• Journal of Oral Medicine and Pain
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• v.32 no.4
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• pp.449-453
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• 2007

Trigeminal neuralgia is defined as "a sudden, usually unilateral, brief stabbing recurrent pain in the distribution of one or more branches of the fifth cranial nerve" by the International Association for the Study of Pain(IASP). Trigeminal neuralgia is classified as an idiopathic trigeminal neuralgia with no apparent cause and a symptomatic trigeminal neuralgia which is caused by a structural lesion such as brain tumor. Over 80% of the tumors are meningioma, acoustic neuroma, and epidermoid tumors. Symptomatic trigeminal neuralgia can not be excluded even if old-aged patient does not have abnormal neurologic sign and symptom, and good response to pharmacotherapy. Therefore, initial examinations such as MRI or CT are essential to exclude symptomatic trigeminal neuralgia. When compared with CT, MRI, especially gadolinium enhanced MRI, has an increased sensitivity in the detection of intracranial lesions. The most effective medical treatment of trigeminal neuralgia is carbamazepine. The most common side effects of carbamazepine include drowsiness, dizziness, unsteadiness, nausea, anorexia. Hepatotoxicity, bone marrow depression are the most feared side effect of carbamazepine therapy but occurs rarely. It require periodic complete blood cell counts as well as hepatic and renal function tests. It has been recommended that complete blood cell counts is done every 2 weeks for the first 2months and then quaterly thereafter. Oxcarbazepine can be used if neutropenia occurs.

• Journal of Oriental Neuropsychiatry
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• v.21 no.4
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• pp.53-68
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• 2010

Objectives : We investigated the effects of Sopungsungj-won(Shufengshunqjvuan) (SSEx1, SSEx2) on the metabolic syndrome in high-fat diet induced obese mice. Methods: 8 weeks old, high fat diet induced obese male mice were divided into 4 groups: C57BL/6 lean control, obese vehicle control, SSEx1, SSEx2. After mice were treated with SSExl, SSEx2 for 12 weeks, we measured body weight gain, food intake, feeding efficiency ratio, fat weight, plasma leptin, insulin, glucose and lipid levels. We also observe the morphology and count for the numbers of Adipocyte and evaluate the weight of organs and it's function. Results: 1. Compared to Obese Control Group, SSEx1 gained significantly lower body weight and showed lower Feeding Efficiency Ratio. 2. Compared to Obese Control Group, SSEx1 showed lower weights of epididymal adipose tissue, troperitoneal adipose tissue, inguinal adipose tissue, brown adipose tissue. SSEx2 showed higher weights of epididymal adipose tissue, troperitoneal adipose tissue, inguinal adipose tissue, brown adipose tissue. 3. Compared to Obese Control Group, the size of adipocytes was significantly decreased by SSEx1, whereas the number of adipocites per unit was significantly increased. Hepatic lipid accumulation was decreased significantly by SSEx1. 4. Concerning the weights of Liver, Heart, Spleen, Kidney and Pancreas, SSEx1, SSEx2 showed little differences with those of Lean Control, Obese Control. 5. Compared to Obese Control Group, SSEX1, SSEx2 showed lower level of plasma triglyceride, but SSEx1 had significance only. SSEx1, SSEx2 showed little lower level of plasma HDL-cholesterol. LDL-cholesterol, total cholesterol, but had no significances. 6. Concerning the levels of plasma glucose, insulin and leptin, SSEx1 and SSEx2 showed littele changes with those of Lean Control, Obese Control. 7. The leves of Plasma AST, AST, ALT, free fatty acid, BUN, creatinine were in the physiological range at 4 groups all: Lean Control, Obese Control, SSEx1, SSEx2. Conclusions : These results showed SSEx1 can be used as therapeutic agent for Obesity and metabolic syndrome caused by long-period high fat diet.

• Journal of Preventive Medicine and Public Health
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• v.33 no.1
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• pp.117-124
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• 2000

Objectives : It is the objective of this study to compare hepatotoxicity of nickel chloride and cadmium chloride with each other through IPRL(Isolated Perfused Rat Liver) method. Methods : Biochemical indicator of hepatic function such as AST(aspartate aminotransferase), ALT(alanine aminotransferase), LDH(lactate dehydrogenase) and perfusion flow rate were used as the indicator of hepatotoxicity. Oxygen consumption rate were used as vability indicator. $300({\pm}50)g$ - weighted rats were allocated randomly to each group($0{\mu}M,\;50{\mu}M,\;200{\mu}M\;NiCl_2\;and\;CdCl_2$ exposure) by 5, totally 25. After Krebs-Ringer bicarbonate butler solution flowed into the penal vein and passed the liver cell, it flowed out of vena cava. Liver was administered with each $NiCl_2\;and\;CdCl_2$ of each concentration and observed with buffer solution sampling time. Butler which got out of liver was sampled and then biochemical indicator of hepatotoxicity was measured. Results : AST, ALT, and LDH in buffer increased with sampling time much more in $CdCl_2$ exposure group than $NiCl_2$ exposure group in both 50 and $200{\mu}M$ and statistical significance w3s verified with 2-way repeated ANOVA. Viability was decreased more and more in all substances during passed time. Conclusions : It is inferred that $CdCl_2$ has stronger hepatotoxicity than $NiCl_2$. IPRL method would be used widely for acute hepatotoxicity when considerating the benefit of it.

• Toxicological Research
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• v.32 no.1
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• pp.73-80
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• 2016

Chronic exposure to cadmium (Cd) is known to adversely affect renal function. Our previous studies indicated that Cd induces p53-dependent apoptosis by inhibiting gene expression of the ubiquitin-conjugating enzyme (Ube) 2d family in both human and rat proximal tubular cells. In this study, the effects of Cd on protein expression of p53 and apoptotic signals in the kidney and liver of mice exposed to Cd for 12 months were examined, as well as the effects of Cd on p53 protein levels and gene expression of the Ube2d family in various cell lines. Results showed that in the kidney of mice exposed to 300 ppm Cd for 12 months, there was overaccumulation of p53 proteins in addition to the induction of apoptosis, which was triggered specifically in the proximal tubules. Interestingly, the site of apoptosis was the same as that of p53 accumulation in the proximal tubules. In the liver of mice chronically exposed to Cd, gene expression of the Ube2d family tended to be slightly decreased, together with slight apoptosis without the accumulation of p53 protein. In rat small intestine epithelial (IEC-6) cells, Cd decreased not only the p53 protein level but also gene expression of Ube2d1, Ube2d2 and Ube2d4. In human brain microvascular endothelial cells (HBMECs), Cd did not suppress gene expression of the Ube2d family, but increased the p53 protein level. In human brain astrocytes (HBASTs), Cd only increased gene expression of UBE2D3. These results suggest that Cd-induced apoptosis through p53 protein is associated with renal toxicity but not hepatic toxicity, and the modification of p53 protein by Cd may vary depending on cell type.

• Journal of Food Hygiene and Safety
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• v.13 no.2
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• pp.171-187
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• 1998

Garlic occupies a special position among the many foods of vegetable origin because it is the sole food for Koreans during the their lives. And vitamin A has been ingested by forms of food or additives. Cadmium has been described as one of the most dangerous trace elements in the food and environment of man and livestocks. Since the de novo synthesis of stress proteins can be detected early after exposure to some agents, analysis of cadmium-induced changes in gene expression , ie. alterations in patterns of protein synthesis, may be useful to develop as biomarkers of exposure and damage for food hygiene. He acute and chronic combine effects of cadmium (Cd, CdCl2 20mg/kg), garlic oil(Dds: diallyl disulfide 50mg/kg, 3 times a week) and vitamin A(Ra: retinol acetate 50,000 IU/kg, 3 times a week) on Wistar male rats were evaluated concerning cadmium contents, tissues enzyme activity, HSP expression histopathological and electron microscopical examinations. The results of the study are as follows ; 1. Less cadmium was absorbed through the digestive tracts, but the ratio of contents in tissue were not changed by the simultaneous adminstration of diallyl disufide or retinol acetate. 2. ALT(alanine aminotransferase) , AST(aspartate aminotransferase), glucose, BUN (blood urea nitrogen), creatinine, the key indices of the clinical changes in hepatic and renal function were significantly hanged by the cadmium treatment after 1 week in liver, after 4 weeks in kidney. 3. Histopathological changes in cadmium treated rats were appeared at 8 weeks age treatment in kidneys. Homogenous eosinophilic material was accumulated in cortical and collecting tubular lumens at 16 weeks. Degenerated or necrotized tubular cells were observed in cortex and medulla. Degenerated seminiferous tubules and homogeneous eosinophilic material was seen in interstitial tissue of rat treated with cadmium for 16 weeks. Calcium deposits were seen in degenerated seminiferous tubules and the tubules showed severe calcification of rat treated with cadmium for 16 weeks. Electron microscope changes in kidney were observed in rats treated with CdCl2 20 mg/kg. Proximal convoluted tubule cells showed selling of cytoplasm and narrow lumen. Capillary endothelial cells showed cytoplasmic vacuoles and swelling. Degenerated epithelial cells were accumulated in tubular lumen of kidney. 4. Enhanced synthesis of 70 KDa relateve molecular mass proteins were detected in 2 hours after cadmium, exposure, with maximum activity occurring at 8~48 hours. Induction of HSP 70 was evident at proximal tubules and glomeruli in kidney. Testicular cells produced enough HSP to be detected normally. From the above results, it could be concluded that HSP70 induction by the cadmium treatment was a rapid reaction to indicated the exposure of xenobiotics, and retinol acetate reduced the cadmium induced nephrotoxicity.

• Journal of Life Science
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• v.30 no.7
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• pp.640-650
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• 2020

Fibroblast growth factor 21 (FGF21) is an atypical member of the FGF protein family which is highly synthesized in the liver, pancreas, and adipose tissue. Depending on the expression tissue, FGF21 uses endo- or paracrine features to regulate several metabolic pathways including glucose metabolism and energy homeostasis. Different physiologically stressful conditions such as starvation, a ketogenic diet, extreme cold, and mitochondrial dysfunction are known to induce FGF21 synthesis in various tissues to exert either adaptive or defensive mechanisms. More specifically, peroxisome proliferator-activated receptor gamma and peroxisome proliferator-activated receptor alpha control FGF21 expression in adipose tissue and liver, respectively. In addition, the pharmacologic administration of FGF21 has been reported to decrease the body weight and improve the insulin sensitivity and lipoprotein profiles of obese mice and type 2 diabetes patients meaning that FGF21 has attracted huge interest as a therapeutic agent for type 2 diabetes, obesity, and non-alcoholic fatty liver disease. However, understanding FGF21 remains complicated due to the paradoxical condition of its tissue-dependent expression. For example, nutrient deprivation largely increases hepatic FGF21 levels whereas adipose tissue-derived FGF21 is increased under feeding condition. This review discusses the issues of interest that have arisen from existing publications, including the tissue-specific function of FGF21 and its action mechanism. We also summarize the current stage of a clinical trial using several FGF21 analogs.

• Journal of Genetic Medicine
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• v.8 no.1
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• pp.53-57
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• 2011

Purpose: Wilson disease is an autosomal recessive disorder which causes excessive copper accumulation in the hepatic region. So far, ATP7B gene is the only disease-causing gene of Wilson disease known to date. However, ATP7B mutations have not been found in ~15% of the patients. This study was performed to identify any causative gene in Wilson disease patients without an ATP7B mutation in either allele. Materials and Methods: The sequence of the coding regions and exon-intron boundaries of the five ATP7B-interacting genes, ATOX1, COMMD1, GLRX, DCTN4, and ZBTB16, were analyzed in the 12 patients with Wilson disease. Results: Three nonsynonymous variants including c.1084A>G (p.Thr362Ala) in the exon 12 of the DCTN4 gene were identified in the patients examined. Among these, only p.Thr362Ala was predicted as possibly damaging protein function by in silico analysis. Examination of allele frequency of c.1084A>G (p.Thr362Ala) variant in the 176 patients with Wilson disease and in the 414 normal subjects revealed that the variant was more prevalent in the Wilson disease patients (odds ratio [OR]=3.14, 95% confidence interval=1.36-7.22, P=0.0094). Conclusion: Our result suggests that c.1084A>G (p.Thr362Ala) in the ATP7B-interacting DCTN4 gene may be associated with the pathogenesis of Wilson disease.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.6
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• pp.1197-1203
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• 2001

This study was conducted to examine the effects of dietary xylooligosaccharide on UDP-glucuronyl transferase (UDP-GTase) activity and excretion of fecal sterols in rat fed high cholesterol diet. Sprague-Dawley male rats weighing 100$\pm$10 g were randomly divided into five groups, one with normal diet and four with high cholesterol diets containing 1% cholesterol (w/w). The high groups with cholesterol diet groups were classified into xylooligosaccharide free diet (C), 5% xylooligosaccharide diet (C5XO), 10% xylooligosaccharide diet (C10XO), and 15% xylooligosaccharide diet (C15XO) group according to the five groups of dietary xylooligosaccharide by weights. The experimental diets were fed ad libidum for 4 weeks. Fecal weights were increased 86% by xylooligosaccharide. Fecal total lipid contents including fecal neutral and acidic sterols in xylooligosaccharide groups were significantly higher than those of the normal and C groups, and especially that of C10XO group was the highest among all experimental groups. Activity of UDP-glucuronyl transferase (UDP-GTase) in liver in C group was 35% higher than that of normal group and the activities in C5XO, C10XO and C15XO groups were 15%, 41%, and 21% higher than in C group, respectively. Fecal bile acid excretions per day were increased 3.1, 3.6 and, 2.8 folds in C5XO, C10XO, and C15XO groups, respectively, compared with that of C group. Contents of neutral sterol, coprostanol, and coprostanone were higher in xylooligosaccharide groups than in C group. These results suggest that dietary xylooligosaccharide may act as potential substitute for a dietary fiber capable of improving a gastrointestinal function and lipid metabolism.

• Journal of the Korean Society of Food Science and Nutrition
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• v.15 no.2
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• pp.136-143
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• 1986

These studies were carried out to investigate effects of Lycii fructus extract on experimentally CC14-induced liver damage and alloxan-induced diabetes in rabbits and acute toxicity using mice. $LD_{50}(mg/kg)$ of Lycii fructus extract(L.F.E.) was 12.17g/kg by intraperitoneal administration in mice. L.F.E. showed more rapid recuperation compared to the control group in CC14-intoxicated rabbits and 800mg/kg was the most effective. Especially GPT activity and total bilirubin level showed an apparant decreasing effect within 6 days and 8 days, respectively in 800mg/kg. But any differences were not observed in alkaline phosphatase and total cholesterol between sample and control group. Large amount administered group exhibited more excellent hypoglycemic effect in alloxan-induced diabetes of rabbits, that is, it was significant to the control group after 4 days and adjacent to the normal level on 12th day. And GPT activity was gradually decreased and showed clear decreasing effect after 6 days. It is suggested that L.F.E. can be administered not only as therapeutic agents (such as liver tonics or antidiabetetics) but also a natural food to shorten the recovery time of hepatic function in liver diseases and decrease the abnormally elevated blood glucose such as Diabetes Mellitus.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.3
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• pp.516-520
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• 2002

This study was designed to investigate the hepatoprotective effects of Semisulcospira libertina and garlic on the acute hepatotoxicity induced by carbon tetrachloride (CCl$_4$) of rats. Male Sprague-Dawley rats weighing 200∼220g were pretreated with dehydrated powder of Semisulcospira libertina (2.1 g/kg, po; SL) and dehydrated powder mixture of Semisulcospira libertina and garlic (3g/kg, 7:3 ratio, po; SG) once daily for 3 consecutive days, and then given a single dose of CCl$_4$(1g/kg in 5ml/kg corn oil, po) and liver function was determined 24 hrs later. Liver damage was assessed by quantitating activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH) and alkaline phosphatase (ALP) as well as by histopathological examination. Pretreatments with SL and SG significantly decleased CCl$_4$-elevated ALT (48% and 61% respectively), AST (32% and 47%) and SDH (51% and 76%), but had no effect on ALP. SL and SG had revealed hepatoprotective effects against CCl$_4$-induced histopathological changes such as severe necrosis, inflammatory cell infiltration and congestion in the central gene of hepatic lobule. These findings demonstrate that SL and SG may haute the hepatoprotective effect on CCl$_4$-induced liver damage.