• Journal of Oriental Neuropsychiatry
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• v.34 no.4
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• pp.335-347
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• 2023

Objectives: The study aimed to understand the current treatment patterns in Korean medicine to develop clinical practice guidelines for autonomic dysfunction in Korean medicine. Methods: This study sent an online survey vai text message to 25,900 Korean medicine doctors whose contact information was registered with the Association of Korean Medicine. A total of 1,410 Korean medical doctors completed the online survey. Results: When autonomic treating dysfunction clinically, 77% of the cases included only a description without entering a diagnosis code. The most commonly used information to diagnose o autonomic dysfunction was history-taking and symptoms (79%), and the main symptoms of autonomic dysfunction were palpitations, dizziness, sleeping difficulties, anxiety/nervousness, and depression/lethargy. The most frequently mentioned cause of autonomic dysfunction was mental problems (54%). The most commonly used Korean medicine treatment method for autonomic dysfunction was herbal medicine (70%), and Soyo-san/Gamisoyo-san is the most frequently used herbal medicine preparation. Liver qi depression used to indicate the most often mentioned Korean medicine pattern identification used to indicate autonomic dysfunction (31%). When asked whether cardiac neurosis in Chinese medicine can be considered autonomic dysfunction, opinions for and against it are determined almost equally. Conclusions: Our results serve are a foundation for developing clinical practice guidelines for autonomic dysfunction in Korean medicine and are expected to catalyst promoting future clinical research on autonomic dysfunction.

• Korean Journal of Community Nutrition
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• v.5 no.4
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• pp.608-614
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• 2000

The purpose of this study was to evaluate the relative importance among various biological and environmental factors on refractive errors. Various factors such as diseases, health related behavior such as drinking, smoking and exercise, as well as dietary factors were considered as a possible determinant. Surveys of 492 residents over 20 years of age in Kuri city were conducted during 1998. The survey included a refractive error test adopting a autokerato-refractometer, dietary survey using a 24 hour recall method, disease survey including blood and other diagnosis tests, and a health behavior survey using questionnaires with variables of smoking, drinking, and exercise. A stepwise logistic regression analysis was adopted to analyse the relative importance among independent variables of health behaviors, disease, and dietary factors on ametropias. As a result, in the case of myopia, liver dysfunction appeared to be the most important factors followed by the health related behavior of smoking and exercise as the second most important factors. Nutrient factors such as carotene and protein appeared to be the third most important factors. Similar results had been shown in the case of the hyperopia. In summary, liver dysfunction and the health related behaviors of drinking and smoking appeared to be more influential factors on abnormal eye sight of myopia and hyperopia than dietary factors.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.22 no.6
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• pp.581-587
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• 2019

Arthrogryposis-renal dysfunction-cholestasis (ARC) syndrome is a rare autosomal recessive multisystemic disease that is associated with the liver, kidney, skin, and central nervous and musculoskeletal systems. ARC occurs as a result of mutations in the VPS33B (Vacuolar protein sorting 33 homolog B) or VIPAR (VPS33B interacting protein, apical-basolateral polarity regulator) genes. A female infant presented with neonatal cholestasis with a severe clinical outcome. She was diagnosed with ARC syndrome using targeted exome sequencing (TES). Exome sequencing revealed compound heterozygous mutations, c.707A>T and c.239+5G>A, in VPS33B, where c.707A>T was a novel variant; the resultant functional protein defects were predicted via in silico analysis. c.239+5G>A, a pathogenic mutation that affects splicing, is found in less than 0.1% of the general population. Invasive techniques, such as liver biopsies, did not contribute to a differential diagnosis of ARC syndrome; thus, early TES together with clinical presentations constituted an apparently accurate diagnostic procedure.

• BMB Reports
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• v.40 no.5
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• pp.814-824
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• 2007

Liver cirrhosis (LC) is defined as comprising diffuse fibrosis and regenerating nodules of the liver. The biochemical and anatomical dysfunction in LC results from both reduced liver cell number and portal vascular derangement. Although several studies have investigated dysregulated genes in cirrhotic nodules, little is known about the genes implicated in the pathophysiologic change of LC or about their relationship with the degree of decompensation. Here, we applied cDNA microarray analysis using 38 HBsAg-positive LC specimens to identify the genes dysregulated in HBV-associated LC and to evaluate their relation to disease severity. Among 1063 known cancer- and apoptosis-related genes, we identified 104 genes that were significantly up- (44) or down- (60) regulated in LC. Interestingly, this subset of 104 genes was characteristically correlated with the degree of decompensation, called the Pugh-Child classification (20 Pugh-Child A, 10 Pugh-Child B, and 8 Pugh-Child C). Patient samples from Pugh-Child C exhibited a distinct pattern of gene expression relative to those of Pugh-Child A and B. Especially in Pugh-Child C, genes encoding hepatic proteins and metabolizing enzymes were significantly down-regulated, while genes encoding various molecules related to cell replication were up-regulated. Our results suggest that subsets of genes in liver cells correspond to the pathophysiologic change of LC according to disease severity and possibly to hepatocarcinogenesis.

• Advances in Traditional Medicine
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• v.7 no.3
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• pp.311-320
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• 2007

The present study was designed to estimate the protective effect of (-) epigallocatechin gallate (EGCG) on ethanol-induced liver injury in rats. Chronic ethanol administration (6 g/kg/day ${\times}$ 60 days) caused liver damage that was manifested by the elevation of markers of liver dysfunction - aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, bilirubin and ${\gamma}$-glutamyl transferase in plasma and reduction in liver glycogen. The activities of alcohol metabolizing enzymes such as alcohol dehydrogenase and aldehyde dehydrogenase were found to be altered in alcohol-treated group. Ethanol administration resulted in the induction of cytochrome p450 and cytochrome-$b_{5}$ activities and reduction of cytochrome-c reductase and glutathione-S-transferase, a phase II drug metabolizing enzyme. Further, ethanol reduced the viability of isolated hepatocytes (ex vivo) as assessed by trypan blue exclusion test and induced hepatocyte apoptosis as assessed by propidium iodide staining. Treatment of alcoholic rats with EGCG restored the levels of markers of liver injury and mitigated the alterations in alcohol metabolizing and drug metabolizing enzymes and cyt-c-reductase. Increased hepatocyte viability and reduced apoptotic nuclei were observed in alcohol + EGCG-treated rats. These findings suggest that EGCG acts as a hepatoprotective agent against alcoholic liver injury.

• Journal of Ginseng Research
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• v.43 no.4
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• pp.606-617
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• 2019

Background: The Panax ginseng berry extract (GBE) is well known to have an antidiabetic effect. The aim of this study is to evaluate and investigate the protective effect of ultrasonication-processed P. ginseng berry extract (UGBE) compared with GBE on liver fibrosis induced by mild bile duct ligation (MBDL) model in rats. After ultrasonication process, the composition ratio of ginsenoside in GBE was changed. The component ratio of ginsenosides Rh1, Rh4, Rg2, Rg3, Rk1, Rk3, and F4 in the extract was elevated. Methods: In this study, the protective effect of the newly developed UGBE was evaluated on hepatotoxicity and neuronal damage in MBDL model. Silymarin (150 mg/kg) was used for positive control. UGBE (100 mg/kg, 250 mg/kg, 500 mg/kg), GBE (250 mg/kg), and silymarin (150 mg/kg) were orally administered for 6 weeks after MBDL surgery. Results: The MBDL surgery induced severe hepatotoxicity that leads to liver inflammation in rats. Also, the serum ammonia level was increased by MBDL surgery. However, the liver dysfunction of MBDL surgery-operated rats was attenuated by UGBE treatment via myeloid differentiation factor 88-dependent Toll-like receptor 4 signaling pathways. Conclusion: UGBE has a protective effect on liver fibrosis induced by MBDL in rats through inhibition of the TLR4 signaling pathway in liver.

• Journal of Nutrition and Health
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• v.48 no.1
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• pp.1-8
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• 2015

Purpose: Anthocyanins from purple sweet potato (PSP) have been investigated in vitro and in animals and found to have a protective effect against oxidative hepatic damage. In this study, we investigated that aqueous extract of PSP can ameliorate the dysfunction of lipid metabolism in mice fed a high fat/cholesterol diet. Methods: Forty C57BL/6J mice were randomly divided into 5 groups (n = 8) and fed one of the following diets for 8 weeks; normal fat (NF) diet; high fat/cholesterol (HFC) diet; HFC with 1.25% PSP (HFPL) diet; HFC with 2.5% PSP (HFPM) diet; HFC with 5% PSP (HFPH) diet. Results: Non-alcoholic fatty liver was manifested in the HFC group by showing increased levels in plasma alanine aminotransferase (ALT) activity, total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C), increased level of TC and presence of many large lipid droplets in the liver, and increased fat cell size in the HFC group compared with the NF group. However, administration of HFC induced a significant decrease in food intake, resulting in decrease in fat mass. Co-administration of PSP did not lead to reversal of body weight changes, ALT activity, and lipid levels in plasma and the liver, but suppressed excess enlargement of the fat cell size through increasing carnitine palmitoyltransferase-1 (CPT-1) gene expression in the liver. Accordingly, the number of fat droplets in the liver was reduced in PSP administered groups. Conclusion: Taken together, these results suggest that PSP may have a protective effect on the dysfunction of lipid metabolism. Conduct of further studies on the coordinated regulation of PSP for lipid metabolic homeostasis at the liver-adipose tissue axis is needed.

• Biomolecules & Therapeutics
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• v.27 no.2
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• pp.222-230
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• 2019

Intestinal barrier dysfunction always accompanies cirrhosis in patients with advanced liver disease and is an important contributor facilitating bacterial translocation (BT), which has been involved in the pathogenesis of cirrhosis and its complications. Several studies have demonstrated the protective effect of Vitamin D on intestinal barrier function. However, severe cholestasis leads to vitamin D depletion. This study was designed to test whether vitamin D therapy improves intestinal dysfunction in cirrhosis. Rats were subcutaneously injected with 50% sterile $CCl_4$ (a mixture of pure $CCl_4$ and olive oil, 0.3 mL/100 g) twice a week for 6 weeks. Next, $1,25(OH)_2D_3$ ($0.5{\mu}g/100g$) and the vehicle were administered simultaneously with $CCl_4$ to compare the extent of intestinal histologic damage, tight junction protein expression, intestinal barrier function, BT, intestinal proliferation, apoptosis, and enterocyte turnover. Intestinal heme oxygenase-1 (HO-1) expression and oxidative stress were also assessed. We found that vitamin D could maintain intestinal epithelial proliferation and turnover, inhibit intestinal epithelial apoptosis, alleviate structural damage, and prevent BT and intestinal barrier dysfunction. These were achieved partly through restoration of HO-1 and inhibition of oxidative stress. Taken together, our results suggest that vitamin D ameliorated intestinal epithelial turnover and improved the integrity and function of intestinal barrier in $CCl_4$-induced liver cirrhotic rats. HO-1 signaling activation was involved in these above beneficial effects.

• Journal of Preventive Medicine and Public Health
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• v.30 no.1 s.56
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• pp.103-128
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• 1997

The object of this study is to evaluate the possibility of chemical-induced liver disorder among workers exposed to various chemicals and to classify the the liver function abnormalities by causes and to analyse the risk factors for each liver disorders. A cross-sectional study including questionnaire survey, physical examination, laboratory tests and ultrasonography of liver was conducted on 1,126 workers, 459 workers in a coal chemical plant(company A) and 667 workers in an insulation material manufacturing factory(company B). An industrial hygienist reviewed the chemicals used in both companies and evaluated the work environments to classify the workers by chemical exposure semiquantitatively. The results are as follows: 1. Of 459 workers in company A, 83 workers(18.1%) are classified as nonexposed, group 163(35,5%) as short-term exposure group, 155(33.8%) as intermediately exposed group and 58(12.6%) as long-term exposed group bared on the mean daily exposure to hepatotoxic chemicals evaluated by an industrial hygienist. Of 667 workers in company B, 484(72.6%) workers were classified as nonexposed and 183(35.5%) as exposed group. 2. Workers with SGOT level higher than 40 IU/l were (10.0%) in company A and 77(11.5%) in company 3, and those with SGPT level higher than 35 IU/l were 118(25.7%) in company A and 198(29.7%) in company B. The differences were not significant between companies and between exposure groups(p>0.05). Workers with $\gamma-GT$ level higher than 62 IU/l were 29(6.3%) in company A and 77(11.5%) in company B (p<0.01). The difference between exposure groups was not significant(p>0.05) within companies. Workers with liver function abnormalities(defined as SGOT higher than 40 IU/l or SGPT higher than 35 IU/l) were 338(30.0%) among 1,126 workers. Of 338 workers with live. function abnormalities 139(12.3%) had fatty liver by ultrasonography, 79(7.0%) had alcoholic liver(defined as workers with liver function abnormalities with weekly alcohol consumption greater than 280 g for more than 5 years), 54(4.8%) had hepatitis B, 12(1.1%) had hepatitis C and the other 114(33.7%) was not otherwise classified. Prevalences of alcoholic liver and fatty liver were significantly lower in company A(prevalence ratio 0.24 for alcoholic liver, p<0.001, prevalence ratio 0.76 for fatty liver, p<0.05) but prevalences of liver disorders between exposure groups within companies were not significant(p>0.05). 3. Summary prevalence ratios(SPR) of live. function abnormalities, fatty live. and other liver disorders, adjusted by age and company were not significantly higher in exposed group in any chemicals(p>0.05) but in some chemicals, SPRs were significantly lower. 4. On simple analysis of risk factors for liver function abnormalities, prevalence odds ratio(POR) of those with age between 30 and 39 was 1.54(p<0.01) and those with age ever 40 was 1.51(p<0.01). POR of those with histories of liver disorders and general anesthesia was 1.77(p<0.001) and 4.02 for those with overweight and 6.23 for those with obesity, defined by body mass index(p<0.001). 5. On logistic regression analysis, risk factors of liver function abnormality were fatty liver(POR 2.92 for grade 1, 12.15 for grade 2), presence of hepatitis B surface antigen(POR 3.62) and obesity(POR 5.38 for overweight and 16.52 for obesity). Presence of hepatitis B surface antigen(POR 0.18) was the only preventive facto. of fatty live. Company(POR 0.30) and obesity(POR 2.49 for overweight, 4.52 for obesity) were related to the alcoholic live. Obesity(POR 2.94 for overweight) was the only significant risk factor of hepatitis B and there was no significant risk factor for liver function abnormality not otherwise classified. It is concluded that the evidence of liver disorder related with chemical exposure is not evident in these factories. It is also postulated that fatty liver and alcoholic liver is most common causes of liver function abnormalities among workers and effort for weight control and improvement of life style should be done.

• Biomedical Science Letters
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• v.16 no.3
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• pp.139-149
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• 2010

The present study was carried out to elucidate whether an environmental strain of Cryptococcus neoformans (environmental C. neoformans) isolated from an environmental source in a park of Busan has an acute pathophysiological effect in rats. On the second day after peritoneal inoculation of environmental C. neoformans, adverse effects occurred from the viewpoint of hematology and biochemistry. Eosinophil damages and crystal formations were found in the blood. Disturbances in cytokines production were observed in the cerebral and pulmonary tissues. Fungal budding existed in the brain, lung, liver and kidney. Tissue injury findings such as inflammation, leukocyte infiltration, bleeding, or degeneration were found in the brain, lung, liver and kidney. The present data suggest that the environmental C. neoformans can cause systematically harmful effects even for short periods of infection (two days of cryptococcal infection) and the adverse effects are summarized as immune derangements and biochemical and/or histological dysfunction and injury on major organ such as the brain, lung, liver and kidney in the immunocompetent hosts. Further studies should be focused on comparing the differences between environmental and clinical strains of C. neoformans.