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https://www.selleckchem.com/ 01). In this small sample, VMAT gives equal coverage with lower OAR and skin surface doses than HDR-BT for both scalp and extremities. VMAT is auseful technique for treating large, superficial volumes with significant curvature in one or more planes. In this small sample, VMAT gives equal coverage with lower OAR and skin surface doses than HDR-BT for both scalp and extremities. VMAT is a useful technique for treating large, superficial volumes with significant curvature in one or more planes.Missing. To examine the effects of small nucleolar RNA host gene 6 (SNHG6) on apoptosis during myocardial ischemic/reperfusion (I/R) injury and its potential molecular mechanisms. In vitro model of I/R was built through exposing mouse HL-1 cardiomyocytes to hypoxia/reoxygenation (H/R) treatment. Quantitative real-time polymerase chain reaction assays were performed to determine gene expression. Cell Counting Kit-8, flow cytometric and western blot assays were conducted to detect cell viability, apoptosis and protein expression. Lactate dehydrogenase (LDH) activity was examined by a commercial detection kit. Dual-luciferase gene reporter and RNA immunoprecipitation experiments were applied for determining the interaction between the molecules. SNHG6 expression was increased in H/R-challenged cardiomyocytes. Depletion of SNHG6 protected against H/R-induced cardiomyocytes apoptosis. SNHG6 could sponge miR-135a-5p to inhibit its expression. Down-regulation of miR-135a-5p reversed the anti-apoptotic effect caused by SNHG6 knockdown in H/R-induced cardiomyocytes. Hypoxia inducible factor 1 subunit alpha inhibitor (HIF1AN) was identified as a direct target of miR-135a-5p, and knockdown of HIF1AN relieved H/R-induced cardiomyocytes apoptosis. Silencing of SNHG6 activated Shh/Gli1 signalling pathway by regulating miR-135a-5p/HIF1AN. Furthermore, inactivation of Shh/Gli signalling abolished the anti-apoptotic effects of SNHG6 knockdown in H/R-induced cardiomyo

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