SiC Conversion Coating Prepared from Silica-Graphite Reaction

The β-SiC conversion coatings were successfully synthesized by the SiO(v)-graphite(s) reaction between silica powder and graphite specimen. This paper is to describe the effects on the characteristics of the SiC conversion coatings, fabricated according to two different reaction conditions. FE-SEM, FE-TEM microstructural morphologies, XRD patterns, pore size distribution, and oxidation behavior of the SiC-coated graphite were investigated. In the XRD pattern and SAD pattern, the coating layers showed cubic SiC peak as well as hexagonal SiC peak. The SiC coatings showed somewhat different characteristics with the reaction conditions according to the position arrangement of the graphite samples. The SiC coating on graphite, prepared in reaction zone (2), shows higher intensity of beta-SiC main peak (111) in XRD pattern as well as rather lower porosity and smaller main pore size peak under 1 μm

Endoplasmic Reticulum Stress in the β-Cell Pathogenesis of Type 2 Diabetes

Type 2 diabetes is a complex metabolic disorder characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency by β-cell failure. Even if the mechanisms underlying the pathogenesis of β-cell failure are still under investigation, recent increasing genetic, experimental, and clinical evidence indicate that hyperactivation of the unfolded protein response (UPR) to counteract metabolic stresses is closely related to β-cell dysfunction and apoptosis. Signaling pathways of the UPR are “a double-edged sword” that can promote adaptation or apoptosis depending on the nature of the ER stress condition. In this paper, we summarized our current understanding of the mechanisms and components related to ER stress in the β-cell pathogenesis of type 2 diabetes

Microstructures and Electrochemical Behavior of Ti-Mo Alloys for Biomaterials

The Ti alloy with 7 wt% Mo revealed a microstructure that contained only the orthorhombic α′′ phase of a fine acicular martensitic structure. The corrosion resistance of the Ti-Mo alloys increased as the Mo content increased. Based on the results obtained from the polarization curve and electrochemical impedance, the Ti-Mo alloys were shown to be corrosion resistant because of the passive films formed on their surfaces. No ion release was detected in SBF (simulated body fluid) solution, while Ti ions were released in 0.1% lactic acid ranging from 0.05 to 0.12 μg/mL for the Ti-Mo alloys. In vitro tests showed that MC3T3-E1 cell proliferation on Ti-7 wt% Mo alloy was rather active compared to other Ti-Mo alloys and commercial-grade pure Ti

Autophagy deficiency leads to protection from obesity and insulin resistance by inducing Fgf21 as a mitokine

Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear. We produced mice with skeletal muscle–specific deletion of Atg7 (encoding autophagy-related 7). Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21). Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response. Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner. We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue. These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance

Polypyrimidine Tract-Binding Protein Enhances the Internal Ribosomal Entry Site-Dependent Translation of p27(Kip1) mRNA and Modulates Transition from G(1) to S Phase

The p27(Kip1) protein plays a critical role in the regulation of cell proliferation through the inhibition of cyclin-dependent kinase activity. Translation of p27(Kip1) is directed by an internal ribosomal entry site (IRES) in the 5′ nontranslated region of p27(Kip1) mRNA. Here, we report that polypyrimidine tract-binding protein (PTB) specifically enhances the IRES activity of p27(Kip1) mRNA through an interaction with the IRES element. We found that addition of PTB to an in vitro translation system and overexpression of PTB in 293T cells augmented the IRES activity of p27(Kip1) mRNA but that knockdown of PTB by introduction of PTB-specific small interfering RNAs (siRNAs) diminished the IRES activity of p27(Kip1) mRNA. Moreover, the G(1) phase in the cell cycle (which is maintained in part by p27(Kip1)) was shortened in cells depleted of PTB by siRNA knockdown. 12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced differentiation in HL60 cells was used to examine PTB-induced modulation of p27(Kip1) protein synthesis during differentiation. The IRES activity of p27(Kip1) mRNA in HL60 cells was increased by TPA treatment (with a concomitant increase in PTB protein levels), but the levels of p27(Kip1) mRNA remained unchanged. Together, these data suggest that PTB modulates cell cycle and differentiation, at least in part, by enhancing the IRES activity of p27(Kip1) mRNA

Sequestration of TRAF2 into Stress Granules Interrupts Tumor Necrosis Factor Signaling under Stress Conditions

The cellular stress response (SR) is a phylogenetically conserved protection mechanism that involves inhibition of protein synthesis through recruitment of translation factors such as eIF4G into insoluble stress granules (SGs) and blockade of proinflammatory responses by interruption of the signaling pathway from tumor necrosis factor alpha (TNF-α) to nuclear factor-κB (NF-κB) activation. However, the link between these two physiological phenomena has not been clearly elucidated. Here we report that eIF4GI, which is a scaffold protein interacting with many translation factors, interacts with TRAF2, a signaling molecule that plays a key role in activation of NF-κB through TNF-α. These two proteins colocalize in SGs during cellular exposure to stress conditions. Moreover, TRAF2 is absent from TNFR1 complexes under stress conditions even after TNF-α treatment. This suggests that stressed cells lower their biological activities by sequestration of translation factors and TRAF2 into SGs through a protein-protein interaction

Effect of Storage Period on the Changes of Odorous Compound Concentrations and Bacterial Ecology for Identifying the Cause of Odor Production from Pig Slurry.

Odor from buildings where pigs are housed is generated by anaerobic fermentation of undigested materials in pig slurry stored for several weeks in pit. The objective of this study was to investigate the effect of storage period on the level of odorous compounds in pig slurry and on its bacterial community. A slurry sample (15 L) was taken from the pit of a finisher pig building and incubated in acryl chambers for six- weeks. Slurry for analysis was sampled every two-week. Levels of odorous compounds in the slurry sample were drastically changed after two weeks of storage period; levels of phenols and short chain fatty acids (SCFAs) were decreased (P<0.05), whereas indoles and branched-chain fatty acids (BCFAs) were increased (P<0.05). Among dominant bacteria, Bacteroides and Porphyromonadacese_uc_g revealed a strong positive correlation with the levels of phenols and SCFAs. Populations of AC160630_g, Acholeplasmatales_uc_g, Mollicutes_uc_g and Cloacamonas_f_uc_g positively correlated with indole and BCFAs content. Taken together, levels of odorous compounds were increased after two weeks of storage, possibly because of changes in the predominant bacterial groups to those that use protein as a carbon source in the hypo-carbohydrate conditions

Extending Task-level to Job-level Fixed Priority Assignment and Schedulability Analysis Using Pseudo-deadlines

Abstract—In global real-time multiprocessor scheduling, a recent analysis technique for Task-level Fixed-Priority (TFP) scheduling has been shown to outperform many of the analyses for Job-level Fixed-Priority (JFP) scheduling on average. Since JFP is a generalization of TFP scheduling, and the TFP analysis technique itself has been adapted from an earlier JFP analysis, this result is counter-intuitive and in our opinion highlights the lack of good JFP scheduling techniques. Towards generalizing the superior TFP analysis to JFP scheduling, we propose the Smallest Pseudo-Deadline First (SPDF) JFP scheduling algorithm. SPDF uses a simple task-level parameter called pseudo-deadline to prioritize jobs, and hence can behave as a TFP or JFP scheduler depending on the values of the pseudodeadlines. This natural transition from TFP to JFP scheduling has enabled us to incorporate the superior TFP analysis technique in an SPDF schedulability test. We also present a pseudo-deadline assignment algorithm for SPDF scheduling that extends the well-known Optimal Priority Assignment (OPA) algorithm for TFP scheduling. We show that our algorithm is optimal for the derived schedulability test, and also present a heuristic to overcome the computational complexity issue of the optimal algorithm. Our simulation results show that the SPDF algorithm with the new analysis significantly outperforms state-of-the-art TFP and JFP analysis. I