BackgroundThe effects of statins in patients with diabetic nephropathy are controversial. With increasing interest in the potential therapeutic role of statins in diabetic nephropathy, it is essential to evaluate its real effects.MethodsPubMed, EMBASE, Web of Science databases, Cochrane Central Register of Controlled Trials and China National Knowledge Infrastructure were systematically searched for randomized controlled trials (RCTs) of statins in patients with diabetic nephropathy.ResultsFourteen trials with 2866 participants were included in our meta-analysis. Compared with placebo, albuminuria and urinary albumin excretion rates in the statin group were reduced by 0.46 [95 % confidence interval (CI),−0.68 to −0.25, P < 0.0001] and 1.68 (95 % CI, −3.23 to −0.12, P = 0.03), respectively. The reduction of albuminuria was greater in patients of type 2 diabetes mellitus with diabetic nephropathy [standardized mean difference (SMD), −0.56; 95 % CI, −0.80 to −0.32, P < 0.00001] and the decrease was significant during the 1 to 3 years period of statin therapy (SMD, −0.57; 95 % CI, −0.95 to −0.19, P = 0.003). Subgroup analysis demonstrated the effects of statins were much stronger in subjects with pathologic albuminuria: change of −0.71 (95 % CI, −1.09 to −0.33, P = 0.0003) for those with urinary protein excretion 30 to 300 mg/day, −0.37 (95 % CI, −0.67 to −0.06, P = 0.02) for those with excretion more than 300 mg/day and −0.29 (95 % CI, −0.78 to 0.21, P = 0.26) for those with excretion less than 30 mg/day. In contrast, statins did not significantly reduce estimated glomerular filtration rate, serum creatinine and blood urea nitrogen levels.ConclusionsStatins decrease the albuminuria and urinary albumin excretion rates significantly. The efficacy of statins on renal function is time dependent and better in type 2 diabetic patients with nephropathy.

Background: Many studies have evaluated the association between matrix metalloproteinase 9 (MMP9) gene promoter polymorphism and diabetic microvascular complications. However, the results are conflicting and inconclusive. The aim of this meta-analysis was to evaluate the association more precisely. Materials and Methods: Studies were retrieved from the PubMed, Embase, Medline, China National Knowledge Infrastructure, Web of Science, and Cochrane databases. All statistical analyses were performed using Review Manager 5.2. Results: Data were abstracted from four case-control studies that included 446 patients with diabetic microvascular complications and 496 diabetic control subjects. The MMP9-1562 C/T genotype was significantly associated with the risk of diabetic nephropathy after stratification by specific type of microvascular complication (CT + TT vs. CC: OR = 0.42, 95% CI = 0.26–0.69, p = 0.0006; TT vs. CC + CT: OR = 0.37, 95% CI = 0.19–0.76, p = 0.006). Conclusions: This study adds to the evidence that MMP9-1562 T gene mutation might reduce the risk of diabetic nephropathy.

Apoptosis of renal proximal tubular epithelial cells (PTECs) plays a vital role in the pathogenesis and progression of diabetic kidney disease (DKD). Calcium dobesilate is a vascular protective compound used for treatment of diabetic retinopathy and chronic venous insufficiency. The aim of this study was to determine whether calcium dobesilate can protect PTECs from glucose-induced apoptosis and the potential mechanism of this effect. It is indicated that high glucose promoted abnormal apoptosis of HK2 cells, which was inhibited by treatment of calcium dobesilate, while Bim expression decreased in response to calcium dobesilate in high-glucose-treated HK2 cells. These findings confirmed the therapeutic effects of calcium dobesilate on DKD and emphasized the importance of it as a potentially crucial drug in treatment of DKD.

The unparalleled heterogeneity in genetic causes of hearing loss along with remarkable differences in prevalence of causative variants among ethnic groups makes single gene tests technically inefficient. Although hundreds of genes have been reported to be associated with nonsyndromic hearing loss (NSHL), GJB2, GJB6, SLC26A4, and mitochondrial (mt) MT-RNR1 and MTTS are the major contributors. In order to provide a faster, more comprehensive and cost effective assay, we constructed a DNA fluidic array, CapitalBioMiamiOtoArray, for the detection of sequence variants in five genes that are common in most populations of European descent. They consist of c.35delG, p.W44C, p.L90P, c.167delT (GJB2); 309kb deletion (GJB6); p.L236P, p.T416P (SLC26A4); and m.1555A>G, m.7444G>A (mtDNA). We have validated our hearing loss array by analyzing a total of 160 DNAs samples. Our results show 100% concordance between the fluidic array biochip-based approach and the established Sanger sequencing method, thus proving its robustness and reliability at a relatively low cost.

Conclusion C/GP hydrogel was demonstrated to be an ideal drug delivery vehicle and scaffold in the vein conduit. Combined use autologous vein and NGF continuously delivered by C/GP-NGF hydrogel can improve the recovery of facial nerve defects. Objective This study investigated the effects of chitosan-β-glycerophosphate-nerve growth factor (C/GP-NGF) hydrogel combined with autologous vein conduit on the recovery of damaged facial nerve in a rat model. Methods A 5 mm gap in the buccal branch of a rat facial nerve was reconstructed with an autologous vein. Next, C/GP-NGF hydrogel was injected into the vein conduit. In negative control groups, NGF solution or phosphate-buffered saline (PBS) was injected into the vein conduits, respectively. Autologous implantation was used as a positive control group. Vibrissae movement, electrophysiological assessment, and morphological analysis of regenerated nerves were performed to assess nerve regeneration. Results NGF continuously released from C/GP-NGF hydrogel in vitro. The recovery rate of vibrissae movement and the compound muscle action potentials of regenerated facial nerve in the C/GP-NGF group were similar to those in the Auto group, and significantly better than those in the NGF group. Furthermore, larger regenerated axons and thicker myelin sheaths were obtained in the C/GP-NGF group than those in the NGF group.

Hearing loss (HL) is a common sensory disorder in humans with high genetic heterogeneity. To date, over 145 loci have been identified to cause nonsyndromic deafness. Furthermore, there are countless families unsuitable for the conventional linkage analysis. In the present study, we used a custom capture panel (MiamiOtoGenes) to target sequence 180 deafness-associated genes in 5 GJB2 negative deaf probands with autosomal recessive nonsyndromic HL from Iran. In these 5 families, we detected one reported and six novel mutations in 5 different deafness autosomal recessive (DFNB) genes (TRIOBP, LHFPL5, CDH23, PCDH15, and MYO7A). The custom capture panel in our study provided an efficient and comprehensive diagnosis for known deafness genes in small families.

Background Up to 70% of patients with advanced ovarian cancer have a relapse after primary therapy. New agents and approaches are urgently needed to avoid or slow down this recurrence.Objectives To investigate the efficacy of PARP inhibitors (PARPis) as maintenance treatment in patients with newly diagnosed advanced ovarian cancer.Search strategy PubMed, MEDLINE, EMBASE, Cochrane Library and Web of Science databases.Selection criteria All randomised clinical trials (RCTs) that compared PARPis with placebo as first-line maintenance therapy in ovarian cancer.Data collection and analysis Two reviewers extracted data. Pooled hazard ratio (HR) and risk ratio (RR) with 95% confidence interval (CI) were calculated.Main results PARPis were associated with significant improvement of progression-free survival (PFS) in advanced epithelial ovarian cancer (AeOC) (HR = 0.53, 95% CI 0.40-0.71; P < 0.0001). The benefit was not only in women with BRCA mutations (HR = 0.35, 95% CI 0.29-0.42; P < 0.00001) and homologous recombination deficiency (HRD) (HR = 0.43, 95% CI 0.32-0.60; P < 0.00001), but also in those with nonmutated BRCA (HR = 0.72, 95% CI 0.63-0.82; P < 0.00001) and even non-HRD (HR = 0.83, 95% CI 0.70-0.99; P = 0.04).Conclusions PARP inhibitors are effective as maintenance therapy among patients with newly diagnosed advanced ovarian cancer after platinum-based chemotherapy, regardless of BRCA mutation or HRD status.

Oxidative stress and excess hepatic lipid accumulation contribute to non-alcoholic fatty liver disease. Radix Hedysari polysaccharides (RHP) have attracted interest due to their antioxidant properties and immunomodulatory effects. However, the effect of RHP on hepatic lipid metabolism remains to be elucidated. In the present study, the response of Sprague-Dawley rat livers to a high-fat diet and RHP treatment was investigated by evaluating body weight, liver histology, hepatic lipid content, adenosine monophosphate-activated protein kinase (AMPK) activity and lipid metabolism gene transcriptional profiles. The present study demonstrated that RHP ameliorated lipid metabolism disorders, regulated hepatic lipid content, improved liver inflammation and damage, activated AMPK via phosphorylation, upregulated peroxisome proliferator-activated receptor α and downregulated the mRNA expression of sterol regulatory element binding protein-1c in rat livers, which reduced lipogenesis and increased lipolysis. Taken together, these results suggested that RHP effectively ameliorates lipid metabolism disorders in rat livers; thus, RHP may be a potential therapeutic agent in the prevention of hepatic steatosis.