• The Journal of Korean Medicine
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• v.27 no.2 s.66
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• pp.253-261
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• 2006

Backgrounds : Hyperlipidemia is a major cause of cardiovascular disease (CVD). Lowering serum cholesterol levels could reduce the risk of CVD. Insamsansa-eum (Renshenshanzha-yin, ISE), composed of Ginseng Radix and Crataegii Fructus, is a new medicine developed to treat hyperlipidemia and CVD. Objectives : In this study, we intended to explore the clinical effects of ISE on patients with hypercholesterolemia, and moreover we also compared its effects according to the pattern identification. Methods : Subjects were administered ISE with the dose of 600 mg three times a day for 4 weeks. Patterns of subjects were identified with diagnostic scoring system for Yin-Yang and the condition of Excess-Deficiency before treatment. Serum lipids were measured at baseline and after 4 weeks of medication. Results : ISE lowered total cholesterol(TC), triglyceride(TG), total lipid(TL), phospholipid(PL) and low density lipoprotein cholesterol(LDL) significantly. Compared with the data of our previous study, it was less effective than Atorvastatin but showed equal lipids-lowering effect to Chunghyul-dan (Qingxue-dan, CHD). In Yang pattern group, ISE was less effective in lowering TG and LDL than it was in not-Yang-not-Yinpattern group. On safety assessment, there was no adverse effect, hepatic or renal toxicity. Conclusions : We suggest that ISE is a safe and useful herbal medicine for hypercholesterolemia, and moreover it could be more useful when it is used for patients with not Yang pattern.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.3
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• pp.117-127
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• 2004

The heterodimeric amino acid transporter family is a subfamily of SLC7 solute transporter family which includes 14-transmembrane cationic amino acid transporters and 12-transmembrane heterodimeric amino acid transporters. The members of heterodimeric amino acid transporter family are linked via a disulfide bond to single membrane spanning glycoproteins such as 4F2hc (4F2 heavy chain) and rBAT $(related\;to\;b^0,\;^+-amino\;acid\;transporter)$. Six members are associated with 4F2hc and one is linked to rBAT. Two additional members were identified as ones associated with unknown heavy chains. The members of heterodimeric amino acid transporter family exhibit diverse substrate selectivity and are expressed in variety of tissues. They play variety of physiological roles including epithelial transport of amino acids as well as the roles to provide cells in general with amino acids for cellular nutrition. The dysfunction or hyperfunction of the members of the heterodimeric amino acid transporter family are involved in some diseases and pathologic conditions. The genetic defects of the renal and intestinal transporters $b^{0,+}AT/BAT1\;(b^{0,+}-type\;amino\;acid\;transporter/b^{0,+}-type\;amino\;acid\;transporter\;1)$ and $y^+LAT1\;(y^+L-type\;amino\;acid\;transporter\;1)$ result in the amino aciduria with sever clinical symptoms such as cystinuria and lysin uric protein intolerance, respectively. LAT1 is proposed to be involved in the progression of malignant tumor. xCT (x-C-type transporter) functions to protect cells against oxidative stress, while its over-function may be damaging neurons leading to the exacerbation of brain damage after brain ischemia. Because of broad substrate selectivity, system L transporters such as LAT1 transport amino acid-related compounds including L-Dopa and function as a drug transporter. System L also interacts with some environmental toxins with amino acid-related structure such as cysteine-conjugated methylmercury. Therefore, these transporter would be candidates for drug targets based on new therapeutic strategies.

• Journal of Veterinary Clinics
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• v.18 no.2
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• pp.116-123
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• 2001

This study was undertaken to find out the effect of Korean safflower seed powder on histopathological changes of cadmium toxicity in mice. Fifty BALB/c mice were divided into a control group(A) and four experimental groups(B, C, D, E) : group A received tap water and basal diet, group B received tap water and diet supplemented with 3% Korean safflower seed powder alone, group C received basal diet and 300 $\mu\textrm{g}$/g of cadmium, group D and E received basal diet supplemented with 3% and 10% Korean safflower seed powder and 300$\mu\textrm{g}$/g of cadmium respectively. Cadmium dissolved in tap water was used, and the Korean safflower seed powder were mixed with feed. All mice were dissected on the 56th day. Histopathological changes in liver, kidney, lung, cortical osseous tissue of femoral shaft, bone trabecular of femur, and epiphyseal cartilage plate of femur were observed. Group B showed no significant changes compared with the control group. But group C showed the unclearness of specific cells in liver, the loss of architecture and focal necrosis of hepatocyte, the glomerular swelling, degeneration and necrosis of convoluted tubules, desquamation and vacuolization of the greater part of the renal tubular epithelium, the marked congestion and thickness of the wall of alveolus in lung, slightly thinning of the cortical osseous tissue in femoral shaft, reduction of cancellous bone volume and marked narrowness of bone trabecular, marked thinning of epiphyseal cartilage plate and irregular arrangement of columnar structure of cartilage cells. On the other hand, Korean safflower seed powder-treated group showed a little convalescent changes and maintained their normal architectures in liner, kidney, lung, cortical osseous tissue of femoral shaft, bone trabecular of femur and epiphyseal cartilage plate of femur.

• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.2
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• pp.71-77
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• 2015

Purpose: Acute endosulfan poisoning is rare but causes significant morbidity and mortality. The aim of our study is to describe complications and features of seizure and determine factors associated with mortality in acute endosulfan poisoning. Methods: Twenty-eight adult patients with acute endosulfan poisoning admitted to our emergency department during a 15-year period were studied retrospectively. The clinical features of seizure, use of antiepileptic drugs during seizure, and hospital courses were evaluated. Clinical factors between survived group and non-survived group were compared for identification of factors associated with mortality. Results: Of the 28 patients with endosulfan poisoning, 4 patients (14.3%) died and 15 (53.6%) patients developed generalized tonic-clonic seizure. Thirteen patients (46.4%) and 5 patients (17.9%) progressed to status epilepticus (SE) and refractory status epilepticus (RSE), respectively. SE and RSE were associated with mortality. Almost all significant complications including shock, acute renal failure, hepatic toxicity, rhabdomyolysis, and cardiac injury developed in SE and RSE patients. Conclusion: SE and RSE were important contributors to death in endosulfan poisoning. Emergency physicians treating endosulfan poisoning should make an effort not to progress seizure following endosulfan poisoning to SE and RSE using a rapid and aggressive antiepileptic drug.

• Journal of The Korean Society of Clinical Toxicology
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• v.10 no.2
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• pp.91-96
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• 2012

Purpose: A retrospective study with a literature review was conducted to identify the clinical characteristics and prognosis after the acute ingestion of glacial acetic acid. Methods: The medical records of 20 patients,who had presented to the emergency department of Ajou University Hospital complaining of the acute ingestion of glacial acetic acid between January 2006 and December 2011, were examined retrospectively. Results: Among the 172 patients admitted for caustics injury, 20 patients ingested glacial acetic acid. The mean age of the patients was $55{\pm}23.5$, and the mean volume of the acid was $84.5{\pm}71.3$ ml. The clinical features included 1) oral ulcers in 12 patients (63.2%), 2) respiratory difficulties in 11 patients (57.9%), 3) oliguria in 8 patients (42.1%), 4) renal toxicity in 7 patients (36.8%), 5) hepatic failure in 7 patients (36.8%), 6) disseminated intravascular boagulopathyin 7 patients (36.8%), 7) low blood pressure in 8 patients (42.1%), and 8) mental changes in 9 patients (47.4%). Ten patients required endotracheal intubation. Nine patients were admitted to the intensive care unit, and 5 patients expired. Conclusion: The ingestion of glacial acetic acid can cause severe symptoms, such as metabolic acidosis, multiple organ failure and upper airway swelling frequently and has a high mortality rate. Therefore, aggressive treatment, including endotracheal intubation, should be considered at the early stages.

• The Journal of Internal Korean Medicine
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• v.37 no.3
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• pp.467-483
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• 2016

Objective: This study was performed to investigate the effect of IUS (Inulsan, an extract of Artemisiae capillaris (茵蔯), Curcumae longae (鬱金), and Crataegi fructus (山査)) on anti-hyperlipidemia, anti-oxidation, and anti-inflammation.Method: We administered water extracts of Artemisiae capillaris, Curcumae longae, and Crataegi fructus for three weeks to db/db mice (C57BL/Ks), animal models induced with type 2 diabetes mellitus. Mice were divided into three groups: normal (C57BL/6J mice group), control group (db/db mice without administration of IUS) and IUS group (db/db mice treated with IUS). Then we measured total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride in the serum after the oral administration of IUS.Results: 1. IUS did not show any cytotoxicity in RAW 264.7 cells. 2. IUS decreased AST, ALP, and creatinine levelsand did not show any liver or renal toxicity in the db/db mice. 3. IUS increased DPPH and ABTS radical scavenging activity and decreased ROS production in RAW 264.7 cells. 4. IUS significantly decreased IL-1β, IL-6, and TNF-α production in RAW 264.7 cells. 5. IUS increased HDL cholesterol and significantly decreased total cholesterol and triglyceride in db/db mice. 6. IUS significantly decreased the atherogenic index and cardiac risk factor. 7. In contrast with the control group, fat infiltration in the liver and aorta decreased in IUS treated mice. The cell nucleus was located in the central area in H&E staining of liver. And endomembranes also were more thinner than the control group in H&E staining of aorta.Conclusions: These results suggest that IUS might be effective in the prevention and treatment of dyslipidemia.

• Toxicological Research
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• v.20 no.3
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• pp.233-239
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• 2004

The present study was designed to determine the impact of mercury on endotoxin-induced inflammatory cytokine expression and corresponding signal transduction in mouse kidney. Male BALB/c mice were exposed continuously to 0, 0.3, 1.5, 7.5, or 37.5 ppm of mercury in drink-ing water for 14 days and at the end of the treatment period, lipopolysaccharide (LPS, 0.5 mg/kg) was injected intraperitoneally 2 h prior to euthanasia. The doses of mercury and LPS did not cause hepatotoxicity or renal toxicity as indicated by unaltered plasma alanine aminotransferase and aspartate aminotransferase levels, and terminal UTP nucleotide end-labeling assay from kidney, respectively. Mercury decreased kidney glutathione (GSH) and with LPS, it additively decreased GSH. Mercury activated p38 mitogen-activated protein kinase (MAPK) and additively increased LPS-induced p38 MAPK phosphorylation. In contrast, mercury inhibited LPS-induced activation of extra-cellular signal-regulated kinase (ERK) but had no effect alone. Mercury increased the gene expression of tumor necrosis factor $\alpha$ (TN F$\alpha$) and potentiated LPS-induced TNF$\alpha$ expression. Mercury did not affect LPS-induced interleukin-1$\beta$ (IL-1$\beta$) expression but decreased LPS-induced IL-6 expression. These results suggest that low levels of mercury might augment LPS-induced TNF$\alpha$ expression by altering GSH and p38 MAPK. Mercury modulates LPS-induced p38 and ERK activation, and downstream TNF$\alpha$ and IL-6 expression in kidney, respectively.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.15
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• pp.6595-6597
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• 2015

Objective: To investigate short- and long-term treatment effects and side reactions of lobaplatin plus 5-Fu combined and concurrent radiotherapy in treating patients with inoperable middle-advanced stage esophageal cancer. Methods: Sixty patients with middle-advanced stage esophageal squamous cell cancer were retrospectively analyzed. All patients were administered lobaplatin (50 mg intravenously) for 2 h on day 1, and 5-Fu ($500mg/m^2$) injected intravenously from day 1 to 5 for 1 cycle, in an interval of 21 days for totally 4 cycles. At the same time, late-course accelerated hyperfractionated three-dimensional conformal radiotherapy was performed. Patients were firstly treated with conventional fractionated irradiation (1.8 Gy/d, 5 times/week, a total of 23 treatments, and DT41.4 Gy), and then treated with accelerated hyperfractionated irradiation (1.5 Gy, 2 times/d, a total of 27 Gy in 9 days, an entire course of 6-7 weeks, and DT 68.4Gy). Results: All patients completed treatment, including 10 complete response (CR), 41 partial response (PR), 7 stable disease (SD), and 2 progressive disease (PD). The total effective rate was 85.0% (51/60). Thirty-nine patients had an increased KPS score. One-, 2-, and 3-year survival rates were 85.3%, 57.5%, and 41.7%, respectively. The median survival time was 27 months. The adverse reactions included myelosuppression, which was mainly degree I and II. The occurrence rate of radiation esophagitis was 17.5%. No significant hepatic or renal toxicity was observed. Conclusion: Lobaplatin plus 5-Fu combined with concurrent radiotherapy is safe and effective in treating patients with middle-advanced stage esophageal cancer. However, this result warrants further evaluation by randomized clinical studies.

• Korean Journal of Environmental Biology
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• v.22 no.1
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• pp.133-140
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• 2004

The histopathologieal effects of his(tri-n-butyltin)oxide (TBTO) on the flounder, Paralichthys otivaceus were examined by means of histological methods. The experimental fishes were exposed to 0.17, 0.36, 0.60, 3.20, 6.30, 12.50 ${\mu}g \;L^{-1}$TBTO concentrations for 42 days. Histopathological change of the fish exposed to TBTO is dependent on the exposure duration and concentration. In the lower concentrations early histological changes included activated mucous cells and chloride cells, capillary hyperemia and epithelial hyperplasia in the gill; hepatocyte activation, degeneration of bile duct and pancyeatic zymogen reduction in the hepatopancreas; and capillary hyperemia, appearance of eosinophilic cell and melano-macrophagocytes in the kidney. At the higher concentrations histological changes of dysfunctionality included epithelial lifting and deformation of the lamellae in the gill; pycnosis and cytoplasmic degeneration of hepatocyte; pycnosis of haemopoietic cell and deformation of renal tubules and glomerulus in the kidney. It is indicated that TBTO induced histopathological changes in the fish as other aquatic pollutants.

• Journal of Yeungnam Medical Science
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• v.28 no.1
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• pp.60-69
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• 2011

Due to its efficacy and tolerability, low dose oral methotrexate (MTX) therapy has been widely used for treatment of rheumatoid arthritis (RA). However, it can rarely cause serious, life-threatening hematologic toxicities, such as pancytopenia. We report here on two patients with chronic kidney disease (CKD), who developed severe pancytopenia after 5 years (cumulative dose 1,240 mg) and 4 years (cumulative dose 1,320 mg) of low dose MTX therapy for treatment of RA, respectively. Both patients presented with renal insufficiency, hypoalbuminemia, concurrent use of nonsteroidal anti-inflammatory drugs, and elevated mean corpuscular volume of red blood cells (RECs), all of which are known as risk factors of MTX-induced pancytopenia. Despite receiving treatment, which included REC and platelet transfusions, antibiotic therapy, granulocyte colony stimulating factor, and leucovorin rescue, one patient died of sepsis. Based on our case study, prompt investigation of risk factors associated with MTX toxicity is required for all patients receiving MTX therapy. MTX treatment, even at a low dose, should be discontinued in patients with advanced CKD.