• Childhood Kidney Diseases
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• 제17권1호
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• pp.13-18
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• 2013

발세포병증은 발세포의 손상을 특징으로 하는 사구체질환이다. 발세포의 손상은 여러 사구체질환에서 관찰될 수 있으나, 미소변화질환과 FSGS에서 주요 병인으로 작용한다. 이 글에서는 FSGS에서 발세포 손상의 형태 변화와 분절경화의 유형을 설명하고자 한다. 발세포가 손상되면 형태 변화로 발돌기의 소실, 발세포 세포질 내 공포, 발세포하 낭 등이 관찰되며, 심하면 발세포의 탈락 및 자멸사가 관찰된다. 그러나 분절경화가 초래되기까지에는 일정 수준 이상의 발세포의 소실이 있어야 하며, 손상된 발세포는 동일한 사구체 소엽 내 주변 발세포로 손상을 전파하여 병변이 커지게 된다. FSGS는 광학현미경 소견을 기초로 NOS형, perihilar형, cellular형, tip형, collapsing형의 다섯 가지 유형으로 나뉜다. 각 아형에 따라 임상 경과나 스테로이드 치료에 대한 반응이 다르고 흔히 동반되는 임상 조건들도 다르다고 보고되었으나 이에 대하여는 아직도 논란이 있는 실정이다. 앞으로 FSGS 발생에 관여하는 유전 정보와 혈액 내 투과인자의 성분 등 관련된 인자들에 대한 체계적인 연구가 이루어지면 FSGS에서 관찰되는 조직 변화나 병태생리를 더 잘 설명할 수 있을 것으로 기대해 본다.

• 대한임상독성학회지
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• 제4권1호
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• pp.78-81
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• 2006

Mad-honey poisoning is mainly brought about by the honey imported from Napal, Turkey, Brazil and other parts of Europe. This mad honey is extracted from Ericaceae plants of Rhododendron species and contains grayanotoxins that causes poisoning. These toxic compounds exert a specific stimulatory action on membrane permeability to Na+ions in various excitable tissues and cause depolarization of cell membranes. The toxic effects of grayanotoxins contained honey are mainly cardiovascular disturbances with bradycardia, cardiac arrhythmia, hypotension. There are Other symptoms like nausea, vomiting, salivation, dizziness, weakness and loss of consciousness. The precise amount for a toxic dose is not known. In general the severity of the honey poisoning depends on the amount ingested. Two cases of mad-honey poisoning are described here. Both patients showed bradycardia and arterial hypotension after ingestion of honey which was brought from Nepal. They were recovered fully within 24 hours after administration of fluids and atropine sulphate.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제35권2호
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• pp.66-73
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• 2009

Tumor angiogenesis is a process leading to formation of blood vessels within tumors and is crucial for maintaining a supply of oxygen and nutrients to support tumor growth and metastasis. Vascular endothelial growth factor(VEGF) plays a key role in tumor angiogenesis including induction of endothelial cell proliferation, migration, survival and capillary tube formation. VEGF binds to two distinct receptors on endothelial cells. VEGFR-2 is considered to be the dominant signaling receptor for endothelial cell permeability, proliferation, and differentiation. Bevacizumab(Avastin, Genetech, USA) is a monoclonal antibody against vascular endothelial growth factor. It is used in the treatment of cancer, where it inhibits tumor growth by blocking the formation of new blood vessels. The goal of this study is to identify the anti-tumor effect of Bevacizumab(Avastin) for oral squamous cell carcinoma cell lines. Human squamous cell carcinoma cell line(HN4) was used in this study. We examined the sensitivity of HN4 cell line to Bevacizumab(Avastin) by using in vitro proliferation assays. The results were as follows. 1. In the result of MTT assay according to concentration of Bevacizumab(Avastin), antiproliferative effect for oral squamous cell carcinoma cell lines was observed. 2. The growth curve of cell line showed the gradual growth inhibition of oral squamous cell carcinoma cell lines after exposure of Bevacizumab(Avastin). 3. In the apoptotic index, groups inoculated Bevacizumab(Avastin) were higher than control groups. 4. In condition of serum starvation, VEGFR-2 did not show any detectable autophosphorylation, whereas the addition of VEGF activated the receptor. Suppression of phosphorylated VEGFR-2 and phosphorylated MAPK was observed following treatment with Bevacizumab(Avastin) in a dose-dependent manner. 5. In TEM view, dispersed nuclear membrane, scattered many cytoplasmic vacuoles and localized chromosomal margination after Bevacizumab(Avastin) treatment were observed. These findings suggest that Bevacizumab(Avastin) has the potential to inhibit MAPK pathway in proliferation of oral squamous cell carcinoma cell lines via inhibition of VEGF-dependent tumor growth.

• 대한의생명과학회지
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• 제7권4호
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• pp.191-196
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• 2001

To evaluate an effect of cyclohexanone (CHO) treatment on the serum levels of glutathione S-transferase (GST) activity in acute liver damaged animals, acute liver damage was induced in rats with pretreatment of 50% $CCl_4$ in olive oil (0.1 ml/100 g body wt) intraperitoneally 14 times every other day. To liver damaged rats, CHO (1.56 g/kg body wt, i. p.) was injected once and then rats were sacrificed at 4 hours after injection of CHO. Increasing rate of GST activity to the control in serum was higher in CHO-treated rats pretreated with CCL$_4$ than the $CCl_4$-pretreated those. All the more, the injection of CHO to the liver damaged rats led to more enhanced liver damage on the basis of liver functional findings, i. e., serum levels of alanine aminotransferase (ALT) activity, liver weight per body weight, and malondialdehyde content. The changing pattern of serum ALT activity was similar with that of GST activity, whereas that of liver in both enzymes differed more or less from each other; the liver GST activity in CHO-treated rats pretreated with $CCl_4$ being more increased tendency than that of $CCl_4$-pretreated rats. Concomitantly the injection of CHO showed a increasing tendency of liver GST activity compared with the control. Furthermore, CHO injection to the liver damaged rats showed somewhat higher Vmax in the kinetics of liver GST enzymes. In conclusion, injection of CHO to the liver damaged animals led to more increased activity of serum GST, and it may be chiefly caused by the alteration of membrane permeability.

• 대한한의학회지
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• 제23권2호
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• pp.164-179
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• 2002

Object: Death rate due to hypertension, atherosclerosis, ischemic heart disease and cerebral infarction induced by Westernized diet and increased average life span is on the rise. Decrease in blood circulation, activation of thrombus generation and intravascular lipid accumulation, cited as the principal causes of the above mentioned diseases in recent studies, result in circulatory disturbance and blood vessel obstruction leading to ischemic cell death of heart, brain and peripheral vessels. Method: We investigated the biochemical changes in microvascular permeability, aggregation of platelet and the intravascular lipid accumulation in induced-diabetic rat using Streptozotocin. We also studied the effects of Woohwangcheongsirn-won after oral administration on blood circulation, platelet function and lipid metabolism. The results are as follows: I. Woohwangcheongsim-won increased blood circulation in microvessels. 2. Woohwangcheongsim-won increased the reduced erythrocyte deformability in diabetes. 3. Woohwangcheongsim-won induced the reduction of contents of 2, 3-DPG, but failed to affect the reduced contents of ATP in erythrocyte in diabetes. 4. Woohwangcheongsim-won reduced the activity of Ca/sup 2+/-ATPase in the membrane of erythrocyte. 5. Woohwangcheongsim-won reduced the platelet aggregation evoked by platelet agglutinin factor. 6. Woohwangcheongsim-won reduced the production of platelet-derived granules. 7. Woohwangcheongsim-won reduced the production of metabolites of arachidonic acid in diabetes, and also reduced the production of increased thromboxane B2. 8. Woohwangcheongsim-won reduced the synthesis of oxidized LDL-cholesterol. In conclusion, Woohwangcheongsim-won enhanced blood circulation in microvesseles, erythrocyte deformability and inhibited the increased platelet aggregation and the synthesis of oxidized LDL-cholesterol in diabetes. Therefore Woohwangcheongsim-won is believed to positively affect blood circulation (J Korean Oriental Med 2002;23(2):164-179)

• Environmental Engineering Research
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• 제17권1호
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• pp.35-39
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• 2012

In this study, multiparametric flow cytometry (FCM) was installed to enumerate the diagnosis of Pseudomonas aeruginosa ATCC 10145 and Escherichia coli K12 (IFO 3301). The nucleic acids (DNA/RNA) were double stained by a LIVE/DEAD bacLight viability kit, involving green SYTO 9 and red propidium iodide (PI), based on the permeability of two chemicals according to the integrity of plasma membrane. As the results showed, the gate for dead bacteria was defined as the range of $0.2{\times}10^0$ to $6.0{\times}10^1$ photo multiplier tube (PMT) 2 fluorescence (X-axis) and $2.0{\times}10^0$ to $2.0{\times}10^2$ PMT 4 fluorescence (Y-axis), and the gate for live bacteria was defined as the range of $6.0{\times}10^0$ to $6.0{\times}10^2$ PMT 2 fluorescence (X-axis) and $2.0{\times}10^0$ to $4.0{\times}10^2$ PMT 4 fluorescence (Y-axis). In the comparison of the number of the tested bacteria detected by FCM (viability assessment) and plate culture (cultivability assessment), the number of bacteria detected by FCM well represented the number of bacteria that was detected by the colony forming unit (CFU) counting method when bacteria were exposed to isopropyl alcohol and silver/copper cations. Consequently, it is concluded that the application of FCM to monitor the functional effect of disinfectants on the physiological status of target bacteria can offer more rapid and reliable data than the plate culture colony counting method.

• Nutrition Research and Practice
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• 제11권2호
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• pp.97-104
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• 2017

BACKGROUND/OBJECTIVE: Although Angelica keiskei (AK) has widely been utilized for the purpose of general health improvement among Asian, its functionality and mechanism of action. The aim of this study was to determine the protective effect of ethanol extract of AK (AK-Ex) on acute hepatotoxicity induced by acetaminophen (AAP) in HepG2 human hepatocellular liver carcinoma cells and HepaRG human hepatic progenitor cells. MATERIALS/METHODS: AK-Ex was prepared HepG2 and HepaRG cells were cultured with various concentrations and 30 mM AAP. The protective effects of AK-Ex against AAP-induced hepatotoxicity in HepG2 and HepaRG cells were evaluated using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide, lactate dehydrogenase (LDH) assay, flow cytometry, and Western blotting. RESULTS: AK-Ex, when administered prior to AAP, increased cell growth and decreased leakage of LDH in a dose-dependent manner in HepG2 and HepaRG cells against AAP-induced hepatotoxicity. AK-Ex increased the level of Bcl-2 and decreased the levels of Bax, Bok and Bik decreased the permeability of the mitochondrial membrane in HepG2 cells intoxicated with AAP. AK-Ex decreased the cleavage of poly (ADP-ribose) polymerase (PARP) and the activation of caspase-9, -7, and -3. CONCLUSIONS: These results demonstrate that AK-Ex downregulates apoptosis via intrinsic and extrinsic pathways against AAP-induced hepatotoxicity. We suggest that AK could be a useful preventive agent against AAP-induced apoptosis in hepatocytes.

• 한국작물학회지
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• 제33권4호
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• pp.375-379
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• 1988

Oxyfluorfen에 내성차이가 있는 것으로 기히 선발된 수도 두 품종(내성 : Chokoto, 감수성 : Weld Pally)을 공시하여 약해반응차이의 근거를 찾을 목적으로 ethylene 발생과 엽록소 함량변화 및 전해질 누출에 의한 세포막 삼투성 차이를 조사하였다. 결과를 요약하면 다음과 같다. 1. Oxyfluorfen $10^{-5}$M 처리의 경우, 감수성 품종은 내성보다 신속하고 않은 ethylene 방출현상을 보였구 $10^{-4}$ M 처리에서는 두 품종간의 ethylene 방출량에 차이가 감소하는 경향이었다. 2. Oxyfluorfen $10^{-6}$ M에서는 두 품종 모두 chorophyll함량차이가 없었으나 $10^{-5}$~$10^{-4}$ M에서는 감수성품종이 내성품종에 비하여 반감하였고, $10^{-3}$ M에서는 품종 차이없이 chlorophyll의 완전분해가 일어나는 양상이었다. 3. Oxyfluorfen 처리에 따른 전도도 증가 반응 및 품종간 차이는 $10^{-4}$ ~$10^{-3}$ M에서 일어났으며 , 감수성 품종이 내성품종보다 무처리대비하여 약 10% 정도 전해질 누출이 높은 경향이었다.

• Journal of Microbiology and Biotechnology
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• 제23권3호
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• pp.343-350
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• 2013

(R)-[3,5-Bis(trifluoromethyl)phenyl] ethanol is a key chiral intermediate for the synthesis of aprepitant. In this paper, an efficient synthetic process for (R)-[3,5- bis(trifluoromethyl)phenyl] ethanol was developed via the asymmetric reduction of 3,5-bis(trifluoromethyl) acetophenone, catalyzed by Leifsonia xyli CCTCC M 2010241 cells using isopropanol as the co-substrate for cofactor recycling. Firstly, the substrate and product solubility and cell membrane permeability of biocatalysts were evaluated with different co-substrate additions into the reaction system, in which isopropanol manifested as the best hydrogen donor of coupled NADH regeneration during the bioreduction of 3,5-bis(trifluoromethyl) acetophenone. Subsequently, the optimization of parameters for the bioreduction were undertaken to improve the effectiveness of the process. The determined efficient reaction system contained 200mM of 3,5-bis(trifluoromethyl) acetophenone, 20% (v/v) of isopropanol, and 300 g/l of wet cells. The bioreduction was executed at $30^{\circ}C$ and 200 rpm for 30 h, and 91.8% of product yield with 99.9% of enantiometric excess (e.e.) was obtained. The established bioreduction reaction system could tolerate higher substrate concentrations of 3,5- bis(trifluoromethyl) acetophenone, and afforded a satisfactory yield and excellent product e.e. for the desired (R)-chiral alcohol, thus providing an alternative to the chemical synthesis of (R)-[3,5-bis(trifluoromethyl)phenyl] ethanol.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2003년도 정기총회 및 학술발표회
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• pp.47-47
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• 2003

The presenilin 1 (PS1) or PS2 is an essential component of the ${\gamma}$-secretase complex, which mediates the intramembrane proteolysis of selected type-I membrane, including the ${\beta}$-amyloid precursor protein (APP) to yield A${\beta}$. Familial Alzheimer's disease (FAD)-associated mutations in presenilins give rise to an increased production of a highly amyloidogenic A${\beta}$42. In addition to their well-documented proteolytic function, the presenilins play a role in calcium signaling. We have previously reported that presenilin FAD mutations cause highly consistent alterations in intracellular calcium signaling pathways, which include deficits in capacitative calcium entry (CCE), the refilling mechanism for depleted internal calcium stores. However, molecular basis for the presenilin-mediated modulation of CCE remains to be elucidated. In the present study, whole-cell patch clamp method was used to identify a specific calcium-permeable ion channel current(s) that is responsible for the CCE deficits associated with FAD-linked PS1 mutants. Unexpectedly, both voltage-activated and conventional store depletion-activated calcium currents I(CRAC), were absent in HEK293 cells, which were stably transfected either with wild-type or FAD mutant (L286V, M146L, and delta E9) forms of PS1. Recently, magnesium-nucleotide-regulated metal cation current, or I(MagNum), has been described and appears to share many common properties with I(CRAC) including calcium permeability and inhibitor sensitivity (e.g. 2-APB). We have detected I(MagNum) in all 293 cells tested. Interestingly, FAD mutant 293 cells developed only about half of currents compared to PS1 wild type cells.