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Objective To investigate the expression of microRNA-138 (miR-138) and forkhead box protein D1 (FOXD1) in oral squamous cell carcinoma (OSCC) tissues and its relationship with pathological parameters and prognosis. Methods Eighty cases of OSCC tissues and corresponding paracancerous tissues from OSCC patients that underwent surgical resection were collected as study subjects, and miR-138 and FOXD1 mRNA expression levels were detected by real-time fluorescence quantitative polymerase chain reaction. We analyzed the relationships between miR-138 and FOXD1 mRNA expression in OSCC tissues and clinicopathological features. OSCC tissues were divided into the high and low expression groups according to the mean values of miR-138 and FOXD1 mRNA expression. The binding sites between miR- 138 and FOXD1 were predicted by TargetScan. Pearson correlation was used to analyze the correlation between miR-138 and FOXD1 mRNA expression in OSCC tissues, Kaplan-Meier method was used to plot the survival curves of OSCC patients with different miR-138 and FOXD1 mRNA expression, and multifactorial Cox regression was used to analyze the influencing factors for the prognosis of OSCC patients. Results Compared with the paracancerous tissues, miR-138 expression decreased and FOXD1 mRNA expression increased in OSCC tissues (both P<0. 05) . MiR-138 had a binding site at the 3' untranslated end of FOXD1 at 2942-2948. Pearson correlation analysis showed that miR-138 was negatively correlated with FOXD1 mRNA expression in OSCC tissues (r = -0. 621, P<0. 001) . Significant differences were found in the miR-138 and FOXD1 mRNA expression levels among OSCC tissues with different degrees of differentiation, TNM stage, depth of infiltration, and lymph node metastasis (all P<0. 05) . The 5-year overall survival rate of 80 patients with OSCC was 55. 00% (44/80) . Kaplan-Meier survival curve analysis showed that the overall survival rate was higher in the miR- 138 high-expression group than in the low-expression group, and the overall survival rate was lower in the FOXD1 mRNA high-expression group than in the low-expression group (both P<0. 05) . Multifactorial Cox regression analysis showed that poor differentiation, TNM stage III, infiltration depth ≥5 cm, lymph node metastasis, and FOXD1 mRNA ≥2. 18 were independent risk factors for death in patients with OSCC, and miR-138 ≥0. 78 was an independent protective factor (all P< 0. 05) . Conclusion MiR-138 is low expressed and FOXD1 mRNA is highly expressed in OSCC tissues, which are associated with the degree of differentiation, TNM stage, depth of infiltration, lymph node metastasis, and prognosis, and may be markers for diagnosis and prognosis of OSCC patients. [ABSTRACT FROM AUTHOR]

Objective To explore the effects of C-reactive protein(CRP) on myocardial ischemia reperfusion injury in rat cardiomyocytes and its mechanisms. Methods We simulated ischemia reperfusion using oxygen-glucose deprivation/reoxygenation(OGD/R) in neonatal Sprague-Dawley rat cardiomyocytes. Cardiomyocytes were treated with CRP, Cyclosporine A(CsA), diazoxide(DZ) and divided into the control group, OGD/R group, CRP + OGD/R group, CRP + CsA +OGD/R group and CRP + DZ + OGD/R group. The myocardial cell viability,Lactic acid dehydrogenase(LDH) level in cell culture medium, mitochondrial membrane permeability transition pore(mPTP) opening level and mitochondrial membrane potential level were measured respectively. Cell viability was calculated as the percentage of the control group. Results Compared with the simple OGD/R group, the cell viability and mitochondrial membrane potential level decreased markedly, and the LDH leakage and mPTP opening level increased significantly in CRP + OGD/R group. All the differences were statistically significant(P < 0. 05). Compared with CRP + OGD/R group, in CRP + CsA + OGD/R group and CRP + DZ + OGD/R group, both cell viability and mitochondrial membrane potential level increased observably, and both LDH leakage and mPTP opening level reduced markedly. Conclusion Our results suggested that CRP directly aggravates myocardial ischemia reperfusion injury in myocardial cells and that this effect is primarily mediated by inhibiting mito KATP channels and promoting mPTP opening. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of cold stress on the sympathetic nerve activity and Stim1 expression of spontaneously hypertensive rats (SHR). Methods Ten male SHR and 10 normal male rats were selected. The normal male rats were randomly divided into the normal control group and cold stress group, and SHR were randomly divided into the SHR model group and SHR cold stress group, with 5 in each. Rats in the normal control group and SHR model group were placed into metabolic cages at room temperature for 6 h, and the rats in the cold stress group and SHR cold stress group were placed into metabolic cages at 4 °C for 6 h. Systolic (SBP) and diastolic (DBP) blood pressure was monitored during room temperature and cold stress by tail-cuff method. Urine norepinephrine excretion was detected by HPLC. The mRNA and protein expression of Stiml in brainstem were detected by quantitative real-time PGR and Western blotting, respectively. Results The SBP, DBP and urinary NE excretion were significantly higher in the cold stress group than in the normal control group; the SBP, DBP, and urinary NE excretion were significantly higher in the SHR cold stress group than in the SHR model group and cold stress group. The Stiml mRNA and protein expression levels in brainstem were significantly lower in the SHR cold stress group than in the SHR model group and cold stress group (all P <0. 01 ). Conclusion In response to cold stress, Stiml may be the key gene to modulate the sympathetic nerve activity. [ABSTRACT FROM AUTHOR]