<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mochamad Yusuf Alsagaff</style></author><author><style face="normal" font="default" size="100%">Melly Susanti</style></author><author><style face="normal" font="default" size="100%">Mochammad Thaha</style></author><author><style face="normal" font="default" size="100%">Christian Jonatan</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Inotropes in Chronic Beta-Blocker Therapy</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Beta-blocker</style></keyword><keyword><style  face="normal" font="default" size="100%">Decompensated heart failure</style></keyword><keyword><style  face="normal" font="default" size="100%">Inotropes</style></keyword><keyword><style  face="normal" font="default" size="100%">Severe sepsis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2021</style></year><pub-dates><date><style  face="normal" font="default" size="100%">May 2021</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">828-834</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;The increasing rate of cardiovascular disorders contributes to rising hospitalized patients receive chronic oral beta-blocker therapy. Beta-blockers remain one of the fundamental therapy for chronic heart failure. Still, their role in decompensated heart failure and severe sepsis during hospitalization is often debated and inconsistent in clinical practice. In recent years, evidence of the efficacy and clinical outcomes of beta-blockers in acute heart failure (AHF) have accumulated. Clinical research indicates that chronic beta-blockade withdrawals should be prevented, or as soon as hemodynamic stabilization and euvolemic condition are reached, it should be reinstituted. As a subset of AHF patients with low cardiac output required inotropes, the choice of proper agent is fundamental. Different inotropic agents such as inhibitors of the phosphodiesterase, levosimendan, and dobutamine also their associations with beta-blockers are discussed.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><work-type><style face="normal" font="default" size="100%">Review Article</style></work-type><section><style face="normal" font="default" size="100%">828</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Mochamad Yusuf Alsagaff&lt;sup&gt;1,&lt;/sup&gt;*, Melly Susanti&lt;sup&gt;1&lt;/sup&gt;, Mochammad Thaha&lt;sup&gt;2&lt;/sup&gt;, Christian Jonatan&lt;sup&gt;2&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Airlangga, Prof Moestopo Street 6-8, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Department of Internal Medicine, Faculty of Medicine, Universitas Airlangga, Prof Moestopo Street 6-8, Surabaya, INDONESIA.&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yudi Her Oktaviono</style></author><author><style face="normal" font="default" size="100%">Melly Susanti</style></author><author><style face="normal" font="default" size="100%">Achmad Lefi</style></author><author><style face="normal" font="default" size="100%">Ferry Sandra</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Human Umbilical Cord Blood-derived Secretome Enhance Endothelial Progenitor Cells Migration on Hyperglycemic Conditions</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Endothelial progenitor cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperglycemia state</style></keyword><keyword><style  face="normal" font="default" size="100%">Mesenchymal stem cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Migration</style></keyword><keyword><style  face="normal" font="default" size="100%">Secretome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2020</style></year><pub-dates><date><style  face="normal" font="default" size="100%">June 2020</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">12</style></volume><pages><style face="normal" font="default" size="100%">793-797</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;Hyperglycemia state is harmful to body’s homeostasis. Uncontrolled hyperglycemic patients, especially patients with diabetes mellitus have a higher mortality risk of heart disease 2 to 4 times compared to non-hyperglycemic patients. Vascular endothelial impairment always been observed and found as a key feature of hyperglycemia state, which is correlated with reduced numbers and dysfunction of endothelial progenitor cells (EPCs). &lt;strong&gt;Objective: &lt;/strong&gt;This paper aims to investigate the effect of hUCB-MSCs derived secretome treatment on the EPCs migration under hyperglycemia state. &lt;strong&gt;Materials and Methods: &lt;/strong&gt;EPCs were isolated and cultured from peripheral blood samples and cultured for three days. Cultured EPCs were cultivated in 6-well plates until confluence and incubated with high glucose for 5 days, then placed in the modified Boyden chamber at the upper chamber with basal media. The lower chamber was supplemented with basal media and secretome at 2%, 10%, and 20% concentration and VEGF treated group as a control. EPCS migration was evaluated using a Boyden chamber assay. Statistical analysis was performed using SPS 25.0. &lt;strong&gt;Results: &lt;/strong&gt;EPCs migration were significantly higher when hUCB-MSCs-derived secretome was given in high glucose concentrations compared to the and control group (79.80 ± 5.07 vs 51.00 ± 5.15, &lt;em&gt;p&lt;/em&gt;&amp;lt;0.000). This study also showed that hUCB-MSCs-derived secretome increase EPCs migration under high glucose concentrations in a dose-dependent manner (&lt;em&gt;p&lt;/em&gt;&amp;lt;0.05). &lt;strong&gt;Conclusion:&lt;/strong&gt; hUCB-MSCsderived secretome enhances EPCs migration under hyperglycemic state. This result may be of relevance for cell-free and regenerative therapeutic modality for a diabetic patient with coronary artery disease (CAD).&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><work-type><style face="normal" font="default" size="100%">Original Article</style></work-type><section><style face="normal" font="default" size="100%">793</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Yudi Her Oktaviono&lt;sup&gt;1,&lt;/sup&gt;*, Melly Susanti&lt;sup&gt;1,&lt;/sup&gt;*, Achmad Lefi&lt;sup&gt;1&lt;/sup&gt;, Ferry Sandra&lt;sup&gt;2,3 &lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Airlangga, Prof Moestopo Street 6-8, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Prodia Stem Cell Laboratory, Kramat 7 No. 11 Street, Jakarta, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;3&lt;/sup&gt;Department of Biochemistry and Molecular Biology, Faculty of Dentistry, Universitas Trisakti, Kyai Tapa Street No.260, Jakarta, INDONESIA.&lt;/p&gt;
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