Clinical characteristics of patients with maintenance hemodialysis affected by COVID‑19: A single‑center retrospective study.

The coronavirus disease 2019 (COVID-19) is spreading continuously worldwide. Maintenance hemodialysis (MHD) patients are a particular group at higher risk of contracting COVID-19. The aim of the present study was to investigate the various risk factors that contribute to the occurrence of co-infection with COVID-19 among patients with MHD.

Whole transcriptome mapping reveals the lncRNA regulatory network of TFP5 treatment in diabetic nephropathy.

Background: TFP5 is a Cdk5 inhibitor peptide, which could restore insulin production. However, the role of TFP5 in diabetic nephropathy (DN) is still unclear.

Objective: This study aims to characterize the transcriptome profiles of mRNA and lncRNA in TFP5-treated DN mice to mine key lncRNAs associated with TFP5 efficacy.

Platelet-to-albumin ratio is a potential biomarker for predicting diabetic nephropathy in patients with type 2 diabetes.

To evaluate whether platelet-to-albumin ratio (PAR) can predict diabetic nephropathy (DN) in type 2 diabetes mellitus (T2DM). A total of 140 patients with T2DM and 40 healthy individuals were enrolled retrospectively. T2DM patients were divided into three groups based on the urinary albumin-to-creatinine ratio, PAR was compared and receiver operating characteristic curve was constructed to evaluate the predictive value of PAR in DN in T2DM.

Cdk5 activation promotes Cos-7 cells transition towards neuronal-like cells.

Objectives: Cyclin-dependent kinase 5 (Cdk5) activity is specifically active in neurogenesis, and Cdk5 and neocortical neurons migration related biomarker are expressed in Cos-7 cells. However, the function of Cdk5 on the transformation of immortalized Cos-7 cells into neuronal-like cells is not clear.

Methods: Cdk5 kinase activity was measured by [γ-P] ATP and p81 phosphocellulose pads based method.

TFP5 attenuates cyclin-dependent kinase 5-mediated islet β-cell damage in diabetes.

Islet β-cell damage and dysfunction represent the pathophysiological basis of diabetes. Excessive activation of cyclin-dependent kinase 5 (CDK5) is involved in the pathogenesis of type 2 diabetes mellitus (T2DM), although the exact mechanism remains unclear. Therefore, this study investigated the role of a CDK5 inhibitor (TFP5) in islet β-cell damage under diabetic conditions by regulating the expression of CDK5 in vitro and in vivo.

TFP5-Mediated CDK5 Activity Inhibition Improves Diabetic Nephropathy NGF/Sirt1 Regulating Axis.

Diabetic nephropathy (DN) is one of the leading causes of chronic kidney disease (CKD), during which hyperglycemia is composed of the major force for the deterioration to end-stage renal disease (ESRD). However, the underlying mechanism triggering the effect of hyperglycemia on DN is not very clear and the clinically available drug for hyperglycemia-induced DN is in need of urgent development. Here, we found that high glucose (HG) increased the activity of cyclin-dependent kinase 5 (CDK5) dependent on P35/25 and which upregulated the oxidative stress and apoptosis of mouse podocytes (MPC-5).

Research development on graphitic carbon nitride and enhanced catalytic activity on ammonium perchlorate.

Recently, graphitic carbon nitride (g-CN) has attracted considerable attention due to its attractive features including excellent electrochemical performance, suitable band gap, nontoxicity, and high mechanical and thermal stability. Such unique advantages endow it with promising applications in batteries, photocatalysts, photodegradation, and so on. In particular, it has been applied to catalyze the thermal decomposition of ammonium perchlorate (AP) and has shown excellent performance.

Early-start and conventional-start peritoneal dialysis: a Chinese cohort study on outcome.

Early-start peritoneal dialysis (PD) is an effective option for patients need unplanned dialysis. However, there are few studies on the long-term prognosis of early-start PD patients. In this retrospective study, 635 eligible patients from 1 March 1996 to 30 September 2016 were included, and divided into three groups according to the duration of break-in period: 3 days or less, 4-13 days and more than 14 days.