• Korean Journal of Clinical Laboratory Science
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• v.54 no.1
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• pp.1-8
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• 2022

Erythrocyte sedimentation rate (ESR) evaluation is a useful tool for monitoring disease activity in various inflammatory and non-inflammatory conditions. ESR is known to be influenced by a multitude of confounding factors. The present study aimed to assess the possible determinants of the ESR and its relationship with various risk factors involved in ischemic stroke. ESR and other hematological and biochemical parameters were investigated in 163 ischemic stroke patients (107 males and 56 females) selected based on imaging techniques including magnetic resonance imaging (MRI) or computed tomography (CT) scans. Statistical analysis was performed using the SPSS 16.0 software. Linear regression analysis showed a significant inverse relationship of hemoglobin (Hb) and hematocrit or packed cell volume (PCV) (P<0.001 for females; P<0.01 for males) with the ESR. It was observed that the red blood cell (RBC) count was not strongly correlated with the ESR (P<0.05 for both males and females). It was also observed that sex significantly affected the variables determining the ESR levels, whereas age had no effect. Gender differences were also observed with respect to Hb, RBC, PCV, mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), and ESR. The possible determinants of higher ESR levels in ischemic stroke may be sex, Hb, hematocrit, and RBC count, but the role of other clinical and laboratory parameters cannot be underestimated.

• Biomolecules & Therapeutics
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• v.30 no.1
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• pp.55-63
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• 2022

Oleanolic acid (OA), a natural pentacyclic triterpenoid, has been reported to exert protective effects against several neurological diseases through its anti-oxidative and anti-inflammatory activities. The goal of the present study was to evaluate the therapeutic potential of OA against acute and chronic brain injuries after ischemic stroke using a mouse model of transient middle cerebral artery occlusion (tMCAO, MCAO/reperfusion). OA administration immediately after reperfusion significantly attenuated acute brain injuries including brain infarction, functional neurological deficits, and neuronal apoptosis. Moreover, delayed administration of OA (at 3 h after reperfusion) attenuated brain infarction and improved functional neurological deficits during the acute phase. Such neuroprotective effects were associated with attenuation of microglial activation and lipid peroxidation in the injured brain after the tMCAO challenge. OA also attenuated NLRP3 inflammasome activation in activated microglia during the acute phase. In addition, daily administration of OA for 7 days starting from either immediately after reperfusion or 1 day after reperfusion significantly improved functional neurological deficits and attenuated brain tissue loss up to 21 days after the tMCAO challenge; these findings supported therapeutic effects of OA against ischemic stroke-induced chronic brain injury. Together, these findings showed that OA exerted neuroprotective effects against both acute and chronic brain injuries after tMCAO challenge, suggesting that OA is a potential therapeutic agent to treat ischemic stroke.

• Biomolecules & Therapeutics
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• v.32 no.3
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• pp.319-328
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• 2024

Lysophosphatidic acid receptor 1 (LPA₁) plays a critical role in brain injury following a transient brain ischemic stroke. However, its role in permanent brain ischemic stroke remains unknown. To address this, we investigated whether LPA₁ could contribute to brain injury of mice challenged by permanent middle cerebral artery occlusion (pMCAO). A selective LPA₁ antagonist (AM152) was used as a pharmacological tool for this investigation. When AM152 was given to pMCAO-challenged mice one hour after occlusion, pMCAO-induced brain damage such as brain infarction, functional neurological deficits, apoptosis, and blood-brain barrier disruption was significantly attenuated. Histological analyses demonstrated that AM152 administration attenuated microglial activation and proliferation in injured brain after pMCAO challenge. AM152 administration also attenuated abnormal neuroinflammatory responses by decreasing expression levels of pro-inflammatory cytokines while increasing expression levels of anti-inflammatory cytokines in the injured brain. As underlying effector pathways, NF-κB, MAPKs (ERK1/2, p38, and JNKs), and PI3K/Akt were found to be involved in LPA₁-dependent pathogenesis. Collectively, these results demonstrate that LPA₁ can contribute to brain injury by permanent ischemic stroke, along with relevant pathogenic events in an injured brain.

• Journal of Chest Surgery
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• v.34 no.11
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• pp.823-830
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• 2001

Background: Paraplegia is a serious complication of thoracic or thoracoabdominal aortic operations, which is related to ischemic injury of the spinal cord induced by low perfusion pressure during cross clamping of the aorta. Ischemic preconditioning of heart or brain with reversible sublethal ischemic injury induces resistance to subsequent lethal ischemia. The aim of this study is to investigate whether ischemic tolerance could be induced by the preconditioning of the spinal cord using swine model. Material and Method: The animals were randomly assigned to three groups: sham group(n=3), control group(n=6) and pre-conditioning group(n=8). In the sham group, we performed the left thoracotomy only without any ischemic injury. In the preconditioning group, the swine received reversible spinal cord ischemic injury by aortic clamping for 20 minutes, whereas control group had no previous aortic cross- clamping. Forty-eight hours later, the aorta was clamped for 30 minutes in both groups. Neurological examination was done 24 hours later, then the animals were euthanized for histopathology and malonedialdehyde(MDA) spectrophotometry assay of the spinal cord. Result: Statistically significant difference in neurological outcome was observed between the control and preconditioning groups at 24 hours after ischemic injury. The incidence of paraplegia and severe paresis was 100% in the control group, and 62.5% in the preconditing group(p=0.028). There was no statistically significant difference in histopathology and MDA assay of the ischemic spinal cord between these two groups with borderline statistical difference in MDA assay(p=0.0745). Conclusion: In the present swine study, ischemic preconditioning could induce tolerance against 30 minute ischemic insult of the spinal cord, although the animals did not completely recover(stand-up or walk). We expect that combining this preconditioning with other currently existing protection methods might lead to a synergistic effect, which warrants further investigation.

• Journal of Chest Surgery
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• v.43 no.3
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• pp.246-253
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• 2010

Background: Our objective was to review the long-term prognosis of patients with preoperative mild to moderate ischemic mitral regurgitation who underwent off-pump coronary artery bypass grafting. Material and Method: We prospectively followed 1,000 consecutive and systematic off-pump coronary artery bypass grafting patients who were operated on between September 1996 and March 2004; follow-up was achieved for 97%. Sixty-seven patients (6.7%) had mild to moderate ischemic mitral regurgitation at the time of surgery. Operative mortality, actuarial survival and major adverse cardiac event free survival were compared to assess the effect of ischemic mitral regurgitation. Result: Average follow-up was $66{\pm}22$ months. Patients with ischemic mitral regurgitation were older (p<0.001), had lower ejection fractions (p<0.001) and more comorbidities. Significantly more female patients presented with ischemic mitral regurgitation (p=0.002). There was no significant difference in operative mortality and perioperative myocardial infarction in ischemic mitral regurgitation patients (p=0.25). Eight-year survival was decreased in ischemic mitral regurgitation patients ($39.6{\pm}11.8%$ vs $76.7{\pm}2.2$, p<0.001). However, after correcting for risk factors, mild to moderate ischemic mitral regurgitation was not found to be a significant independent risk factor for long-term mortality (p=0.42). Major adverse cardiac event free survival at 8 years was significantly lower in ischemic mitral regurgitation patients ($53.12{\pm}12%$ vs $77{\pm}2%$, p<0.001). After correction for risk factors, ischemic mitral regurgitation remained a significant independent cause of major adverse cardiac events (HR: 2.31), especially congestive heart failure and recurrent myocardial infarction. Conclusion: In our series, patients with preoperative mild to moderate ischemic mitral regurgitation had a higher prevalence of preoperative risk factors than patients without ischemic mitral regurgitation. They had comparable perioperative mortality and morbidity, but, in the long term, were found to be at elevated risk for recurrent cardiac events.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.199.1-199.1
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• 2003

Ischemia-induced changes in protein expression may provide important insights into the mechanisms of cellular damage and their potential recovery. In the present study, to investigate protein patterns changed in ischemic condition, the cortical and striatal tissue samples from the permanent and transient ischemic rat brain obtained by middle cerebral occlusion were analysed by proteomic approchese using 20-PAGE and MALOI-MS. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.2
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• pp.145-152
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• 2017

Remote ischemic preconditioning (RIPC) is an intrinsic phenomenon whereby 3~4 consecutive ischemia-reperfusion cycles to a remote tissue (non-cardiac) increases the tolerance of the myocardium to sustained ischemia-reperfusion induced injury. Remote ischemic preconditioning induces the local release of chemical mediators which activate the sensory nerve endings to convey signals to the brain. The latter consequently stimulates the efferent nerve endings innervating the myocardium to induce cardioprotection. Indeed, RIPC-induced cardioprotective effects are reliant on the presence of intact neuronal pathways, which has been confirmed using nerve resection of nerves including femoral nerve, vagus nerve, and sciatic nerve. The involvement of neurogenic signaling has been further substantiated using various pharmacological modulators including hexamethonium and trimetaphan. The present review focuses on the potential involvement of neurogenic pathways in mediating remote ischemic preconditioning-induced cardioprotection.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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• pp.1213-1217
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• 2004

Many ischemic disease patients have been taking herbal medicine and there are some papers that prescription of herbal medicine to ischemic disease patients are useful. Mechanism of herbal medicines on ischmeic disease have been investigated in many ways, but anticougulation or anti platelet effect of herbal medicines is not known obviously. And recently patients receiving anticougulation therapy are discouraged from taking herbal medicines. In this study, we investigate PT, INR, platelet of patients receiving herbal medicine therapy to study whether herbal medicines effect coagulation system of ischemic patients. In PT, INR, platelet values obtained from the patients, before and after administering herbal medicine, there were no significant changes.

• Journal of Chest Surgery
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• v.23 no.1
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• pp.1-8
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• 1990

This experiment was carried out under the postulation that activation of an intracellular calcium-calmodulin complex may play an important role in myocardial injury induced by ischemia and reperfusion. Trifluoperazine[TFP], a calmodulin antagonist, was added to the potassium cardioplegic solution and used just before ischemia, and its protective effect from ischemic injury was investigated, using Langendorff rat heart model. TFP group had better post-ischemic functional recovery and lower post-ischemic contracture after 30 minutes of normothermic ischemia. Creatine kinase leakage was also decreased in TFP group but there was no statistical difference between control group and TFP group. We concluded that TFP has some protective effect from myocardial ischemic injury and its effect might be due to prevention of activation of intracellular calcium-calmodulin complex.

• Journal of Nutrition and Health
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• v.33 no.6
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• pp.668-674
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• 2000

This study was to examine effects of the eight month exercise program at lactate threshold level intensity on 11 women patients of ischemic heart disease. The %body fat and systolic blood pressure were decreased and the aerobic capacioties of oxygen consumption as well as oxygen consumption at lactate threshold were improved through the exercise program arranged by this study. The lipid variables concerned with coronary heart disease were changed a little except that triglyceride was significantly decreased during the exercise program. The effects obtained from exercise program during four months lasted to the end of the exercise program. In case we control the exercise intensity according to increase of oxygen consumption at lactate threshold the exercise program conducted by this study will be effective to the treatment for ischemic heart disease patients.(Korean J Nutrition 33(6) . 668~674, 2000)