<?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%">Muhamad Robiul Fuadi</style></author><author><style face="normal" font="default" size="100%">Jusak Nugraha</style></author><author><style face="normal" font="default" size="100%">I Gde Rurus Suryawan</style></author><author><style face="normal" font="default" size="100%">Hartono Kahar</style></author><author><style face="normal" font="default" size="100%">Aryati</style></author><author><style face="normal" font="default" size="100%">Gwenny Ichsan Prabowo</style></author><author><style face="normal" font="default" size="100%">Budi Utomo</style></author><author><style face="normal" font="default" size="100%">Reny I’tishom</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Correlation of Apo E Gene Polymorphism with Recurrent Acute Coronary Syndrome</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%">Acute Coronary Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">ApoE gene</style></keyword><keyword><style  face="normal" font="default" size="100%">PCR RFLP</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism</style></keyword><keyword><style  face="normal" font="default" size="100%">Public Health</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style  face="normal" font="default" size="100%">June 2023</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">450-453</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;&lt;strong&gt;Background&lt;/strong&gt;: Recurrent cardiovascular disease (CVD) incidence puts patients at higher risk for mortality and morbidity. One of the CVD symptoms is acute coronary syndrome (ACS). Many genetic polymorphisms are CVD risk factors. This study’s purpose was to investigate the correlation between recurrent ACS incidence and apolipoprotein E (ApoE) gene polymorphism.&lt;strong&gt; Method&lt;/strong&gt;: Case-control design was used in this study. About 90 patients who visited the cardiology and internal medicine clinics at UNAIR Hospital in Surabaya, Indonesia, served as the study's subjects. There were 30 patients with recurrent ACS, 30 patients with a single ACS, and 30 patients with no history of cardiovascular disease. Afterward, using the polymerase chain reaction-restriction fragment length method, the ApoE gene polymorphism examination was carried out. The Tropical Disease Center UNAIR Laboratory conducted all laboratory testing. R&lt;strong&gt;esults&lt;/strong&gt;: In the recurrent ACS group, ApoE polymorphism genotype patterns were 5 subjects for ε2ε2 (16.67%), 23 subjects for ε3ε3 (76.66%), and 2 subjects for ε4ε4 (6.67%). Meanwhile, in the single ACS group, ApoE polymorphism genotype patterns were 6 subjects for ε2ε2 (20%), 22 subjects for ε3ε3 (73.4%), 1 subject for ε4ε4 (3.33%), and 1 subject for ε2ε3 (3.33%). And, in the non- ACS group, ApoE polymorphism genotype patterns were4 subjects for ε2ε2 (13.34%), 25 subjects for ε3ε3 (83.33%), and1 subject for ε4ε4 (3.33%). There was no correlation of ApoE gene polymorphism with recurrent ACS incidence by Chi-square analysis (p &amp;gt; 0.05). &lt;strong&gt;Conclusion&lt;/strong&gt;: ApoE gene polymorphism cannot significantly affect recurrent ACS incidence.&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%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">450</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Muhamad Robiul Fuadi&lt;sup&gt;1&lt;/sup&gt;, Jusak Nugraha&lt;sup&gt;2,*&lt;/sup&gt;, I Gde Rurus Suryawan&lt;sup&gt;3&lt;/sup&gt;, Hartono Kahar&lt;sup&gt;2&lt;/sup&gt;, Aryati&lt;sup&gt;2&lt;/sup&gt;, Gwenny Ichsan Prabowo&lt;sup&gt;4&lt;/sup&gt;, Budi Utomo&lt;sup&gt;5&lt;/sup&gt;, Reny I’tishom&lt;sup&gt;6&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Department of Clinical Pathology, Faculty of Medicine, Universitas Airlangga, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;3&lt;/sup&gt;Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Airlangga, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;4&lt;/sup&gt;Department of Physiology and Medical Biochemistry, Faculty of Medicine, Universitas Airlangga, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;5&lt;/sup&gt;Department of Public Health and Preventive Medicine Faculty of Medicine, Universitas Airlangga, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;6&lt;/sup&gt;Department of Medical Biology, Faculty of Medicine, Universitas Airlangga, 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%">I Gde Rurus Suryawan</style></author><author><style face="normal" font="default" size="100%">Andrianto</style></author><author><style face="normal" font="default" size="100%">Ratna Dewi Cahyaningtias</style></author><author><style face="normal" font="default" size="100%">Makhyan Jibril Al-Farabi</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Hypoxic Preconditioning Decrease ROS and Increase SOD Expression in Adipose-Derived Mesenchymal Cell</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%">Antioxidant</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypoxia</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Stem Cells</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%">May 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%">430-435</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Adipose-derived Mesenchymal Stem Cells (AMSCs) have promising ability to differentiate into a cardiomyocyte. However, post-transplantation survival of AMSCs is relatively low due to lethal cellular hypoxia. Hypoxic preconditioning is a sublethal hypoxia condition which may improve AMSCs survival. This research evaluates the effect of hypoxic preconditioning on the expression of reactive oxygen species (ROS) and superoxide dismutase (SOD) of AMSCs. Isolated human AMSCs was cultured to the 4&lt;sup&gt;th&lt;/sup&gt; passage and confirmed with CD45, CD90 and CD105 expression. Cells were divided into control group (normoxia with 21% O&lt;sub&gt;2&lt;/sub&gt;) and hypoxic preconditioning group (with 1% O&lt;sub&gt;2&lt;/sub&gt;). ROS and SOD were evaluated using immunofluorescence and analyzed using SPSS 25. AMSCs was characterized by the CD105 and CD90 without expression of CD44 and CD45. ROS expression is significantly lower in hypoxia group than in controlled group (253,13 ± 67,795 vs 342,13 ± 116,447; p &amp;lt; 0.05) and SOD expression is significantly higher in hypoxia group than in controlled group (340,25 ± 96,476 vs 234,56 ± 38,238; p &amp;lt;0.05). In conclusion, hypoxic preconditioning in human AMSCs induce lower expression of intracellular ROS and higher expression of intracellular SOD.&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%">Original Article</style></work-type><section><style face="normal" font="default" size="100%">430</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p&gt;&lt;strong&gt;I Gde Rurus Suryawan&lt;sup&gt;1,&lt;/sup&gt;*, Andrianto&lt;sup&gt;1&lt;/sup&gt;, Ratna Dewi Cahyaningtias&lt;sup&gt;1&lt;/sup&gt;, Makhyan Jibril Al-Farabi&lt;sup&gt;1,2 &lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Cardiology and Vascular Medicine, Soetomo General Hospital, Airlangga University, Mayjend. Prof. Dr. Moestopo Street No.6-8, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;2&lt;/sup&gt;School of Health Management, University College London, Gower St, Bloomsbury, London WC1E 6BT, UK.&lt;/p&gt;
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