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Long-term peritoneal dialysis (PD) is accompanied by low-grade intraperitoneal inflammation and may eventually lead to peritoneal membrane injury with a high solute transport rate and ultrafiltration failure. Osteopontin (OPN) is highly expressed through the stimulation of pro-inflammatory cytokines in many cell types. This study aimed to investigate the potential of OPN as a new indicator of peritoneal deterioration. One hundred nine continuous ambulatory PD patients were analyzed. The levels of OPN and IL-6 in peritoneal effluents or serum were analyzed by ELISA kits. The mean effluent OPN concentration was 2.39 ± 1.87 ng/mL. The OPN levels in drained dialysate were correlated with D/P Cr (p < 0.0001, R = 0.54) and D/D0 glucose (p < 0.0001, R = 0.39). Logistic regression analysis showed that the OPN levels in peritoneal effluents were an independent predictive factor for the increased peritoneal solute transport rate (PSTR) obtained by the peritoneal equilibration test (p < 0.001). The area under the receiver operating characteristic curve of OPN was 0.84 (95% CI: 0.75–0.92) in predicting the increased PSTR with a sensitivity of 86% and a specificity of 67%. The joint utilization of effluent OPN with age, effluent IL-6, and serum albumin further increased the specificity (81%). Thus, OPN may be a useful indicator of peritoneal deterioration in patients with PD.

Background: Lysosomal cathepsin D (CTSD) can degrade internalized advanced glycation end products (AGEs) in dermal fibroblasts. CTSD expression is decreased in photoaged fibroblasts, which contributes to intracellular AGEs deposition and further plays a role in AGEs accumulation of photoaged skin. The mechanism under downregulated CTSD expression is unclear. Objective: To explore possible mechanism of regulating CTSD expression in photoaged fibroblasts. Methods: Dermal fibroblasts were induced into photoaging with repetitive ultraviolet A (UVA) irradiation. The competing endogenous RNA (ceRNA) networks were constructed to predict candidate circRNAs or miRNAs related with CTSD expression. AGEs‐BSA degradation by fibroblasts was studied with flow cytometry, ELISA, and confocal microscopy. Effects of overexpressing circRNA‐406918 via lentiviral transduction on CTSD expression, autophagy, AGE‐BSA degradation were analyzed in photoaged fibroblasts. The correlation between circRNA‐406918 and CTSD expression or AGEs accumulation in sun‐exposed and sun‐protected skin was studied. Results: CTSD expression, autophagy, and AGEs‐BSA degradation were significantly decreased in photoaged fibroblasts. CircRNA‐406918 was identified to regulate CTSD expression, autophagy, and senescence in photoaged fibroblasts. Overexpressing circRNA‐406918 potently decreased senescence and increased CTSD expression, autophagic flux, and AGEs‐BSA degradation in photoaged fibroblasts. Moreover, circRNA‐406918 level was positively correlated with CTSD mRNA expression and negatively associated with AGEs accumulation in photodamaged skin. Further, circRNA‐406918 was predicted to mediate CTSD expression through sponging eight miRNAs. Conclusion: These findings suggest that circRNA‐406918 regulates CTSD expression and AGEs degradation in UVA‐induced photoaged fibroblasts and might exert a role in AGEs accumulation in photoaged skin. [ABSTRACT FROM AUTHOR]

Objective To explore the relationship between SIRT1 genetic variation (rs1467568, rs4746720) and microscopic polyangiitis (MPA) in Guangxi population. Methods The SIRT1 polymorphisms of 208 patients with microscopic polyangiitis (MPA) and 211 healthy volunteers were genotyped by multiplex polymerase chain reaction (PCR) and high throughput sequencing. The allele frequencies and genotypes were compared. The linkage disequilibrium, haplotype and genetic model were analyzed. The relationship between different genotypes and clinical symptoms and laboratory biochemical indexes was evaluated. Results The results showed no significant difference between the two groups in genotype, allele frequency, and haplotype of SIRT1 rs1467568 and rs4746720(P > 0.05). In the age group ≥ 54 years old, the dominant model(OR = 0.50,95%CI: 0.27 ~ 0.92, P = 0.026), overdominant model(OA = 0.49,95%CI: 0.26 ~ 0.92, P = 0.026) and additive model (OR = 0.57, 95%CI: 0.33 ~ 0.99, P = 0.045) of SIRT1 rs1467568 were associated with lower susceptibility to MPA. In rs1467568, MPA patients with GG genotype had higher levels of glutamic pyruvic transaminase (P = 0.012), while in rs4746720, MPA patients with TT and TC genotypes had higher levels of glutamic oxaloacetic transaminase (P = 0.036). Conclusions In this study, SIRT1 rs4746720 was not related to the susceptibility to MPA in Guangxi population, but rs1467568 may be associated with the susceptibility to MPA in some people (5 54 years old) in Guangxi, and rs1467568 and rs4746720 were associated with the levels of glutamic pyruvic transaminase and glutamic oxaloacetic transaminase in patients with MPA. [ABSTRACT FROM AUTHOR]

Duck hepatitis A virus (DHAV) causes a highly contagious and acute disease in ducklings younger than 3 weeks of age and spreads rapidly by horizontal transmission to all susceptible ducklings in the flock. To date, there is no evidence of vertical transmission of DHAV‐1. In a previous study, we identified a novel DHAV type 1 (DHAV‐1) isolate that could infect adult ducks and induce laying drop. In this study, 30 non‐embryonated duck eggs and 60 17‐day‐old embryos were collected from three breeding duck flocks with egg drop syndrome caused by DHAV‐1 in China, and 30 17‐day‐old embryos were randomly selected from the 60 embryos and allowed to hatch. DHAV‐1 RNA was detected by RT‐PCR in 10 of 30 non‐embryonated eggs, 9 of 30 17‐day‐old embryos, 5 of 7 dead embryos and 5 of 23 newly hatched ducklings. Overall, 29 of 90 (32.2%) eggs and embryos were positive for DHAV‐1. Three DHAV‐1 strains were isolated from the dead duck embryos of the three breeding duck flocks, respectively. Pathogenicity studies showed that the three DHAV‐1 isolates had median embryo lethal doses but were highly pathogenic to healthy ducklings. Compared with the DHAV reference strains, there were two specific amino acid mutation sites (F169 and S220) in VP1 of the three isolates. To the best of our knowledge, this is the first report that DHAV‐1 is isolated from duck embryos. The findings provide evidence of possible vertical transmission of DHAV‐1 from breeding ducks to ducklings. [ABSTRACT FROM AUTHOR]