Background and Purpose-Ischemic postconditioning (Postcond) is defined as a series of intermittent interruptions of blood flow in the early phase of reperfusion that mechanically alters the hydrodynamics of reperfusion. A recent study showed that Postcond reduced infarct size in cerebral ischemia/reperfusion (I/R) injury. However, little is known about the mechanisms of Postcond in cerebral I/R injury. In the present study, we investigated the effects of Postcond in focal cerebral I/R injury in the rat middle cerebral artery occlusion model. Methods-Adult male Sprague-Dawley rats were treated with Postcond after 60 minutes of occlusion (beginning of reperfusion). Neurologic scores and infarct volumes were assessed at 24 and 72 hours. Oxidative stress was evaluated by malondialdehyde assay, and apoptosis-related molecules were studied by Western blotting. Results-Postcond treatment upregulated Bcl-2 and heat-shock protein 70 expression and downregulated cytochrome c release to the cytosol, Bax translocation to the mitochondria, and caspase-3 activity. Postcond treatment also reduced infarct volumes and oxidative stress levels and improved neurologic scores compared with the I/R-only group. Conclusions-These findings indicate that Postcond inhibits focal cerebral I/R injury. This neuroprotective effect is likely achieved by antiapoptotic mechanisms.

Circular RNAs (circRNAs) are ubiquitous endogenous RNA found in various organisms that can regulate gene expression in eukaryotes. However, little is known about potential roles for circRNAs in muscle development. We analyzed circRNA sequencing data of bovine skeletal muscle tissue and found differential expression of circTitin (circTTN) in fetal and adult bovine muscle tissue. We then further studied the role of circTTN in bovine muscle development. Overexpression and inhibition of circTTN together elicited its promoting roles in proliferation and differentiation of bovine primary myoblasts. Mechanistically, circTTN showed interaction with miR-432 by luciferase screening and RNA immunoprecipitation (RIP) assays. Additionally, miR-432 is a regulator of insulin-like growth factor 2 (IGF2), as indicated by luciferase activity, quantitative real-time PCR, and western blotting assays. Increased miR-432 expression inhibited the expression of IGF2, but this effect was remitted by circTTN. Conclusively, our results showed that circTTN promoted proliferation and differentiation of bovine primary myoblasts via competitively combining with miR-432 to activate the IGF2/phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway.

Adipose development is regulated by a series of complex processes, and non-coding RNAs (ncRNAs), including circular RNAs (circRNAs), play important roles in regulating proliferation and differentiation of adipocytes. In this study, we profiled circRNA expression in cattle fat tissue during calf and adult developmental stages and detected 14,274 circRNA candidates. Some circRNAs are differentially expressed between two developmental stages. We characterized circFUT10, named for its host gene FUT10, a highly expressed and abundant circRNA. Luciferase screening, an RNA-binding protein immunoprecipitation (RIP) assay, quantitative real-time PCR, and western blotting assays indicated that circFUT10 directly binds let-7c/let-e, and PPARGC1B (peroxisome proliferator-activated receptor g coactivator 1-b) is identified as a target of let-7c. Flow cytometry, EdU (5-ethynyl-2 0 -deoxyuridine) incorporation, a CCK-8 (cell counting kit-8) assay, oil red O staining, and western blotting assays demonstrated that circFUT10 promotes adipocyte proliferation and inhibits cell differentiation by sponging let-7c. The results demonstrate that circFUT10 binding of let-7c promotes cell proliferation and inhibits cell differentiation by targeting PPARGC1B in cattle adipocytes.

Osteosarcoma (OS) is a tumor with rapid progression, high metastatic potential and poor clinical prognosis. This study was aimed to investigate the function of miR-126 in OS cells. The miR-126 expression in OS cell lines and OS tissues were explored by qRT-PCR. Then, the effects of miR-126 on proliferation, cycle, migration, invasion, and transforming growth factor (TGF)-β1 induced epithelial to mesenchymal transition (EMT) were assessed. Predicted by TargetScan, one of target genes for miR-126 was verified by luciferase activity assay. Meantime, the mRNA and protein expressions of ZEB1 were assessed by qRT-PCR and Western blot assay. Subsequently, the effect of ZEB1 silence on miR-126 down-regulated cells was also evaluated. Finally, the expressions of key kinases involved in c-Jun N-terminal kinase (JNK) and Janus-activated kinase (JAK)-1/signal transducer and activator of transcription (STAT)-3 pathways were detected by Western blot analysis. Result showed that miR-126 was down-regulated in OS tissues and cell lines. Overexpression of miR-126 significantly inhibited cell proliferation, migration, invasion, and TGF-β1 induced EMT. The effect of miR-126 knockdown was just the opposite. ZEB1 was predicted and verified as a target gene of miR-126. Meantime, the influence of miR-126 knockdown was abrogated by ZEB1 silence. Additionally, the phosphorylation levels of c-Jun, JNK, JAK1, and STAT3 were down-regulated in miR-126 over-expressed cells, and the effect of miR-126 knockdown was reversed by ZEB1 silence. In conclusion, miR-126 inhibits proliferation, migration, invasion and EMT in OS by targeting ZEB1 through inactivation of JNK and JAK1/STAT3 pathways. J. Cell. Biochem. 118: 3765-3774, 2017. © 2017 Wiley Periodicals, Inc.

HighlightsOur study can provide a comprehensive assessment on the impacts of the plastic film mulching.We assessed the effects of plastic film mulching on soil physical and biochemical properties.The spring maize yield was significantly increased with plastic film mulching in Northwest China.

Large-scale genomics studies have identified recurrently mutated genes in the ETS gene family, including fusions and copy number variations (CNVs), which are involved in the development of prostate adenocarcinoma (PRAD). However, the aetiology of PRAD remains to be fully elucidated. In the present study, 333 driver genes were identified using four computational tools: OncodriveFM, OncodriveCLUST, iCAGES and DrGaP. In addition, 32 driver pathways were identified using DrGaP. SPOP, TP53, SPTA1, AHNAK, HMCN1, ATM, FOXA1, CSMD3, LRP1B and FREM2 were the 10 most recurrently mutated genes in PRAD. ITGAL, TAGAP, SIGLEC10, RAC2 and ITGA4 were the five hub genes in the yellow module that were associated with the number of positive lymph nodes. Hierarchical clustering analysis of the 20 driver genes with the most frequent CNVs revealed three clusters of patients with PRAD. Cluster 3 tumours exhibited significantly higher numbers of positive lymph nodes, higher Gleason scores, more advanced cancer stages and poorer prognosis than cluster 1 and 2 tumours. A total of 48 genes were significantly associated with the number of positive lymph nodes, Gleason scores and pathologic stage in patients with PRAD. The identified set of cancer genes and pathways sheds light on the tumorigenesis of PRAD and creates avenues for the development of prognostic biomarkers and driver gene-targeted therapies in PRAD.

Spatial heterogeneity in the subsurface of karst environments is high, as evidenced by the multiphase porosity of carbonate rocks and complex landform features that result in marked variability of hydrological processes in space and time. This includes complex exchange of various flows (e.g., fast conduit flows and slow fracture flows) in different locations. Here, we integrate various “state‐of‐the‐art” methods to understand the structure and function of this poorly constrained critical zone environment. Geophysical, hydrometric, and tracer tools are used to characterize the hydrological functions of the cockpit karst critical zone in the small catchment of Chenqi, Guizhou Province, China. Geophysical surveys, using electrical resistivity tomography (ERT), inferred the spatial heterogeneity of permeability in the epikarst and underlying aquifer. Water tables in depression wells in valley bottom areas, as well as discharge from springs on steeper hillslopes and at the catchment outlet, showed different hydrodynamic responses to storm event rainwater recharge and hillslope flows. Tracer studies using water temperatures and stable water isotopes (δD and δ18O) could be used alongside insights into aquifer permeability from ERT surveys to explain site‐ and depth‐dependent variability in the groundwater response in terms of the degree to which “new” water from storm rainfall recharges and mixes with “old” pre‐event water in karst aquifers. This integrated approach reveals spatial structure in the karst critical zone and provides a conceptual framework of hydrological functions across spatial and temporal scales.

1Both these authors contributed equally to this work.Abbreviation used: CBF, cerebral blood flow; I/R, ischemia/reperfusion; ICAM, intercellular adhesion molecule; IL, interleukin; MDA, malondialdehyde; MCA, middle cerebral artery; MCAO, middle cerebral artery occlusion; MPO, myeloperoxidase; Post-cond, post-conditioning; TNF, tumor necrosis factor; TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling. AbstractIschemic post-conditioning (Post-cond) is a phenomenon in which intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/ R) injury. Recent studies demonstrated ischemic Post-cond reduced infarct size in cerebral I/R injury. However, the molecular mechanisms underlying this phenomenon are not completely understood. As inflammation is known to be detrimental to the neurological outcome during the acute phase after stroke, we investigated whether ischemic Post-cond played its protective role in preventing post-ischemic inflammation in the rat middle cerebral artery occlusion model. Rats were treated with ischemic Post-cond after 60 min of occlusion (beginning of reperfusion). The infarct volume and myeloperoxidase activity were assessed at 24 h. The lipid peroxidation levels was evaluated by malondialdehyde assay and the expressions of interleukin-1b, tumor necrosis factor-a, and intercellular adhesion molecule 1 were studied by RT-PCR or western blotting. Ischemic Post-cond decreased myeloperoxidase activity and expressions of interleukin-1b, tumor necrosis factor-a, and intercellular adhesion molecule 1. Ischemic Post-cond also reduced infarct volume and lipid peroxidation levels. These findings indicated that ischemic Post-cond may be a promising neuroprotective approach for focal cerebral I/R injury and it is achieved, at least in part, by the inhibition of inflammation.