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Sepsis is characterized by a systemic inflammatory response to a microbial pathogen. In sepsis, capillary permeability is a tightly regulated feature of microcirculation in all organ beds and is fundamentally altered. We investigated the vascular endothelial growth factor (VEGF) level as a vascular permeability factor and the soluble fms-like tyrosine kinase-1 (Flt-1) level as an antagonist of the VEGF receptors. Serum VEGF and soluble Flt-1 levels in 21 patients with septic shock, who were treated with direct hemoperfusion with a polymyxin B-immobilized fiber column (DHP-PMX), were measured by enzyme-linked immunoassay. The VEGF and the soluble Flt-1 levels were more elevated in patients with septic shock than in controls. Between 14 survivors and 7 non-survivors, there was no significant difference in VEGF level before the DHP-PMX therapy, but the soluble Flt-1 level of survivors was significantly lower than that of non-survivors. Although there was no significant difference between starting and ending VEGF levels in survivors, in non-survivors the VEGF level at the end of DHP-PMX therapy was significantly lower than that at the start. In survivors, the soluble Flt-1 level at the end of DHP-PMX therapy was significantly lower than that at the start. On the other hand, in non-survivors, there was no significant difference between the ending and starting soluble Flt-1 levels. The soluble Flt-1 level may be a suitable marker of disease severity and mortality. [ABSTRACT FROM AUTHOR]

The article reports that staphylococcus aureuscell-envelope antigens are localized in glomeruli from patients with IgA-related nephropathy. Staphylococcus aureus (S. aureus) is a common, normal, and pathogenic flora that colonizes on mucosal tissues. Western blotting analysis showed that the monoclonal antibody reacted with 35 kDa of S. aureus antigens. Histopathological examination was performed in 130 patients with IgA-related nephropathy and 108 patients with other renal diseases using antibodies originated from patients' sera and mouse monoclonal antibody against S. aureus cell membrane antigens.

Introduction: Obesity and inappropriate lifestyle is the major risk factors for liver dysfunction and proteinuria. Nevertheless, previous studies have not described the differential impacts of body weight changes and lifestyle modification on already developed liver dysfunction and proteinuria., Methods: The original cohort was 933,490 individuals from the Japanese general population. In this investigation, we included 36,256 obese individuals with elevated levels of aspartate aminotransferase and/or alanine aminotransferase (≥31 IU/L) or positive proteinuria (+/- or more) in both the first and second years. Outcomes were the first normalization of these data defined as improvement in liver dysfunction and proteinuria. Times to outcomes were assessed using the Cox proportional hazards modeling for -1 kg/m 2 /year change in body mass index (BMI) changes in exercise and alcohol intake., Results: The multivariable-adjusted hazard ratio (HR) for incident improvement in liver dysfunction with BMI change -1.0 kg/m 2 /year was 1.07 (95% confidence interval [CI] 1.05-1.09) in obesity and that with improved proteinuria was 1.04 (95%CI 1.02-1.07). Compared to subjects without exercise habits, subjects who gained exercise habits exhibited a higher rate of improvement in liver dysfunction (HR 1.08; 95%CI 1.01-1.15) but not in proteinuria (HR 0.98; 95%CI 0.88-1.08). Compared to subjects with continuous alcohol intake habits, subjects who quit alcohol intake also showed a higher rate of improvement in liver dysfunction (HR 1.20; 95%CI 1.09-1.32)., Conclusions: This study suggested that weight loss greater than 1 kg/m 2 /year improves liver dysfunction and dipstick proteinuria in obesity. Particularly, liver dysfunction can be remedied by acquiring an exercise habit and quitting alcohol intake., Competing Interests: None, (Copyright © Japan Medical Association.)