The results of our study revealed a strong relationship between microalbuminuria and NAFLD in the patients with prediabetes and newly diagnosed diabetes. Further studies are required to confirm whether NAFLD is a predictor of the development of microalbuminuria in patients with prediabetes and diabetes.

The HP- and C-plans had a similar effect on weight and abdominal fat reduction, but the HP-plan was more effective in reducing body fat among compliant subjects.

Metabolic syndrome is a complex clinical disorder characterized by obesity, a disturbance of glucose metabolism, dyslipidemia, and hypertension, leading to increased cardiovascular risk. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine produced both by innate immune cells and by adipocytes, and it plays an important role in inflammatory and cardiovascular diseases. The goal of this study was to evaluate the expression of circulating MIF in patients with metabolic syndrome. A study was conducted involving 172 persons who attended the Jeju National University Hospital Health Promotion Center. Among the 172 subjects, 88 patients with metabolic syndrome and 84 healthy control subjects were included. Serum MIF levels were considerably higher in patients with metabolic syndrome than in healthy subjects (mean±SEM, 1413.0-pg/ml±102.6 vs. 1077.0-pg/ml±-91.3, p=0.016). Among the metabolic syndrome patients, MIF levels were significantly increased in women (1403.0-pg/ml±114.2 vs. 921.3 pg/ml±117.3, p=0.005), but not in men. Even after further linear regression adjustment for age and body mass index, the expression of MIF for women with metabolic syndrome was still clearly elevated when compared to healthy subjects (p=0.011). Circulating MIF concentrations showed a gender disparity between healthy and metabolic syndrome subjects. An elevation of systemic MIF in women with metabolic syndrome may contribute to pathogenesis of metabolic syndrome or to the development of metabolic syndrome-related diseases, such as atherosclerosis and type 2 diabetes mellitus.

Twenty-five koi (Cyprinus carpio haematopterus) bought from a wholesale fish market in Korea, showed lethargic behaviour and 100% mortality within 20 days. Carp oedema virus (CEV) was detected by PCR in all 25 koi. Results of detailed histopathological and clinical examinations of 17 koi indicated loss of body balance, severe infiltration of inflammatory cells into the inter-lamellar spaces of the gills and vacuolization and inclusion bodies in gill epithelial cells. Sequence analysis of PCR products of these koi showed up to 99% identity to the previously reported sequences, suggesting that the observed mass mortality resulted from koi sleepy disease (KSD) due to CEV infection. To the best of our knowledge, this study is the first report of KSD in the Republic of Korea. Partial sequences of 4a protein from the virus indicated that the present CEV detected in koi from Korea is more closely related to that from the UK and Poland than from Japan. The present findings indicate that the prevalence and spread of KSD must be closely monitored in both European and Asian countries to avoid potential economic losses to the global koi industry.

SUMMARY We conducted an epidemic investigation to discover the route of transmission and the host factors of an outbreak of post-injection abscesses. Of the 2984 patients who visited a single clinic, 77 cases were identified and 208 age- and sex-matched controls were selected for analysis. Injected medications per se were not found to be responsible, and a deviation from safe injection practice suggested the likelihood of diluent contamination. Therefore the injected medications were classified according to whether there was a need for a diluent, and two medications showed a statistically significant association, i.e. injection with pheniramine [adjusted odds ratios (aOR) 5·93, 95% confidence interval (CI) 2·97-11·87] and ribostamycin (aOR 47·95, 95% CI 11·08-207·53). However, when considered concurrently, pheniramine lost statistical significance (aOR 8·71, 95% CI 0·44-171·61) suggesting that normal saline was the causative agent of this outbreak. Epidemiological evidence strongly suggested that this post-injection outbreak was caused by saline contaminated with Mycobacterium massiliense without direct microbiological evidence.