• Journal of Korean Neurosurgical Society
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• 제29권9호
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• pp.1171-1178
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• 2000

Objective : The purpose of the present study was to determine the appropriate time of clinical intervention by observing and analyzing the changes in the size of infarct, penumbra and cerebral edema and the extend of neurological deficit due to reperfusion damage according to time in a reversible cerebral ischemic model of reperfusing blood flow after inducing ischemia by maintaining middle cerebral artery occlusion for 2 hours(h) in rats. Methods : The rats were divided according to reperfusion time into control group(0 h reperfusion time) and experimental groups(0.5, 1, 2, 3, 4, 5, 6, 12, and 24 h of reperfusion time). Results : Changes in the size of infarction due to reperfusion damage were 0.93, 1.48 and 1.16% at 0.5, 1 and 2 h after reperfusion, respectively, and although a statistical significance was not present compared to 1.35% of the control group, damages increased drastically up to 6 h(6.64%), and the size increased were 6.65 and 6.78% at 12 and 24 h, respectively. Also there was no significant difference after 6 h up to 24 h in the size of infarction. In the areas where infarction occurred, reperfusion damage increased significantly with time in cortex than in subcortex. Accordingly, the size of penumbra area also showed a statistically significant decrease from 2 h up to 6 h after reperfusion, and 6 h after reperfusion, the area almost disappeared, becoming permanent infarction. Thus, reperfusion damage showed a significant increase from 2 h up to 6 h after reperfusion, and became steady thereafter. As for the mean ratio of the extend of cerebral edema, the control group and reperfusion 0.5 h group were 1.073 and 1.081, respectively ; up to 2 h thereafter, the ratio decreased to 1.01 but increased again with time ; and in reperfusion 12 h and reperfusion 24 h, the ratios were 1.070 and 1.075, respectively, showing similar size with that of control group. As for neurological deficit scores, the score of the control group was 2.67, that of reperfusion 2 h was 2, those of reperfusion 3 h and 6 h groups were 3.2 and 3.8, respectively, and those of reperfusion 12 h and 24 h groups were 4.2 and 4.6, respectively. Thus, as for the test results, the neurological deficit increased with time 2 h after reperfusion, and in reperfusion 12 and 24 h groups, almost all the symptoms appeared. Conclusion : As shown in these results, although the changes in the size of infarction due to reperfusion damage did not increase up to 2 h after reperfusion in the experimental groups compared to the control group, damage increased significantly thereafter up to 6 h, and the size remained about the same from 6 h to 24 h after reperfusion, becoming permanent infarction ; thus, the appropriate time of intervention according to the present study is at least 6 h before after maintaining reperfusion, including the time of cerebral artery occlusion.

• Journal of Yeungnam Medical Science
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• 제20권1호
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• pp.1-12
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• 2003

Ischemic stroke is among the principal causes of death and disability in the elderly. Although control of blood pressure, decreased cigarette smoking, and modified dietary habits are among important reasons for stroke decline, the use of antithrombotic therapy, rigorously prescribed. Several antiplatelet agents are approved to reduce the risk of recurrent stroke. Aspirin is the best-studied and most widely used antiplatelet agent for stroke prevention; it provides approximately 15% to 25% relatively risk reduction for secondary prevention of stroke or the major vascular death. Combining 2 antiplatelet agents with different mechanism of action was demonstrated to provide a substantial increase in efficacy in several studies. Anticoagulation should be considered first with potential cardiac sources of embolism. Heparin reduces development of erythrocyte-fibrin thrombi that form in regions of vascular stasis especially within the heart, in severely stenosed arteries sometimes engrafted on white thrombi, in acute arterial occlusion. Heparin should not be indiscriminately given to all acute brain ischemia patients, but may contribute to treatment of large artery occlusion and severe stenosis, cardiogenic embolism with a high acute recurrence risk, and dural sinus and cerebral venous thromobosis.

• 동의신경정신과학회지
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• 제10권2호
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• pp.115-126
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• 1999

This study was conducted to find out the effects of Woohwangchungsimwon on learning and memory in the NOS inhibitor treated rats. The Morris water maze was used in evaluating them. The result of the study was summarized as follows. 1. In the learning test, three groups have showed a gradual improvement of learning ability by repeating the trials in Morris water maze. WHCS group have showed statistical improvement than control group at 4,5,6 trial(p<0.05, p<0.01, p<0.01). 2. In the memory test, the first latency of WHCH group was statistically shortened than that of control group(p<0.05). 3. In the memory test, there was no statistical difference in the entry number between WHCH group and control. 4. In the memory test, there was no statistical difference in the memory score between WHCH group and control. The result of this experimental study presents that Woohwangchungsimwon has the improving effect on impaired learning and memory in NOS inhibitor treated rats, and implies that Woohwangchungsimwon may be one of the useful prescription for the treatment of vascular dementia after cerebral ischemia.

• The Korean Journal of Pain
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• 제12권2호
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• pp.263-267
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• 1999

We have observed retroperitoneal hematoma after trigger point injections of quadratus lumborum in a patient with chronic low back pain. Severe flank pain and dyspnea was observed three hours after injection of local anesthetic and steroid to the trigger point of quadratus lumborum muscle. There was fuge hematoma in abdominal CT image around the right kidney, which displaced and compressed the kidney anteriorly. Following infusion of contrast media, extravasation through renal vein and IVC was notified. Patient had a past history of having been treated with platelet aggregation inhibitor and lower dose aspirin treatment after cerebral ischemia for a year, but coagulative function was within normal range. Patient was admitted 12 days for bed rest, pain control and transfusion. We need to take greater care with a frequent aspiration and exact direction of needle, during trigger point injection of quadratus lumborum, particu right side, to avoid vascular injury.

• The Korean Journal of Physiology and Pharmacology
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• 제10권3호
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• pp.123-129
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• 2006

In several experimental models, estrogens protect neurons against ischemic insults. However, the recent clinical studies of hormone replacement showed negative results to prevent stroke. Therefore, optimal models to study estrogen replacement for neuroprotection are needed before its clinical ap-plication. Organotypic hippocampal slice under oxygen-glucose deprivation (OGD) has been established as a model of cerebral ischemia and has advantages to study drug effects. We investigated whether estrogen protected CAI neurons and affected activation of Akt (pAkt) in CAI region under OGD. Thus, rat hippocampal slices on day 7 of culture were treated with $17-{\beta}$ estradiol (E, 1 nM) for 7 days before 30 min OGD, and cell death of CAI neurons was quantified by propidium iodide (PI) staining and expression of pAkt was studied by Western blot and immunofluorescence. PI intensity in slices treated with E was significantly reduced 72 hour after OGD compared to that of non-treated slices (p < 0.05). E pretreatment also increased the expression of pAkt 72 hour after OGD compared to that of no treatment (p<0.01). These data suggest that estrogen pretreatment may rescue neurons from ischemic insults through the activation of Akt and also indicate that our model would be a useful alternative method to study the mechanisms and effects of estrogen replacement treatment for neuroprotection.

• Journal of Magnetics
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• 제19권2호
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• pp.197-204
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• 2014

A transcranial magnetic stimulation device is a complicated appliance that employs a switching power device designed for discharging and charging a capacitor to more than 1 kV. For a simple transcranial magnetic stimulation device, this study used commercial power and controlled the firing angle using a Triac power device. AC 220V 60 Hz, the power device was used directly on the tanscranial magnetic stimulation device. The power supply device does not require a current limiting resistance in the rectifying device, energy storage capacitor or discharge circuit. To control the output power of the tanscranial magnetic stimulation device, the pulse repetition rate was regulated at 60 Hz. The change trigger of the Triac gate could be varied from $45^{\circ}$ to $135^{\circ}$. The AVR 182 (Zero Cross Detector) Chip and AVR one chip microprocessor could control the gate signal of the Triac precisely. The stimulation frequency of 50 Hz could be implemented when the initial charging voltage Vi was 1,000 V. The amplitude, pulse duration, frequency stimulation, train duration and power consumption was 0.1-2.2T, $250{\sim}300{\mu}s$, 0.1-60 Hz, 1-100 Sec and < 1 kW, respectively. Based on the results of this study, TMS can be an effective method of treating dysfunction and improving function of brain cells in brain damage caused by ischemia.

• 약학회지
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• 제45권4호
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• pp.419-425
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• 2001

The neuronal cell death induced by excess glutamate (Glu) has been implicated in many acute and chronic neurodegenerative diseases including cerebral ischemia. Glu-induced elevation of intra-cellular $Ca^{2+}$ plays a critical role in the excitotoxicity, partly through the activation of a variety of $Ca^{2+}$ dependent enzymes. In the present study, we investigated the Glu-induced modulation of $Ca^{2+}$/calmodulin-dependent protein kinase IV (CaMK IV), a multifunctional enzyme abundantly present in the nuclei of neurons. The exposure of cultured rat cortical neurons to $100{\mu}$M Glu for 3 min dramatically increased CaMK IV activity up to 4.5-fold of the control-treated enzyme activity. The activation was very rapid, reaching peak at 3 min and then declined gradually. Under the same experimental conditions, time-dependent acute and delayed neuronal cell death was observed. Immunoblot analyses using specific antibodies showed that the expressions of CaMK IV and $CaMKK_{\alpha}$ were time-dependently modulated by Glu. Taken together, these results imply that the modulation of CaMK IV activity by Glu may be involved in the cascade of events resulting in neuronal cell death in cortical cultures.

• Journal of Chest Surgery
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• 제33권8호
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• pp.676-680
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• 2000

To minimize the period of brain ischemia and the potential for neurologic damage during aortic arch replacement, we used the arch-first technique. First case was a 28-year-old female with extensive aneurysm involving ascending, arch and descending thoracic aorta. Exposure was obtained via a bilateral via a bilateral thoracotomy (clamshell incision) in the anterior 4th right and 3rd left intercostal space with oblique sternotomy. To prepare for arch perfusion, the side-arm graft(10mm) was anastomosed to the aortic graft, opposite the site of the planned anastomosis to the arch vessels. After completing the arch anastomosis under total circulatory arrest(37min) and retrograde cerebral perfusion(12min), aortic graft was clamped on either side and the arch was perfused via side-arm graft for 36min. When distal aortic anastomosis was finished, distal clamp of aortic graft was released and arch vessels were perfused via common femoral artery, and the proximal aortic anastomosis was accomplished. The patient was discharged with no event. Second case was a 48-year-old male with extensive aneurysm involving ascending, arch, and aortic regurgitaiton(grade III/IV). This case was also done using the clamshell incision. Aortic valve replacement was done by valved-conduit(Vascutek 30mm), both coronary artery anastomosis using Cabrol's procedure. Last operation procedure was the same as the 1st case.

• Investigative Magnetic Resonance Imaging
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• 제22권2호
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• pp.131-134
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• 2018

Susceptibility-weighted imaging (SWI) is well known for detecting the presence of hemorrhagic transformation, microbleeds and the susceptibility of vessel signs in acute ischemic stroke. But in some cases, it can provide the tissue perfusion state as well. We describe a case of a patient with hyperacute ischemic infarction that had a slightly hypodense, patchy lesion at the left thalamus on the initial SWI, with a left proximal posterior cerebral artery occlusion on a magnetic resonance (MR) angiography and delayed time-to-peak on an MR perfusion performed two hours after symptom onset. No obvious abnormal signals at any intensity were found on the initial diffusion-weighted imaging (DWI). On a follow-up MR image (MRI), an acute ischemic infarction was seen on DWI, which is the same location as the lesion on SWI. The hypointensity on the initial SWI reflects the susceptibility artifact caused by an increased deoxyhemoglobin in the affected tissue and vessels, which reflects the hypoperfusion state due to decreasing arterial flow. It precedes the signal change on DWI that reflects a cytotoxic edema. This case highlights that, in some hyperacute stages of ischemic stroke, hypointensity on an SWI may be a finding before the hyperintensity is seen on a DWI.

• Journal of Ginseng Research
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• 제45권5호
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• pp.599-609
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• 2021

Ginseng has long been considered as an herbal medicine. Recent data suggest that ginseng has antiinflammatory properties and can improve learning- and memory-related function in the central nervous system (CNS) following the development of CNS neuroinflammatory diseases such as Alzheimer's disease, cerebral ischemia, and other neurological disorders. In this review, we discuss the role of ginseng in the neurovascular unit, which is composed of endothelial cells surrounded by astrocytes, pericytes, microglia, neural stem cells, oligodendrocytes, and neurons, especially their blood-brain barrier maintenance, anti-inflammatory effects and regenerative functions. In addition, cell-cell communication enhanced by ginseng may be attributed to regeneration via induction of neurogenesis and angiogenesis in CNS diseases. Thus, ginseng may have therapeutic potential to exert cognitive improvement in neuroinflammatory diseases such as stroke, traumatic brain injury, multiple sclerosis, Parkinson's disease, and Alzheimer's disease.