Emodin Ameliorates High Glucose-Induced Podocyte Apoptosis via Regulating AMPK/mTOR-Mediated Autophagy Signaling Pathway.

Objective: To investigate the effect of emodin on high glucose (HG)-induced podocyte apoptosis and whether the potential anti-apoptotic mechanism of emodin is related to induction of adenosine-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)-mediated autophagy in podocytes (MPC5 cells) in vitro.

Methods: MPC5 cells were treated with different concentrations of HG (2.5, 5, 10, 20, 40, 80 and 160 mmol/L), emodin (2, 4, 8 µ mol/L), or HG (40 mmol/L) and emodin (4 µ mol/L) with or without rapamycin (Rap, 100 nmol/L) and compound C (10 µ mol/L).

An Improved Electronic Image Motion Compensation (IMC) Method of Aerial Full-Frame-Type Area Array CCD Camera Based on the CCD Multiphase Structure and Hardware Implementation.

In this paper, the performance of the electronic conventional image motion compensation (IMC) method based on the time delay integration (TDI) mode was analyzed using the optical injection formula of charge coupled devices (CCDs). The result shows that the non-synchronous effect of charge packet transfer caused by line-by-line transfer during exposure makes the compensated image dissatisfying. Then an improved electronic IMC method based on the CCD multiphase structure was proposed.

Efficacy of lifestyle interventions in patients with type 2 diabetes: A systematic review and meta-analysis.

Background: The current meta-analysis evaluated the outcomes of various lifestyle interventions, including diet modifications (DIET), physical activity (PA), and patient education (EDU) in reducing the risk of cardiovascular disease in patients with type 2 diabetes.

Methods: Randomized clinical trials comparing lifestyle intervention with "usual care" (control) in type 2 diabetes patients were hand-searched from medical databases by two independent reviewers using the terms "diabetes, cardiovascular risk, lifestyle, health education, dietary, exercise/physical activities, and behavior intervention".

Results: Of the 235 studies identified, 17 were chosen for the meta-analysis.

Hepatocyte-Specific Arid1a Deficiency Initiates Mouse Steatohepatitis and Hepatocellular Carcinoma.

ARID1A, encoding a subunit of chromatin remodeling SWI/SNF complexes, has recently been considered as a new type of tumor suppressor gene for its somatic mutations frequently found in various human tumors, including hepatocellular carcinoma (HCC). However, the role and mechanism of inactivated ARID1A mutations in tumorigenesis remain unclear. To investigate the role of ARID1A inactivation in HCC pathogenesis, we generated hepatocyte-specific Arid1a knockout (Arid1aLKO) mice by crossing mice carrying loxP-flanked Arid1a exon 8 alleles (Arid1af/f) with albumin promoter-Cre transgenic mice.