The investigation aims to analyze the effect of homogenization heat treatment on the quantity, distribution, morphology, and chemical composition of δ ferrite and sigma phase in the 316L austenitic stainless steel cast billet. Microstructures of the cast billet at different locations, center, 0.5 R, R, and the subsequent 2/6-hour homogenization heat treatment at 1240 oC were examined. The microstructure at the radius R was much more uniform and expected a better performance in the following hot/cold forging processes due to the highest cooling rate compared with those at 0.5R and center. The δ ferrite often accompanies the generation of the sigma phase, and the transformation of δ ferrite into the sigma/(austenite) and retained δ ferrite is strongly related to the cooling rate after homogenization heat treatment. The sigma phase is hard and detrimental to the subsequent hot/cold forgings. It must be removed from the homogenization heat treatment before forging. Fast air cooling from 850 oC to room temperature after homogenization heat treatment cannot prohibit the sigma phase formation. Rapid cooling between 850 and 1240 oC after homogenization treatment is required to avoid the sigma phase formation in the 316L stainless steel cast billet.

Wireless sensor networks are usually applied in hostile areas where nodes are easy to be moni-tored and captured by adversary. Key distribution is an essential primitive to provide most of security mechanism. However, the characteristic of limited resources of sensors restricts the direct use of conventional key distribution schemes. In this paper, a complete security key distribution scheme based on asymmetric cryptography technology is proposed in both static and mobile scenarios. Mutual authentication is guaranteed using challenge-response mechanism. The per-formance evaluation and security analysis show that the proposed scheme with low complexity not only provides better security for wireless sensor networks, but also reduces storage overhead and key exposure risks.

Laminopathies are a spectrum of diseases caused by LMNA mutations. In familial partial lipodystrophy of Dunnigan (FPLD), LMNA plays role in the differentiation and development of adipocytes and lipid metabolism. Changes in LMNA predict not only the differentiation of adipose-derived mesenchymal stem cells (AD-MSCs) but also the transformation of cancer cells. Hence, our in-depth study aimed to identify the molecular connection between disordered lipid metabolism and hepatic carcinogenesis. We first discovered significant positive correlations between pLMNA and two key rate-limiting enzymes in de novo fatty acid synthesis, acetyl-CoA-carboxylase 1 (ACC1) and fatty acid synthase (FASN), in the liver tissue but not in adipose tissue of obese model rats. Moreover, LMNA knockdown (KD) in rat AD-MSCs prevented the differentiation and maturation of adipocytes. To clarify the mechanistic relationship with lipogenesis, gain- and loss-of-function experiments in which functional changes and the related molecular pathways were investigated in a normal hepatocyte line (7701 cells). Adenosine 5'-monophosphate activated protein kinase α (AMPKα) was found to be activated by abnormalities in the LMNA structure under conditions of LMNA deletion, farnesyltransferase inhibitor (FTI) treatment and LMNA mutations associated with clinical FPLD pathogenic phenotype. Active AMPKα could directly phosphorylate ACC1 and thus inhibit lipid synthesis but induced glycolysis in both HCC cells and normal cells. The HCC cells could not survive with LMNA knockout (KO) or even KD. Lonafarnib (an FTI) combined with low-glucose conditions significantly decreased the proliferation of HepG2 and MHCC cells by inhibiting glycolysis and the maturation of prelamin A.

Malignant gliomas are heterogeneous neoplasms. Glioma stem-like cells (GSCs) are undifferentiated and self-renewing cells that develop and maintain these tumors. These cells are the main population that resist current therapies. Genomic and epigenomic analyses has identified various molecular subtypes. Bone morphogenetic protein 4 (BMP4) reduces the number of GSCs through differentiation and induction of apoptosis, thus increasing therapeutic sensitivity. However, the short half-life of BMP4 impedes its clinical application. We have previously reviewed BMP4 signaling in central nervous system development and glioma tumorigenesis and its’ potential as a treatment target in human gliomas. Recent advances in understanding both adult and pediatric malignant gliomas highlight critical roles of BMP4 signaling pathways in the regulation of tumor biology, and indicate its’ potential as a therapeutic molecule. Furthermore, significant progress has been made on synthesizing BMP4 biocompatible delivery materials, which can bind to and markedly extend BMP4 half-life. Here, we review current research associated with BMP4 in brain tumors, especially in pediatric malignant gliomas. We also summarize BMP4 delivery strategies, with a focus on biocompatible BMP4 binding peptide amphiphile nanostructures as promising novel delivery platforms for treatment of these devastating tumors.