Experimental analysis for the effect of dynamic capillarity on stress transformation in porous silicon

The evolution of real-time stress in porous silicon(PS) during drying is investigated using micro-Raman spectroscopy. The results show that the PS sample underwent non-negligible stress when immersed in liquid and suffered a stress impulsion during drying. Such nonlinear transformation and nonhomogeneneous distribution of stress are regarded as the coupling effects of several physical phenomena attributable to the intricate topological structure of PS. The effect of dynamic capillarity can induce microcracks and even collapse in PSstructures during manufacture and storage.This work is funded by the National Natural Science Foundation of China Contract Nos. 10732080 and 10502014

SIRT3 Protects Rotenone-induced Injury in SH-SY5Y Cells by Promoting Autophagy through the LKB1-AMPK-mTOR Pathway.

SIRT3 is a class III histone deacetylase that modulates energy metabolism, genomic stability and stress resistance. It has been implicated as a potential therapeutic target in a variety of neurodegenerative diseases, including Parkinson's disease (PD). Our previous study demonstrates that SIRT3 had a neuroprotective effect on a rotenone-induced PD cell model, however, the exact mechanism is unknown. In this study, we investigated the underlying mechanism. We established a SIRT3 stable overexpression cell line using lentivirus infection in SH-SY5Y cells. Then, a PD cell model was established using rotenone. Our data demonstrate that overexpression of SIRT3 increased the level of the autophagy markers LC3 II and Beclin 1. After addition of the autophagy inhibitor 3-MA, the protective effect of SIRT3 diminished: the cell viability decreased, while the apoptosis rate increased; α-synuclein accumulation enhanced; ROS production increased; antioxidants levels, including SOD and GSH, decreased; and MMP collapsed. These results reveal that SIRT3 has neuroprotective effects on a PD cell model by up-regulating autophagy. Furthermore, SIRT3 overexpression also promoted LKB1 phosphorylation, followed by activation of AMPK and decreased phosphorylation of mTOR. These results suggest that the LKB1-AMPK-mTOR pathway has a role in induction of autophagy. Together, our findings indicate a novel mechanism by which SIRT3 protects a rotenone-induced PD cell model through the regulation of autophagy, which, in part, is mediated by activation of the LKB1-AMPK-mTOR pathway

Poly[diaqua­(μ2-oxalato-κ4 O 1,O 2:O 1′,O 2′)(μ2-pyrazine-2-carboxyl­ato-κ4 N 1,O:O,O′)neodymium(III)]

In the title complex, [Nd(C5H3N2O2)(C2O4)(H2O)2]n, the NdIII atom is ten-coordinated by one N atom and three O atoms from two pyrazine-2-carboxyl­ate ligands, four O atoms from two oxalate ligands and two water mol­ecules in a distorted bicapped square-anti­prismatic geometry. The two crystallographically independent oxalate ligands, each lying on an inversion center, act as bridging ligands, linking Nd atoms into an extended zigzag chain. Neighboring chains are linked by the pyrazine-2-carboxyl­ate ligands into a two-dimensional layerlike network in the (10) plane. The layers are further connected by O—H⋯O and O—H⋯N hydrogen bonds, forming a three-dimensional supra­molecular network

Erythromycin Enhances CD4+Foxp3+ Regulatory T-Cell Responses in a Rat Model of Smoke-Induced Lung Inflammation

Heavy smoking can induce airway inflammation and emphysema. Macrolides can modulate inflammation and effector T-cell response in the lungs. However, there is no information on whether erythromycin can modulate regulatory T-cell (Treg) response. This study is aimed at examining the impact of erythromycin on Treg response in the lungs in a rat model of smoking-induced emphysema. Male Wistar rats were exposed to normal air or cigarette smoking daily for 12 weeks and treated by gavage with 100 mg/kg of erythromycin or saline daily beginning at the forth week for nine weeks. The lung inflammation and the numbers of inflammatory infiltrates in bronchoalveolar lavage fluid (BALF) were characterized. The frequency, the number of Tregs, and the levels of Foxp3 expression in the lungs and IL-8, IL-35, and TNF-α in BALF were determined by flow cytometry, RT-PCR and ELISA, respectively. Treatment with erythromycin reduced smoking-induced inflammatory infiltrates, the levels of IL-8 and TNF-α in the BALF and lung damages but increased the numbers of CD4+Foxp3+ Tregs and the levels of Foxp3 transcription in the lungs, accompanied by increased levels of IL-35 in the BALF of rats. Our novel data indicated that erythromycin enhanced Treg responses, associated with the inhibition of smoking-induced inflammation in the lungs of rats

4-(4-Pyrid­yl)pyridinium 3′,4,4′-tricarboxy­biphenyl-3-carboxyl­ate dihydrate

In the title compound, C10H9N2 +·C16H9O8 −·2H2O, both the cation and anion possess crystallographically imposed centres of symmetry, causing the nitro­gen-bound H atom in the 4-(4-pyrid­yl)pyridinium cation and the acidic H atom of the carboxyl­ate groups at the 3 and 3′ positions in the anion to be disordered over two positions with equal occupancies. In the crystal packing, the cations, anions and water mol­ecules are connected by O—H⋯O, C—H⋯O and N—H⋯N hydrogen bonds, forming layers parallel to (20). These layer are further connected into a three-dimensional supra­molecular network by O—H⋯O hydrogen bonds involving the water mol­ecules as H-atom donors and by weak π–π stacking inter­actions between neighbouring benzene and pyridine rings, with centroid–centroid distances of 3.756 (5) Å

Protective Role of Hydrogen Sulfide against Noise-Induced Cochlear Damage: A Chronic Intracochlear Infusion Model

Background: A reduction in cochlear blood flow plays an essential role in noise-induced hearing loss (NIHL). The timely regulation of cochlear perfusion determines the progression and prognosis of NIHL. Hydrogen sulfide (H 2S) has attracted increasing interest as a vasodilator in cardiovascular systems. This study identified the role of H2S in cochlear blood flow regulation and noise protection. Methodology/Principal Findings: The gene and protein expression of the H2S synthetase cystathionine-c-lyase (CSE) in the rat cochlea was examined using immunofluorescence and real-time PCR. Cochlear CSE mRNA levels varied according to the duration of noise exposure. A chronic intracochlear infusion model was built and artificial perilymph (AP), NaHS or DLpropargylglycine (PPG) were locally administered. Local sodium hydrosulfide (NaHS) significantly increased cochlear perfusion post-noise exposure. Cochlear morphological damage and hearing loss were alleviated in the NaHS group as measured by conventional auditory brainstem response (ABR), cochlear scanning electron microscope (SEM) and outer hair cell (OHC) count. The highest percentage of OHC loss occurred in the PPG group. Conclusions/Significance: Our results suggest that H2S plays an important role in the regulation of cochlear blood flow and the protection against noise. Further studies may identify a new preventive and therapeutic perspective on NIHL and othe

GraphGrind: addressing load imbalance of graph partitioning

The incidence of HCAIs before and after antimicrobial stewardship. Incidence of VAP, CRBSI and CAUTI were defined as the number of VAP, CRBSI and CAUTI patients per 1000 ventilation days, per 1000 central venous catheter days and per 1000 urine-catheter days, respectively. (DOCX 15 kb