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). The viability and apoptosis of MPC5 cells were detected using cell counting kit-8 (CCK-8) assay and flow cytometry analysis, respectively. The expression levels of cleaved caspase-3, autophagy marker light chain 3 (LC3) I/II, and AMPK/mTOR signaling pathway-related proteins were determined by Western blot. The changes of morphology and RFP-LC3 fluorescence were observed under microscopy. RESULTS: HG at 20, 40, 80 and 160 mmol/L dose-dependently induced cell apoptosis in MPC5 cells, whereas emodin (4 µ mol/L) significantly ameliorated HG-induced cell apoptosis and caspase-3 cleavage (P<0.01). Emodin (4 µ mol/L) significantly increased LC3-II protein expression levels and induced RFP-LC3-containing punctate structures in MPC5 cells (P<0.01). Furthermore, the protective effects of emodin were mimicked by rapamycin (100 nmol/L). Moreover, emodin increased the phosphorylation of AMPK and suppressed the phosphorylation of mTOR. The AMPK inhibitor compound C (10 µ mol/L) reversed emodin-induced autophagy activation. CONCLUSION: Emodin ameliorated HG-induced apoptosis of MPC5 cells in vitro that involved induction of autophagy through the AMPK/mTOR signaling pathway, which might provide a potential therapeutic option for diabetic nephropathy.

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. In this method, a series of proper driving clocks were applied to drive the charge packet to move electrode-by-electrode during the exposure time, which results in a minimum non-synchronous effect of charge packet transfer. The mismatch of velocity between charge packet transfer and image motion was decreased. The performance of the improved electronic IMC method was also analyzed using the optical injection formula. The modulation degrees of the two methods were compared. The average value of the modulation degree of the improved electronic IMC method was 47/96, greater than the conventional electronic IMC method, which was 1/3. To achieve the improved electronic IMC, the driver timing diagram of the improved electronic IMC method was proposed. This paper presented an improved hardware implementation method for the improved electronic IMC method. Based on the basic FTF4052M drive circuit system, an IMC pulse pattern generator that worked together with the main pulse pattern generator (SAA8103) was added to achieve the improved electronic IMC. Then, the internal structure of the IMC pulse pattern generator was given. A dual pulse pattern generator drive circuit system was proposed. After computer simulation and indoor real shot verification, the compensation effect of the improved electronic IMC method was better than the compensation effect of the conventional electronic IMC method.

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. The average age of patients ranged from 50-67.3 years. Results reveal no significant difference between the groups, with respect to BMI, while PA and DIET yielded a greater reduction in HbA1c. Significant reduction in both systolic and diastolic pressures in the DIET group, and diastolic pressure in the PA group, was observed. HDL-c in the DIET group was significantly higher than the control group, while no change in LDL-c levels, was seen in all three intervention subtypes. There was no difference between the EDU vs. the control group in terms of HbA1c, blood pressure or HDL-c and LDL-c. CONCLUSION: DIET intervention showed an improvement in HbA1c, systolic/diastolic blood pressure and HDL-c, with an exception of LDL-c and BMI, suggesting that nutritional intervention had a significant impact on the quality of life by reducing the cardiovascular risk in type 2 diabetes patients.

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. Significantly, the hepatocyte-specific Arid1a deficiency results in mouse steatohepatitis and HCC development. In Arid1aLKO mice, we found that innate immune cells, including F4/80+ macrophages and CD11c+ neutrophil cells, infiltrate into the liver parenchyma, accompanied by the increased tumor necrosis factor (TNF)-α and interleukin (IL)-6, and activation of STAT3 and NF-κB pathways. In conclusion, hepatocyte-specific Arid1a deficiency could lead to mouse steatohepatitis and HCC development. This study provides an alternative mechanism by which Arid1a deficiency contributes to HCC tumorigenesis.

Multiple dens evaginatus of premolars and molars in Chinese dentition: a case report and literature review / 国际口腔科学杂志·英文版

Dens evaginatus (DE) is a dental anomaly that occurs as an accessory tubercle on the occlusal or lingual surface of a tooth. The authors provide a literature review and report a rare case in which DE occurs on multiple mandibular premolars and maxillary molars. The patient is a 26-year-old Chinese woman, with a chief complaint of gingival bleeding. DE affecting teeth 17, 27, 35, and 45 was found during clinical examination. For treatment of the patient, we reduced the opposing occluding teeth, while undertaking progressive grinding of the tubercles for six months. We followed-up for a year. This suggests the importance of examining for multiple DE during clinical practice.