Objective To investigate the effect of surgical treatment combined with 131I in the treatment of thyroid papillary carcinoma.Methods45 cases of papillary thyroid cancer patients were selected from January 2008 to January 2012 in our hospital.All of the patients were treated with total thyroidectomy surgical,postoperative underwent thyroid hormone and 131I radionuclide therapy,The patients were followed up.ResultsAt 3 months or 6 months after operation,the levels of serum P53,Fas and TNF-a were significantly higher than immediate time after surgery (P<0.05) and cyclin E protein levels were significantly lower than immediate time after surgery (P<0.05).There were no difference of serum P53,Fas,TNF-and Cyclin E protein levels between at 3 months and 6 months after operation.During five years of follow-up, the 5-year recurrence rate of 4.4%,and the distant metastasis rate was 2.2%.ConclusionOperation combined with 131I radionuclide therapy has good clinical results,could be used as the first choice for clinical treatment.

Objective:To study the effect of levosimendan on coronary microembolization (CME)-induced myocardial injury and LOX-1/p38MAPK pathway.Methods:Microspheres were injected into coronary anterior descending branch to construct swine CME model, swine was given levosimendan by continuous intravenous drip for 24 h before modeling, and myocardial-specific overexpression of lectin-like oxidized low density lipoprotein receptor 1 (LOX-1) was achieved through coronary artery injection of adeno-associated virus (AAVs) at 2 weeks before modeling. Then, echocardiography was used to measure cardiac function; HE staining and HBFP staining were used to observe the pathological changes of myocardium and myocardial microinfarction area, respectively; ELISA was used to detect the serum level of cTnI; TUNLE staining was used to detect cardiomyocyte apoptotic index; the LOX-1, Bax, caspase-3 p12, Bcl-2, and p-p38 MAPK protein in myocardial tissue was observed by immunofluorescence method.Results:Compared to the sham group, the LVEF, LVFS, and CO value in the CME group were decreased, while the LVEDd value was increased significantly (all P<0.05); the area of myocardial micro-infarction, serum cTnI level and cardiomyocyte apoptotic rate in the CME group were increased significantly (all P<0.05); the protein levels of Bax, caspase-3 p12, LOX-1, and p-p38 MAPK were increased significantly, while the Bcl-2 level was decreased significantly ( P<0.05). Levosimendan pretreatment significantly improved cardiac dysfunction, reduced the area of myocardial micro-infarction and serum cTnI level, alleviated cardiomyocyte apoptosis, and significantly reduced the LOX-1 and p-p38 MAPK protein expression levels following CME (all P<0.05); while pretreatment with levosimendan and LOX-1 overexpression AAVs simultaneously abolished the effects of pretreatment with levosimendan alone (all P<0.05). Conclusion:Levosimendan alleviates CME-induced myocardial injury through inhibiting cardiomyocyte apoptosis mediated by LOX-1/p38 MAPK signaling pathway.