IgA nephropathy (IgAN), membranous nephropathy (MN), and lupus nephritis (LN) represent important causes of chronic kidney disease. They belong to the immune-mediated glomerulonephritis (GNs), and have distinct pathogenesis, distinct clinical courses, and variable responses to treatment. Therefore, specific diagnostic procedures are necessary for more effective patient management. Recently, a role for oxidative stress has been proposed in various renal disorders. Thus, molecules related to oxidative stress, such as 2-Cys-peroxiredoxins (PRDXs), may represent plausible candidates for biomarkers in renal pathologies. The aim of this study was to assess whether there are differences between individual GNs and healthy controls in the context of PRDXs serum concentration. We enrolled 108 patients with biopsy-proven IgAN (47), MN (26), LN (35) and 30 healthy age- and sex-matched controls. The serum concentrations of PRDX 1–5 were measured with ELISA assays and correlated with demographic and clinical data. The PRDXs’ concentration varied depending on the GN type. We also observed an association of PRDXs with lower estimated glomerular filtration rates, complement, hemoglobin, and body mass index. Our study indicates that individual PRDX can play roles in pathophysiology of selected GNs and that their serum concentrations may become useful as a new supplementary diagnostic markers in IgAN, MN as well as LN. The results of this study open a new avenue for prospective research on PRDXs in renal diseases.

International Press of Boston - publishers of scholarly mathematical and scientific journals and books

Background/Objectives: The aim of this study was to evaluate the association between various clinical and laboratory findings and in-hospital mortality in community-acquired bacterial meningitis (BM). Methods: We retrospectively analyzed 339 adult (≥18 years old) patients with bacterial meningitis who were admitted to the Hospital for Infectious Diseases in Warsaw between January 2010 and December 2017. Results: Altogether, 56 patients (16.5%) died during hospitalization. On admission, the non-survivors scored lower on the Glasgow Coma Scale (GCS) (median 7 vs. 13, p < 0.001) and higher on the Sequential Organ Failure Assessment (SOFA) score (median 6 vs. 2, p < 0.001) and were less likely to complain about headaches (18.75% vs. 54.21%, p < 0.001) and nausea and/or vomiting (1.89% vs. 36.2%, p < 0.001), but were more likely to manifest peripheral nerve palsies (21.43% vs. 9.61%, p = 0.02). The patients who died were also more likely to be immunocompromised (53.57% vs. 34.28%, p = 0.01), have Streptococcus pneumoniae etiology (35.71% vs. 16.25%, p = 0.001), higher concentrations of procalcitonin (median 5.035 ng/mL vs. 2.245 ng/mL, p = 0.003) and urea (median 10.7 mmol/L vs. 5.865 mmol/L, p < 0.001) in the blood and higher protein (median 4.57 g/L vs. 2.605 g/L, p = 0.014) and lower glucose levels (median 0.765 mmol/L vs. 1.89 mmol/L, p = 0.006) in the cerebrospinal fluid (CSF). In a multiple logistic regression analysis, which was conducted separately for the GCS and SOFA, both scoring systems (OR = 0.67, OR 95% CI 0.59–0.75, p < 0.001 for GCS and OR = 1.42, OR 95% CI 1.29–1.60, p < 0.001 for SOFA) as well as an age over 70 years (OR = 3.99, OR 95% CI 1.39–12.93, p = 0.014) and Streptococcus pneumoniae etiology (OR = 2.38, OR 95% CI 1.12–4.99, p = 0.022) were associated with in-hospital deaths. Conclusions: The survivors and non-survivors with BM differed with respect to a number of signs and symptoms, etiology, the results of blood and CSF laboratory tests, and the immune deficiency status, as well as the GCS and SOFA scores. In the multiple logistic regression analysis, both of the GCS and SOFA scoring systems, age and Streptococcus pneumoniae etiology showed high associations with the in-hospital deaths.

We study residue formulas for push-forward in K-theory of homogeneous spaces. First we review formulas for classical groups, which we derive from a formula for the classical Grassmannian case. Next we consider the homogeneous spaces for G2. One of them embeds in the Grassmannian Gr(2,7). We find its fundamental class in the equivariant K-theory and obtain the residue formula for the push-forward. This formula is valid for G2/B as well.

We revisit residue formulas for the push-forward in the cohomology of the even orthogonal Grassmannian. This space has two components, and the formula for a single component demands separate attention. We correct errors spread throughout the literature.