Commentary on the Regulation of Viral Proteins in Autophagy Process

The ability to subvert intracellular antiviral defenses is necessary for virus to survive as its replication occurs only in the host cells. Viruses have to modulate cellular processes and antiviral mechanisms to their own advantage during the entire virus life cycle. Autophagy plays important roles in cell regulation. Its function is not only to catabolize aggregate proteins and damaged organelles for recycling but also to serve as innate immunity to remove intracellular pathogenic elements such as viruses. Nevertheless, some viruses have evolved to negatively regulate autophagy by inhibiting its formation. Even more, some viruses have employed autophagy to benefit their replication. To date, there are more and more growing evidences uncovering the functions of many viral proteins to regulate autophagy through different cellular pathways. In this review, we will discuss the relationship between viruses and autophagy and summarize the current knowledge on the functions of viral proteins contributing to affect autophagy process

The Interplay of Reovirus with Autophagy

Autophagy participates in multiple fundamental physiological processes, including survival, differentiation, development, and cellular homeostasis. It eliminates cytoplasmic protein aggregates and damaged organelles by triggering a series of events: sequestering the protein substrates into double-membrane vesicles, fusing the vesicles with lysosomes, and then degrading the autophagic contents. This degradation pathway is also involved in various disorders, for instance, cancers and infectious diseases. This paper provides an overview of modulation of autophagy in the course of reovirus infection and also the interplay of autophagy and reovirus

Tidal Effects on Circulation in and near the East China Sea

We incorporate tidal currents into a previously validated, three-dimensional, subtidal circulation model to assess tidal effects on the circulation in and around the East China Sea. Of particular interest is the tide-enhanced Changjiang plume dispersal and circulation in the southern East China Sea. The modeling results show that without tides, the Changjiang plume in summer presents itself as a stagnant, expansive pool in regions bordering the northern East China Sea and Yellow Sea, too far north and too accumulating relative to observations. The winter plume dispersal pushed by the north-northeast monsoon follows the China coastline southeastward as a coastal current that matches more closely with observations with or without tides. Incorporating the effect of tides brings the model closer to observation, especially in summer. During summer the Taiwan Warm Current shifts to lower latitudes, enhances upwelling off southeast China and induces a southward tidal residual coastal flow off southeast China. Tides also induce the observed seaward detachment of the summer plume. In winter, the prevailing north-northeast monsoon suppresses the Taiwan Warm Current to the minimum. However, if the winter monsoon is weakened for a few weeks, the Taiwan Warm Current reappears and these three mechanisms begin to operate as in summer. CTD surveys and satellite observations south of the Changjiang River estuary contribute to a better understanding of the tidal effects on regional ocean currents

Bacteroides fragilis aortic arch pseudoaneurysm: case report with review

We present a case of 58-year-old woman with underlying diabetes mellitus, hepatitis C virus-related liver cirrhosis, and total hysterectomy for uterine myoma 11 moths ago, who was diagnosed ruptured aortic arch mycotic pseudoaneurysm after a certain period of survey for her unknown fever cause. After emergent surgery with prosthetic graft interposition, all her blood cultures and tissue cultures revealed pathogen with Bacteroides fragilis. Although mycotic aneurysms have been well described in literatures, an aneurysm infected solely with Bacteroides fragilis is unusual, with only eight similar cases in the literature. Here we reported the only female case with her specific clinical and management course and summarized all reported cases of mycotic aneurysm caused by Bacteroides fragilis to clarify their conditions and treatments, alert the difficulty in diagnosis, and importance of highly suspicious

AGE-BSA down-regulates endothelial connexin43 gap junctions

<p>Abstract</p> <p>Background</p> <p>Advanced glycation end products generated in the circulation of diabetic patients were reported to affect the function of vascular wall. We examined the effects of advanced glycation end products-bovine serum albumin (AGE-BSA) on endothelial connexin43 (Cx43) expression and gap-junction communication.</p> <p>Results</p> <p>In human aortic endothelial cells (HAEC) treated with a series concentrations of AGE-BSA (0-500 μg/ml) for 24 and 48 hours, Cx43 transcript and Cx43 protein were reduced in a dose dependent manner. In addition, gap-junction communication was reduced. To clarify the mechanisms underlying the down-regulation, MAPKs pathways in HAEC were examined. Both a MEK1 inhibitor (PD98059) and a p38 MAPK inhibitor (SB203580) significantly reversed the reductions of Cx43 mRNA and protein induced by AGE-BSA. Consistently, phosphorylation of ERK and p38 MAPK was enhanced in response to exposure to AGE-BSA. However, all reversions of down-regulated Cx43 by inhibitors did not restore the functional gap-junction communication.</p> <p>Conclusions</p> <p>AGE-BSA down-regulated Cx43 expression in HAEC, mainly through reduced Cx43 transcription, and the process involved activation of ERK and p38 MAPK.</p

Emodin, a Naturally Occurring Anthraquinone Derivative, Ameliorates Dyslipidemia by Activating AMP-Activated Protein Kinase in High-Fat-Diet-Fed Rats

The aim of this study was to investigate the antiobesity and antihyperlipidaemic effects of emodin on high-fat diet (HFD)-induced obese rats, and on the regulation of the expression of the genes involved in lipid metabolism to elucidate the mechanisms. After being fed HFD for two weeks, Wistar rats were dosed orally with emodin (40 and 80 mg kg−1) or pioglitazone (20 mg kg−1), once daily for eight weeks. Emodin (80 mg kg−1 per day) displayed similar characteristics to pioglitazone (20 mg kg−1 per day) in reducing body weight gain, plasma lipid levels as well as coronary artery risk index and atherogenic index of HFD-fed rats. Emodin also caused dose related reductions in the hepatic triglyceride and cholesterol contents and lowered hepatic lipid droplets accumulation in HFD-fed rats. Emodin and pioglitazone enhanced the phosphorylation of AMP-activated protein kinase (AMPK) and its primary downstream targeting enzyme, acetyl-CoA carboxylase, up-regulated gene expression of carnitine palmitoyl transferase 1, and down-regulated sterol regulatory element binding protein 1 and fatty acid synthase protein levels in hepatocytes of HFD-fed rats. Our findings suggest emodin could attenuate lipid accumulation by decreasing lipogenesis and increasing mitochondrial fatty acid β-oxidation mediated by activation of the AMPK signaling pathway