Limb remote ischemic preconditioning (RIPC) is an effective means of protection against ischemia/reperfusion (IR)–induced injury to multiple organs. Many studies are focused on identifying endocrine mechanisms that underlie the cross-talk between muscle and RIPC-mediated organ protection. We report that RIPC releases irisin, a myokine derived from the extracellular portion of fibronectin domain–containing 5 protein (FNDC5) in skeletal muscle, to protect against injury to the lung. Human patients with neonatal respiratory distress syndrome show reduced concentrations of irisin in the serum and increased irisin concentrations in the bronchoalveolar lavage fluid, suggesting transfer of irisin from circulation to the lung under physiologic stress. In mice, application of brief periods of ischemia preconditioning stimulates release of irisin into circulation and transfer of irisin to the lung subjected to IR injury. Irisin, via lipid raft–mediated endocytosis, enters alveolar cells and targets mitochondria. Interaction between irisin and mitochondrial uncoupling protein 2 (UCP2) allows for prevention of IR-induced oxidative stress and preservation of mitochondrial function. Animal model studies show that intravenous administration of exogenous irisin protects against IR-induced injury to the lung via improvement of mitochondrial function, whereas in UCP2-deficient mice or in the presence of a UCP2 inhibitor, the protective effect of irisin is compromised. These results demonstrate that irisin is a myokine that facilitates RIPC-mediated lung protection. Targeting the action of irisin in mitochondria presents a potential therapeutic intervention for pulmonary IR injury.

Classical force fields have been broadly used in studies of metal–organic framework crystals. However, processes involving bond breaking or forming are prohibited due to the nonreactive nature of the potentials. With emerging trends in the study of zeolitic imidazolate frameworks (ZIFs) that include glass formation, defect engineering, and chemical stability, enhanced computational methods are needed for efficient computational screening of ZIF materials. Here, we present simulations of three ZIF compounds using a ReaxFF reactive force field. By simulating the melt–quench process of ZIF-4, ReaxFF can reproduce the atomic structure, density, thermal properties, and pore morphology of the glass formed (a gZIF-4), showing remarkable agreement with experimental and first-principles molecular dynamics results. The predictive capability of ReaxFF is further exemplified in the melting of ZIF-62, where the balancing of electronic and steric effects of benzimidazolate yields a lower T m. On the basis of the electron-withdrawing effect of the −NO2 group, ReaxFF simulations predict that ZIF-77 has an even lower T m in terms of Zn–N interaction, but its low chemical stability makes it unsuitable as a glass former. Because of its low computational cost and transferability, ReaxFF will enable the computational design of ZIF materials by accounting for properties associated with disorder/defects.

We have previously shown that the integrin ␤ 6 is neoexpressed in invasive oral squamous cell carcinoma (SCC) and is correlated with oral tumor progression. However, the mechanism by which the integrin ␤ 6 promotes oral tumor progression is not well understood. The purpose of the present study was to determine whether integrin ␤ 6 signaling activates Fyn and thus promotes oral squamous cell carcinoma progression. We analyzed the integrin ␤ 6 signaling complex and investigated the function of these signaling molecules in oral SCC cells. We found that, upon ligation of the integrin ␤ 6 with fibronectin, ␤ 6 complexed with Fyn and activated it. The activation of Fyn recruited and activated focal adhesion kinase to this complex. This complex was necessary to activate Shc and to couple ␤ 6 signaling to the Raf-ERK/MAPK pathway. This pathway transcriptionally activated the matrix metalloproteinase-3 gene and promoted oral SCC cell proliferation and experimental metastasis in vivo. These findings indicate that integrin ␤ 6 signaling activates Fyn and thus promotes oral cancer progression.

IntroductionEpidemiological evidence suggests that overweight and obesity have been associated with acute myocardial infarction (AMI). However, data on this issue are controversial. This study aims to use meta-analysis to determine whether overweight and obesity are related to AMI.Material and methodsWe searched PubMed and Embase databases up to October 23rd, 2013 for related literature. The association of overweight and obesity with AMI was assessed by odd ratio (OR) with 95% confidence interval (CI) as the effect size. Then subgroup analysis was performed according to gender, area and study type.ResultsFive primary studies (one cohort study and four case-control studies) were included in this meta-analysis involving 36 803 participants, 14 883 of whom had an AMI. There was a significant association between overweight and AMI (OR = 1.27, 95% CI: 1.21–1.33, p < 0.001). Similar results revealed a relation between obesity and AMI (OR = 1.22, 95% CI: 1.07–1.40, p = 0.003). Subgroup analysis showed that overweight and obesity were positively associated with AMI risk except for obese subjects in Europe. There was no publication bias (Begg's test p = 0.972, Egger's test p = 0.858).ConclusionsBoth overweight and obesity increased the incidence of AMI, and it is necessary to control weight to prevent AMI. A large number of studies is needed to explore the mechanisms that link overweight and obesity with AMI.

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conclusionsOur results suggest that dietary capsaicin protects against cardiac hypertrophy and fibrosis in pressure overload mice through TRPV1.