O Antigens ; immunology ; Serotyping ; Shigella flexneri ; immunology

BACKGROUND: The purpose of this study is to prove that human infection of Yersinia pseudotuberculosis might be occurred by drinking of mountain spring water contaminated with wild mice excreta through epidemiological tool. METHOD: Y. pseudotuberculosis strains which were isolated from patient stools, mountain spring water and mice excreta were analysed by serotyping of O antigen and plasmid DNA profile (Restriction Endonuclease Analysis of Plasmic DNA analysis REAP) assay Also reservoir rate of Y. pseudotuberculosis was calculated from wild mice which were captured throughout Korean mountains. RESULTS: Reservoir rate of Y. pseudotuberculosis from wild mice in Korea was 0.85% and was not higher than that in other country. The analysis of 66 strains of Y. pseudotuberculosis showed that 36 strains of serotype 15, REAP B type, 24 strains of serotype 4b, REAP D type, and 1 strain of serotype 4b, REAP new unclassifiable type, but 5 strains didn't have plasmic (serotype 15:3, 11 :2) .Especially same 4b, D type of Y. pseudotuberculosis was isolated from patient stools, mountain spring water and wild mouse (Apodemus agrarius) excretion and this fact was considered that Y. pseudotuberculosis strains from 3 groups were closely correlated epidemiologically. Also serotype 15, REAP B strains were isolated from patient stools and mountain spring water, but were not isolated from wild mice yet and 15, B type was isolated from Korea only and considered as native Korean strain which had not isolated in other countries yet. CONCLUSIONS: Human Y. pseudotuberculosis infection in Korea was occurred by drinking of contaminated mountain spring water and A. agrarius was one of main reservoir which contaminates mountain spring waters in Korea, Also above antigenic distribution of Y. pseudotuberculosis would be useful for development of ELISA kit of Korean type.
Animals ; DNA ; Drinking ; Enzyme-Linked Immunosorbent Assay ; Humans ; Korea ; Mice ; O Antigens ; Plasmids ; Serotyping ; Yersinia pseudotuberculosis* ; Yersinia*

In Korea, all domestic made test systems for detecting antibodies in HIV-1 contain the antigens from human immunodeficiency type 1 (HIV-1) subtype B. However, because HIV-1 subtype O is significantly different in amino acid sequences from all other subtypes of HIV-1, there has been a need for developing a test for detecting antibodies in subtype O. For this purpose, the entire nucleotide sequence corresponding to the extracellular domain of the transmembrane glycoprotein of HIV-1 subtype O was synthesized with consideration of Escherichia coli cordon usage. Various regions of the extracellular domain were cloned into E. coli expression vectors and tested for levels of protein production. The nucleotide sequence, named ECTM, that can encode a 129 amino acid-long peptide, was found to be expressed at a high level in E. coli. The protein of approximately 17 kDa specifically reacted with sera from individuals infected with HIV-1 subtype O. The ECTM protein was purified to near homogeneity by the CM-T gel chromatography, using concentrated, denatured inclusion bodies. In Western blot analysis, the purified viral antigen reacted with sera from individuals infected with subtype O more efficiently than subtype B. The enzyme linked immunoabsorbent assay (ELISA) system was developed using the subtype O viral protein and compared with the commercially available kit lacking the antigens from subtype O. The ELISA kit containing the subtype O antigen ECTM alone efficiently reacted with sera from individuals infected with subtype O. The subtype O antigen-containing kit produced a positive absorbence even when sera were diluted 512-fold, suggesting a high sensitivity. The commercially available kit also reacted with subtype O sera, but produced a negative result at a dilution of 8-fold. Our results suggest that the currently available kit may not be able to efficiently detect subtype O sera and that the viral protein developed in this study may be added to the current system to maximize the detection of sera from individuals infected with subtype O.
Amino Acid Sequence ; Antibodies ; Base Sequence ; Blotting, Western ; Chromatography, Gel ; Clone Cells ; Enzyme-Linked Immunosorbent Assay ; Escherichia coli ; Glycoproteins ; HIV* ; HIV-1* ; Humans* ; Inclusion Bodies ; Korea ; O Antigens

This study was conducted to determine if humoral antibody response of foot-and-mouth disease (FMD) vaccine improved in 8-week-old growing pigs born to well-vaccinated sows pre-treated with 60 mg of poly-γ-glutamic acid (γ-PGA) three days before vaccination. Antibody against FMD virus serotype O was measured 0, 2, 4 and 6 weeks post-vaccination, using a PrioCHECK FMDV type O ELISA kit. The results showed that positive antibody reactions against FMDV serotype O antigen among a component of the vaccine significantly increased in response to pre-injection with γ-PGA.
Animals ; Antibody Formation* ; Enzyme-Linked Immunosorbent Assay ; Foot-and-Mouth Disease Virus* ; Foot-and-Mouth Disease* ; Immunity, Humoral ; O Antigens ; Serogroup ; Swine* ; Vaccination

BACKGROUND: During the past 10 years, there has been an increased incidence of gastrointestinal infections caused by salmonellae in Korea. In 1999, there were several outbreaks and sporadic occurrences of food borne infections due to Salmonella enterica serotype Enteritidis in Gwangju. Thus, there is a need for careful monitoring of its occurrence. METHODS: Salmonella Enteritidis were isolated from feces samples of patients with foodborne diarrhea in Gwangju, 1999. We performed antigen typing, examination of biochemical properties, anibiotic susceptibility test, plasmid typing and RAPD analysis to characterize of S. Enteritidis isolates. RESULTS: There were three Salmonella outbreaks (April, July, October), and 203 isolates of S. Enteritidis were isolated from the 286 patients. Eighteen isolates were obtained from the patients of sporadic occurrences. Antigenic types of the isolates were O antigen; D1 (1, 9, 12), H antigen phase 1; (g, m), serotype; Enteritidis. The isolates were susceptible to most of the antibiotics. We performed plasmid DNA analysis of the isolates, and the results showed 3 plasmids (8, 6, 3.8 kb) in 14 of 14 strains from outbreaks; 3 plasmids (8, 6, 3.8 kb) in 2 isolates from sporadic cases; 4 plasmids (8, 6, 3.8, 2 kb) in 10 isolates from sporadic occurrences, and 2 isolates from food specimens. However, 1 isolate from patients and 2 isolates from Ham-Yang, Kyung Nam, did not contain plasmids. RAPD analysis showed that all isolates from Gwangju in 1999 showed relatively uniform characteristics which were different from those derived from Ham-Yang, Kyung-Nam. CONCLUSION: The present data demonstrated that most food poisoning cases by S. Enteritidis in Gwangju, 1999, were originated from the same Salmonella Enteritidis strains.
Anti-Bacterial Agents ; Diarrhea ; Disease Outbreaks* ; DNA* ; Epidemiologic Studies* ; Feces ; Foodborne Diseases ; Gwangju* ; Humans ; Incidence ; Korea ; O Antigens ; Plasmids* ; Salmonella enterica* ; Salmonella enteritidis ; Salmonella*

BACKGROUND: During the past 10 years, there has been an increased incidence of gastrointestinal infections caused by salmonellae in Korea. In 1999, there were several outbreaks and sporadic occurrences of food borne infections due to Salmonella enterica serotype Enteritidis in Gwangju. Thus, there is a need for careful monitoring of its occurrence. METHODS: Salmonella Enteritidis were isolated from feces samples of patients with foodborne diarrhea in Gwangju, 1999. We performed antigen typing, examination of biochemical properties, anibiotic susceptibility test, plasmid typing and RAPD analysis to characterize of S. Enteritidis isolates. RESULTS: There were three Salmonella outbreaks (April, July, October), and 203 isolates of S. Enteritidis were isolated from the 286 patients. Eighteen isolates were obtained from the patients of sporadic occurrences. Antigenic types of the isolates were O antigen; D1 (1, 9, 12), H antigen phase 1; (g, m), serotype; Enteritidis. The isolates were susceptible to most of the antibiotics. We performed plasmid DNA analysis of the isolates, and the results showed 3 plasmids (8, 6, 3.8 kb) in 14 of 14 strains from outbreaks; 3 plasmids (8, 6, 3.8 kb) in 2 isolates from sporadic cases; 4 plasmids (8, 6, 3.8, 2 kb) in 10 isolates from sporadic occurrences, and 2 isolates from food specimens. However, 1 isolate from patients and 2 isolates from Ham-Yang, Kyung Nam, did not contain plasmids. RAPD analysis showed that all isolates from Gwangju in 1999 showed relatively uniform characteristics which were different from those derived from Ham-Yang, Kyung-Nam. CONCLUSION: The present data demonstrated that most food poisoning cases by S. Enteritidis in Gwangju, 1999, were originated from the same Salmonella Enteritidis strains.
Anti-Bacterial Agents ; Diarrhea ; Disease Outbreaks* ; DNA* ; Epidemiologic Studies* ; Feces ; Foodborne Diseases ; Gwangju* ; Humans ; Incidence ; Korea ; O Antigens ; Plasmids* ; Salmonella enterica* ; Salmonella enteritidis ; Salmonella*

Escherichia coli (E. coli) O157:H7 is an important cause of hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS). LPS-based vaccines need improvement since the anti-LPS antibodies raised by the vaccines are bactericidal and release toxin that may precipitate the development of HUS. Despite huge efforts, the treatment of infection with E. coli O157 has been difficult because antibiotics do not change the course of the enteritis caused by E. coli O157 and may increase the incidence of HUS through the release of Shiga-like toxin (Stx)-I. For this aim we tried the conjugate of E. coli O157 OSP bound to the nontoxic B subunit of Stx-I B as a vaccine that can induce both serum IgG anti-LPS antibody with bactericidal activity and neutralizing antibody to Stx-I. Mice were immunized s.c. with OSP-Stx-I B conjugate. Anti-sera were analyzed for the anti-LPS antibody, anti-Stx-I B antibody, complement-dependent bactericidal activity, and Stx-I neutralization activity. Mice injected with the bivalent conjugate elicited both bactericidal antibodies to E. coli O157 and neutralization antibodies to Stx-1. We also analyzed the distributional, functional changes of T lymphocytes in vitro and in vivo. After the injection of Stx-I, splenocytes showed a decrease in proliferation when stimulated with phytohemagglutinin (PHA) or LPS, and the number of CD4+ and CD8+ T cells also decreased. Interleukin (IL)-2, IL-4 and IFN-gamma productions by CD3+ T cells were slightly increased in the Stx-I injected mice.
Animals ; Anti-Bacterial Agents ; Antibodies ; Antibodies, Neutralizing ; Colitis ; Enteritis ; Escherichia coli O157* ; Escherichia coli* ; Escherichia* ; Hemolytic-Uremic Syndrome ; Immunoglobulin G ; Immunotoxins* ; Incidence ; Interleukin-4 ; Interleukins ; Mice ; O Antigens ; T-Lymphocytes ; Vaccines*

OBJECTIVETo study the changes of serum neuron specific enolase in rats with septic shock.

METHODSThe model of septic shock was set up by injection of lipopolysaccharide (LPS, from Escherichia coil O55: B5) at a dose of 25 mg/kg through femoral vein. Twenty male Wistar rats were randomly divided into 2 groups: normal control group (LPS was substituted by same volume of normal saline solution) and septic shock group. Six hours after the septic shock model formed, whole blood was taken for measuring the serum neuron specific enolase (NSE). The brains of the rats were taken for histopathological examination.

RESULTSThe serum NSE of septic shock group was significantly higher than that of control group [(10.0781 +/- 0.526) microg/L vs. (3.7188 +/- 0.602) microg/L, P < 0.05]. Neurons were severely damaged 6 hours after injection of LPS. Neuronal necrosis and the damage of blood-brain barrier were seen by light and electron microscope in septic shock group but not in the control group.

CONCLUSIONNSE in serum increased when septic encephalopathy occurred, which indicated that NSE might become a marker of neural damage in septic shock.

Animals ; Biomarkers ; blood ; Blood Pressure ; Blood-Brain Barrier ; ultrastructure ; Brain ; cytology ; pathology ; Cell Death ; Disease Models, Animal ; Male ; Microscopy, Electron ; Neurons ; pathology ; ultrastructure ; O Antigens ; toxicity ; Phosphopyruvate Hydratase ; blood ; Rats ; Rats, Inbred BB ; Shock, Septic ; blood ; enzymology ; pathology

OBJECTIVETo study the effect of Jinlida on changes in expression of skeletal muscle lipid transport enzymes in fat-induced insulin resistance ApoE -/- mice.

METHODEight male C57BL/6J mice were selected in the normal group (NF), 40 male ApoE -/- mice were fed for 16 weeks, divided into the model group (HF), the rosiglitazone group ( LGLT), the Jinlida low-dose group (JLDL), the Jinlida medium-dose group (JLDM), the Jinlida high-dose group (JLDH) and then orally given drugs for 8 weeks. The organization free fatty acids, BCA protein concentration determination methods were used to determine the skeletal muscle FFA content. The Real-time fluorescent quantitative reverse transcription PCR ( RT-PCR) and Western blot method were adopted to determine mRNA and protein expressions of mice fatty acids transposition enzyme (FAT/CD36), carnitine palm acyltransferase 1 (CPT1), peroxide proliferators-activated receptor α( PPAR α).

RESULTJinlida could decrease fasting blood glucose (FBG), cholesterol (TC), triglyceride (TG), free fatty acid (FFA) and fasting insulin (FIns) and raise insulin sensitive index (ISI) in mice to varying degrees. It could also up-regulate mRNA and protein expressions of CPT1 and PPARα, and down-regulate mRNA and protein levels of FAT/CD36.

CONCLUSIONJinlida can improve fat-induced insulin resistance ApoE -/- in mice by adjusting the changes in expression of skeletal muscle lipid transport enzymes.

Animals ; Apolipoproteins E ; deficiency ; genetics ; Blood Glucose ; metabolism ; CD36 Antigens ; genetics ; metabolism ; Carnitine O-Palmitoyltransferase ; genetics ; metabolism ; Dietary Fats ; adverse effects ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Hypoglycemic Agents ; administration & dosage ; Insulin ; metabolism ; Insulin Resistance ; Lipid Metabolism ; drug effects ; Male ; Metabolic Diseases ; drug therapy ; enzymology ; genetics ; metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Skeletal ; drug effects ; metabolism

The aim of this study is to establish a simple and stable model like poloxamer 407 (P-407)-induced dyslipidemia of golden hamster model, and investigate the mechanism of lipid metabolism disturbance in this model. PPARalpha agonist and HMG-CoA reductase inhibitor were administrated to validate the efficacy on regulating lipid metabolism in the dyslipidemia golden hamster model. Six weeks male golden hamsters were chosen to inject P-407 intraperitoneally at a bolus dose of 300 mg x kg(-1), an intermittent injection at a dose of 200 mg x kg(-1) every 72 hours after the bolus. The results showed that P-407-induced golden hamster model characterized as increased serum triglyceride (TG), total cholesterol (TC), free cholesterol (free-CHO), cholesteryl ester (CE), free fatty acids (FFA) and apoB levels, and the hyperlipidemia state maintained at a stable level persistently. Meanwhile, augmented malondialdehyde (MDA) and nitric oxide (NO) level was observed. LCAT and SR-B I mRNA levels in liver of model group were down-regulated (expression ratio is 0.426; 0.783), while HMG-CoA reductase mRNA level was up-regulated (expression ratio is 1.493) compared with those of the normal group. The serum cholesterol and triglyceride levels were significantly lower in P-407-induced dyslipidemia hamster model after treated with atorvastatin (Ato) at a dose of 50 mg x kg(1) or fenofibrate (Fen) at 100 mg x kg(-1) for two weeks. These findings suggest that serum lipid distribution in dyslipidemia golden hamster is similar to that of human, and which may be relevant to the disturbance of the enzymes expression involved in lipid metabolism in liver. Results obtained from this study support the concept that dyslipidemia golden hamster may be an adequate animal model to evaluate the efficacy of lipid-lowering agents.
Animals ; Anticholesteremic Agents ; pharmacology ; Atorvastatin Calcium ; CD36 Antigens ; genetics ; metabolism ; Cricetinae ; Disease Models, Animal ; Dyslipidemias ; chemically induced ; metabolism ; Fenofibrate ; pharmacology ; Heptanoic Acids ; pharmacology ; Hydroxymethylglutaryl CoA Reductases ; genetics ; metabolism ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; pharmacology ; Hypolipidemic Agents ; pharmacology ; Lipid Metabolism ; Liver ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mesocricetus ; Nitric Oxide ; metabolism ; PPAR alpha ; agonists ; Phosphatidylcholine-Sterol O-Acyltransferase ; genetics ; metabolism ; Poloxamer ; Pyrroles ; pharmacology ; RNA, Messenger ; metabolism ; Superoxide Dismutase ; metabolism