• Journal of the East Asian Society of Dietary Life
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• v.15 no.5
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• pp.606-612
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• 2005

This study was performed to provide basic data that predict the application of Saengmaegsan(SMS) as medicinal food. SMS has been used in oriental medicine for many years as a therapeutic agent for cerebral disease. We examined the effects of SMS on physiological function in isolated abdominal aorta and femoral artery from rabbit and measured the changes of regional cerebral hood flow(rCBF), which was continually monitored by laser-doppler flowmeter and pressure transducer in anesthetized adult Spargue-Dawley rats through the data acquisition system composed of MacLab and Macintosh computer. The contraction forces by injection of norephinephrine in isolated abdominal aorta and femoral artery were significantly decreased in each concentration of SMS treatment compared with control. rCBF was increased by SMS in a dose-dependent manner. These results suggest that SMS causes a diverse response of rCBF and arterial diameter. These mechanism in rCBF increase may be mediated by prostaglandis, cyclic GMP and adrenergic $\beta-receptor$. Also mechanism in artery contraction decrease is also mediated by prostaglandis and cyclic GMP. These results indicate that SMS can be nsed as a safe and clinically applicable as a supplementation of diet therapy for cerebral cardiovascular disease patients.

• Proceedings of the Korea Society of Environmental Biology Conference
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• 2003.11a
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• pp.111-115
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• 2003

Tannic acid (0.5mg/ml, 1.0mg/ml, 2.0mg/ml)와 카드뮴(20mg/kg)을 마우스에 경구 투여한 결과는 다음과 같다. 1. Tannic acid와 카드뮴을 투여한 마우스의 증체량과 음수소비량에 변화가 있었으나, 카드뮴투여에 의한 변화는 tannic acid투여에 의하여 감소되었다. 2. 카드뮴투여에 의하여 간장의 상대중량과 뇌 상대중량이 대조군에 비하여 유의한 변화가 있었으며, tannic acid 1.0mg/ml 투여군에서는 간장의 상대중량, 폐장의 상대중량, 흉선의 상대중량도 유의하게 변화하였다. (P < 0.05) 3. Hemoglobin contents, packed cell volume, platelet count, neutrophill count 등의 혈액학적인 변화는 대조군에 비하여 카드뮴투여군에서 유의한 변화가 인정되었다. 그러나, 이러한 유의한 변화가 tannic acid를 동시 투여한 군에서는 나타나지 않았다. 4. 카드뮴을 투여한 군에서는 혈청학적 변화(ALT, AST, BUN와 creatinine)가 있었으나 tannic acid 0.5, 1.0, 2.0mg/ml을 동시투여한 군에서는 회복되는 경향이 나타났다. 위의 결과로 미루어 카드뮴 투여에 의한 독성이 tannic acid을 2.0 mg/ml/day 이상 4주간 투여하였을 때 경감효과가 나타날 수 있었다. 그러나, 카드뮴과 같은 중금속의 독성에 tannic acid가 어떻게 경감효과를 나타내는지에 관한 작용기전의 연구가 더 필요할 것으로 사료된다.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.6
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• pp.1538-1542
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• 2006

The study was designed to investigate the effects of MokhwyangJoki-san Extract (MJSE) on the change of regional cerebral blood flow (rCBF) and mean arterial blood pressure (MABP) in normal rats, and further to determine the mechanism of MJSE. The results in normal rats were as follows ; MJSE significantly increased rCBF in a dose-dependent manner, and MABP did not change in a dose-dependent manner. This results were suggested that MJSE significantly increased rCBF by dilating pial arterial diameter. The MJSE-induced increase in rCBF was significantly inhibited by pretreatment with methylene blue (10 ${\mu}g/kg$, i.p.), an inhibitor of guanylate cyclase, and was not changed by indomethacin (1 ${\mu}g/kg$, i.p.), an inhibitro of cyclooxygenase. The MJSE-was not changed MABP was decreased by pretreatment with indomethacin but was not changed by methylene blue. This results were suggested that the mechanism of MJSE was mediated by guanylate cyclase.

• Journal of the Korean Society of Radiology
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• v.84 no.4
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• pp.792-808
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• 2023

Trauma to the head and neck region can have serious consequences for vital organs such as the brain, and injuries to blood vessels can cause permanent neurological damage or even death. Thus, prompt treatment of head and neck vessels is crucial. Although the level of evidence is moderate, an increasing amount of research indicates that endovascular treatments can be a viable alternative to traditional surgery or medical management. Embolization or reconstructive endovascular procedures can significantly improve patient outcomes. This article provides an overview of various endovascular options available for specific clinical scenarios, along with examples of cases in which they were employed.

• Journal of Hospice and Palliative Care
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• v.16 no.4
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• pp.205-215
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• 2013

Most terminally ill cancer patients experience various physical and psychological symptoms during their illness. In addition to pain, they commonly suffer from fatigue, anorexia-cachexia syndrome, nausea, vomiting and dyspnea. In this paper, I reviewed some of the common non-pain symptoms in terminally ill cancer patients, based on the National Comprehensive Cancer Network (NCCN) guidelines to better understand and treat cancer patients. Cancer-related fatigue (CRF) is a common symptom in terminally ill cancer patients. There are reversible causes of fatigue, which include anemia, sleep disturbance, malnutrition, pain, depression and anxiety, medical comorbidities, hyperthyroidism and hypogonadism. Energy conservation and education are recommended as central management for CRF. Corticosteroid and psychostimulants can be used as well. The anorexia and cachexia syndrome has reversible causes and should be managed. It includes stomatitis, constipation and uncontrolled severe symptoms such as pain or dyspnea, delirium, nausea/vomiting, depression and gastroparesis. To manage the syndrome, it is important to provide emotional support and inform the patient and family of the natural history of the disease. Megesteol acetate, dronabinol and corticosteroid can be helpful. Nausea and vomiting will occur by potentially reversible causes including drug consumption, uremia, infection, anxiety, constipation, gastric irritation and proximal gastrointestinal obstruction. Metoclopramide, haloperidol, olanzapine and ondansetron can be used to manage nausea and vomiting. Dyspnea is common even in terminally ill cancer patients without lung disease. Opioids are effective for symptomatic management of dyspnea. To improve the quality of life for terminally ill cancer patients, we should try to ameliorate these symptoms by paying more attention to patients and understanding of management principles.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.273-289
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• 1994

Reversible brain ischemia was produced by occluding both common carotid arteries for 5 min, and the effects of aminoguanidine (AG), $DL-{\alpha}-difluoromethylornithine$ (DFMO), MK-801, and nimodipine (NM) on the ischemia induced changes of the polyamine, glutamate and acetylcholine levels in the hippocampus CA1 subfield and the specific $[^3H]\;MK-801$ binding to the hippocampus synaptosomal membranes were studied with a histological reference of the cresyl violet stained hippocampus. The basal putrescine level $(PT:\;74.4{\pm}8.8\;nM)$ showed a rapid increase (up to 1.7 fold) for 5 min of ischemia, remained significantly increased for 6 h, and then resumed the further increase to amount gradually up to about 3 fold 96 h after recirculation. However, the level of spermidine was little changed, and the spermine level showed a transient increase during ischemia followed by a sustained decrease to about 40% of the preischemic level after recirculation. The increase of PT level induced by brain ischemia was enhanced with AG or MK-801, but it was reduced by DFMO or NM. The basal glutamate level $(GT:\;0.90{\pm}0.l4\;{\mu}M)$ rapidly increased to a peak level of $8.19{\pm}1.14\;{\mu}M$ within 5 min after onset of the ischemia and then decreased to the preischemic level in about 25 min after recirculation. And NM reduced the ischemia induced increase of GT level by about 25%, but AG, DFMO and MK-801 did not affect the GT increase. The basal acetylcholine level $(ACh:\;118.0{\pm}10.5\;{\mu}M)$ did little change during/after brain ischemia and was little affected by AG or NM. But DFMO and MK-801, respectively, produced the moderate decrease of ACh level. The specific $[^3H]\;MK-801$ binding to the hippocampus synaptosomal membrane was little affected by brain ischemia for 5 min. The control value (78.9 fmole/mg protein) was moderately decreased by AG and MK-801, respectively but was little changed by DFMO or NM. The microscopic findings of the brains extirpated on day 7 after ischemia showed severe neuronal damage of the hippocampus, particularly CA1 subfield. NM and AG moderately attenuated the delayed neuronal damage, and DFMO, on the contrary, aggravated the ischemia induced damage. However, MK-801 did not protect the hippocampus from ischemic damage. These results suggest that unlike to the mode of anti-ischemic action of NM, AG might protect the hippocampus from ischemic injury as being negatively regulatory on the N-methyl-D-aspartate (NMDA) receptor function in the hippocampus.

• The Korean Journal of Nuclear Medicine
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• v.34 no.3
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• pp.169-182
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• 2000

Purpose: To investigate the various ictal perfusion patterns and find the relationships between clinical factors and different perfusion patterns. Materials and Methods: Interictal and ictal SPECT and SPECT subtraction were performed in 61 patients with partial epilepsy. Both positive images showing ictal hyperperfusion and negative images revealing ictal hypoperfusion were obtained by SPECT subtraction The ictal perfusion patterns of subtracted SPECT were classified into focal hyperperfusion, hyperperfusion-plus, combined hyperperfusion-hypoperfusion, and focal hypoperfusion only. Results: The concordance rates with epileptic focus were 91.8% in combined analysis of ictal hyperperfusion and hypoperfusion images of subtracted SPECT, 85.2% in hyperperfusion images only of subtracted SPECT, and 68.9% in conventional ictal SPECT analysis. Ictal hypoperfusion occurred less frequently in temporal lobe epilepsy (TLE) than extratemporal lobe epilepsy. Mesial temporal hyperperfusion alone was seen only in mesial TLE while lateral temporal hyperperfusion alone was observed only in neocortical TLE. Hippocampal sclerosis had much lower incidence of ictal hypoperfusion than any other pathology. Some patients showed ictal hypoperfusion at epileptic focus with ictal hyperperfusion in the neighboring brain regions where ictal discharges propagated. Conclusion: Hypoperfusion as well as hyperperfusion in ictal SPECT should be considered for localizing epileptic focus. Although the mechanism of ictal hypoperfusion could be an intra-ictal early exhaustion of seizure focus or a steal phenomenon by the propagation of ictal discharges to adjacent brain areas, further study is needed to elucidate it.

• Korean Journal of Acupuncture
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• v.31 no.1
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• pp.20-32
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• 2014

Objectives : There has been some controversy about the modulatory effects on brain function during acupuncture on each side of the same acupoint. This study was designed to investigate and compare the blood oxygen level-dependent(BOLD) responses of acupuncture on each side of ST36. Methods : Fourteen healthy subjects were recruited for imaging and received acupuncture or placebo stimulations either on the left or on the right acupoint of ST36 in each scan. For the voxel-wise statistical analysis, one sample T-test and the within-subject analysis of variance(ANOVA) test were performed using SPM8 software. Results : This study showed that acupuncture on each side of ST36 showed different BOLD signal patterns. Higher BOLD responses after acupuncture stimulations at the left ST36 compared to the right were observed mainly in the parahippocampal gyrus(BA 28), dorsolateral prefrontal cortex(DLPFC, BA 44), thalamus, culmen and claustrum. We investigated the different neural responses between rest and activation periods of placebo and acupuncture stimulations on each side of ST36. Acupuncture at the right ST36 elicited activation mainly in the insula, supplementary motor area(SMA) and anterior cingulate cortex(ACC), while acupuncture at the left ST36 elicited activation mainly in the insula, primary somatosensory cortex(SI, BA 2) and DLPFC(BA 44). Conclusions : To our knowledge, this is the first reported functional MRI study directly comparing when needling at the right and at the left side of ST36. This study's preliminary results proved to be evidence of acupuncture's different effects when performed on opposite sides of an acupoint.

• Journal of Life Science
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• v.16 no.2 s.75
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• pp.266-273
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• 2006

This study is investigated the effect of selenium against neurotoxicity induced by MPTP(1-methy-4-phenyl-propion-oxypiperidine) in mice. In order to demonstrate neuroprotective activity of selenium, mice were administrated orally with selenium(25, 50, 100 ${\mu}g/kg$, once/day) for 10 days, and MPTP(10 mg/kg) was injected subcutaneously into the mice for 6 days from the beginning 1hr before selenium treatment. Test of rota road activity was inhibited by treatment with selenium in MPTP-induced neurotoxicity group when compared to MPTP treatment group in normal mice. Monoamine oxidase(MAO)-B activity and cerebral lipid peroxide content were significantly decreased in the treatment of selenium in MPTP-induced neurotoxicity group when compared to MPTP treatment group in normal mice and MAO-A was not affected. Activities of cerebral superoxide dismutase, catalase and glutathione peroxidase were significantly increased in the treatment of selenium in MPTP-induced neurotoxicity group when compared to MPTP treatment group in normal mice. These results suggest that selenium might be estimated the result from the cooperative action of its inhibitory effect on monoamine oxidase-B with that of the enhancement of antioxidant(SOD, catalase, GSH-Px) defence ability.

• Journal of Life Science
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• v.26 no.12
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• pp.1367-1375
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• 2016

Cilostazol is known to be a selective inhibitor of phosphodiesterase III and is generally used to treat stroke. Our previous findings showed that cilostazol enhanced capillary density through angiogenesis after focal cerebral ischemia. Angiogenesis is an important physiological process for promoting revascularization to overcome tissue ischemia. It is a multistep process consisting of endothelial cell proliferation, migration, and tubular structure formation. Here, we examined the modulatory effect of cilostazol at each step of the angiogenic mechanism by using human brain microvascular endothelial cells (HBMECs). We found that cilostazol increased the migration of HBMECs in a dose-dependent manner. However, it did not enhance HBMEC proliferation and capillary-like tube formation. We used a cDNA microarray to analyze the mechanisms of cilostazol in cell migration. We picked five candidate genes that were potentially related to cell migration, and we confirmed the gene expression levels by real-time PCR. The genes phosphoserine aminotransferase 1 (PSAT1) and CCAAT/enhancer binding protein ${\beta}$ ($C/EBP{\beta}$) were up-regulated. The genes tissue factor pathway inhibitor 2 (TFPI2), retinoic acid receptor responder 1 (RARRES1), and RARRES3 were down-regulated. Our observations suggest that cilostazol can promote angiogenesis by promoting endothelial migration. Understanding the cilostazol-modulated regulatory mechanisms in brain endothelial cells may help stimulate blood vessel formation for the treatment of ischemic diseases.