• Journal of The Korean Society of Integrative Medicine
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• v.4 no.1
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• pp.21-29
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• 2016

Purpose : The purpose of this study was to evaluate the influence of LOTCA-G and ADL by individualized cognitive program in elderly with vascular dementia, alzheimer dementia and mild cognitive impairment. Method : The subjects of this study, old man and woman diagnosed with vascular dementia, alzheimer dementia and mild cognitive impairment, 24 patients were picked up, who were agreed with this research and were having hospital care for 3weeks at nursing care centers. Individualized cognitive program was applied to 8 patients of vascular dementia, 8 patients of alzheimer dementia and 8 patients of mild cognitive impairment. Cognitive function measured by LOTCA-G and performance measured by FIM. The SPSS Ver. 22.0 statistical program was used for data processing. The significance level for statistical inspection was set as 0.05. Result : In comparison of LOTCA-G was significant increased after intervention and among three groups were significant difference. But FIM was no significant difference after intervention and among three groups were no significant difference. Conclusion : Therefore, the individualized cognitive program is useful to improve the cognitive function in elderly with dementia and mild cognitive impairment.

• YAKHAK HOEJI
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• v.50 no.4
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• pp.293-299
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• 2006

The aim of present study was to investigate the possible influence of Rho-kinase inhibition on the plant-derived estrogen-like compounds-induced arterial relaxation. Agonist- or depolarization-induced vascular smooth muscle contractions involve the activation of Rho-kinase pathway. However there are no reports addressing the question whether this pathway is involved in genistein-or daidzein-induced vascular relaxation in rat aortae precontracted with phenylephrine or thromboxane $A_2$ mimetic U-46619. We hypothesized that Rho-kinase inhibition plays a role in vascular relaxation evoked by genistein or daidzein in rat aortae. Endothelium-intact and denuded arterial rings from male Sprague-Dawley rats were used and isometric contractions were recorded using a computerized data acquisition system. Genistein concentration-dependently inhibited phenylephrine or thromboxane $A_2-induced$ contraction regardless of endothelial function. Surprisingly, in the agonists-induced contraction, similar results were also observed in aortae treated with daidzein, the inactive congener for protein tyrosine kinase inhibition, suggesting that Rho-kinase might act upstream of tyrosine kinases in phenylephrine-induced contraction. In conclusion, in the agonists-precontracted rat aortae, genistein and daidzein showed similar relaxant response regardless of tyrosine kinase inhibition or endothelial function.

• International Journal of Oral Biology
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• v.41 no.4
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• pp.217-223
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• 2016

Porphyromonas gingivalis, a foremost periodontal pathogen, has been known to cause periodontal diseases. Epidemiologic evidences have indicated the involvement of P. gingivalis in the development of cardiovascular diseases. In this study, we show that the P. gingivalis lipopolysaccharide increases the mRNA expression and protein secretion of interleukin-6 in vascular smooth muscle cells. We demonstrate that P. gingivalis LPS activates the extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and Akt, which mediate the IL-6 expression in vascular smooth muscle cells. Also, P. gingivalis LPS stimulates the vascular smooth muscle cell migration, which is a critical step for the progression of atherosclerosis. Moreover, neutralization of the IL-6 function inhibits the migration of vascular smooth muscle cells induced by P. gingivalis LPS. Taken together, these results indicate that P. gingivalis LPS promotes the expression of IL-6, which in turn increases the migration of vascular smooth muscle cells.

• BMB Reports
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• v.49 no.5
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• pp.255-262
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• 2016

The disease known as cerebral cavernous malformations mostly occurs in the central nervous system, and their typical histological presentations are multiple lumen formation and vascular leakage at the brain capillary level, resulting in disruption of the blood-brain barrier. These abnormalities result in severe neurological symptoms such as seizures, focal neurological deficits and hemorrhagic strokes. CCM research has identified 'loss of function' mutations of three ccm genes responsible for the disease and also complex regulation of multiple signaling pathways including the WNT/β-catenin pathway, TGF-β and Notch signaling by the ccm genes. Although CCM research is a relatively new and small scientific field, as CCM research has the potential to regulate systemic blood vessel permeability and angiogenesis including that of the blood-brain barrier, this field is growing rapidly. In this review, I will provide a brief overview of CCM pathogenesis and function of ccm genes based on recent progress in CCM research.

• Molecules and Cells
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• v.37 no.6
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• pp.435-440
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• 2014

Hemodynamic shear stress, the frictional force acting on vascular endothelial cells, is crucial for endothelial homeostasis under normal physiological conditions. When discussing blood flow effects on various forms of endothelial (dys)function, one considers two flow patterns: steady laminar flow and disturbed flow because endothelial cells respond differently to these flow types both in vivo and in vitro. Laminar flow which exerts steady laminar shear stress is atheroprotective while disturbed flow creates an atheroprone environment. Emerging evidence has provided new insights into the cellular mechanisms of flowdependent regulation of vascular function that leads to cardiovascular events such as atherosclerosis, atherothrombosis, and myocardial infarction. In order to study effects of shear stress and different types of flow, various models have been used. In this review, we will summarize our current views on how disturbed flow-mediated signaling pathways are involved in the development of atherosclerosis.

• Journal of Yeungnam Medical Science
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• v.40 no.3
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• pp.225-232
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• 2023

Cognitive dysfunction is relatively less considered a complication of hypertension. However, there is sufficient evidence to show that high blood pressure in middle age increases the risk of cognitive decline and dementia in old age. The greatest impact on cognitive function in those with hypertension is on executive or frontal lobe function, similar to the area most damaged in vascular dementia. Possible cognitive disorders associated with hypertension are vascular dementia, Alzheimer disease, and Lewy body dementia, listed in decreasing strength of association. The pathophysiology of cognitive dysfunction in individuals with hypertension includes brain atrophy, microinfarcts, microbleeds, neuronal loss, white matter lesions, network disruption, neurovascular unit damage, reduced cerebral blood flow, blood-brain barrier damage, enlarged perivascular damage, and proteinopathy. Antihypertensive drugs may reduce the risk of cognitive decline and dementia. Given the high prevalence of dementia and its impact on quality of life, treatment of hypertension to reduce cognitive decline may be a clinically relevant intervention.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.6
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• pp.431-436
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• 2011

Vascular smooth muscle cells can obtain a proliferative function in environments such as atherosclerosis in vivo or primary culture in vitro. Proliferation of vascular smooth muscle cells is accompanied by changes in ryanodine receptors (RyRs). In several studies, the cytosolic $Ca^{2+}$ response to caffeine is decreased during smooth muscle cell culture. Although caffeine is commonly used to investigate RyR function because it is difficult to measure $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) directly, caffeine has additional off-target effects, including blocking inositol trisphosphate receptors and store-operated $Ca^{2+}$ entry. Using freshly dissociated rat aortic smooth muscle cells (RASMCs) and cultured RASMCs, we sought to provide direct evidence for the operation of RyRs through the $Ca^{2+}$- induced $Ca^{2+}$ -release pathway by directly measuring $Ca^{2+}$ release from SR in permeabilized cells. An additional goal was to elucidate alterations of RyRs that occurred during culture. Perfusion of permeabilized, freshly dissociated RASMCs with $Ca^{2+}$ stimulated $Ca^{2+}$ release from the SR. Caffeine and ryanodine also induced $Ca^{2+}$ release from the SR in dissociated RASMCs. In contrast, ryanodine, caffeine and $Ca^{2+}$ failed to trigger $Ca^{2+}$ release in cultured RASMCs. These results are consistent with results obtained by immunocytochemistry, which showed that RyRs were expressed in dissociated RASMCs, but not in cultured RASMCs. This study is the first to demonstrate $Ca^{2+}$ release from the SR by cytosolic $Ca^{2+}$ elevation in vascular smooth muscle cells, and also supports previous studies on the alterations of RyRs in vascular smooth muscle cells associated with culture.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.8 no.1
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• pp.1-19
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• 1995

Seungmagalgeuntang-gamibang has long been known to have anti-allergic effect. However, the mechanism of action of Seungmagalgeuntang-gamibang is not well investigated. The author analysed the effects of Seungmagalgeuntang-gamibang on the vascular permeability, delayed-type and contact hypersensitivities, and phagocytic function, the results obtained are as follows: 1. Administration of Seungmagalgeungtang-gamibang decreased the vascular permeability induced by serotonin in the mouse. 2. Administration of Seungmagalgeuntang-gamibang decreased the vascular permeability induced by histamine without statistical significant. 3. Administration of Seungmagalgeuntang-gamibang decreased the delayed-type hypersensitivity induced by sheep red blood cells. 4. Administration of Seungmagalgeungtang-gamibang decreased the contact hypersensitivity induced by dinitrochlorobenzene. 5. Seungmagalgeungtang-gamibang increased the phagocytic-activities of macrophages in vitro and in vivo. 6. Seungmagalgeungtang-gamibang enhanced the formation of reactive oxygen intermediates in vitro and in vivo. The above results demonstrate that Seungmagalgeuntang-gamibang suppresses the hypersensitivity reactions with increasing the phagocytic functions and formations of reactive oxygen intermediates from macrophages.

• Annals of Surgical Treatment and Research
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• v.95 no.5
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• pp.278-285
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• 2018

Purpose: We investigated the clinical outcomes of deceased donor kidney transplantation (KT) using kidneys with terminal acute kidney injury (AKI). Methods: Between February 2000 and December 2013, we performed 202 deceased donor renal transplants from 159 brain dead donors. According to the expanded criteria donor (ECD) and AKI network criteria, we divided 202 recipients into 4 groups: Group I: Non-AKI & standard criteria donor (SCD) (n = 97); group II: Non-AKI & ECD (n = 15); group III: AKI & SCD (n = 52); and group IV: AKI & ECD (n = 38). Results: The incidence of delayed graft function (DFG) was significantly higher in patients with AKI than it was in the non-AKI group (P = 0.008). There were no significant differences among the 4 groups in graft survival (P = 0.074) or patient survival (P = 0.090). However, the long-term allograft survival rate was significantly lower in group IV than it was in other groups (P = 0.024). Conclusion: Allografts from deceased donors with terminal AKI had a higher incidence of DGF than did those from donors without AKI. However, there is no significant difference in graft and patient survival rates among the groups. So, the utilization of renal grafts from ECDs with terminal AKI is a feasible approach to address the critical organ shortage.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.51-66
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• 1989

Mammalian cardiocytes secrete atrial natriuretic peptides (ANPs) into plasma, which cause marked natriuresis, diuresis, vasorelaxation and inhibition of hormone secretions. Aging influences the ability of the kidney both to conserve and to excrete sodium; i.e., in old animals, the excretory capacity of sodium is reduced and the time required to excrete sodium load is prolonged. Therefore, it is possible that animals differing in ages may respond differently to ANP. In the present study, we determined whether the renal, hormonal and vascular effects of ANP may be influenced by aging in conscious rabbits. The plasma renin concentration decreased with aging but plasma ANP concentration was significantly lower only in 24-month-old rabbits. Plasma aldosterone concentration and atrial ANP content did not change by aging. In 1-month-old rabbits, ANP (atriopeptin III, 3 ug/kg) administered intravenously caused hypotension and decreased in plasma renin and aldosterone concentrations, but did not cause diuresis and natriuresis. In 2 to 5 month-old rabbits, ANP caused hypotension, decreases in Plasma renin and aldosterone concentrations and marked renal effects. However, in 24-month-old rabbits, all the above effects of ANP was blunted. With hydration of physiological saline at a rate of 15 ml/kg/h for 2hr, urine volume and glomerular filtration rate did not change but the electrolyte excretion as well as fractional excretion of sodium significantly increased. The plasma concentrations of active renin and aldosterone were decreased but plasma inactive renin and ANP concentrations were increased. The changes in renal function and plasma level of hormone showed no differences in different ages. These results suggest that the peripheral vascular receptors to ANP may develop earlier than those in the kidney, and the attenuated vascular and renal responses to ANP in the old age may be due to age-related modifications in renal function and blood vessel.