• The Journal of Korean Physical Therapy
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• 제13권3호
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• pp.529-535
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• 2001

The purpose of this study was to test that the exercise adaptive training enhance behavioral outcome significantly after focal brain ischemia in rats. After occlusion of middle cerebral artery in rats, they were housed in individual standard cages fur 24 hours. The control group was sacrificed 24 hours after ischemic event. The experimental group I was housed in standard cages for 7days. The experimental group ll was housed in enriched environment and had got exercise adaptive training fur 7days. The rats were examined five motor behavioral tests. In motor behavioral tests :postural reflex test, limb placement test, beam-walking test, rotarod test, horizontal wire test. The outcomes of control group and group I were significantly lower than the group II. The conclusion was that exercise adaptive training induced functional repair.

• Journal of Chest Surgery
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• 제28권12호
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• pp.1113-1121
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• 1995

From August, 1986 to December, 1993, mitral valve replacement was performed in 178 patients. Of the valve implanted, 114 were St.Jude Medical, 47 Duromedics, 16 Carpenter-Edward and 1 Ionesc-Shiley. The hospital mortality rate was 2.8%[5 patients and the late mortality rate was 7.5%[13 patients . The causes of hospital death were LV rupture in 1, renal failure in 1, cardiac tamponade in 1, valve malfunction in 1 and hypoxic brain damage in 1. The causes of late death were sudden death in 6, congestive heart failure in 4, brain ischemic injury in 3. Follow-up was done on 155 surviving patients : mean follow-up period was 50.94$\pm$8.04 months. The actual survival rate was 88.2% at 8 years. We concluded, therefore, that good clinical results could be achieved with mitral valve replacement in mid-term follow-up, and long-term follow-up is also necessary.

• Animal cells and systems
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• 제10권2호
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• pp.79-83
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• 2006

Tissue plasminogen activator (tPA) is used to lyse clots and reperfuse brain in ischemic stroke. However, sideeffects of intracerebral hemorrhage (ICH) and edema limit their clinical application. In part, these phenomena has been linked with elevations in matrix metalloproteinase-9 (MMP-9) in neurovascular unit. However little is known about their regulatory signaling pathways in brain cells. Here, I examine the role of MAP kinase pathways in tPA-induced MMP-9 regulation in rat cortical astrocytes. tPA $(1-10\;{\mu}g/ml)$ induced dose-dependent elevations in MMP-9 and MMP-2 in conditioned media. Although tPA increased phosphorylation in two MAP kinases (ERK, JNK), only inhibition of the JNK pathway by the JNK inhibitor SP600126 significantly reduced MMP-9 upregulation. Neither ERK inhibition with U0126 nor p38 inhibition with SB203580 had any significant effects. Taken together, these results suggest that c-jun N-terminal kinase (JNK) plays an essential role for tPA-induced MMP-9 upregulation.

• Biomolecules & Therapeutics
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• 제7권3호
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• pp.234-241
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• 1999

The present study assessed the cerebroprotective effect of platelet-activating factor(PAF) antagonists in transient cerebral ischemia of rats. Right middle cerebral artery (MCA) of Sprague-Dawley rats was occluded for 2 hours using an intraluminal filament technique, and was reperfused for 6 hours following cerebral ischemia. The infarct area of seven coronal brain slices was measured morphometrically following stain ing in the 2% 2,3,5-triphenyltetrazolium chloride solution. The changes in regional cerebral blood flow (rCBF) and pial arteriolar diameter were measured by laser-Doppler flowmetry and by a videomicroscopy, respectively. The infarct size was significantly reduced by PAF antagonists, BN 52021 and CV-6209, which were administered i.p. 10 min before MCA occlusion. Pretreatment with PAF antagonists significantly restored the changes in pial arterial diameter as well as those in rCBF during the period of cerebral ischemia-reperfusion. PAF antagonists significantly inhibited the inducible nitric oxide synthase activity in the pial arteries ipsilateral to ischemia. These results suggest that PAF antagonists exert a cerebroprotective effect against ischemic brain damage through an improvement of postocclusive cerebral blood flow.

• Journal of Chest Surgery
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• 제55권4호
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• pp.283-287
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• 2022

The shortage of donor lungs has become a serious obstacle to implementing lung transplantation (LTx). Donation after circulatory death (DCD) donors are among the several donor pools utilized to overcome the problem posed by the shortage of donation after brain death (DBD) donors. The active use of DCD donors is expected to significantly reduce mortality on the waiting list for LTx, as LTx from DCD donors has comparable outcomes to LTx from DBD donors. Further studies on efforts to shorten the warm ischemic time and use uncontrolled DCD are required.

• The Korean Journal of Physiology and Pharmacology
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• 제1권5호
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• pp.495-504
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• 1997

Water transport is mediated by two distinct pathways, diffusional and channel-mediated water transport. The first molecular water channel was identified from human erythrocytes in 1992. Genetically-related proteins from other mammalian tissues have subsequently been identified to transport water, and the group is referred to as th "Aquaporins". Aquaporin-4 (AQP4) is most abundant in the brain, which may be involved in CSF reabsorption and osmoregulation. However, ontogeny and regulatory mechanisms of AQP4 channels have not been reported. Northern blot analysis showed that AQP4 mRNA began to be expressed in the brain just before birth and that its expression gradually increased by PN7 and then decreased at adult level. AQP4 was expressed predominantly in the ependymal cells of ventricles in newborn rats. And then its expression decreased in ependymal cells and increased gradually in other regions including supraoptic and paraventricular nuclei. AQP4 is also expressed in the subfornical organ, in which the expression level is not changed after birth. Cryogenic brain injury did not affect expression of AQP4 mRNA, while ischemic brain injury decreased it. Osmotic water permeability of AQP4 channel expressed in Xenopus oocytes was inhibited by the pretreatment of BAPTA/AM and calmidazolium, a $Ca^{2+}/Calmodulin$ kinase inhibitor, in a dose-dependent manner. These results indicate that the expression and the function of AQP4 channel are regulated by developmental processes and various pathophysiological conditions. These results will contribute to the understanding of fluid balance in the central nervous system and the osmoregulatory mechanisms of the body.

• 동의생리병리학회지
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• 제17권3호
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• pp.728-737
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• 2003

This study was investigated to prove the effect of GMGHT on the gultamate receptor, free radical and brain damage in rats sujected to Brain Ischemia The results were as follows; 1, GMGHT showed significant inhibitory effect of GMGHT on LDH release induced by NMDA, AMPA, and kinate. 2. GMGHT showed significant inhibitory effect of GMGHT on LDH release induced by BSO and Fe/sup 2+/. 3. GMGHT decreased coma duration time in a infatal dose of KCN and showed 30% of survival rate in a fatal dose. 4. GMGHT decreased ischemic area and edema incited by the MCA blood flow block. 5. GMGHT showed improvement of forelimb and hindlimb test after MCA occulusion in neurological exemination. 6. GMGHT showed no significant change after MCA occulusion in pathological observation as normal group. These results indicate that GMGHT can be used in the brain damage sujected to Brain Ischemia. Further study will be needed about the functional mechanism and etc.

• 한국자기공명학회논문지
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• 제13권2호
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• pp.64-83
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• 2009

The purpose of this study was to evaluate the usefulness of in vivo 3T $^1H$ MRS with short TE for prescreening various brain diseases. Together with ten normal volunteers, 12 brain tumor patients(2 lymphomas, 5 malignant gliomas) and 5(benign meningiomas) and 10 brain ischemic disease patients(6 acute and 4 subacute infarctions) participated. Lymphomas showed increased intensities of Cho and Lac. Likewise, gliomas showed increased Cho and Lac, but with decreased NAA and ${\beta}\;{\gamma}$-Glx; in higher grade of gliomas, Lac, Cho, mI and Lip predominantly increased with decrease of NAA. Benign meningiomas showed increased Cho, Lac and ${\beta}\;{\gamma}$-Glx; with decreased of NAA. The alanine peak at 1.47 ppm is a neuronal marker for meningiomas. Infarctions showed increased Lac and Lip and decreased NAA, ${\alpha}$-Glx and ${\beta}\;{\gamma}$-Glx where Lac increased with decreased of ${\alpha}$-Glx in acute, and Cho, Lac and Lip increased with decrease of NAA in subacute. Elevated Lac and decreased NAA levels were more aggravated in subacute. Clinical application of the $^1H$ MRS with short TE at 3T is able to povide valuable spectral information for prescreening various brain diseases by monitoring the changes of disease-specific cerebral metabolite concentrations in vivo, and consequently, it can be applicable to assessment of differential diagnosis and malignancy as well.

• 대한본초학회지
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• 제35권1호
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• pp.1-8
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• 2020

Objectives : This study was conducted to evaluate the effects of Corni Fructus, the dried fruits of Cornus officinalis Sieb., on unilateral common carotid artery occlusion (UCCAO) in mouse model. Methods : The Corni Fructus used in the experiment was extracted with anhydrous methanol, then filtered and freeze-dried. C57BL/6 mice used in the experiments were conducted left UCCAO surgery to set up UCCAO rodent model for mice. The mice were divided into five groups for evaluate the effect of methanol extract of Corni Fructus (COM) on UCCAO induced ischemic brain injury. The expression levels of nitric oxide in cerebrum and serum, body weight change were measured. To determine the effect of UCCAO and COM administration on brain neurons, morphological changes of the cerebrum through a microscope was conducted. And western blot was performed to confirm the underlying mechanism of neuroprotective effect of COM administration. Results : COM administered UCCAO groups (CO50, CO150, and CO500) had no significant effects on nitric oxide production in ipsilateral hemisphere proteins and sera. The CO500, 500 mg/kg COM administration, attenuated UCCAO-induced p38 inflammatory signaling pathway and inflammatory mediators such as iNOS and COX-2. The CO500 group showed resilient morphological changes of hippocampus neuronal cells about brain damage caused by decreased flow of blood. These group also showed decreased inflammation and cellular stress response in neuronal cells. Conclusions : From these results, COM has a neuroprotective property via moderating inflammatory factors and cellular stress inducing factors in brain cells.

• The Korean Journal of Physiology and Pharmacology
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• 제17권4호
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• pp.275-281
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• 2013

Astrocytes are reported to have critical functions in ischemic brain injury including protective effects against ischemia-induced neuronal dysfunction. Na-K ATPase maintains ionic gradients in astrocytes and is suggested as an indicator of ischemic injury in glial cells. Here, we examined the role of the Na-K ATPase in the pathologic process of ischemic injury of primary cultured astrocytes. Chemical ischemia was induced by sodium azide and glucose deprivation. Lactate dehydrogenase assays showed that the cytotoxic effect of chemical ischemia on astrocytes began to appear at 2 h of ischemia. The expression of Na-K ATPase ${\alpha}1$ subunit protein was increased at 2 h of chemical ischemia and was decreased at 6 h of ischemia, whereas the expression of ${\alpha}1$ subunit mRNA was not changed by chemical ischemia. Na-K ATPase activity was time-dependently decreased at 1, 3, and 6 h of chemical ischemia, whereas the enzyme activity was temporarily recovered to the control value at 2 h of chemical ischemia. Cytotoxicity at 2 h of chemical ischemia was significantly blocked by reoxygenation for 24 h following ischemia. Reoxygenation following chemical ischemia for 1 h significantly increased the activity of the Na-K ATPase, while reoxygenation following ischemia for 2 h slightly decreased the enzyme activity. These results suggest that the critical time for ischemia-induced cytotoxicity of astrocytes might be 2 h after the initiation of ischemic insult and that the increase in the expression and activity of the Na-K ATPase might play a protective role during ischemic injury of astrocytes.