IncRNA XIST Promotes Cardiac Fibrosis in Mice with Diabetic Nephropathy via Sponging miR-106a-5p to Target RUNX1.

Diabetic nephropathy (DN) accompanied by cardiac fibrosis (CF) increases the mortality rate among people with diabetes. This study sought to explore the molecular mechanism of long non-coding RNA X inactive specific transcript (lncRNA XIST) in CF in DN mice. The animal model of DN was established by streptozocin (STZ).

WITHDRAWN: Overexpression of NR4A2 Alleviates Renal and Myocardial Injury in Diabetic Nephropathy in Rats Through the HDAC11/ SPRY1 Pathway.

Unlabelled: Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn. Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused. The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.

Treatment of pyogenic liver abscess by surgical incision and drainage combined with platelet-rich plasma: A case report.

Background: Pyogenic liver abscesses are insidious in the early stage. Some cases progress rapidly, and the patient's condition can worsen and even become life-threatening if timely treatment is not provided. Surgery and prolonged antibiotic treatment are often required if the abscess is large and liquefied and becomes separated within the lumen.

Dynamic co-expression network analysis of lncRNAs and mRNAs associated with venous congestion.

Venous congestion and volume overload are important in cardiorenal syndromes, in which multiple regulated factors are involved, including long non‑coding RNAs (lncRNAs). To investigate the underlying role of lncRNAs in regulating the development of venous congestion, an Affymetrix microarray associated with peripheral venous congestion was annotated, then a bipartite dynamic lncRNA-mRNA co-expression network was constructed in which nodes indicated lncRNAs or mRNAs. The nodes were connected when the lncRNAs or mRNAs were dynamically co‑expressed.

Heme oxygenase‑1 protects H2O2‑insulted glomerular mesangial cells from excessive autophagy.

Increasing evidence has demonstrated that the activation of heme oxygenase (HO)‑1 reduces autophagy stimulated by oxidative stress injury, in which the supraphysiological production of reactive oxygen species (ROS) is detected. However, the potential mechanism underlying this effect remains unclear. The present study aimed to investigate the function of HO‑1 activation in the regulation of autophagy in glomerular mesangial cells subjected to H2O2‑induced oxidative stress injury.