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A growing body of literature has documented that job stress is associated with the development of cardiovascular disease. Nevertheless, the pathophysiological mechanism of this association remains unclear. The purpose of this study is to elucidate the relationship between job stress, heart rate variability, and metabolic syndrome. The study design was cross-sectional, and a total of 169 industrial workers were recruited. A structured-questionnaire was used to assess the general characteristics and job characteristics (work demand, decision latitude). Heart rate variability (HRV) was recorded using SA-2000 (medi-core), and was assessed by time-domain and by frequency-domain analyses. Time domain analysis was performed using SDNN (Standard Deviation of normal to normal interval), and spectral analysis using low-frequency (LF), high-frequency (HF), and total frequency power. Metabolic syndrome was defined on the basis of risk factors being clustered when three or more of the following cardiovascular risk factors were included in the fifth quintile: glucose, systolic blood pressure, high-density lipoprotein cholesterol (bottom quintile), triglyceride, and waist-hip ratio. The results showed that job characteristics were not associated with cardiovascular risk factors. Compared to the lower strain group (low strain+passive+active group), the high strain group had a less favorable cardiovascular risk profile with higher levels of blood pressure, glucose, homocysteine, and clotting factor, but the difference was not statistically significant. The SDNN of HRV was significantly lower in the high strain group than in the low strain group. The prevalence of metabolic syndrome in the lower strain group and high strain group was 13.2% and 23.8%, respectively. In the high strain group, the metabolic syndrome was significantly related to a decreased SDNN. However, we could not find a significant association in LF/HF ratio. This result suggests that decreased HRV found in the high-strain group are not a direct indicator of disease. However, it can induce cardiovascular abnormalities or dysfunctions related to the onset of heart disease among high risk groups.

N,N-dimethylformamide (DMF) is metabolized by the microsomal cytochrome p-450 into mainly N-hydroxymethyl- N-methylformamide (HMMF), which further breaks down to N-methyformamide (NMF). However, the detailed mechanism of its toxicity remains unclear. We investigated the metabolism and the toxicity of DMF using the isolated perfused liver model. DMF was added to the recirculating perfusate of the isolated perfused rat liver at concentrations of 0, 10 and 25 mM. Samples were collected from the inferior vena cava at 0, 30, 45, 60, 75, and 90 minutes following addition of the DMF. The metabolites of DMF were analyzed using Gas-chromatography (GC). The changes in the rate of oxygen consumption by the DMF were monitored during perfusion. The enzyme activities (aspartic aminotransferase:AST, alanine aminotransferase:ALT, and lactic dehydrogenase:LDH)) in the perfusate were monitored to see if DMF caused hepatotoxicity. As the perfusion progressed, the DMF concentration in the perfusate decreased, but the level of NMF increased to a maximum of 1.16 mM. The rate of oxygen consumption increased at DMF concentrations of 10 mM and 25 mM. However, when a known inhibitor of cytochrome p-450, SKF 525A (300 micro M), was used to pretreat the perfusate prior to the addition of the DMF, the rate of oxygen consumption was significantly inhibited, indicating the cytochrome p-450 system was responsible for the conversion of DMF to NMF. On addition of the DMF, the activities of the enzymes AST, ALT and LDH were significantly increased a time and dose dependent manner. However, following pretreatment with SKF 525A, their releases were inhibited.

Purpose Growing evidence suggests that hypoadiponectinemia may play a significant role in the development of metabolic syndrome (MetS). Therefore, the relationships between serum adiponectin with MetS and components of MetS were investigated in non-diabetic samples of drawn from the Koreans general population. Materials and Methods We performed a cross-sectional study in samples of older Koreans (age > 40 years) including 2,471 men and 3,463 women. MetS was defined according to the Asian modified criteria of the National Cholesterol Education Program Adult Treatment Panel III report. Serum adiponectin concentrations were measured by radioimmunoassay. Results The median adiponectin level in MetS was significantly lower than that in non-MetS subjects in men (6.00 vs. 8.00 µg/mL, p < 0.001) and women (10.12 vs. 11.74 µg/mL, p < 0.001). Adiponectin concentration was negatively correlated with waist circumference and levels of triglyceride, C-reactive protein (CRP), fasting glucose, and insulin, and positively correlated with high-density lipoprotein and age in both genders (p < 0.001). In a multivariate regression model after adjustment for age, body mass index, smoking, CRP, and lipid profiles, the odds ratio of MetS comparing extreme quartiles of adiponectin distribution was 0.32 [95% confidence interval (CI), 0.20 to 0.50] in men and 0.57 (95% CI, 0.43 to 0.76) in women. Conclusion Adiponectin levels are independently associated with the phenotype of MetS, as well as components of MetS in the non-diabetic Korean general population.

Epidemiologic studies were conducted on 31 cases of Salmonella group E infection detected in 2000 through a laboratory-based pathogen surveillance in Gangwon Province, Korea. Data were collected on the environmental exposures and the patients' foods, including the brand(s) of milk consumed before the onset of diarrhea. The patients' medical records were also reviewed. All of the patients were infants under 10 months of age except one 7-year old child. Surprisingly, all of the infants were fed with infant formulas from Company A, although two infants were fed with infant formulas from both Company A and Company B. Antimicrobial susceptibility test and pulsed-field gel electrophoresis (PFGE) were performed in 25 out of 31 isolates from the patients and in 1 isolate from an opened packet of infant formula collected from the home of an infected infant. All of the 26 isolates were Salmonella enterica serovar London. They showed a single PFGE pattern, and all of the isolates were susceptible to the 18 antibiotics tested. The causative agent of the salmonella outbreaks in the Gangwon Province and its surrounding areas was Salmonella London, and the highly likely source of the infection was infant formula from Company A.