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With a network structure formed by cross-linking process, epoxy resins possess excellent mechanical properties. Among them, SU-8 photoresist (bisphenol-A epoxy resin) is widely used as coatings in microelectronic applications. This paper reports molecular dynamics simulations of the cross-linking process of SU-8 photoresist with detailed scripts and illustrates fracture behaviors of cross-linked network with in situ visualizations of atomistic details. The epoxy molecular models with the cross-linking degree of 20%, 40%, 60% and 80% are constructed, which possess density, glass transition temperature, and mechanical properties in a good agreement with existing experimental studies on SU-8. 1-Methyl-3-nitro-1-nitrosoguanidine supplier For the models with cross-linking degree of 60% and 80%, uncoiling phenomena observed during large-strain tensile deformations are proved to be associated with significant drops of stress and the dissipation of local concentrated energy developed within the stretched structure, which indicates that the coiling of molecular chains is a critical structure for strength of epoxy molecules. The findings from this paper enrich our understandings of molecular details of SU-8 photoresist upon fracture and contribute as a useful reference to atomistic modeling database of cross-linked polymers.Coronavirus disease 2019 caused by SARS-CoV-2 originated from China and spread across every corner of the world. The scientific interest on COVID-19 increased after WHO declared it a pandemic in the early February of 2020. In fact, this pandemic has had a worldwide impact on economy, health, and lifestyle like no other in the last 100 years. SARS-CoV-2 belongs to Coronaviridae family and causes the deadliest clinical manifestations when compared to other viruses in the family. COVID-19 is an emerging zoonotic disease that has resulted in over 383,000 deaths around the world. Scientists are scrambling for ideas to develop treatment and prevention strategies to thwart the disease condition. In this review, we have attempted to summarize the latest information on the virus, disease, prevention, and treatment strategies. The future looks promising.Bone provides skeletal support and functions as an endocrine organ by producing osteocalcin, whose uncarboxylated form (GluOC) increases the metabolism of glucose and lipid by activating its putative G protein-coupled receptor (family C group 6 subtype A). Low doses (≤10 ng/ml) of GluOC induce the expression of adiponectin, adipose triglyceride lipase and peroxisome proliferator-activated receptor γ, and promote active phosphorylation of lipolytic enzymes such as perilipin and hormone-sensitive lipase via the cAMP-PKA-Src-Rap1-ERK-CREB signaling axis in 3T3-L1 adipocytes. Administration of high-dose (≥20 ng/ml) GluOC induces programmed necrosis (necroptosis) through a juxtacrine mechanism triggered by the binding of Fas ligand, whose expression is induced by forkhead box O1, to Fas that is expressed in adjacent adipocytes. Furthermore, expression of adiponectin and adipose triglyceride lipase in adipocytes is triggered in the same manner as following low-dose GluOC stimulation; these effects protect mice from diet-induced accumulation of triglycerides in hepatocytes and consequent liver injury through the upregulation of nuclear translocation of nuclear factor-E2-related factor-2, expression of antioxidant enzymes, and inhibition of the c-Jun N-terminal kinase pathway. Evaluation of these molecular mechanisms leads us to consider that GluOC might have potential as a treatment for lipid metabolism disorders. Indeed, there have been many reports demonstrating the negative correlation between serum osteocalcin levels and obesity or non-alcoholic fatty liver disease, a common risk factor for which is dyslipidemia in humans. The present review summarizes the effects of GluOC on lipid metabolism as well as its possible therapeutic application for metabolic diseases including obesity and dyslipidemia.Cellular membranes are critical platforms for intracellular signaling that involve complex interfaces between lipids and proteins, and a web of interactions between a multitude of lipid metabolic pathways. Membrane lipids impart structural and functional information in this regulatory circuit that encompass biophysical parameters such as membrane thickness and fluidity, as well as chaperoning the interactions of protein binding partners. Phosphatidylinositol and its phosphorylated derivatives, the phosphoinositides, play key roles in intracellular membrane signaling, and these involvements are translated into an impressively diverse set of biological outcomes. The phosphatidylinositol transfer proteins (PITPs) are key regulators of phosphoinositide signaling. Found in a diverse array of organisms from plants, yeast and apicomplexan parasites to mammals, PITPs were initially proposed to be simple transporters of lipids between intracellular membranes. It now appears increasingly unlikely that the soluble versions of these proteins perform such functions within the cell. Rather, these serve to facilitate the activity of intrinsically biologically insufficient inositol lipid kinases and, in so doing, promote diversification of the biological outcomes of phosphoinositide signaling. The central engine for execution of such functions is the lipid exchange cycle that is a fundamental property of PITPs. How PITPs execute lipid exchange remains very poorly understood. Molecular dynamics simulation approaches are now providing the first atomistic insights into how PITPs, and potentially other lipid-exchange/transfer proteins, operate.PKC isozymes have been put in place as oncoproteins since the discovery that they can function as receptors for potent tumor-promoting phorbol esters in the 1980s. Despite nearly two decades of research, a clear in vivo proof of that concept was missing. The availability of so-called knock out mouse lines of individual PKC genes provided a tool to investigate isozyme specific in vivo functions in the context of tumor initiation, development and progression. This review aims to provide a limited overview of how the application of these mouse lines in combination with a cancer mouse model helped to understand PKC's in vivo function during tumorigenesis. The focus of this review will be on skin, colon and lung cancer.
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