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Background. M-type phospholipase A2 receptor (PLA2R) is the first autoantigen responsible for idiopathic membranous nephropathy (IMN). However, serum PLA2R antibody (PLA2R-Ab) can be inaccurate in distinguishing between IMN and secondary membranous nephropathy, while renal PLA2R antigen (PLA2R-Ag) emerges as an ancillary diagnostic. The present study is aimed at examining the associations between PLA2R-Ab in sera and PLA2R-Ag in kidneys in IMN patients. Methods. A total of 93 patients with IMN were retrospectively identified. Their serum PLA2R-Ab and renal PLA2R-Ag expression levels were determined, and the clinical correlations between these parameters and clinical features were examined. Results. The sensitivities of serum PLA2R-Ab and renal PLA2R-Ag for diagnosing IMN were 74.2% and 88.2%, respectively (P < 0.001), with poor consistency. Higher serum PLA2R-Ab levels were correlated to stronger renal PLA2R-Ag expression (P = 0.048). Patients with positive PLA2R-Ab significantly differed from those with negative levels, in terms of proteinuric levels over 24 hours (4.54 vs. 3.46 g/day, P = 0.015) and serum albumin (23.28 vs. 27.95 g/L, P = 0.038). Among patients with positive renal PLA2R-Ag, patients with positive PLA2R-Ab had significantly higher 24-hour proteinuria, when compared to patients with negative PLA2R-Ab (4.57 vs. 3.08 g/day, P = 0.005). Among those with positive PLA2R-Ab in sera, their PLA2R-Ab levels were correlated with the estimated glomerular filtration and serum creatinine. Conclusion. Serum PLA2R-Ab exhibits a closer correlation with proteinuric severity and renal function, when compared to renal PLA2R-Ag. [ABSTRACT FROM AUTHOR]

Abstract: The present study investigated the protective effects of ginsenoside Rb1 (GRb1) against genotoxicity induced by cyclophosphamide (CP). Single cell gel electrophoresis, flow cytometry assay with annexin V-FITC/propidine iodide (PI) and acridine orange (AO)/ethidium bromide (EB) staining assay were employed to measure DNA damage and cell apoptosis, respectively. The activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GPx) and the malondialdehyde (MDA) content were also investigated by a number of colormetric methods. The results showed that the CP produced significant DNA damage and cell apoptosis in mouse bone marrow cells or peripheral blood leukocytes, markedly inhibited the activities of T-SOD and GPx, and markedly increased the MDA content. GRb1 significantly inhibited DNA damages and cell apoptosis in mouse bone marrow cells or peripheral blood leukocytes induced by CP and antagonized the reduction of CP-induced T-SOD and GPx activities, and inhibited the increase in MDA content induced by CP. The anti-tumor study of GRb1 showed that GRb1 did not affect the anti-tumor activities of CP. In conclusion, GRb1 had significant protective effects against DNA damage and apoptosis induced by CP. [Copyright &y& Elsevier]

d-Pantolactone is a key chiral intermediate for the synthesis of d-pantothenic acid and its derivatives. Biocatalytic kinetic resolution of d,l-pantoyl lactone using d-lactonase is an efficient route to synthesize d-pantolactone. In this study, we report the expression of a novel d-lactonase TSDL in Escherichia coli host. The recombinant TSDL exhibited high hydrolysis activity and enantioselectivity toward d-pantolactone. The reaction conditions of the recombinant TSDL-catalyzed kinetic resolution of d,l-pantolactone was systematically investigated by whole cell biocatalysis. In addition, a preparative-scale reaction for bioproduction of d-pantoic acid was examined under optimized reaction conditions. This study presented an alternative enzymatic process for kinetic resolution of d,l-pantolactone., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

Background: That nimodipine (NMD) is potentially useful for ophthalmic treatment. However, the effect of NMD is unknown on retinal degenerative diseases., Objective: The purpose of the present study was to investigate the effect of NMD on N-methyl-N-nitrosourea (MNU)-induced retinal degeneration (RD) and elucidate its possible mechanisms., Materials and Methods: Morphological observation of NMD on MNU-induced RD was evaluated by light microscopy and electron microscopy. Nonenzymatic antioxidant glutathione (GSH) was measured by a colorimetric method. Transforming growth factor-beta (TGF-β) was measured by enzyme-linked immunosorbent assay (ELISA). Telomerase was detected by reverse transcriptase polymerase chain reaction (RT-PCR)., Results: The significantly protective effect of NMD on MNU-induced RD was demonstrated morphologically. NMD increased the content of GSH and decreased the level of TGF-β in rat retina. RT-PCR analysis demonstrated that NMD treatment significantly decreased mRNA level of telomerase., Conclusion: These data suggest that NMD inhibit MNU-induced RD in rats. The expressions of TGF-β, telomerase and GSH contents might partially contribute to its protective effects on MNU-induced RD.

The present study investigated the protective effects of ginsenoside Rb(1) (GRb(1)) against genotoxicity induced by cyclophosphamide (CP). Single cell gel electrophoresis, flow cytometry assay with annexin V-FITC/propidine iodide (PI) and acridine orange (AO)/ethidium bromide (EB) staining assay were employed to measure DNA damage and cell apoptosis, respectively. The activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GPx) and the malondialdehyde (MDA) content were also investigated by a number of colormetric methods. The results showed that the CP produced significant DNA damage and cell apoptosis in mouse bone marrow cells or peripheral blood leukocytes, markedly inhibited the activities of T-SOD and GPx, and markedly increased the MDA content. GRb(1) significantly inhibited DNA damages and cell apoptosis in mouse bone marrow cells or peripheral blood leukocytes induced by CP and antagonized the reduction of CP-induced T-SOD and GPx activities, and inhibited the increase in MDA content induced by CP. The anti-tumor study of GRb(1) showed that GRb(1) did not affect the anti-tumor activities of CP. In conclusion, GRb(1) had significant protective effects against DNA damage and apoptosis induced by CP., (Copyright © 2009 Elsevier B.V. All rights reserved.)