Medical science monitor : international medical journal of experimental and clinical research
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BACKGROUND For coronary artery disease, percutaneous coronary intervention (PCI) is the preferred treatment. Reperfusion injury is a common and serious complication of PCI. Studies showed that early statin therapy has a favorable prognostic impact for patients undergoing PCI. ⋯ The pooled analysis showed that high-dose statin pretreatment before PCI significantly improved the final TIMI flow grade compared with the control group (OR=0.61, 95% CI: 0.46 to 0.80, p=0.0005), and showed reduced incidence of MACE (OR=0.53, 95%CI: 0.39 to 0.71, p<0.0001). In subgroup analysis, the beneficial effect of high-dose statin was significant in statin-naive treatment patients, ACS patients, and patients on atorvastatin therapy, but no difference occurred in rosuvastatin, previous statin therapy, and stable angina patients. CONCLUSIONS High-dose statin pretreatment has an important effect on postprocedure myocardial perfusion by improving the TIMI flow in patients undergoing PCI, and high-dose statin preloading also reduces the incidence of MACE.
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BACKGROUND As a nuclear protein and a secreted protein, HMGB1 is involved in many cellular processes such as proliferation, transcription, and inflammation. The overexpression of HMGB1 in various types of cancers is reported, but its clinical significance and prognostic value in glioblastoma multiforme (GBM) has not been well defined. MATERIAL AND METHODS The expression of HMGB1 in 116 patients with GBM was investigated with immunohistochemistry, and was detected with qRT-PCR in 12 pairs of tumor tissues and adjacent tissues. ⋯ In hypoxia, intracellular HMGB1 of GBM cells was released out and activated AKT and ERK signaling pathways, thus promoting GBM cell invasion in this autocrine pathway. CONCLUSIONS HMGB1 is an independent prognostic biomarker for unfavorable prognosis of patients with GBM. Released HMGB1 of GBM cells can activate AKT and ERK signaling pathways and promote GBM cells invasion in this autocrine pathway, indicating that anti-HMGB1 therapy may be a promising treatment for GBM.