The Approaches from National Literature to World Literature

The paper explores the approaches from national literature to world one. The first approach to the world literature is literary translation and translated literature, the former refers to the faithful translation of original national works, and the latter means a creative treason of translation, or a kind of rewriting, based on the original text; the second is to gain the Nobel Award for Literature; The third is travel, exile or Diaspora of literature; and the last one is literary communication. In the end, the author stresses that the world literature is a literary garden of diversional and different dimension

Additional file 1 of A comparative study to determine the association of gut microbiome with schizophrenia in Zhejiang, China

Additional file 1: Figure S1. (A) Rarefaction curve analysis of archaeal 16S rRNA gene clone libraries. (B) Rank abundance curves of archaeal 16S rRNA gene clone libraries. Sample color codes are presented in the legend. Figure S2. Microbial composition and abundance at phylum level (A) and genus level (B) for gut microbiota in SZ (Case) and NC (Control) groups. The bars represent the average relative abundance of each genera, having significant differences between the two groups, with 95% confidence interval distribution and p value shown on their right

Branched Chain Amino Acids Cause Liver Injury in Obese/Diabetic Mice by Promoting Adipocyte Lipolysis and Inhibiting Hepatic Autophagy

The Western meat-rich diet is both high in protein and fat. Although the hazardous effect of a high fat diet (HFD) upon liver structure and function is well recognized, whether the co-presence of high protein intake contributes to, or protects against, HF-induced hepatic injury remains unclear. Increased intake of branched chain amino acids (BCAA, essential amino acids compromising 20% of total protein intake) reduces body weight. However, elevated circulating BCAA is associated with non-alcoholic fatty liver disease and injury. The mechanisms responsible for this quandary remain unknown; the role of BCAA in HF-induced liver injury is unclear. Utilizing HFD or HFD + BCAA models, we demonstrated BCAA supplementation attenuated HFD-induced weight gain, decreased fat mass, activated mammalian target of rapamycin (mTOR), inhibited hepatic lipogenic enzymes, and reduced hepatic triglyceride content. However, BCAA caused significant hepatic damage in HFD mice, evidenced by exacerbated hepatic oxidative stress, increased hepatic apoptosis, and elevated circulation hepatic enzymes. Compared to solely HFD-fed animals, plasma levels of free fatty acids (FFA) in the HFD + BCAA group are significantly further increased, due largely to AMPKα2-mediated adipocyte lipolysis. Lipolysis inhibition normalized plasma FFA levels, and improved insulin sensitivity. Surprisingly, blocking lipolysis failed to abolish BCAA-induced liver injury. Mechanistically, hepatic mTOR activation by BCAA inhibited lipid-induced hepatic autophagy, increased hepatic apoptosis, blocked hepatic FFA/triglyceride conversion, and increased hepatocyte susceptibility to FFA-mediated lipotoxicity. These data demonstrated that BCAA reduces HFD-induced body weight, at the expense of abnormal lipolysis and hyperlipidemia, causing hepatic lipotoxicity. Furthermore, BCAA directly exacerbate hepatic lipotoxicity by reducing lipogenesis and inhibiting autophagy in the hepatocyte