Small hepatitis delta antigen selectively binds to target mRNA in hepatic cells: a potential mechanism by which hepatitis D virus downregulates glutathione S-transferase P1 and induces liver injury and hepatocarcinogenesis.

Liver coinfection by hepatitis B virus (HBV) and hepatitis D virus (HDV) can result in a severe form of hepatocellular carcinoma with poor prognosis. Coinfection with HDV and HBV causes more deleterious effects than infection with HBV alone. Clinical research has shown that glutathione S-transferase P1 (GSTP1), a tumor suppressor gene, is typically downregulated in liver samples from hepatitis-infected patients.

miR-17-92 ameliorates renal ischemia reperfusion injury.

There is limited information on the role of miR-17-92 in renal tubular pathophysiology. Therefore, the present study was performed to determine whether miR-17-92 plays a role in ischemia-reperfusion injury (IRI)-induced acute kidney injury. We originally demonstrated that miR-17-92 is up-regulated following IRI in vivo.

[Effects of Cellular Density on the Induction of Suspension Globe of Ovarian Cancer Stem Cells].

Objective: To determine the effect of cellular density on the separation and identification of cancer stem cells from human ovarian clear cell carcinoma cell line ES-2 and adenocarcinoma cell line A2780.

Methods: ES-2 and A2780 cells were cultured with human recombinant epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) and bovine serum albumin and insulin in serum free medium. The cancer stem cells were obtained through serial passages.

Kidneys from Older Living Donors Provide Excellent Short and Intermediate Outcomes--A Single China Center's Experience.

Background: Transplantation with kidneys from older living donors is on the rise, yet controversy still exists over whether the outcomes are as satisfactory as with kidneys from younger donors.

Methods: We retrospectively analyzed 1009 living donor kidney transplants performed at our center between 2006 and 2013. Graft and patient outcomes were compared between transplants with kidneys from old living donors (OLD, 55-65 years) (n = 264) and from young living donors (YLD, <55 years) (n = 745).

A modified TALEN-based strategy for rapidly and efficiently generating knockout mice for kidney development studies.

The transcription activator-like effector nucleases (TALENs) strategy has been widely used to delete and mutate genes in vitro. This strategy has begun to be used for in vivo systemic gene manipulation, but not in an organ-specific manner. In this study, we developed a modified, highly efficient TALEN strategy using a dual-fluorescence reporter.

Comparative proteomics and correlated signaling network of kidney in ApoE deficient mouse.

Purpose: Apolipoprotein E knockout (apoE-/- ) mouse is one of the most popular models for cardiovascular research, especially in the study of atherosclerosis. Naturally, large amount of studies try to uncover the role of apoE in atherosclerosis, and indeed apoE plays an important role in this pathogenesis. Kidney is an organ that contains lots of capillaries and also largely expresses apoE.

Comparative proteomic analysis suggests that mitochondria are involved in autosomal recessive polycystic kidney disease.

Autosomal recessive polycystic kidney disease (ARPKD), characterized by ectatic collecting duct, is an infantile form of PKD occurring in 1 in 20 000 births. Despite having been studied for many years, little is known about the underlying mechanisms. In the current study, we employed, for the first time, a MS-based comparative proteomics approach to investigate the differently expressed proteins between kidney tissue samples of four ARPKD and five control individuals.

PKHD1 post-transcriptionally modulated by miR-365-1 inhibits cell-cell adhesion.

Autosomal recessive polycystic kidney disease (ARPKD) is a severe inherited disorder with an incidence of 1/20 000 live births. Mutations of PKHD1 (polycystic kidney and hepatic disease gene 1) gene were identified to be responsible for ARPKD. However, the underlying molecular mechanisms remain largely unknown.

The miR-17-92 cluster regulates FOG-2 expression and inhibits proliferation of mouse embryonic cardiomyocytes.

MicroRNAs (miRNAs) have gradually been recognized as regulators of embryonic development; however, relatively few miRNAs have been identified that regulate cardiac development. A series of recent papers have established an essential role for the miRNA-17-92 (miR-17-92) cluster of miRNAs in the development of the heart. Previous research has shown that the Friend of Gata-2 (FOG-2) is critical for cardiac development.

FLNA and PGK1 are two potential markers for progression in hepatocellular carcinoma.

Background/aims: Hepatocellular carcinoma (HCC) is one of the most deadly diseases; metastasis and recurrence are the most important factors that affect the therapy of HCC chronically. Until now, the prognosis for the metastasis of HCC had not improved. Recently, several proteins that are related to metastasis and invasion of HCC were identified, but the effective markers still remain to be elucidated.

Overexpression of FoxO1 causes proliferation of cultured pancreatic beta cells exposed to low nutrition.

Multiple lines of evidence have shown that the functional defect of pancreatic beta cells is the root cause of type 2 diabetes. FoxO1, a key transcription factor of fundamental cellular physiology and functions, has been implicated in this process. However, the underlying molecular mechanism is still largely unknown.