• Molecules and Cells
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• 제45권4호
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• pp.216-230
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• 2022

SERTA domain-containing protein 1 (Sertad1) is upregulated in the models of DNA damage and Alzheimer's disease, contributing to neuronal death. However, the role and mechanism of Sertad1 in ischemic/hypoxic neurological injury remain unclear. In the present study, our results showed that the expression of Sertad1 was upregulated in a mouse middle cerebral artery occlusion and reperfusion model and in HT22 cells after oxygen-glucose deprivation/reoxygenation (OGD/R). Sertad1 knockdown significantly ameliorated ischemia-induced brain infarct volume, neurological deficits and neuronal apoptosis. In addition, it significantly ameliorated the OGD/R-induced inhibition of cell viability and apoptotic cell death in HT22 cells. Sertad1 knockdown significantly inhibited the ischemic/hypoxic-induced expression of p-Rb, B-Myb, and Bim in vivo and in vitro. However, Sertad1 overexpression significantly exacerbated the OGD/R-induced inhibition of cell viability and apoptotic cell death and p-Rb, B-Myb, and Bim expression in HT22 cells. In further studies, we demonstrated that Sertad1 directly binds to CDK4 and the CDK4 inhibitor ON123300 restores the effects of Sertad1 overexpression on OGD/R-induced apoptotic cell death and p-Rb, B-Myb, and Bim expression in HT22 cells. These results suggested that Sertad1 contributed to ischemic/hypoxic neurological injury by activating the CDK4/p-Rb pathway.

• 대한한방내과학회지
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• 제25권4호
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• pp.105-116
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• 2004

Objective : In this study, we used the aged bilateral common carotid artery occlusion (BCAO) rats were used to measure the effect of Bupleuri Radix (Si-Ho) on the brain ischemic injury, because aging is an important factor in storke, Method : The brian ischemic injury was induced by temporary closing of carotids on both sides in a low blood pressure state. Bupleuri Radix (Si-Ho) was orally administered in 18-month-old BCAO rats. Result : The Ischemic Damaged Hippocampus and HSP expression were analyzed by the immunohistochemical staining and the result were as follows: 1. The low numbers of pyramid cells in the hippocampus CA1 area for the ischemically injured experimental group rose to numbers simillar to those of the control group. 2. The thin neuronal cell layer in the hippocampus CA1 area for the ischemically injured experimental group returned to thickness simillar to those of the control group. 3. The normalized optical density of HSP70 expression was suppressed in CA2, DG and CA1 expression was significantly suppressed in the experimental group compared to the control group. Conclusion : These results suggested that Bupleuri Radix (Si-Ho) has a neuroprotective effect by reducing neural cell injury in the initial ischemic state.

• Journal of Chest Surgery
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• 제22권6호
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• pp.901-913
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• 1989

This study was investigated under the postulation that activation of intracellular calcium- calmodulin complex during ischemia-reperfusion leads to myocardial injury. The protective effects of calcium channel blocker, diltiazem and calmodulin inhibitors, trifluoperazine, flunarizine and calmidazolium from ischemic injury in rat hearts were observed by using Langendorff apparatus when the antagonists were infused for 3 min in the beginning of ischemia. Thereby, an increase in resting tension developed during 30-min ischemia was analyzed with regard to [1] the degree of cardiac functional recovery following 60-min reperfusion, [2] changes in biochemical variables evoked during 30-min ischemia. The results obtained were as follows: l. In the ischemic group, the resting tension was increased by 4.1*0.2 g at 30-min ischemia. However, the increase in resting tension was markedly reduced not only by pretreatment with diltiazem [3.3 p M] but also with calmodulin inhibitors, trifluoperazine [3.3 p M], flunarizine [0.5 p M] and calmidazolium [0.5 p M], respectively. 2. Recovery of myocardial contractility, +dF /dt and coronary flow were much reduced when evoked by reperfusion in the ischemic group. These variables were significantly improved either by pretreatment with diltiazem or with calmodulin inhibitors. 3. The resting tension increment evoked during ischemia was significantly inversely correlated with the degree of cardiac function recovered during reperfusion. 4. Following 30-min ischemia, the production of malondialdehyde and release of lysosomal enzyme were much increased in association with a decrease in creatine kinase activity. 5. The increases in malondialdehyde production and release of free lysosomal enzyme were suppressed by pretreatment with calmodulin inhibitors as well as diltiazem. Likewise, the decrease of creatine kinase activities was prevented by these calcium antagonists. With these results, it is indicated that a increase in resting tension observed during ischemia has an inverse relationship to the cardiac function recovered following reperfusion, and further, the later may be significantly dependent on the degree of biochemical alterations occurred during ischemia such as decrease in creatine kinase activity, increased production of malondialdehyde and increased release of free lysosomal enzyme. Thus it is concluded that calmodulin plays a pivotal role in the process of ischemic injury.

• Journal of Korean Biological Nursing Science
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• 제23권3호
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• pp.217-226
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• 2021

Purpose: The aim of this study was to investigate the risk factors for brain reperfusion injury in ischemic stroke patients and to analyze the clinical outcomes. Methods: A retrospective study was conducted in 168 patients who underwent mechanical thrombectomy. The data were analyzed using descriptive statistics, t-test, Mann-Whitney U test, Chi-Square test, Fisher's exact test, and logistic regression with IBM SPSS/WIN 24.0. Results: Brain reperfusion injury occurred in 67 patients (39.9%) with a low favored outcome (𝛘²=6.01, p=.014). On multivariable analysis, blood urea nitrogen (Odds ratio [OR]=1.14, 95% Confidence interval [CI]=1.06-1.23), aphasia (OR=6.16, CI=1.62-23.40), anosognosia (OR=4.84, CI=1.13-20.79), presence of both aphasia and anosognosia (OR=7.33, CI=1.20-44.60), and time required to achieve targeted blood pressure (OR=1.00, CI=1.00-1.00) were identified as risk factors for brain reperfusion injury. A statistically significant difference was detected in clinical outcomes, including hemorrhagic transformation (𝛘²=6.32, p=.012), intensive care unit length of stay (Z=-2.08, p=.038), National Institute of Health Stroke scale score at discharge (Z=-3.14, p=.002), and modified Rankin Scale score at discharge (Z=-2.93, p=.003). Conclusion: This study identified the risk factors and presented the clinical outcomes of brain reperfusion injury. It is necessary to consider these risk factors for evaluating the patients and to establish nursing interventions and strategies.

• BMB Reports
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• 제35권1호
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• pp.67-86
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• 2002

Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of $Ca^{2+}$ and $Na^+$ that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Apoptosis or programmed cell death that often occurs during developmental process has been coined as additional route to pathological neuronal death in the mature nervous system. Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury. Thus, the therapeutic intervention of hypoxic-ischemic neuronal injury should be aimed to prevent excitotoxicity, oxidative stress, and apoptosis in a concerted way.

• 한방안이비인후피부과학회지
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• 제17권3호
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• pp.138-145
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• 2004

The clinical features and therapeutic results of alopecia areata are variable and unpredictable. For example, genetic, psychic, immunologic factors are regarded as the reason of alopecia areata. For the relationship between alopecia and whiplash injury, Dr. Guun explained that whiplash injury by the traffic accident produces cervical muscle spasm, and it makes autonomic nerve change. The tropical changes accompanied with ischemic change of scalp vessels made by this mechanism cause alopecia areata. And Yesudian reported the case of scalp alopecia as the result of ischemic change following traffic accident. We have experienced a 25-year-old woman with Alopecia areata following whiplash injury by traffic accident, and who had no risk factor of it. The patient was treated by acupuncture and physical treatment. Her hair loss, cervical angle and pain were improved through acupuncture treatment. This case of alopecia areata following whiplash injury is uncommon, so we report the mechanism of it, but should collect more cases and observations.

• Natural Product Sciences
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• 제25권2호
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• pp.136-142
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• 2019

Ischemia/reperfusion-induced myocardial injury is the main cause of acute myocardial infarction. Dendropanax morbifera $L{\acute{e}}veille$ has been used in traditional medicines for the treatment of various diseases such as headache, infectious diseases, and general debility. However, the effect of extract from D. morbifera (EDM) on myocardial ischemic injury is still unknown. In this study, the effects of EDM on neonatal rat cardiomyocytes with hypoxia/reoxygenation (H/R) injury were investigated. The viability of cardiomyocytes with H (30 min)/R (1 h) decreased; however, treatment with EDM significantly inhibited H/R injury-induced cardiomyocyte death. Further, we observed that reactive oxygen species (ROS) generation and intracellular calcium concentration ($Ca^{2+}{_i}$) were significantly reduced in EDM-treated cardiomyocytes compared with that in H/R-injured positive control. In addition, western blotting results showed that EDM attenuated abnormal changes of RyR2 and SERCA2a genes in hypoxic cardiomyocytes. These results suggest that EDM ameliorates ROS generation and $Ca^{2+}{_i}$ homeostasis to prevent dysregulation of calcium regulatory proteins in the heart, thereby exerting cardioprotective effects and reducing hypoxia-induced cardiomyocyte damage, which verifies the potential use of EDM as a new therapeutic agent for the treatment of myocardial ischemic injury.

• Archives of Plastic Surgery
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• 제50권2호
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• pp.188-193
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• 2023

Vascular injury following traumatic knee injury quoted in the literature ranges from 3.3 to 65%, depending on the magnitude and pattern of the injury. Timely recognition is crucial to ensure the revascularization is done within 6 to 8 hours from the time of injury to avoid significant morbidity, amputation, and medicolegal ramifications. We present a case of an ischemic limb following delayed diagnosis of popliteal artery injury after knee dislocation. Even though we have successfully repaired the popliteal artery, the evolving ischemia over the distal limb poses a reconstruction challenge. Multiple surgical debridement procedures were performed to control the local tissue infection. Free tissue transfer with chimeric latissimus dorsi flap was done to resurface the defect. However, the forefoot became gangrenous despite a free muscle flap transfer. His limb appeared destined for amputation in the vicinity of tissue and recipient vessels, but we chose to use a cross-leg free flap as an option for limb salvage.

• The Korean Journal of Physiology and Pharmacology
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• 제6권3호
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• pp.155-160
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• 2002

It is not known whether gender differences play a role in susceptibility to ischemic acute renal failure. Thus, we examined if there were any differences in susceptibility between male and female mice to kidney ischemic injury, and if so, whether it is due to differences in mitogen activated protein kinases (MAPKs) or inflammatory responses to ischemia. Female mice were protected against kidney ischemia when compared with males. Thirty minutes of bilateral ischemia resulted in marked functional and morphological damages in males, but not in females. The ischemia-induced phosphorylation of c-jun N-terminal stress-activated protein kinases (JNKs) was higher in males than in females. Phosphorylation of extracellular signal-regulated kinases (ERKs) was lower in males than in females. Post- ischemia medullary infiltration of RAW 264.7 cell, a monocyte-macrophage cell, and intercellular adhesion molecule-1 (ICAM-1) were greater in males than in females. In conclusion, males were much more susceptible to ischemia than females. The enhanced propensity to ischemic injury in males was correlated with greater activation of JNKs, greater expression of ICAM-1, and greater trapping of leukocytes in the medulla.

• Journal of Korean Neurosurgical Society
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• 제47권2호
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• pp.89-94
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• 2010

Objective : To evaluate the role of cranial sonography and computed tomography in the diagnosis of neonatal intracranial hemorrhage and hypoxic-ischemic injury in an Indian set-up. Methods : The study included 100 neonates who underwent cranial sonography and computed tomography (CT) in the first month of life for suspected intracranial ischemia and hemorrhage. Two observers rated the images for possible intracranial lesions and a kappa statistic for interobserver agreement was calculated. Results : There was no significant difference in the kappa values of CT and ultrasonography (USG) for the diagnosis of germinal matrix hemorrhage/intraventricular hemorrhage (GMH/IVH) and periventricular leucomalacia (PVL) and both showed good interobserver agreement. USG, however detected more cases of GMH/IVH (24 cases) and PVL (19) cases than CT (22 cases and 16 cases of IVH and PVL, respectively). CT had significantly better interobserver agreement for the diagnosis of hypoxic ischemic injury (HII) in term infants and also detected more cases (33) as compared to USG (18). CT also detected 6 cases of extraaxial hemorrhages as compared to 1 detected by USG. Conclusion : USG is better modality for imaging preterm neonates with suspected IVH or PVL. However, USG is unreliable in the imaging of term newborns with suspected HII where CT or magnetic resonance image scan is a better modality.