Rabbit Anti-Human VIM (Phospho-Ser72) polyclonal antibody

Corona discharge, or gas breakdown, is undesired in superalloy vacuum induction melting (VIM) applications as it can damage insulation, produce ozone and subsequently oxidize and contaminate the melt. Gas breakdown also introduces uncontrolled variations to the casting process and increases the risk of needing to scrap the end product. To reduce the risk of corona, a rule-of-thumb of 150 to 1000 micron (150 mTorr to 1 Torr) was developed in the past as a No-Go Pressure Zone. Operating within this zone has been observed to create an unwanted, readily ionizable environment. An analytical model is developed within this work to evaluate the historical rule-of-thumb. The analytical model incorporates the following elements: Paschen's law, gas compressibility, gas and insulation permittivity, and electric field non-uniformity. The model is then applied to a sampling of VIM furnace designs to evaluate the shifts of the No-Go Pressure Zone due to variations in configuration and other operating conditions. In the end, the objective is to improve VIM furnace design and operation to reduce the risk of corona discharge-thereby improving the casting process, practice of alloy melting and quality of the end product.

Persimmon (Diospyros kaki L.f.) trees are widely cultivated for their edible fruits in Asia. D. kaki leaves are abundant in phytochemicals that have numerous medicinal properties. Hepatocyte growth factor (HGF) and its receptor met lead to poor prognosis via the promotion of metastasis and chemoresistance in hepatocellular carcinoma (HCC). Therefore, inhibitors targeting the HGF/Met pathway are regarded as promising drugs against HCC. Here, we investigated the effects of D. kaki leaves on HGF-induced epithelial-to-mesenchymal transition (EMT) and stemness traits in HCC. The ethanol extract of D. kaki leaves (EEDK) markedly suppressed HGFmediated cell migration and invasion through upregulation of CDH1 and downregulation of SNAI1, VIM, MMP1, MMP2, and MMP9. Moreover, EEDK increased the cytotoxicity of sorafenib, which was reduced by HGF, and decreased the expression of the stemness markers KRT19 and CD44. Additionally, we found a clear correlation between stemness and EMT markers in HCC patients. Importantly, EEDK reduced met activity and attenuated HGF-mediated activation of JNK/c-Jun. Our findings provide new evidence that EEDK can ameliorate HCC with poor prognosis and aggressive phenotype by blocking HGF/Met signaling.