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To detect the effects of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) on SIRT1 expression and p53 deacetylation, involving cell senescence, in activated human hepatic stellate cell (HSC) in vitro, human HSC LX-2 was cultured with TWEAK for 24 h. The result showed that the expression of membrane receptor Fn14 was remarkably increased by TWEAK, which upregulated SIRT1 in LX-2 cells, detected by Western blotting and real-time PCR. The expression of p53 was not significantly altered; however, the ac-p53 was decreased. Furthermore, the viability of LX-2 cells was significantly enhanced by TWEAK. The activity of SA-β-Gal was notably inhibited, showing a suppressing effect of TWEAK on the senescence of activated HSC. Primary cultured HSC on days 7 and 11 was used to examine the expression of TWEAK, Fn14, SIRT1, and the activity of SA-β-Gal. The result indicated that the mRNA of TWEAK, SIRT1, and Fn14 was all decreased on day 11 compared to that on day 7, and the activity of SA-β-Gal was higher on day 11 than that on day 7. The present study suggested that TWEAK enhanced the expression of SIRT1 and decreased the acetylation of p53, probably inhibiting the senescence of activated HSC in vitro, which provides a molecular basis for TWEAK as a potential target in the therapy of liver fibrosis. [ABSTRACT FROM AUTHOR]

Lithium-sulfur (Li−S) batteries are one of the most promising candidates for the next generation of energy-storage devices owing to their high theoretical energy and low cost. However, low practical energy density and poor cycling life are obstacles to the practical application of Li−S batteries. A highly conductive and lightweight poly(3,4-ethylenedioxythiophene):polystyrene sulfonate-carbon nanotube (PEDOT:PSS-CNT) interlayer for Li−S batteries has been fabricated. The PEDOT:PSS-CNT interlayer not only acts as a soft buffer to scavenge excess lithium polysulfides in the pores and restricts polysulfides from migrating to the lithium anode by chemical absorption, but also serves as an assisted 'current collector' to improve the electronic conductivity for the sulfur cathode. With these synergistic contributions, pure sulfur cathode with the PEDOT:PSS-CNT interlayer shows a high capacity (921 mA h g−1at 0.5 C; 1 C=1675 mA h g−1), enhanced cycling performance (a capacity retention of 70.9 % after 200 cycles), and good rate performance. The excellent electrochemical performance of the sulfur cathode plus the easy fabrication of such a functional interlayer bring feasible Li−S batteries for practical applications one step closer. [ABSTRACT FROM AUTHOR]

As a cancer stem cell marker, CD44 variant 6 (CD44v6) has been implicated in carcinogenesis, tumor progression, and metastasis in a variety of human carcinomas. However, little is known about the expression of CD44v6 in Gastric Carcinoma (GC). Therefore we investigated CD44v6 expression in clinical specimen and further explore the underlying molecular mechanisms. In this study, we systemically investigated CD44v6 expression by immunohistochemistry in normal, premalignant gastric mucosa (low and high grade intraepithelial neoplasia), and GC at various stages. The correlation of CD44v6 expression with clinicopathological characteristics, and prognosis in GC was also analyzed. Next, we investigated cell proliferation, migration and invasion in GC cell lines. Furthermore, we explored a novel mechanism by which CD44V6 was upregulated in GC cell. The immunohistochemistry results showed that enhanced expression of CD44v6 was closely associated with tumor differentiation, lymph node metastasis, TNM stage and poor prognosis in GC patients. In gastric cancer cell lines, CD44v6 involved in cell proliferation, invasion and metastasis in Next, report on a novel mechanism by which interleukin-6/signal transducer and activator of transcription 3 (IL-6/STAT3) signaling up-regulates expression of CD44v6. RNA interference silencing of STAT3 resulted in decrease of CD44v6 levels. We also found that STAT3 inhibitor AG490 decrease expression of CD44v6 by blocking activation of STAT3, even in the presence of IL-6. Targeting STAT3-mediated CD44v6 up-regulation may represent a novel, effective treatment by eradicating the stomach tumor microenvironment., Version of Record