<?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 Syahroni Fardiansyah</style></author><author><style face="normal" font="default" size="100%">Tomy Lesmana</style></author><author><style face="normal" font="default" size="100%">Edwin Danardono</style></author><author><style face="normal" font="default" size="100%">Denny Septarendra</style></author><author><style face="normal" font="default" size="100%">Ismu Nugroho</style></author><author><style face="normal" font="default" size="100%">Adhitya Angga Wardhana</style></author><author><style face="normal" font="default" size="100%">Anton Sugianto</style></author><author><style face="normal" font="default" size="100%">Rena Normasari</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Association of CRP, Procalcitonin, Lactate, and Albumin Levels with In-Hospital Mortality Post-Definitive Laparotomy in Patients with Complicated Intra-Abdominal Infections</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%">Complicated intraabdominal infection</style></keyword><keyword><style  face="normal" font="default" size="100%">Damage control laparotomy</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammatory mediators</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">August 2024</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">805-808</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;!-- x-tinymce/html --&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Introduction:&lt;/strong&gt; Complicated intra-abdominal infection (cIAI) still has a high mortality rate due to organ dysfunction despite advances in supportive care. Unlike other sources of septicemia, cIAI requires source control surgery, which is crucial for improving outcomes. The strategy for source control varies depending on the degree of inflammation associated with cIAI; the more severe the inflammation, the less aggressive the surgery needs to be. Therefore, we need a reliable parameter to predict the degree of inflammation before any physiological rearrangement or organ dysfunction occurs due to excessive inflammation from surgery. The literature shows that CRP, procalcitonin, lactate, and albumin are associated with the degree of inflammation. Thus, it’s necessary to study about mentioned parameters for being reference determination strategy of surgery in cIAI, classical definitive laparotomy, or rapid source control laparotomy (RSCL). &lt;strong&gt;Methods: &lt;/strong&gt;We have collected data from CIAI patients at Dr. Soetomo Regional General Hospital in Surabaya, Indonesia, covering November 2022 to April 2024. Our primary focus is assessing the inflammation level associated with the compensated or decompensated phase. The decompensated phase signifies an excessive inflammatory response, with one indication being in-hospital mortality. Subsequently, we performed univariate and multivariate analyses using the SPSS program to determine which laboratory parameters (CRP, Procalcitonin, Lactate, and Albumin) are most associated with in-hospital mortality. &lt;strong&gt;Results:&lt;/strong&gt; Between November 2022 and April 2024, there were 309 patients with complicated intra-abdominal infections (cIAI). Among the patients, 61.8% were male and 38.2% were female. The majority of patients (27.17%) were aged 61-70. The causes of cIAI included perforated appendicitis (22.65%), perforated peptic ulcer (21.69%), complications from previous surgeries (18.13%), large bowel perforation (12.29%), small bowel perforation (11.33%), intraperitoneal abscess (11.33%), and other causes (2.58%). Statistically, lactate was found to be the most accurate predictor of intraoperative hemodynamic instability (p-value &amp;lt; 0.001; correlation coefficient of 0.481), followed by albumin (p-value &amp;lt; 0.001; correlation coefficient of 0.357). CRP and Procalcitonin were less accurate, with correlation coefficients of 0.182 and 0.272, respectively. The determined cut-off points for lactate and albumin were 1.94 and 2.73, for CRP and Procalcitonin were 23,24 and 47,95. Abnormal laboratory finding in our study mean CRP above cut off point, Procalcitonin above cut off point, lactate above cut off point and albumin below cut off point. More than 2 laboratories finding, in-hospital mortality 66,7%, 2 laboratory finding in-hospital mortality 42,8% and only 1 laboratory finding in-hospital mortality 28,4%. &lt;strong&gt;Conclusions&lt;/strong&gt;: CRP, Procalcitonin, Lactate and Albumin have relation statistically significant with in-hospital mortality. Lactate and albumin are better than CRP and procalcitonin in our study, and consider RSCL for more than 2 parameter abnormal laboratory findings CRP, procalcitonin, lactate or albumin.&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%">805</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p&gt;&lt;!-- x-tinymce/html --&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Mochamad Syahroni Fardiansyah&lt;sup&gt;1&lt;/sup&gt;, Tomy Lesmana&lt;sup&gt;2*&lt;/sup&gt;, Edwin Danardono&lt;sup&gt;2&lt;/sup&gt;, Denny Septarendra&lt;sup&gt;2&lt;/sup&gt;, Ismu Nugroho&lt;sup&gt;2&lt;/sup&gt;, Adhitya Angga Wardhana&lt;sup&gt;2&lt;/sup&gt;, Anton Sugianto&lt;sup&gt;2&lt;/sup&gt;, Rena Normasari&lt;sup&gt;3&lt;/sup&gt; &lt;/strong&gt;&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;1&lt;/sup&gt;Trainee of Digestive Surgery, Medical Faculty, Universitas Airlangga, Soetomo General Academic Hospital, Surabaya INDONESIA&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;2&lt;/sup&gt;Consultant of Digestive Surgery, Medical Faculty, Universitas Airlangga, Soetomo General Academic Hospital, Surabaya INDONESIA.&lt;/p&gt;

&lt;p class=&quot;rtejustify&quot;&gt;&lt;sup&gt;3&lt;/sup&gt;Pathology Anatomy Department, Medical Faculty, Universitas Jember, 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%">Rena Normasari</style></author><author><style face="normal" font="default" size="100%">Bambang Purwanto</style></author><author><style face="normal" font="default" size="100%">Damayanti Tinduh</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Protective Effects of Rutinoside on Oxidative Induced Articular Cartilage Damage and Catabolic Activity in Rat Chondrocyte</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%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoarthritis</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Rutinoside</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">April 2024</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">360-365</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;Objective:&lt;/strong&gt; This study aimed to look into the therapeutic potential of rutinoside in reducing articular cartilage degeneration in a rat model of osteoarthritis generated by monosodium iodoacetate (MIA). &lt;strong&gt;Methods:&lt;/strong&gt; We formed three groups of male Wistar rats: the OA, rutinoside, and control groups. Monosodium iodoacetate (3.0 mg) was injected intra-articularly into the knee joint to cause osteoarthritis. For four weeks, oral administration of rutinoside at 100 mg/kg/day was given to the groups that were given the treatment. Histological examination, immunohistochemistry, and biochemical tests were used to assess the level of articular cartilage injury, oxidative damage, catabolic activity, and biomarker expression. &lt;strong&gt;Results:&lt;/strong&gt; The results showed that treatments with rutinoside significantly reduced the damage to articular cartilage in rats with MIA-induced osteoarthritis. Compared to the osteoarthritis group, the rutinoside-treated groups showed enhanced cartilage structure, proteoglycan content, and chondrocyte organization. Immunohistochemistry revealed reduced NFκB, IL-1β, and MMP-13 expressions in the rutinosidetreated groups, indicating suppressed inflammatory and catabolic activity in chondrocytes. Additionally, rutinoside treatment increased SOD activity and decreased MDA levels, which showed less oxidative damage to the joint. A substantial drop in CTX-II levels was found by biochemical research, indicating less type II collagen breakdown. &lt;strong&gt;Conclusion: &lt;/strong&gt;According to a study, rutinoside effectively reduces oxidative damage and catabolic activity in chondrocytes, which can lead to decreased articular cartilage loss in a rat model of MIA-induced osteoarthritis. The study also found that rutinoside can control critical biomarkers such as NFκB, IL-1β, SOD, MDA, MMP-13, and CTX-II, highlighting its potential as a treatment for osteoarthritis. These findings provide valuable insights into using natural chemicals as a promising treatment for OA and suggest that rutinoside could potentially modulate the critical interplay between oxidative stress, inflammation, and chondrocyte catabolism in osteoarthritis. However, further research is required to understand the underlying molecular mechanisms and evaluate rutinoside's translational potential for OA therapy.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">360</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p&gt;&lt;strong&gt;Rena Normasari&lt;sup&gt;1,2&lt;/sup&gt;, Bambang Purwanto&lt;sup&gt;3*&lt;/sup&gt;, Damayanti Tinduh&lt;sup&gt;4&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Doctoral Program, Faculty of Medicine, Airlangga University, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;2&lt;/sup&gt;Pathology Anatomy Department, Medical Faculty, Jember University, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;3&lt;/sup&gt;Physiology Department, Faculty of Medicine, Airlangga University, INDONESIA. 4Physical Medicine and Rehabilitation Department, Faculty of Medicine, Airlangga University, 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%">Rena Normasari</style></author><author><style face="normal" font="default" size="100%">Bambang Purwanto</style></author><author><style face="normal" font="default" size="100%">Damayanti Tinduh</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A Comparative Study of CFA and MIA Induction Models in Rat  Knee Arthritis</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%">CFA</style></keyword><keyword><style  face="normal" font="default" size="100%">CTX-II</style></keyword><keyword><style  face="normal" font="default" size="100%">IL-1β</style></keyword><keyword><style  face="normal" font="default" size="100%">MIA</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoarthritis</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%">December 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%">1197-1201</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;This study presents another comparative review of knee joint arthritis induction in rats using two distinct methods: Complete Freund's Adjuvant (CFA) and monosodium iodoacetate (MIA). Different variables are assessed, including bodyweight changes, knee bend scores, and knee diameter measurements, as well as the quantification of interleukin-1β (IL-1β) and C-telopeptide of type II collagen (CTX-II) levels. CFA or MIA induction was used on rats, and 14 days were observed. Our data show that the impact of arthritis induction varies significantly across the two models. Both the CFA and MIA groups showed different changes in terms of bodyweight changes, knee bend scores, and knee diameter variations. Furthermore, the levels of IL-1β and CTX-II, both known indicators of inflammation and cartilage degeneration, were measured. Notably, IL-1β levels in the CFA group were considerably higher than in the MIA-induced rats, although CTX-II concentrations showed a contrary pattern. These findings highlight the need to carefully consider the induction approach when performing arthritis investigations in rats since the model used has a major impact on the reported physiological alterations. This study's comparative analysis provides useful information for researchers looking to use rat knee joint arthritis models, laying the groundwork for a better-informed selection of the best induction strategy depending on desired outcome metrics.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">1197</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Rena Normasari&lt;sup&gt;1&lt;/sup&gt; , Bambang Purwanto&lt;sup&gt;2,&lt;/sup&gt;*, Damayanti Tinduh&lt;sup&gt;3&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Doctoral Program, Medical Faculty, Airlangga University, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;2&lt;/sup&gt;Physiology Department, Medical Faculty, Airlangga University, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;3&lt;/sup&gt;Physical Medicine and Rehabilitation Department, Medical Faculty, Airlangga University, Surabaya, INDONESIA.&lt;/p&gt;
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