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reperfusion injury</title> <meta name="description" content="Search results for: myocardial reperfusion injury"> <meta name="keywords" content="myocardial reperfusion injury"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button 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action="https://publications.waset.org/abstracts/search"> <div id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="myocardial reperfusion injury"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 986</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: myocardial reperfusion injury</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">986</span> Myocardial Reperfusion Injury during Percutaneous Coronary Intervention in Patient with Triple-Vessel Disease in Limited Resources Hospital: A Case Report</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Fanniyah%20Anis">Fanniyah Anis</a>, <a href="https://publications.waset.org/abstracts/search?q=Bram%20Kilapong"> Bram Kilapong</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Myocardial reperfusion injury is defined as the cellular damage that results from a period of ischemia, followed by the reestablishment of the blood supply to the infarcted tissue. Ventricular tachycardia is one of the most commonly encountered reperfusion arrhythmia as one of the types of myocardial perfusion injury. Prompt and early treatment can reduce mortality, despite limited resources of the hospital in high risk patients with history of triple vessel disease. Case report, Male 53 years old has been diagnosed with NSTEMI with 3VD and comorbid disease of Hypertension and has undergone revascularization management with Percutaneous coronary intervention. Ventricular tachycardia leading to cardiac arrest occurred right after the stent was inserted. Resuscitation was performed for almost 2 hours until spontaneous circulation returned. Patient admitted in ICU with refractory cardiac shock despite using combination of ionotropic and vasopressor agents under standard non-invasive monitoring due to the limitation of the hospital. Angiography was performed again 5 hours later to exclude other possibilities of blockage of coronary arteries and conclude diagnosis of myocardial reperfusion injury. Patient continually managed with combination of antiplatelet agents and maintenance dose of anti-arrhythmia agents. The handling of the patient was to focus more on supportive and preventive from further deteriorating of the condition. Patient showed clinically improvement and regained consciousness within 24 hours. Patient was successfully discharged from ICU within 3 days without any neurological sequela and was discharge from hospital after 3 days observation in general ward. Limited Resource of hospital did not refrain the physician from attaining a good outcome for this myocardial reperfusion injury case and angiography alone can be used to confirm the diagnosis of myocardial reperfusion injury. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=limited%20resources%20hospital" title="limited resources hospital">limited resources hospital</a>, <a href="https://publications.waset.org/abstracts/search?q=myocardial%20reperfusion%20injury" title=" myocardial reperfusion injury"> myocardial reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=prolonged%20resuscitation" title=" prolonged resuscitation"> prolonged resuscitation</a>, <a href="https://publications.waset.org/abstracts/search?q=refractory%20cardiogenic%20shock" title=" refractory cardiogenic shock"> refractory cardiogenic shock</a>, <a href="https://publications.waset.org/abstracts/search?q=reperfusion%20arrhythmia" title=" reperfusion arrhythmia"> reperfusion arrhythmia</a>, <a href="https://publications.waset.org/abstracts/search?q=revascularization" title=" revascularization"> revascularization</a>, <a href="https://publications.waset.org/abstracts/search?q=triple-vessel%20disease" title=" triple-vessel disease"> triple-vessel disease</a> </p> <a href="https://publications.waset.org/abstracts/63220/myocardial-reperfusion-injury-during-percutaneous-coronary-intervention-in-patient-with-triple-vessel-disease-in-limited-resources-hospital-a-case-report" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/63220.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">304</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">985</span> A Review of Pharmacological Prevention of Peri-and Post-Procedural Myocardial Injury After Percutaneous Coronary Intervention</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Syed%20Dawood%20Md.%20Taimur">Syed Dawood Md. Taimur</a>, <a href="https://publications.waset.org/abstracts/search?q=Md.%20Hasanur%20Rahman"> Md. Hasanur Rahman</a>, <a href="https://publications.waset.org/abstracts/search?q=Syeda%20Fahmida%20Afrin"> Syeda Fahmida Afrin</a>, <a href="https://publications.waset.org/abstracts/search?q=Farzana%20Islam"> Farzana Islam</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The concept of myocardial injury, although first recognized from animal studies, is now recognized as a clinical phenomenon that may result in microvascular damage, no-reflow phenomenon, myocardial stunning, myocardial hibernation and ischemic preconditioning. The final consequence of this event is left ventricular (LV) systolic dysfunction leading to increased morbidity and mortality. The typical clinical case of reperfusion injury occurs in acute myocardial infarction (MI) with ST segment elevation in which an occlusion of a major epicardial coronary artery is followed by recanalization of the artery. This may occur either spontaneously or by means of thrombolysis and/or by primary percutaneous coronary intervention (PCI) with efficient platelet inhibition by aspirin (acetylsalicylic acid), clopidogrel and glycoprotein IIb/IIIa inhibitors. In recent years, percutaneous coronary intervention (PCI) has become a well-established technique for the treatment of coronary artery disease. PCI improves symptoms in patients with coronary artery disease and it has been increasing the safety of procedures. However, peri- and post-procedural myocardial injury, including angiographical slow coronary flow, microvascular embolization, and elevated levels of cardiac enzyme, such as creatine kinase and troponin-T and -I, has also been reported even in elective cases. Furthermore, myocardial reperfusion injury at the beginning of myocardial reperfusion, which causes tissue damage and cardiac dysfunction, may occur in cases of the acute coronary syndrome. Because patients with myocardial injury is related to larger myocardial infarction and have a worse long-term prognosis than those without myocardial injury, it is important to prevent myocardial injury during and/or after PCI in patients with coronary artery disease. To date, many studies have demonstrated that adjunctive pharmacological treatment suppresses myocardial injury and increases coronary blood flow during PCI procedures. In this review, we highlight the usefulness of pharmacological treatment in combination with PCI in attenuating myocardial injury in patients with coronary artery disease. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=coronary%20artery%20disease" title="coronary artery disease">coronary artery disease</a>, <a href="https://publications.waset.org/abstracts/search?q=percutaneous%20coronary%20intervention" title=" percutaneous coronary intervention"> percutaneous coronary intervention</a>, <a href="https://publications.waset.org/abstracts/search?q=myocardial%20injury" title=" myocardial injury"> myocardial injury</a>, <a href="https://publications.waset.org/abstracts/search?q=pharmacology" title=" pharmacology "> pharmacology </a> </p> <a href="https://publications.waset.org/abstracts/2256/a-review-of-pharmacological-prevention-of-peri-and-post-procedural-myocardial-injury-after-percutaneous-coronary-intervention" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/2256.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">451</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">984</span> Grape Seed Extract and Zinc Containing Multivitamin-Mineral Nutritional Food Supplement Protects Heart against Myocardial Ischemic-Reperfusion Injury in Wistar Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=S.%20M.%20Satyam">S. M. Satyam</a>, <a href="https://publications.waset.org/abstracts/search?q=K.%20L.%20Bairy"> K. L. Bairy</a>, <a href="https://publications.waset.org/abstracts/search?q=R.%20Pirasanthan"> R. Pirasanthan</a>, <a href="https://publications.waset.org/abstracts/search?q=R.%20L.%20Vaishnav"> R. L. Vaishnav</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Zincovit tablets have been used as nutritional food supplement over a prolonged period of time. The aim of the present study was to investigate the cardio-protective effect of combined formulation of grape seed extract and Zincovit tablets (40, 80 and 160 mg/kg) using a Langendorff model of ischemia-reperfusion in Wistar rats. Following 21 days of pre-treatment, combined formulation of grape seed extract and Zincovit tablets significantly attenuated ischemia-reperfusion induced cardiac injury in terms of increased coronary flow rate (p < 0.01), decreased creatine kinase activity in coronary effluent (p < 0.05), decreased MDA (p < 0.001), 4-HNE (p < 0.001) and increased protein thiol content (p < 0.01) in comparison with the untreated (control) group. This study opens an avenue to clinical studies to demonstrate the validity of this paradigm as a nutritional food supplement, which could improve the clinical outcome of patients subjected to percutaneous angioplasty. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=grape%20seed%20extract" title="grape seed extract">grape seed extract</a>, <a href="https://publications.waset.org/abstracts/search?q=myocardial%20ischemia-reperfusion%20injury" title=" myocardial ischemia-reperfusion injury"> myocardial ischemia-reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=Zincovit%20tablets" title=" Zincovit tablets "> Zincovit tablets </a> </p> <a href="https://publications.waset.org/abstracts/13015/grape-seed-extract-and-zinc-containing-multivitamin-mineral-nutritional-food-supplement-protects-heart-against-myocardial-ischemic-reperfusion-injury-in-wistar-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/13015.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">376</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">983</span> Possible Role of Fenofibrate and Clofibrate in Attenuated Cardioprotective Effect of Ischemic Preconditioning in Hyperlipidemic Rat Hearts</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Gurfateh%20Singh">Gurfateh Singh</a>, <a href="https://publications.waset.org/abstracts/search?q=Mu%20Khan"> Mu Khan</a>, <a href="https://publications.waset.org/abstracts/search?q=Razia%20Khanam"> Razia Khanam</a>, <a href="https://publications.waset.org/abstracts/search?q=Govind%20Mohan"> Govind Mohan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objective: The present study has been designed to investigate the beneficial role of Fenofibrate & Clofibrate in attenuated the cardioprotective effect of ischemic preconditioning (IPC) in hyperlipidemic rat hearts. Materials & Methods: Experimental hyperlipidemia was produced by feeding high fat diet to rats for a period of 28 days. Isolated langendorff鈥檚 perfused normal and hyperlipidemic rat hearts were subjected to global ischemia for 30 min followed by reperfusion for 120 min. The myocardial infarct size was assessed macroscopically using triphenyltetrazolium chloride staining. Coronary effluent was analyzed for lactate dehydrogenase (LDH) and creatine kinase-MB release to assess the extent of cardiac injury. Moreover, the oxidative stress in heart was assessed by measuring thiobarbituric acid reactive substance, superoxide anion generation and reduced form of glutathione. Results: The ischemia-reperfusion (I/R) has been noted to induce oxidative stress by increasing TBARS, superoxide anion generation and decreasing reduced form of glutathione in normal and hyperlipidemic rat hearts. Moreover, I/R produced myocardial injury, which was assessed in terms of increase in myocardial infarct size, LDH and CK-MB release in coronary effluent and decrease in coronary flow rate in normal and hyperlipidemic rat hearts. In addition, the hyperlipidemic rat hearts showed enhanced I/R-induced myocardial injury with high degree of oxidative stress as compared with normal rat hearts subjected to I/R. Four episodes of IPC (5 min each) afforded cardioprotection against I/R-induced myocardial injury in normal rat hearts as assessed in terms of improvement in coronary flow rate and reduction in myocardial infarct size, LDH, CK-MB and oxidative stress. On the other hand, IPC mediated myocardial protection against I/R-injury was abolished in hyperlipidemic rat hearts. However, Treatment with Fenofibrate (100 mg/kg/day, i.p.), Clofibrate (300mg/kg/day, i.p.) as a agonists of PPAR-伪 have not affected the cardioprotective effect of IPC in normal rat hearts, but its treatment markedly restored the cardioprotective potentials of IPC in hyperlipidemic rat hearts. Conclusion: It is noted that the high degree of oxidative stress produced in hyperlipidemic rat heart during reperfusion and consequent down regulation of PPAR-伪 may be responsible to abolish the cardioprotective potentials of IPC. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hyperlipidemia" title="Hyperlipidemia">Hyperlipidemia</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia-reperfusion%20injury" title=" ischemia-reperfusion injury"> ischemia-reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemic%20preconditioning" title=" ischemic preconditioning"> ischemic preconditioning</a>, <a href="https://publications.waset.org/abstracts/search?q=PPAR-%CE%B1" title=" PPAR-伪"> PPAR-伪</a> </p> <a href="https://publications.waset.org/abstracts/41455/possible-role-of-fenofibrate-and-clofibrate-in-attenuated-cardioprotective-effect-of-ischemic-preconditioning-in-hyperlipidemic-rat-hearts" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41455.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">288</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">982</span> Protective Role of Peroxiredoxin V against Ischemia/Reperfusion-Induced Acute Kidney Injury in Mice</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Eun%20Gyeong%20Lee">Eun Gyeong Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Ji%20Young%20Park"> Ji Young Park</a>, <a href="https://publications.waset.org/abstracts/search?q=Hyun%20Ae%20Woo"> Hyun Ae Woo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Reactive oxygen species (ROS) production is involved in ischemia/reperfusion (I/R) injury in kidney of mice. Oxidative stress develops from an imbalance between ROS production and reduced antioxidant defenses. Many enzymatic and nonenzymatic antioxidant systems including peroxiredoxins (Prxs) are present in kidney to maintain an appropriate level of ROS and prevent oxidative damage. Prxs are a family of peroxidases that reduce peroxides, with a conserved cysteine residue serving as the site of oxidation by peroxides. In this study, we examined the protective role of Prx V against I/R-induced acute kidney injury (AKI) using Prx V wild type (WT) and knockout (KO) mice. We compared the response of Prx V WT and KO mice in mice model of I/R injury. Renal structure, functions, oxidative stress markers, protein levels of oxidative damage marker were worse in Prx V KO mice. Ablation of Prx V enhanced susceptibility to I/R-induced oxidative stress. Prx V KO mice were seen to have more severe renal damage than Prx V WT mice in mice model of I/R injury. Our results demonstrate that Prx V is protective against I/R-induced AKI. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=peroxiredoxin" title="peroxiredoxin">peroxiredoxin</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia%2Freperfusion" title=" ischemia/reperfusion"> ischemia/reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=kidney" title=" kidney"> kidney</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/47859/protective-role-of-peroxiredoxin-v-against-ischemiareperfusion-induced-acute-kidney-injury-in-mice" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/47859.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">386</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">981</span> Possible Neuroprotective Mechanism of Remote Limb Ischemic Post Conditioning against Global Cerebral Ischemic Injury</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sruthi%20Ramagiri">Sruthi Ramagiri</a>, <a href="https://publications.waset.org/abstracts/search?q=Rajeev%20Taliyan"> Rajeev Taliyan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background and purpose: Recent investigations on ischemia and reperfusion injury postulate that transient ischemia of remote organs after a prolonged ischemic insult confers neuroprotection. However, the molecular mechanisms of the remote limb ischemic post-conditioning (RIPOC) are yet to be elucidated. The current study was designed to investigate the protective mechanism of RIPOC against cerebral ischemic injury using global model of stroke. Materials and methods: Global ischemic reperfusion injury (IR) was achieved by 30 minutes ischemia of cerebral artery, followed by reperfusion for 24 hours. Induction of global ischemia was followed by 4 brief episodes (30 seconds each) of ischemia and reperfusion of femoral artery to accomplish RIPOC. 5-Hydroxy Decanoic acid (5-HD), a KATP channel blocker (20 mg/kg) was administered after induction of global ischemia and RIPOC intervention. Results: IR injury ensue significant behavioural deficits as manifested by rotarod performance and spontaneous locomotor activity when compared to sham control. Furthermore, IR injury significantly increased oxidonitrative stress and infarct volume as evidenced by biochemical parameters (MDA, GSH, Nitrite, SOD) and 2,3,5-triphenyltetrazolium chloride (TTC) staining respectively. Moreover, RIPOC intervention ameliorated the behavioural performance, attenuated the oxidative stress and infarct volume when compared to IR injury group. However, administration of 5-HD increased the oxidative stress and infarct size while deteriorating the behavioural parameters when compared to RIPOC group. Conclusions: In a nutshell, cerebral IR injury has significantly induced the neuronal damage, whereas RIPOC intervention decreased the neuronal injury. Moreover, 5-HD abolished the neuroprotection offered by RIPOC indicating the putative role of KATP channel opening in RIPOC against cerebral ischemic injury. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=RIPOC" title="RIPOC">RIPOC</a>, <a href="https://publications.waset.org/abstracts/search?q=cerebral%20injury" title=" cerebral injury"> cerebral injury</a>, <a href="https://publications.waset.org/abstracts/search?q=KATP%20channel" title=" KATP channel"> KATP channel</a>, <a href="https://publications.waset.org/abstracts/search?q=neuroprotection" title=" neuroprotection"> neuroprotection</a> </p> <a href="https://publications.waset.org/abstracts/16163/possible-neuroprotective-mechanism-of-remote-limb-ischemic-post-conditioning-against-global-cerebral-ischemic-injury" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/16163.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">470</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">980</span> Hydroxy Safflower Yellow A (HSYA) Mediated Neuroprotective Effect against Ischemia Reperfusion (I/R) Injury in Cerebral Stroke</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sruthi%20Ramagiri">Sruthi Ramagiri</a>, <a href="https://publications.waset.org/abstracts/search?q=Rajeev%20T."> Rajeev T.</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Free radical damage has been entailed as the major culprit in the ischemic stroke contributing for oxidative damage. Recent investigations on Hydroxy Safflower Yellow A (HSYA) suggested its role in cerebral ischemia and various neurodegenerative disorders with unidentified molecular mechanisms. The current study was designed to investigate putative therapeutic role and possible molecular mechanisms of HSYA administration during the onset of reperfusion in cerebral ischemia-reperfusion (I/R) injury in cerebral stroke. Cerebral stroke was achieved by focal ischemic model. HSYA (10 mg/kg) was injected intravenously via the tail vein 5 minutes before reperfusion. Losses of sensorimotor abilities were evaluated by neurological scoring, spontaneous locomotor activity, and rotarod performance. Extent of oxidative stress was evaluated by biochemical parameters i.e., malondialdehyde (MDA), Glutathione (GSH), Super Oxide Dismutase (SOD) and catalase levels. The infarct volume of brain was assessed by 2,3,5-triphenyl tetrazolium chloride (TTC) staining technique. Increased cerebral injury (I/R) was evidenced by motor impairment, increased infarct volume and elevation of MDA levels along with significant reduction in antioxidant i.e.,MDA levels along with significant reduction in antioxidant i.e., GSH, SOD and catalase levels when compared to sham control. However, post conditioning with HSYA (10 mg/kg, i.v.) at the onset of reperfusion has significantly ameliorated sensorimotor abilities, attenuated MDA levels and reduced the infarct volume as compared with vehicle treated I/R injury group. Moreover, HSYA treatments improved antioxidant enzyme levels as compared with vehicle treated I/R-injury group. In conclusion, it may be suggested that HSYA post conditioning could be novel therapeutic approach against I/R injury in cerebral stroke possibly through its anti-oxidant mechanism. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=HSYA" title="HSYA">HSYA</a>, <a href="https://publications.waset.org/abstracts/search?q=Ischemia%20reperfusion%20injury" title=" Ischemia reperfusion injury"> Ischemia reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=stroke" title=" stroke"> stroke</a> </p> <a href="https://publications.waset.org/abstracts/19618/hydroxy-safflower-yellow-a-hsya-mediated-neuroprotective-effect-against-ischemia-reperfusion-ir-injury-in-cerebral-stroke" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19618.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">427</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">979</span> The Impact of Intestinal Ischaemia-Reperfusion Injury upon the Biological Function of Mesenteric Lymph</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Beth%20Taylor">Beth Taylor</a>, <a href="https://publications.waset.org/abstracts/search?q=Kojima%20Mituaki"> Kojima Mituaki</a>, <a href="https://publications.waset.org/abstracts/search?q=Atsushi%20Senda"> Atsushi Senda</a>, <a href="https://publications.waset.org/abstracts/search?q=Koji%20Morishita"> Koji Morishita</a>, <a href="https://publications.waset.org/abstracts/search?q=Yasuhiro%20Otomo"> Yasuhiro Otomo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Intestinal ischaemia-reperfusion injury drives systemic inflammation and organ failure following trauma/haemorrhagic shock (T/HS), through the release of pro-inflammatory mediators into the mesenteric lymph (ML). However, changes in the biological function of ML are not fully understood, and therefore, a specific model of intestinal ischaemia-reperfusion injury is required to obtain ML for the study of its biological function upon inflammatory cells. ML obtained from a model of intestinal ischaemia-reperfusion injury was used to assess biological function upon inflammatory cells and investigate changes in the biological function of individual ML components. An additional model was used to determine the effect of vagal nerve stimulation (VNS) upon biological function. Rat ML was obtained by mesenteric lymphatic duct cannulation before and after occlusion of the superior mesenteric artery (SMAO). ML was incubated with human polymorphonuclear neutrophils (PMNs), monocytes and lymphocytes, and the biological function of these cells was assessed. ML was then separated into supernatant, exosome and micro-vesicle components, and biological activity was compared in monocytes. A model with an additional VNS phase was developed, in which the right cervical vagal nerve was exposed and stimulated, and ML collected for comparison of biological function with the conventional model. The biological function of ML was altered by intestinal ischaemia-reperfusion injury, increasing PMN activation, monocyte activation, and lymphocyte apoptosis. Increased monocyte activation was only induced by the exosome component of ML, with no significant changes induced by the supernatant or micro-vesicle components. VNS partially attenuated monocyte activation, but no attenuation of PMN activation was observed. Intestinal ischaemia-reperfusion injury induces changes in the biological function of ML upon both innate and adaptive inflammatory cells, supporting the role of intestinal ischaemia-reperfusion injury in driving systemic inflammation following T/HS. The exosome component of ML appears to be critical to the transport of pro-inflammatory mediators in ML. VNS partially attenuates changes in innate inflammatory cell biological activity observed, presenting possibilities for future novel treatment development in multiple organ failure patients. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=exosomes" title="exosomes">exosomes</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=intestinal%20ischaemia" title=" intestinal ischaemia"> intestinal ischaemia</a>, <a href="https://publications.waset.org/abstracts/search?q=mesenteric%20lymph" title=" mesenteric lymph"> mesenteric lymph</a>, <a href="https://publications.waset.org/abstracts/search?q=vagal%20stimulation" title=" vagal stimulation"> vagal stimulation</a> </p> <a href="https://publications.waset.org/abstracts/111415/the-impact-of-intestinal-ischaemia-reperfusion-injury-upon-the-biological-function-of-mesenteric-lymph" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/111415.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">134</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">978</span> Albendazole Ameliorates Inflammatory Response in a Rat Model of Acute Mesenteric Ischemia Reperfusion Injury</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Kamyar%20Moradi">Kamyar Moradi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Acute mesenteric ischemia is known as a life-threatening condition. Re-establishment of blood flow in this condition can lead to mesenteric ischemia reperfusion (MIR) injury, which is accompanied by inflammatory response. Still, clear blueprint of inflammatory mechanism underlying MIR injury has not been provided. Interestingly, Albendazole has exhibited notable effects on inflammation and cytokine production. In this study, we aimed to evaluate outcomes of MIR injury following pretreatment with Albendazole with respect to assessment of mesenteric inflammation and ischemia threshold. Methods: Male rats were randomly divided into sham operated, vehicle treated, Albendazole 100 mg/kg, and Albendazole 200 mg/kg groups. MIR injury was induced by occlusion of superior mesenteric artery for 30 minutes followed by 120 minutes of reperfusion. Samples were utilized for assessment of epithelial survival and villous height. Immunohistochemistry study revealed intestinal expression of TNF-伪 and HIF-1-伪. Gene expression of NF-魏B/TLR4/TNF-伪/IL-6 was measured using RTPCR. Also, protein levels of inflammatory cytokines in serum and intestine were assessed by ELISA method. Results: Histopathological study demonstrated that pretreatment with Albendazole could ameliorate decline in villous height and epithelial survival following MIR injury. Also, systemic inflammation was suppressed after administration of Albendazole. Analysis of possible participating inflammatory pathway could demonstrate that intestinal expression of NF-魏B/TLR4/TNF-伪/IL-6 is significantly attenuated in treated groups. Eventually, IHC study illustrated concordant decline in mesenteric expression of HIF-1-伪/TNF-伪. Conclusion: Single dose pretreatment with Albendazole could ameliorate inflammatory response and enhance ischemia threshold following induction of MIR injury. Still, more studies would clarify existing causality in this phenomenon. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=albendazole" title="albendazole">albendazole</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia%20reperfusion%20injury" title=" ischemia reperfusion injury"> ischemia reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=mesenteric%20ischemia" title=" mesenteric ischemia"> mesenteric ischemia</a> </p> <a href="https://publications.waset.org/abstracts/146614/albendazole-ameliorates-inflammatory-response-in-a-rat-model-of-acute-mesenteric-ischemia-reperfusion-injury" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/146614.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">169</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">977</span> Neuroprotective Effects of Allium Cepa Extract Against Ischemia Reperfusion Induced Cognitive Dysfunction and Brain Damage in Mice</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jaspal%20Rana">Jaspal Rana</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Oxidative stress has been identified as an underlying cause of ischemia-reperfusion (IR) related cognitive dysfunction and brain damage. Therefore, antioxidant based therapies to treat IR injury are being investigated. Allium cepa L. (onion) is used as culinary medicine and is documented to have marked antioxidant effects. Hence, the present study was designed to evaluate the effect of A. cepa outer scale extract (ACE) against IR induced cognition and biochemical deficit in mice. ACE was prepared by maceration with 70% methanol and fractionated into ethylacetate and aqueous fractions. Bilateral common carotid artery occlusion for 10 min followed by 24 h reperfusion was used to induce cerebral IR injury. Following IR injury, ACE (100 and 200 mg/kg) was administered orally to animals for 7 days once daily. Behavioral outcomes (memory and sensorimotor functions) were evaluated using Morris water maze and neurological severity score. Cerebral infarct size, brain thiobarbituric acid reactive species, reduced glutathione, and superoxide dismutase activity was also determined. Treatment with ACE significantly ameliorated IR mediated deterioration of memory and sensorimotor functions and rise in brain oxidative stress in animals. The results of the present investigation revealed that ACE improved functional outcomes after cerebral IR injury which may be attributed to its antioxidant properties. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ischemia-reperfusion" title="ischemia-reperfusion">ischemia-reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=neuroprotective" title=" neuroprotective"> neuroprotective</a>, <a href="https://publications.waset.org/abstracts/search?q=stroke" title=" stroke"> stroke</a>, <a href="https://publications.waset.org/abstracts/search?q=antioxidant" title=" antioxidant"> antioxidant</a> </p> <a href="https://publications.waset.org/abstracts/148184/neuroprotective-effects-of-allium-cepa-extract-against-ischemia-reperfusion-induced-cognitive-dysfunction-and-brain-damage-in-mice" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/148184.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">115</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">976</span> Raman Spectroscopic of Cardioprotective Mechanism During the Metabolic Inhibition of Heart Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=A.%20Almohammedi">A. Almohammedi</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20J.%20Hudson"> A. J. Hudson</a>, <a href="https://publications.waset.org/abstracts/search?q=N.%20M.%20Storey"> N. M. Storey</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Following ischaemia/reperfusion injury, as in a myocardial infraction, cardiac myocytes undergo oxidative stress which leads to several potential outcomes including; necrotic or apoptotic cell death or dysregulated calcium homeostasis or disruption of the electron transport chain. Several studies have shown that nitric oxide donors protect cardiomyocytes against ischemia and reperfusion. However until present, the mechanism of cardioprotective effect of nitric oxide donor in isolated ventricular cardiomyocytes is not fully understood and has not been investigated before using Raman spectroscopy. For these reasons, the aim of this study was to develop a novel technique, pre-resonance Raman spectroscopy, to investigate the mechanism of cardioprotective effect of nitric oxide donor in isolated ventricular cardiomyocytes exposed to metabolic inhibition and re-energisation. The results demonstrated the first time that Raman microspectroscopy technique has the capability to monitor the metabolic inhibition of cardiomyocytes and to monitor the effectiveness of cardioprotection by nitric oxide donor prior to metabolic inhibition of cardiomyocytes. Metabolic inhibition and reenergisation were used in this study to mimic the low and high oxygen levels experienced by cells during ischaemic and reperfusion treatments. A laser wavelength of 488 nm used in this study has been found to provide the most sensitive means of observe the cellular mechanisms of myoglobin during nitric oxide donor preconditioning, metabolic inhibition and re-energisation and did not cause any damage to the cells. The data also highlight the considerably different cellular responses to metabolic inhibition to ischaemia. Moreover, the data has been shown the relationship between the release of myoglobin and chemical ischemia where that the release of myoglobin from the cell only occurred if a cell did not recover contractility. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ex%20vivo%20biospectroscopy" title="ex vivo biospectroscopy">ex vivo biospectroscopy</a>, <a href="https://publications.waset.org/abstracts/search?q=Raman%20spectroscopy" title=" Raman spectroscopy"> Raman spectroscopy</a>, <a href="https://publications.waset.org/abstracts/search?q=biophotonics" title=" biophotonics"> biophotonics</a>, <a href="https://publications.waset.org/abstracts/search?q=cardiomyocytes" title=" cardiomyocytes"> cardiomyocytes</a>, <a href="https://publications.waset.org/abstracts/search?q=ischaemia%20%2F%20reperfusion%20injury" title=" ischaemia / reperfusion injury"> ischaemia / reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=cardioprotection" title=" cardioprotection"> cardioprotection</a>, <a href="https://publications.waset.org/abstracts/search?q=nitric%20oxide%20donor" title=" nitric oxide donor"> nitric oxide donor</a> </p> <a href="https://publications.waset.org/abstracts/29502/raman-spectroscopic-of-cardioprotective-mechanism-during-the-metabolic-inhibition-of-heart-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/29502.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">352</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">975</span> Melatonin Suppresses the Brain Injury after Cerebral Ischemia/Reperfusion in Hyperglycemic Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Dalia%20O.%20Saleha">Dalia O. Saleha</a>, <a href="https://publications.waset.org/abstracts/search?q=Gehad%20A.%20Abdel%20Jaleela"> Gehad A. Abdel Jaleela</a>, <a href="https://publications.waset.org/abstracts/search?q=Sally%20W.%20Al-Awdana"> Sally W. Al-Awdana</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Diabetes mellitus (DM) is known to exacerbate cerebral ischemic injury. The present study aimed to investigate the anti-oxidant and anti-inflammatory effects of oral supplementation of melatonin (MLN) on cerebral injury caused by middle cerebral artery occlusion and reperfusion (MCAO/Re) in streptozotocin (STZ)-induced hyperglycemic rats. Hyperglycemia was induced by a single injection of STZ (55mg/kg; i.p.), six weeks later the cerebral injury was induced by MCAO/Re. Twenty-four hours after the MCAO/Re the MLN (10 mg/kg) was injected for 14 consecutive days. Results of the present study revealed that MCAO/Re in STZ-induced hyperglycemia in rats causes an increase in the oxidative stress biomarkers; it increased brain lipid peroxidation (measured as malondialdehyde; MDA) and brain level of nitric oxide (NO). Moreover, MCAO/Reproduces a prominent increase in the brain inflammatory markers viz. interleukin-6 (IL-6), interleukin-1尾 (IL-1尾) and tumor necrosis nuclear factor-alpha (TNF-伪). Oral treatment of MCAO/Re in STZ-induced hyperglycemic rats with MLN (10 mg/kg) for two weeks restored the brain levels of MDA, GSH, NO, IL-6, IL-1尾 and the TNF-伪. MLN succeeded to suppress the exacerbation of damage in the brain of hyperglycemic rats. These results suggest that daily intake of MLN attenuates the exacerbation of cerebral ischemic injury in a diabetic state, which may be attributed to anti-oxidant and anti-inflammatory effects in the brain. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=melatonin" title="melatonin">melatonin</a>, <a href="https://publications.waset.org/abstracts/search?q=brain%20injury" title=" brain injury"> brain injury</a>, <a href="https://publications.waset.org/abstracts/search?q=cerebral%20ischemia%2Freperfusion" title=" cerebral ischemia/reperfusion"> cerebral ischemia/reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=hyperglycemia" title=" hyperglycemia"> hyperglycemia</a>, <a href="https://publications.waset.org/abstracts/search?q=rats" title=" rats"> rats</a> </p> <a href="https://publications.waset.org/abstracts/89295/melatonin-suppresses-the-brain-injury-after-cerebral-ischemiareperfusion-in-hyperglycemic-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/89295.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">158</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">974</span> The Effect of 尾-Cryptoxanthin on Testicular Ischemia-Reperfusion Injury in a Rat Model: Evidence from Testicular Histology</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Kianoush%20Mohammadnejad">Kianoush Mohammadnejad</a>, <a href="https://publications.waset.org/abstracts/search?q=Rahim%20Mohammadi"> Rahim Mohammadi</a>, <a href="https://publications.waset.org/abstracts/search?q=Ali%20Soleimanzadeh"> Ali Soleimanzadeh</a>, <a href="https://publications.waset.org/abstracts/search?q=Ali%20Shalizar%20Jalai"> Ali Shalizar Jalai</a>, <a href="https://publications.waset.org/abstracts/search?q=Farshid%20Sareafzadeh%20Rezaei"> Farshid Sareafzadeh Rezaei</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Testicular torsion and detorsion are significant clinical issues for infertile men. Torsion of the spermatic cord is an emergency condition resulting from the rotation of the testis and epididymis around the axis of the spermatic cord. A rat testis model was used to assess the effects of 尾-cryptoxanthin on ischemia-reperfusion injury. Twenty healthy male Wistar rats were included and randomized into four investigational groups (n = 5): Group SHAM: In this group, midline incision of the scrotum was performed, and the testicles were taken out for 2 hours with a 720-degree rotation. Group ISCHEMIA: In this group, a midline incision of the scrotum was performed, and the testicles were taken out and underwent ischemia for 2 hours with a 720-degree rotation. Group IS/REP/Oil: In this group, a midline scrotum cut was performed the testicles were taken out, and ischemia was created for 2 hours with a 720-degree rotation and at the end of ischemia 100 碌L of corn oil (尾-cryptoxanthin solvent) was injected intraperitoneally. Group IS/REP/CRPTXNTN 2.5: The same as group IS/REP/Oil as well as intraperitoneal administration of 100 碌L of 尾-cryptoxanthin (2.5 碌g/kg) at the end of ischemia. In all groups, the testes were returned back to the scrotum and, after 60 days, were dissected out and removed for histopathological analyses. 尾-cryptoxanthin at the dose of 2.5 碌g/kg significantly improved histologic indices compared to other treatment groups (p<0.05). 尾-cryptoxanthin could be helpful in minimizing ischemia-reperfusion injury in testicular tissue exposed to ischemia. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=beta-cryptoxanthin" title="beta-cryptoxanthin">beta-cryptoxanthin</a>, <a href="https://publications.waset.org/abstracts/search?q=testis" title=" testis"> testis</a>, <a href="https://publications.waset.org/abstracts/search?q=Ischemia-reperfusion" title=" Ischemia-reperfusion"> Ischemia-reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=Intraperitoneal" title=" Intraperitoneal"> Intraperitoneal</a> </p> <a href="https://publications.waset.org/abstracts/189306/the-effect-of-v-cryptoxanthin-on-testicular-ischemia-reperfusion-injury-in-a-rat-model-evidence-from-testicular-histology" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/189306.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">18</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">973</span> Allium Cepa Extract Provides Neuroprotection Against Ischemia Reperfusion Induced Cognitive Dysfunction and Brain Damage in Mice</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jaspal%20Rana">Jaspal Rana</a>, <a href="https://publications.waset.org/abstracts/search?q=Alkem%20Laboratories"> Alkem Laboratories</a>, <a href="https://publications.waset.org/abstracts/search?q=Baddi"> Baddi</a>, <a href="https://publications.waset.org/abstracts/search?q=Himachal%20Pradesh"> Himachal Pradesh</a>, <a href="https://publications.waset.org/abstracts/search?q=India%20Chitkara%20University"> India Chitkara University</a>, <a href="https://publications.waset.org/abstracts/search?q=Punjab"> Punjab</a>, <a href="https://publications.waset.org/abstracts/search?q=India"> India</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Oxidative stress has been identified as an underlying cause of ischemia-reperfusion (IR) related cognitive dysfunction and brain damage. Therefore, antioxidant based therapies to treat IR injury are being investigated. Allium cepa L. (onion) is used as culinary medicine and is documented to have marked antioxidant effects. Hence, the present study was designed to evaluate the effect of A. cepa outer scale extract (ACE) against IR induced cognition and biochemical deficit in mice. ACE was prepared by maceration with 70% methanol and fractionated into ethylacetate and aqueous fractions. Bilateral common carotid artery occlusion for 10 min followed by 24 h reperfusion was used to induce cerebral IR injury. Following IR injury, ACE (100 and 200 mg/kg) was administered orally to animals for 7 days once daily. Behavioral outcomes (memory and sensorimotor functions) were evaluated using Morris water maze and neurological severity score. Cerebral infarct size, brain thiobarbituric acid reactive species, reduced glutathione, and superoxide dismutase activity was also determined. Treatment with ACE significantly ameliorated IR mediated deterioration of memory and sensorimotor functions and rise in brain oxidative stress in animals. The results of the present investigation revealed that ACE improved functional outcomes after cerebral IR injury, which may be attributed to its antioxidant properties. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=stroke" title="stroke">stroke</a>, <a href="https://publications.waset.org/abstracts/search?q=neuroprotection" title=" neuroprotection"> neuroprotection</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia%20reperfusion" title=" ischemia reperfusion"> ischemia reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=herbal%20drugs" title=" herbal drugs"> herbal drugs</a> </p> <a href="https://publications.waset.org/abstracts/148736/allium-cepa-extract-provides-neuroprotection-against-ischemia-reperfusion-induced-cognitive-dysfunction-and-brain-damage-in-mice" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/148736.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">106</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">972</span> The Protective Role of Decoy Receptor 3 Analogue on Rat Steatotic Liver against Ischemia-Reperfusion Injury by Blocking M1/Th1 Polarization and Multiple Upstream Pathogenic Cascades</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Tzu-Hao%20Li">Tzu-Hao Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Shie-Liang%20Hsieh"> Shie-Liang Hsieh</a>, <a href="https://publications.waset.org/abstracts/search?q=Han-Chieh%20Lin"> Han-Chieh Lin</a>, <a href="https://publications.waset.org/abstracts/search?q=Ying-Ying%20Yang"> Ying-Ying Yang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> TNF superfamily-stimulated pathogenic cascades and macrophage (M1)/kupffer cells (KC) polarization are important in the pathogenesis of ischemia-reperfusion (IR) liver injury in animals with hepatic steatosis (HS). Decoy receptor 3 (DcR3) is a common upstream inhibitor of the above-mentioned pathogenic cascades. The study evaluated whether modulation of these DcR3-related cascades was able to protect steatotic liver from IR injury. Serum and hepatic DcR3 levels were lower in patients and animals with HS. Accordingly, the effects of pharmacologic and genetic DcR3 replacement on the IR-related pathogenic changes were measured. Significantly, DcR3 replacement protected IR-Zucker(HS) rats and IR-DcR3-Tg(HS) mice from IR liver injury. The beneficial effects of DcR3 replacement were accompanied by decreased serum/hepatic TNF, soluble TNF-like cytokine 1A (TL1A), Fas ligand (Fas-L) and LIGHT, T-helper-cell-1 cytokine (INF) levels, neutrophil infiltration, M1 polarization, neutrophil-macrophage/KC-T-cell interaction, hepatocyte apoptosis and improved hepatic microcirculatory failure among animals with IR-injured steatotic livers. Additionally, TL1A, Fas-L, LIGHT and TLR4/NFB signals were found to mediate the DcR3-related protective effects of steatotic livers from IR injury. Using multimodal in vivo and in vitro approaches, we found that DcR3 was a potential agent to protect steatotic livers from IR injury by simultaneous blocking the multiple IR injury-related pathogenic changes. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Decoy%203%20receptor" title="Decoy 3 receptor">Decoy 3 receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia-reperfusion%20injury" title=" ischemia-reperfusion injury"> ischemia-reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=M1%20polarization" title=" M1 polarization"> M1 polarization</a>, <a href="https://publications.waset.org/abstracts/search?q=TNF%20superfamily" title=" TNF superfamily"> TNF superfamily</a> </p> <a href="https://publications.waset.org/abstracts/77043/the-protective-role-of-decoy-receptor-3-analogue-on-rat-steatotic-liver-against-ischemia-reperfusion-injury-by-blocking-m1th1-polarization-and-multiple-upstream-pathogenic-cascades" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/77043.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">208</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">971</span> The Impact of Co-Administration of Phosphodiesterase-5 Inhibitor and Sodium Selenite on Ischemia/Reperfusion Injury in a Rat Ovary Model: Biochemical and Histopathologic Evaluation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Waleed%20Aly%20Sayed%20Ahmed">Waleed Aly Sayed Ahmed</a>, <a href="https://publications.waset.org/abstracts/search?q=Eman%20Kishk"> Eman Kishk</a>, <a href="https://publications.waset.org/abstracts/search?q=Tahani%20%20Shams"> Tahani Shams</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aim: To study the effects of co-administration of phosphodiesterase-5 inhibitor (PDE-5) and sodium selenite against the damage induced by ovarian ischemia-reperfusion in rats. Materials and Methods: A total of forty-two sexually mature, virgin, female rats were divided randomly into six groups of seven each: sham group (C), ischemia group (I), ischemia/reperfusion group (I/R), ischemia/reperfusion plus 1.4mg/kg sildenafil (I/R+S) group, ischemia/reperfusion plus 0.2mg/kg selenium (I/R+Se) group and ischemia/reperfusion plus combination of sildenafil and selenium (I/R+S+Se) group. In ischemia group (I), rats were exposed to ischemia for 3 hours (h). In ischemia/reperfusion group (I/R), rats were exposed to ischemia for 3 h followed by 6 h of reperfusion. Treated groups received 1.4mg/kg sildenafil or 0.2 mg/kg selenium or both 30 min before reperfusion. Both ovaries were surgically removed carefully. One ovary was examined for histopathological changes and the other was subject to biochemical analysis including malondialdehyde (MDA), catalase (CAT) and glutathione peroxidase (GPx). Results: Assessment of ovarian tissue damage using a scoring system showed marked vascular congestion, interstitial edema, leukocyte infiltration, hemorrhage, and follicular degeneration in ischemia and ischemia/reperfusion groups. Tissue damage score for I, IR and all treated groups were significantly higher than those of the sham group (p<0.001), while tissue damage score decreased significantly in I/R+S and I/R+Se groups compared to I/R group (p<0.05), and notably, the difference was highly significant in I/R+S+Se group (p<0.001). There was significant increase in MDA levels and reduction in activities of CAT and GPx in I/R group compared to the sham group (p < 0.05). In I/R+S and I/R+Se groups, MDA was significantly decreased compared to the I/R group (p<0.05) and the difference was highly significant with co-administration of sildenafil and selenium (p<0.001). CAT and GPx were higher in all treated groups compared to I/R group (p<0.05). Conclusion: The co-administration of sildenafil citrate and selenium are highly protective against damage induced by ovarian ischemia/reperfusion in rats. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=phosphodiesterase-5%20inhibitor" title="phosphodiesterase-5 inhibitor">phosphodiesterase-5 inhibitor</a>, <a href="https://publications.waset.org/abstracts/search?q=sildenafil" title=" sildenafil"> sildenafil</a>, <a href="https://publications.waset.org/abstracts/search?q=antioxidant" title=" antioxidant"> antioxidant</a>, <a href="https://publications.waset.org/abstracts/search?q=selenium" title=" selenium"> selenium</a>, <a href="https://publications.waset.org/abstracts/search?q=ovarian%20ischemia" title=" ovarian ischemia"> ovarian ischemia</a> </p> <a href="https://publications.waset.org/abstracts/64362/the-impact-of-co-administration-of-phosphodiesterase-5-inhibitor-and-sodium-selenite-on-ischemiareperfusion-injury-in-a-rat-ovary-model-biochemical-and-histopathologic-evaluation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/64362.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">312</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">970</span> Inhibition of Glutamate Carboxypeptidase Activity Protects Retinal Ganglionic Cell Death Induced by Ischemia-Reperfusion by Reducing the Astroglial Activation in Rat</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Dugeree%20Otgongerel">Dugeree Otgongerel</a>, <a href="https://publications.waset.org/abstracts/search?q=Kyong%20Jin%20Cho"> Kyong Jin Cho</a>, <a href="https://publications.waset.org/abstracts/search?q=Yu-Han%20Kim"> Yu-Han Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Sangmee%20Ahn%20Jo"> Sangmee Ahn Jo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Excessive activation of glutamate receptor is thought to be involved in retinal ganglion cell (RGC) death after ischemia- reperfusion damage. Glutamate carboxypeptidase II (GCPII) is an enzyme responsible for the synthesis of glutamate. Several studies showed that inhibition of GCPII prevents or reduces cellular damage in brain diseases. Thus, in this study, we examined the expression of GCPII in rat retina and the role of GCPII in acute high IOP ischemia-reperfusion damage of eye by using a GCPII inhibitor, 2-(phosphonomethyl) pentanedioic acid (2-PMPA). Animal model of ischemia-reperfusion was induced by raising the intraocular pressure for 60 min and followed by reperfusion for 3 days. Rats were randomly divided into four groups: either intra-vitreous injection of 2-PMPA (11 or 110 ng per eye) or PBS after ischemia-reperfusion, 2-PMPA treatment without ischemia-reperfusion and sham-operated normal control. GCPII immunoreactivity in normal rat retina was detected weakly in retinal nerve fiber layer (RNFL) and retinal ganglionic cell layer (RGL) and also inner plexiform layer (IPL) and outer plexiform layer (OPL) strongly where are co-stained with an anti-GFAP antibody, suggesting that GCPII is expressed mostly in Muller and astrocytes. Immunostaining with anti-BRN antibody showed that ischemia- reperfusion caused RGC death (31.5 %) and decreased retinal thickness in all layers of damaged retina, but the treatment of 2-PMPA twice at 0 and 48 hour after reperfusion blocked these retinal damages. GCPII level in RNFL layer was enhanced after ischemia-reperfusion but was blocked by PMPA treatment. This result was confirmed by western blot analysis showing that the level of GCPII protein after ischemia- reperfusion increased by 2.2- fold compared to control, but this increase was blocked almost completely by 110 ng PMPA treatment. Interestingly, GFAP immunoreactivity in the retina after ischemia- reperfusion followed by treatment with PMPA showed similar pattern to GCPII, increase after ischemia-reperfusion but reduction to the normal level by PMPA treatment. Our data demonstrate that increase of GCPII protein level after ischemia-reperfusion injury is likely to cause glial activation and/or retinal cell death which are mediated by glutamate, and GCPII inhibitors may be useful in treatment of retinal disorders in which glutamate excitotoxicity is pathogenic. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=glutamate%20carboxypepptidase%20II" title="glutamate carboxypepptidase II">glutamate carboxypepptidase II</a>, <a href="https://publications.waset.org/abstracts/search?q=glutamate%20excitotoxicity" title=" glutamate excitotoxicity"> glutamate excitotoxicity</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia-reperfusion" title=" ischemia-reperfusion"> ischemia-reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=retinal%20ganglion%20cell" title=" retinal ganglion cell"> retinal ganglion cell</a> </p> <a href="https://publications.waset.org/abstracts/39644/inhibition-of-glutamate-carboxypeptidase-activity-protects-retinal-ganglionic-cell-death-induced-by-ischemia-reperfusion-by-reducing-the-astroglial-activation-in-rat" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/39644.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">340</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">969</span> Antioxidant Mediated Neuroprotective Effects of Allium Cepa Extract Against Ischemia Reperfusion Induced Cognitive Dysfunction and Brain Damage in Mice</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jaspal%20Rana">Jaspal Rana</a>, <a href="https://publications.waset.org/abstracts/search?q=Varinder%20Singh"> Varinder Singh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Oxidative stress has been identified as an underlying cause of ischemia-reperfusion (IR) related cognitive dysfunction and brain damage. Therefore, antioxidant based therapies to treat IR injury are being investigated. Allium cepa L. (onion) is used as culinary medicine and is documented to have marked antioxidant effects. Hence, the present study was designed to evaluate the effect of A. cepa outer scale extract (ACE) against IR induced cognition and biochemical deficit in mice. ACE was prepared by maceration with 70% methanol and fractionated into ethylacetate and aqueous fractions. Bilateral common carotid artery occlusion for 10 min, followed by 24 h reperfusion, was used to induce cerebral IR injury. Following IR injury, ACE (100 and 200 mg/kg) was administered orally to animals for 7 days once daily. Behavioral outcomes (memory and sensorimotor functions) were evaluated using Morris water maze and neurological severity score. Cerebral infarct size, brain thiobarbituric acid reactive species, reduced glutathione, and superoxide dismutase activity were also determined. Treatment with ACE significantly ameliorated IR mediated deterioration of memory and sensorimotor functions and rose in brain oxidative stress in animals. The results of the present investigation revealed that ACE improved functional outcomes after cerebral IR injury which may be attributed to its antioxidant properties. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=allium%20cepa" title="allium cepa">allium cepa</a>, <a href="https://publications.waset.org/abstracts/search?q=cerebral%20ischemia" title=" cerebral ischemia"> cerebral ischemia</a>, <a href="https://publications.waset.org/abstracts/search?q=memory" title=" memory"> memory</a>, <a href="https://publications.waset.org/abstracts/search?q=sensorimotor" title=" sensorimotor"> sensorimotor</a> </p> <a href="https://publications.waset.org/abstracts/117211/antioxidant-mediated-neuroprotective-effects-of-allium-cepa-extract-against-ischemia-reperfusion-induced-cognitive-dysfunction-and-brain-damage-in-mice" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/117211.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">113</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">968</span> Investigation of Ezetimibe Administration on Cell Survival Markers in Kidney Ischemia</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Zahra%20Heydari">Zahra Heydari</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: One of the major clinical issues is acute renal failure, which is caused by ischemia-reperfusion of the kidney and is associated with high mortality. Despite advances in this area, important issues such as tissue necrosis, cell apoptosis, and so on in damaged tissue are suggestive for more researches and study on this subject. Objective: Evaluation of the potential utility of Ezetimibe in reducing injuries and cell death induced by kidney ischemia/ reperfusion through inducing expression changes of different cellular pathways in adult Sprague-Dawley rats. Materials and methods: Forty rats weighing 180-200g were divided into 4 groups. For this purpose, the first right kidneys of the rats were removed during surgery. After 20 days, the left renal artery was closed with a soft clamp and reperfusion was performed. After 24 hours, blood samples were collected and sent to the laboratory with kidneys to measure bax and bcl-2 by Western blotting and histopathological tests. Results: Quantitative damage reviews of Kidney tissue indicates damage Acute and severe tubular lesions were observed in the ischemia group. Also, the amount of injury was significantly reduced in the treatment group. There was also a significant difference between the ischemia and sham groups. In general, the results show that a single dose of 1.2 mg/kg of ezetimibe can reduce the bax/ bcl-2 ratio compared to the ischemia group. In general, the results showed Ezetimibe is effective in reducing cell damage and death due to ischemia/ reperfusion after renal ischemia through changes in the expression of various cellular pathways in rats. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=acute%20renal%20failure" title="acute renal failure">acute renal failure</a>, <a href="https://publications.waset.org/abstracts/search?q=renal%20ischemia-reperfusion%20injury" title=" renal ischemia-reperfusion injury"> renal ischemia-reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=ezetimibe" title=" ezetimibe"> ezetimibe</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a> </p> <a href="https://publications.waset.org/abstracts/140497/investigation-of-ezetimibe-administration-on-cell-survival-markers-in-kidney-ischemia" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/140497.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">196</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">967</span> Syndecan -1 as Regulator of Ischemic-Reperfusion Damage Limitation in Experiment</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=M.%20E.%20Kolpakova">M. E. Kolpakova</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20A.%20Jakovleva"> A. A. Jakovleva</a>, <a href="https://publications.waset.org/abstracts/search?q=L.%20S.%20Poliakova"> L. S. Poliakova</a>, <a href="https://publications.waset.org/abstracts/search?q=H.%20El%20Amghari"> H. El Amghari</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20Soliman"> S. Soliman</a>, <a href="https://publications.waset.org/abstracts/search?q=D.%20R.%20Faizullina"> D. R. Faizullina</a>, <a href="https://publications.waset.org/abstracts/search?q=V.%20V.%20Sharoyko"> V. V. Sharoyko</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Brain neuroplasticity is associated with blood-brain barrier vascular endothelial proteoglycans and post-stroke microglial activation. The study of the mechanisms of reperfusion injury limitation by remote ischemic postconditioning (RC) is of interest due to the effects on functional recovery after cerebral ischemia. The goal of the study is the assessment of the role of syndecan-1 (SDC-1) in restriction of ischemic-reperfusion injury on middle cerebral artery model in rats using RC protocol. Randomized controlled trials were conducted. Ischemia was performed by middle cerebral artery occlusion by Belayev L. (1996) on the Wistar rat-males (n= 87) weighting 250 卤 50 g. under general anesthesia (Zoletil 100 懈 Xylazine 2%). Syndecan-1 (SDC-1) concentration difference in plasma samples of false operated animals and animals with brain ischemia was 30% (30 min. 袦小袗芯: 41.4 * 卤 1.3 ng/ml). SDC-1 concentration in animal plasma samples with ischemia + RC protocol was 112% (30 min 袦小袗芯+ RC): 67.8**卤 5.8 ng/ml). Calculation of infarction volume in the ischemia group revealed brain injury in 31.97 卤 2.5%; the volume of infarction was 13.6 卤 1.3% in 30 min. 袦C袗芯 + RC group. Swelling of tissue in the group 30 min. 袦C袗芯 + RC was 16 卤 2.1%; it was 47 卤 3.3%. in 30 min. 袦C袗芯 group. Correlation analysis showed a high direct correlation relationship between infarct area and muscle strength in the right forelimb (袣袣=0.72) in the 30 min. 袦C袗芯 + RC group. Correlation analysis showed very high inverse correlation between infarct area and capillary blood flow in the 30 min. 袦C袗芯 + RC group (p <0.01; r = -0.98). We believe the SDC-1 molecule in blood plasma may play role of potential messenger of ischemic-reperfusion injury restriction mechanisms. This leads to infarct-limiting effect of remote ischemic postconditioning and early functioning recovery. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ischemia" title="ischemia">ischemia</a>, <a href="https://publications.waset.org/abstracts/search?q=%D0%9C%D0%A1%D0%90%D0%BE" title=" 袦小袗芯"> 袦小袗芯</a>, <a href="https://publications.waset.org/abstracts/search?q=remote%20ischemic%20postconditioning" title=" remote ischemic postconditioning"> remote ischemic postconditioning</a>, <a href="https://publications.waset.org/abstracts/search?q=syndecan-1" title=" syndecan-1"> syndecan-1</a> </p> <a href="https://publications.waset.org/abstracts/179202/syndecan-1-as-regulator-of-ischemic-reperfusion-damage-limitation-in-experiment" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/179202.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">61</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">966</span> Antioxidant Effects of C-Phycocyanin on Oxidized Astrocyte in Brain Injury Using 2D and 3D Neural Nanofiber Tissue Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Seung%20Ju%20Yeon">Seung Ju Yeon</a>, <a href="https://publications.waset.org/abstracts/search?q=Seul%20Ki%20Min"> Seul Ki Min</a>, <a href="https://publications.waset.org/abstracts/search?q=Jun%20Sang%20%20Park"> Jun Sang Park</a>, <a href="https://publications.waset.org/abstracts/search?q=Yeo%20Seon%20Kwon"> Yeo Seon Kwon</a>, <a href="https://publications.waset.org/abstracts/search?q=Hoo%20Cheol%20Lee"> Hoo Cheol Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Hyun%20Jung%20Shim"> Hyun Jung Shim</a>, <a href="https://publications.waset.org/abstracts/search?q=Il-Doo%20Kim"> Il-Doo Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Ja%20Kyeong%20Lee"> Ja Kyeong Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Hwa%20Sung%20Shin"> Hwa Sung Shin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In brain injury, depleting oxidative stress is the most effective way to reduce the brain infarct size. C-phycocyanin (C-Pc) is a well-known antioxidant protein that has neuroprotective effects obtained from green microalgae. Astrocyte is glial cell that supports the nerve cell such as neuron, which account for a large portion of the brain. In brain injury, such as ischemia and reperfusion, astrocyte has an important rule that overcomes the oxidative stress and protect from brain reactive oxygen species (ROS) injury. However little is known about how C-Pc regulates the anti-oxidants effects of astrocyte. In this study, when the C-Pc was treated in oxidized astrocyte, we confirmed that inflammatory factors Interleukin-6 and Interleukin-3 were increased and antioxidants enzyme, Superoxide dismutase (SOD) and catalase was upregulated, and neurotrophic factors, brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) was alleviated. Also, it was confirmed to reduce infarct size of the brain in ischemia and reperfusion because C-Pc has anti-oxidant effects in middle cerebral artery occlusion (MCAO) animal model. These results show that C-Pc can help astrocytes lead neuroprotective activities in the oxidative stressed environment of the brain. In summary, the C-PC protects astrocytes from oxidative stress and has anti-oxidative, anti-inflammatory, neurotrophic effects under ischemic situations. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=c-phycocyanin" title="c-phycocyanin">c-phycocyanin</a>, <a href="https://publications.waset.org/abstracts/search?q=astrocyte" title=" astrocyte"> astrocyte</a>, <a href="https://publications.waset.org/abstracts/search?q=reactive%20oxygen%20species" title=" reactive oxygen species"> reactive oxygen species</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia%20and%20reperfusion" title=" ischemia and reperfusion"> ischemia and reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=neuroprotective%20effect" title=" neuroprotective effect"> neuroprotective effect</a> </p> <a href="https://publications.waset.org/abstracts/50872/antioxidant-effects-of-c-phycocyanin-on-oxidized-astrocyte-in-brain-injury-using-2d-and-3d-neural-nanofiber-tissue-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/50872.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">320</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">965</span> Delicate Balance between Cardiac Stress and Protection: Role of Mitochondrial Proteins</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Zuzana%20Tatarkova">Zuzana Tatarkova</a>, <a href="https://publications.waset.org/abstracts/search?q=Ivana%20Pilchova"> Ivana Pilchova</a>, <a href="https://publications.waset.org/abstracts/search?q=Michal%20Cibulka"> Michal Cibulka</a>, <a href="https://publications.waset.org/abstracts/search?q=Martin%20Kolisek"> Martin Kolisek</a>, <a href="https://publications.waset.org/abstracts/search?q=Peter%20Racay"> Peter Racay</a>, <a href="https://publications.waset.org/abstracts/search?q=Peter%20Kaplan"> Peter Kaplan</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Normal functioning of mitochondria is crucial for cardiac performance. Mitochondria undergo mitophagy and biogenesis, and mitochondrial proteins are subject to extensive post-translational modifications. The state of mitochondrial homeostasis reflects overall cellular fitness and longevity. Perturbed mitochondria produce less ATP, release greater amounts of reactive molecules, and are more prone to apoptosis. Therefore mitochondrial turnover is an integral aspect of quality control in which dysfunctional mitochondria are selectively eliminated through mitophagy. Currently, the progressive deterioration of physiological functions is seen as accumulation of modified/damaged proteins with limiting regenerative ability and disturbance of such affected protein-protein communication throughout aging in myocardial cells. Methodologies: For our study was used immunohistochemistry, biochemical methods: spectrophotometry, western blotting, immunodetection as well as more sophisticated 2D electrophoresis and mass spectrometry for evaluation protein-protein interactions and specific post-translational modification. Results and Discussion: Mitochondrial stress response to reactive species was evaluated as electron transport chain (ETC) complexes, redox-active molecules, and their possible communication. Protein-protein interactions revealed a strong linkage between age and ETC protein subunits. Redox state was strongly affected in senescent mitochondria with shift in favor of more pro-oxidizing condition within cardiomyocytes. Acute myocardial ischemia and ischemia-reperfusion (IR) injury affected ETC complexes I, II and IV with no change in complex III. Ischemia induced decrease in total antioxidant capacity, MnSOD, GSH and catalase activity with recovery in some extent during reperfusion. While MnSOD protein content was higher in IR group, activity returned to 95% of control. Nitric oxide is one of the biological molecules that can out compete MnSOD for superoxide and produce peroxynitrite. This process is faster than dismutation and led to the 10-fold higher production of nitrotyrosine after IR injury in adult with higher protection in senescent ones. 2D protein profiling revealed 140 mitochondrial proteins, 12 of them with significant changes after IR injury and 36 individual nitrotyrosine-modified proteins further identified by mass spectrometry. Linking these two groups, 5 proteins were altered after IR as well as nitrated, but only one showed massive nitration per lowering content of protein after IR injury in adult. Conclusions: Senescent cells have greater proportion of protein content, which might be modulated by several post-translational modifications. If these protein modifications are connected to functional consequences and protein-protein interactions are revealed, link may lead to the solution. Assume all together, dysfunctional proteostasis can play a causative role and restoration of protein homeostasis machinery is protective against aging and possibly age-related disorders. This work was supported by the project VEGA 1/0018/18 and by project 'Competence Center for Research and Development in the field of Diagnostics and Therapy of Oncological diseases', ITMS: 26220220153, co-financed from EU sources. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=aging%20heart" title="aging heart">aging heart</a>, <a href="https://publications.waset.org/abstracts/search?q=mitochondria" title=" mitochondria"> mitochondria</a>, <a href="https://publications.waset.org/abstracts/search?q=proteomics" title=" proteomics"> proteomics</a>, <a href="https://publications.waset.org/abstracts/search?q=redox%20state" title=" redox state"> redox state</a> </p> <a href="https://publications.waset.org/abstracts/87281/delicate-balance-between-cardiac-stress-and-protection-role-of-mitochondrial-proteins" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/87281.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">167</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">964</span> An Empirical Study to Predict Myocardial Infarction Using K-Means and Hierarchical Clustering </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Md.%20Minhazul%20%20%20Islam">Md. Minhazul Islam</a>, <a href="https://publications.waset.org/abstracts/search?q=Shah%20Ashisul%20Abed%20%20Nipun"> Shah Ashisul Abed Nipun</a>, <a href="https://publications.waset.org/abstracts/search?q=Majharul%20%20Islam"> Majharul Islam</a>, <a href="https://publications.waset.org/abstracts/search?q=Md.%20Abdur%20Rakib%20Rahat"> Md. Abdur Rakib Rahat</a>, <a href="https://publications.waset.org/abstracts/search?q=Jonayet%20Miah"> Jonayet Miah</a>, <a href="https://publications.waset.org/abstracts/search?q=Salsavil%20Kayyum"> Salsavil Kayyum</a>, <a href="https://publications.waset.org/abstracts/search?q=Anwar%20Shadaab"> Anwar Shadaab</a>, <a href="https://publications.waset.org/abstracts/search?q=Faiz%20Al%20Faisal"> Faiz Al Faisal</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The target of this research is to predict Myocardial Infarction using unsupervised Machine Learning algorithms. Myocardial Infarction Prediction related to heart disease is a challenging factor faced by doctors & hospitals. In this prediction, accuracy of the heart disease plays a vital role. From this concern, the authors have analyzed on a myocardial dataset to predict myocardial infarction using some popular Machine Learning algorithms K-Means and Hierarchical Clustering. This research includes a collection of data and the classification of data using Machine Learning Algorithms. The authors collected 345 instances along with 26 attributes from different hospitals in Bangladesh. This data have been collected from patients suffering from myocardial infarction along with other symptoms. This model would be able to find and mine hidden facts from historical Myocardial Infarction cases. The aim of this study is to analyze the accuracy level to predict Myocardial Infarction by using Machine Learning techniques. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Machine%20Learning" title="Machine Learning">Machine Learning</a>, <a href="https://publications.waset.org/abstracts/search?q=K-means" title=" K-means"> K-means</a>, <a href="https://publications.waset.org/abstracts/search?q=Hierarchical%20Clustering" title=" Hierarchical Clustering"> Hierarchical Clustering</a>, <a href="https://publications.waset.org/abstracts/search?q=Myocardial%20Infarction" title=" Myocardial Infarction"> Myocardial Infarction</a>, <a href="https://publications.waset.org/abstracts/search?q=Heart%20Disease" title=" Heart Disease"> Heart Disease</a> </p> <a href="https://publications.waset.org/abstracts/121240/an-empirical-study-to-predict-myocardial-infarction-using-k-means-and-hierarchical-clustering" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/121240.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">203</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">963</span> Conduction System Disease and Atrioventricular Block in Victims of COVID-19</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Shirin%20Sarejloo">Shirin Sarejloo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Electrophysiological-related manifestation of COVID-19 is a matter of debate in the literature nowadays. A wide spectrum of arrhythmias was observed among patients who have been infected with COVID-19. Objectives: This study discussed the prevalence of arrhythmias and conduction system disease in patients with COVID-19. Method: In this retrospective study, demographic and electrocardiographic data of 432 expired COVID-19 patients who had been admitted to Faghihi Hospital of Shiraz University of Medical Sciences from August2020 until December 2020 were reviewed. Results: Atrioventricular nodal block (AVB) was found in 40(9.3%) patients. Furthermore, 28(6.5%) of them suffered from the first degree of AVB, and 12(2.8%) suffered from complete heart block (CHB). Among 189 cases (59.0%), ST-T changes agreed with myocardial infarction or localized myocarditis. Findings of myocardial injury, including fragmented QRS and prolonged QTc were observed among 91 (21.1%) and 28 (6.5%), respectively. In victims of COVID-19, conduction disease was not related to any comorbidities. Fragmented QRS, axis deviation, presence of S1Q3T3, and poor R wave progression were significantly related to conduction system abnormalities in victims of COVID-19 (P-value > 0.05). Conclusion: Our findings can serve in future studies that aim to develop a risk stratification method for susceptible COVID-19 patients. The myocardial injury appears to role significantly in COVID-19 morbidity and mortality. Consequently, we recommend health policymakers consider separate catheterization laboratories that provide service only to COVID-19 patients. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=COVID-19" title="COVID-19">COVID-19</a>, <a href="https://publications.waset.org/abstracts/search?q=conduction%20system" title=" conduction system"> conduction system</a>, <a href="https://publications.waset.org/abstracts/search?q=ECG" title=" ECG"> ECG</a>, <a href="https://publications.waset.org/abstracts/search?q=atrioventricular%20block" title=" atrioventricular block"> atrioventricular block</a> </p> <a href="https://publications.waset.org/abstracts/154521/conduction-system-disease-and-atrioventricular-block-in-victims-of-covid-19" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/154521.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">87</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">962</span> Silent Myocardial Infarction Presented with Homonymous Hemianopia in a Non-Diabetic Middle Aged Man</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Seyed%20Fakhroddin%20Hejazi">Seyed Fakhroddin Hejazi</a>, <a href="https://publications.waset.org/abstracts/search?q=Mohammad%20Saleh%20Sadeghi"> Mohammad Saleh Sadeghi</a>, <a href="https://publications.waset.org/abstracts/search?q=Leili%20Iranirad"> Leili Iranirad</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Silent myocardial infarction is defined as the appearance of pathological Q waves in the electrocardiogram, without objective signs of myocardial infarction and any minimal or atypical symptoms. Although this condition has been known for a long time, but little is known about its phenomenon and the mechanisms of it remain unclear. Its coincidence with stroke is also still controversial. This case report introduces a middle-aged man with silent myocardial infarction presented with homonymous hemianopia, which except stage 1 hypertension, had no other major cardiovascular risk factors including diabetes mellitus, hypercholesterolemia, family history of cardiac diseases and smoking. In conclusion, this case report indicated that existence of only one cardiovascular risk factor would lead to the development of MI or stroke. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=silent%20myocardial%20infarction" title="silent myocardial infarction">silent myocardial infarction</a>, <a href="https://publications.waset.org/abstracts/search?q=homonymous%20hemianopia" title=" homonymous hemianopia"> homonymous hemianopia</a>, <a href="https://publications.waset.org/abstracts/search?q=stroke" title=" stroke"> stroke</a>, <a href="https://publications.waset.org/abstracts/search?q=hypertension" title=" hypertension"> hypertension</a> </p> <a href="https://publications.waset.org/abstracts/52813/silent-myocardial-infarction-presented-with-homonymous-hemianopia-in-a-non-diabetic-middle-aged-man" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/52813.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">288</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">961</span> An Autopsy Case of Blunt Chest Trauma from a Traffic Accident Complicated by Chest Compression Due to Resuscitation Attempts</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Satoshi%20Furukawa">Satoshi Furukawa</a>, <a href="https://publications.waset.org/abstracts/search?q=Satomu%20Morita"> Satomu Morita</a>, <a href="https://publications.waset.org/abstracts/search?q=Katsuji%20Nishi"> Katsuji Nishi</a>, <a href="https://publications.waset.org/abstracts/search?q=Masahito%20Hitosugi"> Masahito Hitosugi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Coronary artery dissection leading to acute myocardial infarction after blunt chest trauma is extremely rare. A 67-year-old woman suffered blunt chest trauma following a traffic accident. The electrocardiogram revealed acute posterior ST-segment elevation and myocardial infarction and coronary angiography demonstrated acute right coronary artery dissection. Following the death of the victim an autopsy was performed after cardiopulmonary support had been carried out. In this case report, we describe the case of a woman with blunt chest trauma, who developed an acute myocardial infarction secondary to right coronary artery dissection. Although there was additional the blunt chest trauma due to chest compression, we confirmed the injury at autopsy and by histological findings. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=blunt%20chest%20trauma" title="blunt chest trauma">blunt chest trauma</a>, <a href="https://publications.waset.org/abstracts/search?q=right%20coronary%20artery%20dissection" title=" right coronary artery dissection"> right coronary artery dissection</a>, <a href="https://publications.waset.org/abstracts/search?q=coronary%20angiography" title=" coronary angiography"> coronary angiography</a>, <a href="https://publications.waset.org/abstracts/search?q=autopsy" title=" autopsy"> autopsy</a>, <a href="https://publications.waset.org/abstracts/search?q=histological%20examination" title=" histological examination "> histological examination </a> </p> <a href="https://publications.waset.org/abstracts/13624/an-autopsy-case-of-blunt-chest-trauma-from-a-traffic-accident-complicated-by-chest-compression-due-to-resuscitation-attempts" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/13624.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">634</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">960</span> Modelling Sudden Deaths from Myocardial Infarction and Stroke</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Y.%20S.%20Yusoff">Y. S. Yusoff</a>, <a href="https://publications.waset.org/abstracts/search?q=G.%20Streftaris"> G. Streftaris</a>, <a href="https://publications.waset.org/abstracts/search?q=H.%20R%20Waters"> H. R Waters</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Death within 30 days is an important factor to be looked into, as there is a significant risk of deaths immediately following or soon after, Myocardial Infarction (MI) or stroke. In this paper, we will model the deaths within 30 days following a Myocardial Infarction (MI) or stroke in the UK. We will see how the probabilities of sudden deaths from MI or stroke have changed over the period 1981-2000. We will model the sudden deaths using a Generalized Linear Model (GLM), fitted using the R statistical package, under a Binomial distribution for the number of sudden deaths. We parameterize our model using the extensive and detailed data from the Framingham Heart Study, adjusted to match UK rates. The results show that there is a reduction for the sudden deaths following a MI over time but no significant improvement for sudden deaths following a stroke. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sudden%20deaths" title="sudden deaths">sudden deaths</a>, <a href="https://publications.waset.org/abstracts/search?q=myocardial%20infarction" title=" myocardial infarction"> myocardial infarction</a>, <a href="https://publications.waset.org/abstracts/search?q=stroke" title=" stroke"> stroke</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemic%20heart%20disease" title=" ischemic heart disease"> ischemic heart disease</a> </p> <a href="https://publications.waset.org/abstracts/4355/modelling-sudden-deaths-from-myocardial-infarction-and-stroke" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/4355.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">286</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">959</span> Stromal Vascular Fraction Regenerative Potential in a Muscle Ischemia/Reperfusion Injury Mouse Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Anita%20Conti">Anita Conti</a>, <a href="https://publications.waset.org/abstracts/search?q=Riccardo%20Ossanna"> Riccardo Ossanna</a>, <a href="https://publications.waset.org/abstracts/search?q=Lindsey%20A.%20Quintero"> Lindsey A. Quintero</a>, <a href="https://publications.waset.org/abstracts/search?q=Giamaica%20Conti"> Giamaica Conti</a>, <a href="https://publications.waset.org/abstracts/search?q=Andrea%20Sbarbati"> Andrea Sbarbati</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Ischemia/reperfusion (IR) injury induces muscle fiber atrophy and skeletal muscle fiber death with subsequently functionality loss. The heterogeneous pool of cells, especially mesenchymal stem cells, contained in the stromal vascular fraction (SVF) of adipose tissue could promote muscle fiber regeneration. To prevent SVF dispersion, it has been proposed the use of injectable biopolymers that work as cells carrier. A significant element of the extracellular matrix is hyaluronic acid (HA), which has been widely used in regenerative medicine as a cell scaffold given its biocompatibility, degradability, and the possibility of chemical functionalization. Connective tissue micro-fragments enriched with SVF obtained from mechanical disaggregation of adipose tissue were evaluated for IR muscle injury regeneration using low molecular weight HA as a scaffold. IR induction. Hindlimb ischemia was induced in 9 athymic nude mice through the clamping of the right quadriceps using a plastic band. Reperfusion was induced by cutting the plastic band after 3 hours of ischemic period. Contralateral (left) muscular tissue was used as healthy control. Treatment. Twenty-four hours after the IR induction, animals (n=3) were intramuscularly injected with 100 碌l of SVF mixed with HA (SVF-HA). Animals treated with 100 碌l of HA (n=3) and 100 碌l saline solution (n=3) were used as control. Treatment monitoring. All animals were in vivo monitored by magnetic resonance imaging (MRI) at 5, 7, 14 and 18 days post-injury (dpi). High-resolution morphological T2 weighed, quantitative T2 map and Dynamic Contrast-Enhanced (DCE) images were acquired in order to assess the regenerative potential of SVF-HA treatment. Ex vivo evaluation. After 18 days from IR induction, animals were sacrificed, and the muscles were harvested for histological examination. At 5 dpi T2 high-resolution MR images clearly reveal the presence of an extensive edematous area due to IR damage for all groups identifiable as an increase of signal intensity (SI) of muscular and surrounding tissue. At 7 dpi, animals of the SVF-HA group showed a reduction of SI, and the T2relaxation time of muscle tissue of the HA-SVF group was 29卤0.5ms, comparable with the T2relaxation time of contralateral muscular tissue (30卤0.7ms). These suggest a reduction of edematous overflow and swelling. The T2relaxation time at 7dpi of HA and saline groups were 84卤2ms and 90卤5ms, respectively, which remained elevated during the rest of the study. The evaluation of vascular regeneration showed similar results. Indeed, DCE-MRI analysis revealed a complete recovery of muscular tissue perfusion after 14 dpi for the SVF-HA group, while for the saline and HA group, controls remained in a damaged state. Finally, the histological examination of SVF-HA treated animals exhibited well-defined and organized fibers morphology with a lateralized nucleus, similar to contralateral healthy muscular tissue. On the contrary, HA and saline-treated animals presented inflammatory infiltrates, with HA slightly improving the diameter of the fibers and less degenerated tissue. Our findings show that connective tissue micro-fragments enriched with SVF induce higher muscle homeostasis and perfusion restoration in contrast to control groups. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ischemia%2Freperfusion%20injury" title="ischemia/reperfusion injury">ischemia/reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=regenerative%20medicine" title=" regenerative medicine"> regenerative medicine</a>, <a href="https://publications.waset.org/abstracts/search?q=resonance%20imaging" title=" resonance imaging"> resonance imaging</a>, <a href="https://publications.waset.org/abstracts/search?q=stromal%20vascular%20fraction" title=" stromal vascular fraction"> stromal vascular fraction</a> </p> <a href="https://publications.waset.org/abstracts/151594/stromal-vascular-fraction-regenerative-potential-in-a-muscle-ischemiareperfusion-injury-mouse-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/151594.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">127</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">958</span> Neuroprotective Effect of Vildagliptin against Cerebral Ischemia in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Salma%20A.%20El-Marasy">Salma A. El-Marasy</a>, <a href="https://publications.waset.org/abstracts/search?q=Rehab%20F.%20Abdel-Rahman"> Rehab F. Abdel-Rahman</a>, <a href="https://publications.waset.org/abstracts/search?q=Reham%20M.%20Abd-Elsalam"> Reham M. Abd-Elsalam</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The burden of stroke is intensely increasing worldwide. Brain injury following transient or permanent focal cerebral ischemia develops ischemic stroke as a consequence of a complex series of pathophysiological events. The aim of this study is to evaluate the possible neuroprotective effect of a dipeptidyl peptidase-4 inhibitor, vildagliptin, independent on its insulinotropic properties in non-diabetic rats subjected to cerebral ischemia. Anaesthetized Wistar rats were subjected to either left middle cerebral artery occlusion (MCAO) or sham operation followed by reperfusion after 30 min of MCAO. The other three groups were orally administered vildagliptin at 3 dose levels (2.5, 5, 10 mg/kg) for 3 successive weeks before subjected to left focal cerebral ischemia/reperfusion and till the end of the study. Neurological deficit scores and motor activity were assessed 24h following reperfusion. 48h following reperfusion, rats were euthanized and their left brain hemispheres were harvested and used in the biochemical, histopathological, and immunohistochemical investigations. Vildagliptin pretreatment improved neurological score deficit, locomotor activity and motor coordination in MCAO rats. Moreover, vildagliptin reduced malondialdehyde (MDA), elevated reduced glutathione (GSH), phosphotylinosital 3 kinase (PI3K), phosphorylated of protein kinase B (p-AKT), and mechanistic target of rapamycin (mTOR) brain contents in addition to reducing protein expression of caspase-3. Also, vildagliptin showed a dose-dependent attenuation in neuronal cell loss and histopathological alterations in MCAO rats. This study proves that vildagliptin exerted the neuroprotective effect in a dose-dependent manner as shown in amelioration of neuronal cell loss and histopathological damage in MCAO rats, which may be mediated by attenuating neuronal and motor deficits, it鈥檚 anti-oxidant property, activation of PI3K/AKT/mTOR pathway and its anti-apoptotic effect. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=caspase-3" title="caspase-3">caspase-3</a>, <a href="https://publications.waset.org/abstracts/search?q=cerebral%20ischemia" title=" cerebral ischemia"> cerebral ischemia</a>, <a href="https://publications.waset.org/abstracts/search?q=dipeptidyl%20peptidase-4%20inhibitor" title=" dipeptidyl peptidase-4 inhibitor"> dipeptidyl peptidase-4 inhibitor</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=PI3K%2FAKT%2FmTOR%20pathway" title=" PI3K/AKT/mTOR pathway"> PI3K/AKT/mTOR pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=rats" title=" rats"> rats</a>, <a href="https://publications.waset.org/abstracts/search?q=vildagliptin" title=" vildagliptin"> vildagliptin</a> </p> <a href="https://publications.waset.org/abstracts/90168/neuroprotective-effect-of-vildagliptin-against-cerebral-ischemia-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/90168.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">155</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">957</span> Effects of Preparation Caused by Ischemic-Reperfusion along with Sodium Bicarbonate Supplementation on Submaximal Dynamic Force Production</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sara%20Nasiri%20Semnani">Sara Nasiri Semnani</a>, <a href="https://publications.waset.org/abstracts/search?q=Alireza%20Ramzani"> Alireza Ramzani</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background and Aims: Sodium bicarbonate is a supplementation that used to reduce fatigue and increase power output in short-term training. On the other hand, the Ischemic Reperfusion Preconditioning (IRPC) is an appropriate stimulus to increase the submaximal contractile response. Materials and methods: 9 female student-athletes in double-blind randomized crossover design were three mode, sodium bicarbonate + IRPC, sodium bicarbonate and placebo+ IRPC. Participants moved forward single arm dumbbell hand with a weight of 2 kg can be carried out most frequently. Results: The results showed that plasma lactate concentration and records of sodium bicarbonate + IRPC and sodium bicarbonate conditions were significantly different compared to placebo + IRPC (Respectively p=0.001, p=0/02). Conclusion: According to the research findings, bicarbonate supplementation in IRPC training condition increased force and delay fatigue in submaximal dynamic contraction. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ischemic%20reperfusion" title="ischemic reperfusion">ischemic reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=preconditioning" title=" preconditioning"> preconditioning</a>, <a href="https://publications.waset.org/abstracts/search?q=sodium%20bicarbonate" title=" sodium bicarbonate"> sodium bicarbonate</a>, <a href="https://publications.waset.org/abstracts/search?q=submaximal%20dynamic%20force" title=" submaximal dynamic force"> submaximal dynamic force</a> </p> <a href="https://publications.waset.org/abstracts/89111/effects-of-preparation-caused-by-ischemic-reperfusion-along-with-sodium-bicarbonate-supplementation-on-submaximal-dynamic-force-production" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/89111.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">303</span> </span> </div> </div> <ul class="pagination"> <li class="page-item disabled"><span class="page-link">&lsaquo;</span></li> <li class="page-item active"><span class="page-link">1</span></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=myocardial%20reperfusion%20injury&page=2">2</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=myocardial%20reperfusion%20injury&page=3">3</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=myocardial%20reperfusion%20injury&page=4">4</a></li> <li class="page-item"><a class="page-link" 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