Correlation Between Thymus Radiology and Myasthenia Gravis in Clinical Practice

Background: The ability to distinguish between a normal thymus, thymic hyperplasia, and thymoma should aid in clinical management and decision making for patients with myasthenia gravis (MG). We sought to determine the accuracy of routine radiological examinations in predicting thymic pathology.Methods: We retrospectively analyzed the records of patients with MG who had undergone thymectomy from the Second Affiliated Hospital of Zhengzhou University. Each patient received at least one initial radiological diagnosis and one histological diagnosis, and the patients were classified into the all-patient, CT, contrast CT, and MRI groups. The sensitivity, accuracy and specificity of each group were calculated for different histological types.Results: This study included 114 patients. All sensitivity, specificity and accuracy values except for sensitivity to hyperplasia in each group for different histological types were satisfactory. MRI had higher sensitivity (68.4, 95% CI: 43.5–87.4%) to histological hyperplasia than did CT (14.3, 95% CI: 0.4–57.9%) and contrast CT (26.7, 95% CI: 7.8–55.1%). Contrast CT had higher specificity (97.9, 95% CI: 88.9–99.95%) for histological hyperplasia than did MRI (88.5, 95% CI: 69.9–97.6%).Discussion: For patients with MG, CT, contrast CT, and MRI examinations can effectively identify thymoma. Additionally, compared with CT or contrast CT, MRI may have a stronger ability to distinguish thymoma and detect hyperplasia

Participation Of Protein Kinase C In The Activation Of Nrf2 Signaling By Ischemic Preconditioning In The Isolated Rabbit Heart

Activation of protein kinase C (PKC) is a critical intracellular signaling triggered by ischemic preconditioning (IPC), but the precise mechanisms underlying the actions of PKC in IPC-mediated cardioprotection remain unclear. Here, we investigated the role of PKC activation on the antioxidant activity by IPC in rabbit hearts. Isolated rabbit hearts were subjected to 60 min of global ischemia by cold cardioplegic arrest (4 °C) and 60 min of reperfusion (37 °C). IPC was induced by three cycles of 2-min ischemia following 3 min of reperfusion (37 °C) before cardioplegic arrest. IPC resulted in a better recovery of mechanical function, increased tissue reduced glutathione-to- oxidized glutathione ratio (GSH/GSSG), superoxide dismutase and catalase content, and decreased tissue malondialdehyde (MDA) content compared to control hearts subjected to 60 min of cardioplegic ischemia and 60 min of reperfusion. IPC also significantly induced activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and the inductions of antioxidant genes heme oxygenase-1 (HO-1) and manganese superoxide dismutase (MnSOD). Injection of phorbol 12-myristate 13 acetate, an activator of PKC, before cardioplegic ischemia induced translocation of PKC-δ and -ε isoforms to membrane fraction, nuclear accumulation of Nrf2, and conferred cardioprotection similar to IPC. Polymyxin B, an inhibitor of PKC, blocked the membrane translocation of PKC-δ and -ε during IPC, inhibited Nrf2 nuclear accumulation, and significantly diminished the IPC-induced cardioprotection when administrated before IPC. These results indicate that the activation of PKC induces the translocation of Nrf2 and the enhancement of endogenous antioxidant defenses in the IPC hearts and suggest that PKC may target Nrf2 to confer cardioprotection. © 2012 Springer Science+Business Media New York

MicroRNA-145 Aggravates Hypoxia-Induced Injury by Targeting Rac1 in H9c2 Cells

Background/Aims: Myocardial infarction (MI) is a leading cause of morbidity and mortality. Here, we sought to explore the potential role and underlying mechanism of miR-145 in MI. Methods: H9c2 cells were cultured under persistent hypoxia to simulate MI. The hypoxia-induced injury was assessed on the basis of cell viability, migration, invasion and apoptosis. The expression of miR-145 was evaluated by qRT-PCR and the influence of aberrantly expressed miR-145 on H9c2 cells under hypoxia was also estimated. Utilizing bioinformatics methods, the target genes of miR-145 were verified by luciferase reporter assay. Then, effects of abnormally expressed target gene on miR-145 silenced H9c2 cells were assessed. Finally, the phosphorylation levels of key kinases in the phosphatidylinositol-3-kinase (PI3K)/AKT and the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathways were detected by Western blot analysis. Results: Hypoxia remarkably lowered viability, migration and invasion but promoted cell apoptosis. Meantime, the miR-145 level was up-regulated in H9c2 cells under hypoxia. Following experiments suggested that hypoxia-induced injury was exacerbated by miR-145 overexpression while was alleviated by miR-145 silence. Rac1 was predicted and further validated to be a target gene of miR-145. The influence of miR-145 silencing on H9c2 cells under hypoxia could be reversed by down-regulation of Rac1. Additionally, the phosphorylation levels of PI3K, AKT, MAPK and ERK were all elevated in miR-145 silenced cells and these alterations were reversed by down-regulation of Rac1. Conclusion: miR-145 silencing could protect H9c2 cells against hypoxia-induced injury by targeting Rac1, in which PI3K/AKT and MAPK/ERK pathways might be involved