Time-moisture superposition principle in creep behavior of white oak with various earlywood vessel locations

Creep behavior of wood plays a fundamental role in precision processing of wood. In this work, experi- mental creep tests have been conducted to determine the influence of earlywood vessel location and moisture content on creep behavior of Quercus alba (white oak). Time-moisture superposition principle was applied to predict long-term creep behavior of white oak. Results revealed that both of instantaneous and 45-min strain of specimens increased with the increasing of moisture content and decreased with increasing distance between earlywood vessel belt and load-bearing surface significantly. Additionally, the time-moisture superposition principle was found to have feasibility to predict creep behavior of white oak with various earlywood vessel locations and moisture content ranges (6 % - 18 %). We believe that the proposed investigation was beneficial for the processing precision and civil engineering applications of wood

Vitamin D binding protein variants associate with asthma susceptibility in the Chinese han population

<p>Abstract</p> <p>Background</p> <p>Asthma is a genetically heterogeneous disease. Polymorphisms of genes encoding components of the vitamin D pathway have been reported to associate with the risk of asthma. We have previously demonstrated that vitamin D status was associated with lung function in Chinese asthma patients. In this study, we tested whether polymorphisms of genes encoding for vitamin D receptor (<it>VDR</it>), vitamin D 25-hydroxylase (<it>CYP2R1</it>) and vitamin D binding protein (<it>GC</it>) were associated with asthma in the Chinese Han population.</p> <p>Methods</p> <p>We sequenced all 8 exons of <it>VDR </it>and all 5 exons of <it>CYP2R1 </it>in a Chinese case-control cohort of asthma consisting of 467 cases and 288 unrelated healthy controls. Two mutations were identified in these regions. These variants were specified as rs2228570 in exon 2 of <it>VDR </it>and rs12794714 in exon 1 of <it>CYP2R1</it>. We also genotyped two common polymorphisms in <it>GC </it>gene (rs4588 and rs7041) by a PCR-restriction fragment length polymorphism (RFLP) method. We analyzed the association between these 4 polymorphisms and asthma susceptibility and asthma-related traits.</p> <p>Results</p> <p>Polymorphic markers in <it>VDR </it>and <it>CYP2R1 </it>were not associated with asthma in the Chinese Han cohort. Importantly, variants in <it>GC </it>gene, which give rise to the two most common electrophoretic isoforms of the vitamin D binding protein, were associated with asthma susceptibility. Compared with isoform Gc1, Gc2 was significantly associated with the risk of asthma (OR = 1.35, 95% CI = 1.01-1.78 p = 0.006).</p> <p>Conclusions</p> <p>The results provide supporting evidence for association between <it>GC </it>variants and asthma susceptibility in the Chinese Han population.</p

Exposure time relevance of response to nitrite exposure: Insight from transcriptional responses of immune and antioxidant defense in the crayfish, Procambarus clarkii

Abstract(#br)To understand the toxic effects of nitrite exposure on crayfish, expression of genes involved in the immune system, the antioxidant defense, and the heat shock protein 70 (HSP70) was measured after 12, 24, and 48 h of different nitrite concentrations exposure in the hepatopancreas and hemocytes of Procambarus clarkii . Nitrite exposure up-regulated mRNA levels of cytoplasmic Mn superoxide dismutase (cMn-SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST), after 24 h nitrite exposure. At 48 h, nitrite exposure decreased the mRNA levels of mitochondrial MnSOD (mMn-SOD), CAT, and GPx. High concentrations of nitrite at 48 h of exposure decreased expression of β-1,3-glucan-bingding protein in the hepatopancreas, and lysozyme expression in hemocytes. Nitrite exposure caused little effect on the heat shock protein 70 (HSP70) in hemocytes. Through overall clustering analysis, we found that 24 h of nitrite exposure caused stronger transcriptional responses. Our study indicated that the response of P. clarkii to acute nitrite exposure was exposure time-dependent. These results will help to understand the dynamic response pattern of crustaceans to nitrite pollution, and improve our understanding of the toxicological mechanisms of nitrite in crustaceans

IRE1α Determines Ferroptosis Sensitivity Through Regulation of Glutathione Synthesis

Cellular sensitivity to ferroptosis is primarily regulated by mechanisms mediating lipid hydroperoxide detoxification. We show that inositol-requiring enzyme 1 (IRE1α), an endoplasmic reticulum (ER) resident protein critical for the unfolded protein response (UPR), also determines cellular sensitivity to ferroptosis. Cancer and normal cells depleted of IRE1α gain resistance to ferroptosis, while enhanced IRE1α expression promotes sensitivity to ferroptosis. Mechanistically, IRE1α\u27s endoribonuclease activity cleaves and down-regulates the mRNA of key glutathione biosynthesis regulators glutamate-cysteine ligase catalytic subunit (GCLC) and solute carrier family 7 member 11 (SLC7A11). This activity of IRE1α is independent of its role in regulating the UPR and is evolutionarily conserved. Genetic deficiency and pharmacological inhibition of IRE1α have similar effects in inhibiting ferroptosis and reducing renal ischemia-reperfusion injury in mice. Our findings reveal a previously unidentified role of IRE1α to regulate ferroptosis and suggests inhibition of IRE1α as a promising therapeutic strategy to mitigate ferroptosis-associated pathological conditions

Impact of GADD34 on Apoptosis of Tonsillar Mononuclear Cells from IgA Nephropathy Patients by Regulating Eif2α Phosphorylation

Background/Aims: Tonsillectomy may be an important method to achieve a long-term remission of IgAN, but patients’ physical status may limit their access to this surgery. We proposed an encouraging solution through inhibiting GADD34 expression in order to promote tonsillar mononuclear cells (TMCs) apoptosis and reduce nephropathic IgA secretion. Methods: A total of 12 IgAN and 9 non-IgAN patients were involved from March 2015 to May 2016. After TMCs were extracted by density gradient centrifugation and stimulated by inactivated hemolytic streptococcus, the mRNA and protein expression of GADD34, GRP78, CHOP, Bcl-2, Bcl-XL, AID, Iα-Cα, and cleaved caspase-3 were examined by fluorescent RT-PCR and Western blotting. Guanabenz treatment and siRNA interference were applied to downregulate GADD34 in tonsillar mononuclear cells from IgAN patients, and P-eIF2α expression was examined by Western Blotting. Cell apoptosis was evaluated by Annexin V FITC/PI flowcytometry, and IgA secretion in cultural supernatant was inspected by enzyme linked immunosorbent assay. Results: After stimulation, the expression of GADD34 was significantly increased in IgAN patients (P&#x3c; 0.05). Cell apoptosis was mitigated and IgA secretion level was elevated (P&#x3c; 0.05). To be noticed, CHOP expression had no significant difference between two groups. After guanabenz treatment and siRNA interference, a prolonged elevation of P-eIF2α expression was observed. Cell apoptosis was reinforced and IgA secretion level was decreased (P&#x3c; 0.05). Conclusion: GADD34 may be a potential therapeutic target for IgAN treatment due to its effect on cell apoptosis

Development of a synchronous recording and photo-stimulating electrode in multiple brain neurons

The investigation of brain networks and neural circuits involves the crucial aspects of observing and modulating neurophysiological activity. Recently, opto-electrodes have emerged as an efficient tool for electrophysiological recording and optogenetic stimulation, which has greatly facilitated the analysis of neural coding. However, implantation and electrode weight control have posed significant challenges in achieving long-term and multi-regional brain recording and stimulation. To address this issue, we have developed a mold and custom-printed circuit board-based opto-electrode. We report successful opto-electrode placement and high-quality electrophysiological recordings from the default mode network (DMN) of the mouse brain. This novel opto-electrode facilitates synchronous recording and stimulation in multiple brain regions and holds promise for advancing future research on neural circuits and networks

YY1 directly interacts with myocardin to repress the triad myocardin/SRF/CArG box-mediated smooth muscle gene transcription during smooth muscle phenotypic modulation

Yin Yang 1 (YY1) regulates gene transcription in a variety of biological processes. In this study, we aim to determine the role of YY1 in vascular smooth muscle cell (VSMC) phenotypic modulation both in vivo and in vitro. Here we show that vascular injury in rodent carotid arteries induces YY1 expression along with reduced expression of smooth muscle differentiation markers in the carotids. Consistent with this finding, YY1 expression is induced in differentiated VSMCs in response to serum stimulation. To determine the underlying molecular mechanisms, we found that YY1 suppresses the transcription of CArG box-dependent SMC-specific genes including SM22α, SMα-actin and SMMHC. Interestingly, YY1 suppresses the transcriptional activity of the SM22α promoter by hindering the binding of serum response factor (SRF) to the proximal CArG box. YY1 also suppresses the transcription and the transactivation of myocardin (MYOCD), a master regulator for SMC-specific gene transcription by binding to SRF to form the MYOCD/SRF/CArG box triad (known as the ternary complex). Mechanistically, YY1 directly interacts with MYOCD to competitively displace MYOCD from SRF. This is the first evidence showing that YY1 inhibits SMC differentiation by directly targeting MYOCD. These findings provide new mechanistic insights into the regulatory mechanisms that govern SMC phenotypic modulation in the pathogenesis of vascular diseases