creator>Zhaohui Zhong</dc:creator>
  1096.      <dc:creator>Shalesh Kaushal</dc:creator>
  1097.      <dc:creator>Xiufen Zheng</dc:creator>
  1098.      <dc:creator>Xiubao Ren</dc:creator>
  1099.      <dc:creator>Xishan Hao</dc:creator>
  1100.      <dc:creator>James A Joyce</dc:creator>
  1101.      <dc:creator>Harold H Hanley</dc:creator>
  1102.      <dc:creator>Neil H Riordan</dc:creator>
  1103.      <dc:creator>James Koropatnick</dc:creator>
  1104.      <dc:creator>Vladimir Bogin</dc:creator>
  1105.      <dc:creator>Boris R Minev</dc:creator>
  1106.      <dc:creator>Wei-Ping Min</dc:creator>
  1107.      <dc:creator>Richard H Tullis</dc:creator>
  1108.      <dc:date>2008-07-23</dc:date>
  1109.      <dc:source>Journal of translational medicine</dc:source>
  1110.      <dc:title>Exosomes as a tumor immune escape mechanism: possible therapeutic implications</dc:title>
  1111.      <dc:identifier>pmid:18644158</dc:identifier>
  1112.      <dc:identifier>pmc:PMC2504474</dc:identifier>
  1113.      <dc:identifier>doi:10.1186/1479-5876-6-37</dc:identifier>
  1114.    </item>
  1115.    <item>
  1116.      <title>Immune effects of mesenchymal stem cells: implications for Charcot-Marie-Tooth disease</title>
  1117.      <link>https://pubmed.ncbi.nlm.nih.gov/18627903/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  1118.      <description>Mesenchymal stem cell (MSC) therapy is the most clinically advanced form of cell therapy, second to hematopoietic stem cell transplants. To date, MSC have been used for immune modulation in conditions such as Graft Versus Host Disease (GVHD) and Crohn's Disease, for which Phase III clinical trials are currently in progress. Here, we review the immunological properties of MSC and make a case for their use in treatment of Charcot-Marie-Tooth disease type 1 (CMT1), a group of inherited peripheral...</description>
  1119.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Immunol. 2008 May-Jun;253(1-2):11-5. doi: 10.1016/j.cellimm.2008.06.003. Epub 2008 Jul 15.</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">Mesenchymal stem cell (MSC) therapy is the most clinically advanced form of cell therapy, second to hematopoietic stem cell transplants. To date, MSC have been used for immune modulation in conditions such as Graft Versus Host Disease (GVHD) and Crohn's Disease, for which Phase III clinical trials are currently in progress. Here, we review the immunological properties of MSC and make a case for their use in treatment of Charcot-Marie-Tooth disease type 1 (CMT1), a group of inherited peripheral neuropathies. CMT1 is characterized by demyelination and aberrant immune activation making this condition an ideal target for exploration of MSC therapy, given the ability of these cells to promote sheath regeneration as well as suppress inflammation. Studies supporting this hypothesis will be presented and placed into the context of other cell-based approaches that are theoretically feasible. Given that MSCs selectively home to areas of inflammation, as well as exert effects in an allogeneic manner, the possibility of an "off the shelf" therapy for CMT1 will be discussed.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/18627903/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">18627903</a> | DOI:<a href=https://doi.org/10.1016/j.cellimm.2008.06.003>10.1016/j.cellimm.2008.06.003</a></p></div>]]></content:encoded>
  1120.      <guid isPermaLink="false">pubmed:18627903</guid>
  1121.      <pubDate>Thu, 17 Jul 2008 06:00:00 -0400</pubDate>
  1122.      <dc:creator>Alejandro Leal</dc:creator>
  1123.      <dc:creator>Thomas E Ichim</dc:creator>
  1124.      <dc:creator>Annette M Marleau</dc:creator>
  1125.      <dc:creator>Fabian Lara</dc:creator>
  1126.      <dc:creator>Shalesh Kaushal</dc:creator>
  1127.      <dc:creator>Neil H Riordan</dc:creator>
  1128.      <dc:date>2008-07-17</dc:date>
  1129.      <dc:source>Cellular immunology</dc:source>
  1130.      <dc:title>Immune effects of mesenchymal stem cells: implications for Charcot-Marie-Tooth disease</dc:title>
  1131.      <dc:identifier>pmid:18627903</dc:identifier>
  1132.      <dc:identifier>doi:10.1016/j.cellimm.2008.06.003</dc:identifier>
  1133.    </item>
  1134.    <item>
  1135.      <title>Placental mesenchymal and cord blood stem cell therapy for dilated cardiomyopathy</title>
  1136.      <link>https://pubmed.ncbi.nlm.nih.gov/18549704/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&amp;fc=None&amp;ff=20240507135650&amp;v=2.18.0.post9+e462414</link>
  1137.      <description>Regenerative treatment of dilated, non-ischaemic cardiomyopathy represents a significant unmet clinical need. Intracoronary administration of autologous bone marrow stem cells has demonstrated positive results in treatment of post-infarct and chronic ischaemic patients. Limitations of this procedure include: invasiveness of bone marrow extraction and cardiac catheterization, and dependence on stem cell populations that are aged and possibly senescent. Here, the use of intravenously administered...</description>
  1138.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Reprod Biomed Online. 2008 Jun;16(6):898-905. doi: 10.1016/s1472-6483(10)60159-9.</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">Regenerative treatment of dilated, non-ischaemic cardiomyopathy represents a significant unmet clinical need. Intracoronary administration of autologous bone marrow stem cells has demonstrated positive results in treatment of post-infarct and chronic ischaemic patients. Limitations of this procedure include: invasiveness of bone marrow extraction and cardiac catheterization, and dependence on stem cell populations that are aged and possibly senescent. Here, the use of intravenously administered allogeneic placental matrix derived mesenchymal stem cells for treatment of dilated cardiomyopathy is discussed. Safety of this cell population has already been established in completed Phase I and II trials; however, to date, clinical implementation for dilated cardiomyopathy has not been reported. Preclinical studies have demonstrated that mesenchymal stem cells: (i) inhibit myocardial inflammation; (ii) inhibit cardiomyocyte apoptosis; (iii) stimulate angiogenesis; and (iv) display therapeutic activity in models of dilated cardiomyopathy. Clinical studies have demonstrated the ability of mesenchymal stem cells to inhibit post-infarct remodelling, as well as potently block inflammatory processes in graft versus host and Crohn disease. Presented here is case report of a patient with dilated cardiomyopathy treated with intravenous allogeneic mesenchymal stem cells and expanded umbilical cord blood CD34 cells who underwent a profound clinical improvement.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/18549704/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1n_ssa6lDEVUzfl88acuw-y9KQmTLlQcpqlVmmv4pTyfw5oEPg&ff=20240507135650&v=2.18.0.post9+e462414">18549704</a> | DOI:<a href=https://doi.org/10.1016/s1472-6483(10)60159-9>10.1016/s1472-6483(10)60159-9</a></p></div>]]></content:encoded>
  1139.      <guid isPermaLink="false">pubmed:18549704</guid>
  1140.      <pubDate>Sat, 14 Jun 2008 06:00:00 -0400</pubDate>
  1141.      <dc:creator>Thomas E Ichim</dc:creator>
  1142.      <dc:creator>Fabio Solano</dc:creator>
  1143.      <dc:creator>Roberto Brenes</dc:creator>
  1144.      <dc:creator>Eduardo Glenn</dc:creator>
  1145.      <dc:creator>Junbiao Chang</dc:creator>
  1146.      <dc:creator>Kyle Chan</dc:creator>
  1147.      <dc:creator>Neil H Riordan</dc:creator>
  1148.      <dc:date>2008-06-14</dc:date>
  1149.      <dc:source>Reproductive biomedicine online</dc:source>
  1150.      <dc:title>Placental mesenchymal and cord blood stem cell therapy for dilated cardiomyopathy</dc:title>
  1151.      <dc:identifier>pmid:18549704</dc:identifier>
  1152.      <dc:identifier>doi:10.1016/s1472-6483(10)60159-9</dc:identifier>
  1153.    </item>
  1154.  </channel>
  1155. </rss>
  1156.  

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