Background: Intestinal ischemia reperfusion (I/R) occurs in various diseases, such as trauma and intestinal transplantation. Excessive reactive oxygen species (ROS) accumulation and subsequent apoptotic cell death in intestinal epithelia are important causes of I/R injury. PTEN-induced putative kinase 1 (PINK1) and phosphorylation of dynamin-related protein 1 (DRP1) are critical regulators of ROS and apoptosis.
View Article and Find Full Text PDFPurpose: In this era of life highly comminuted and multi planar tibial plateau fractures involving the posterior corners are more commonly seen and addressed in the literature than before. Among these several types have not been described in the currently used classification systems. In fact simple classification systems ignore several fracture types and leniently grouped the fractures with different mechanism, morphology, treatment modalities and prognosis in same category.
View Article and Find Full Text PDFWe report regarding a young lady who presented with recurrent syncopal episodes associated with palpitations, documented to be due to rapid wide QRS tachycardia, subsequently detected to have thyrotoxicosis and who responded promptly to appropriate medication to become free from arrhythmia.
View Article and Find Full Text PDFBackground/aims: Ischemic postconditioning (iPoC) represents a promising strategy to mitigate ischemia/reperfusion (I/R) injury of the intestine, yet the mechanisms of this treatment remain to be elucidated. Circular RNAs (circRNAs), a novel class of endogenous non-coding RNAs, have recently been recognized as important regulators of gene expression and pathological processes. Here, we aimed to investigate the expression patterns of circRNAs after intestinal I/R with and without iPoC and, furthermore, to explore the potential mechanisms of iPoC in relation to the differentially expressed circRNAs.
View Article and Find Full Text PDFImpairment in gut barrier function induced by intestinal ischemia/reperfusion (I/R) injury is associated with high morbidity and mortality. Intestinal barrier function requires the tight coordination of epithelial migration, proliferation and differentiation. We previously observed that nuclear receptor-related protein 1 (nurr1)-mediated proliferative pathway was impaired in intestinal I/R injury.
View Article and Find Full Text PDFBackground: Clinically there are different fixation methods used for fixation of the posterior malleolar fractures (PMF), but the best treatment modality is still not clear. Few studies have concentrated on this issue, least of all using a biomechanical comparison. The purpose of this study was to carry out a computational comparative biomechanics of three different commonly used fixation constructs for the fixation of PMF by finite element analysis (FEA).
View Article and Find Full Text PDFIntestinal ischemia-reperfusion (I/R) is a common clinical problem that occurs during various clinical pathological processes. Excessive apoptosis has an indispensable role in intestinal I/R injury. Tumor necrosis factor receptor-associated factor 2 (TRAF2) and PKCζ have an essential role in apoptosis.
View Article and Find Full Text PDFPurpose: Appropriate fixation method for the posterior malleolar fractures (PMF) according to the fracture size is still not clear. Aim of this study was to evaluate the outcomes of the different fixation methods used for fixation of PMF by finite element analysis (FEA) and to compare the effect of fixation constructs on the size of the fracture computationally.
Materials And Methods: Three dimensional model of the tibia was reconstructed from computed tomography (CT) images.
Intestinal epithelial oxidative stress and apoptosis constitute key pathogenic mechanisms underlying intestinal ischemia/reperfusion (I/R) injury. We previously reported that the adaptor 66 kDa isoform of the adaptor molecule ShcA (p66Shc)-mediated pro-apoptotic pathway was activated after intestinal I/R. However, the upstream regulators of the p66Shc pathway involved in intestinal I/R remain to be fully identified.
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