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ObjectiveThe local recurrence or distant metastasis of colorectal cancer (CRC) after surgical resection still directly affects the prognosis of CRC patients.This study aims to investigate the clinical significance of preoperative peripheral blood fibrinogen (Fbg) level combined with platelet-to-lymphocyte ratio (PLR) in the prognosis of CRC.MethodsThe clinicopathological characteristics of 108 CRC patients who were diagnosed by pathology and underwent surgical resection in Wujin hospital affiliated to Jiangsu University from January 2013 to December 2015 were analyzed. Fbg and PLR thresholds were determined by ROC curve, and the patients were grouped according to Fbg combined with PLR (F-PLR) to analyze the relationship between different F-PLR scores and the clinicopathological characteristics and prognosis of CRC patients.ResultsPLR showed statistically significant difference in the left and right half of the tumor (P0.05). Multivariate analysis using COX regression showed that F-PLR score, TNM stage and lymph node metastasis were independent risk factors for the prognosis of CRC patients (P<0.05).ConclusionThe F-PLR score (Fbg and PLR combined) can be used as a predictor of treatment effect and prognosis of CRC patients to guide clinical treatment decisions and prognoses.
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Objective To investigate the expression of CDKN1C in bone marrow in myelodysplastic syndromes and clinical significance of the detection of syndrome and secondary acute myeloid leukemia patients.Methods 125 patients with MDS/ AML were selected as the research object,and selected 20 cases of healthy people as healthy control group,and to investigate the mRNA and protein expression in CD34+ cells in bone marrow the expression of MDS/AML in patients and the survival rate of different expression of CDKN1C,to analyze the factors for survival rate of patients with MDS by Cox regression,and analyze the different treatment methods in patients with MDS/AML.Results The expression lcvcls of CDKN1C mRNA and protein of bone marrow CD34 + cells in the patients with MDS/AML were significantly higher than the healthy control group (t=5.324,7.326;P=0.002,0.000),and which was positive with BM count (r=2.014,P=0.004);the survival rate of CDKN1C high expression levels in patients with MDS/AML was significantly lower than that of the low expression of CDKN1C group and intermediate CDKN1C expression group (P＜0.05).Cox regression analysis showed that age,high BM count,cytogenetic risk difference and CDKN1C positive significantly affect the survival rate of patients with MDS/AML (95％CI=1.10～1.32,1.92～4.40,1.18～2.67,1.03～2.32,P=0.034～0.000).MDS/AML chemotherapy in CDKN1C positive group was significantly lower than the survival rate of patients with CDKN1C negative expression group (t=5.314,P=0.002).Conclusion The expression of CDKN1C in bone marrow of patients with MDS/AML was significantly increased,and the high expression of CDKN1CMDS/AML effect of chemotherapy on the survival rate of patients with MDS/AML.
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OBJECTIVE@#To investigate the protective effect of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury and the potential mechanism in rabbits.@*METHODS@#Thirty New Zealand male white rabbits were randomly assigned to 3 groups: Control group; I/R group; and 2.0% isoflurane group. Isoflurane group was exposed to 2.0% isoflurane-100% oxygen for 2 hours. Control group and I/R group were exposed to 100% oxygen for 2 hours and served as untreated controls. Twenty-four hours later I/R group and isoflurane group underwent 40 minutes of coronary occlusion followed by 2 hours of reperfusion. Blood samples were taken from the arterial line at 20 minutes before the occlusion(T1), 20 minutes after the occlusion(T2), 40 minutes after the occlusion(T3), 1 hours after the reperfusion(T4), and 2 hours after the reperfusion(T5) to determine the plasma level of TNF-alpha. At the end of the reperfusion, infarct size and area at risk were defined by Evans and TTC staining. The heart was harvested and levels of the p38MAPK activity were determined by Western blot, and ultrastructures were observed under the electron microscope.@*RESULTS@#The p38MAPK activity of isoflurane group was significantly lower than that of I/R group (P<0.05). Isoflurane significantly (P<0.05) reduced the infarct size(19.7%+/-2.8% in isoflurane group) of the left ventricular area at risk as compared with the controls (37.8%+/-1.7% in I/R group).The injury of I/R group was worse than that of isoflurane group under the light microscope. Isoflurane group had a lower level of TNF-alpha than I/R group.@*CONCLUSION@#Isoflurane can inhibit p38MAPK activity during myocardial ischemia reperfusion and modulate the cytokine expression, which may be one of the molecular mechanisms of isoflurane delayed preconditioning on cardioprotection.
Subject(s)
Animals , Male , Rabbits , Ischemic Preconditioning, Myocardial , Methods , Isoflurane , Pharmacology , Myocardial Reperfusion Injury , Pathology , Myocardium , Random Allocation , Tumor Necrosis Factor-alpha , Metabolism , p38 Mitogen-Activated Protein Kinases , MetabolismABSTRACT
OBJECTIVE@#To explore the effect of ulinastain on the expression of hemeoxy genase-1 (HO-1) in oil acid-induced acute lung injury in rats.@*METHODS@#The animal model of acute lung injury was established by oil acid. Thirty SD rats were randomly divided into 3 groups: the blank control group (A), the acute lung injury group (B) and the acute lung injury group (C) followed by injecting 100 mL/kg ulinastatin. Each group consisted of 10 rats. Group A were given 0.2 mL/kg natural solution through the trial vein; Group B and C were given 0.2 mL/kg oil-acid through trial vein, while group C were injected 100mL/kg ulinastatin by the peritoneal cavity after injecting oil acid. After 4 hours, the rates of respiration were counted and blood samples were cramped out through the heart puncture for blood gas analysis. The expressions of hemeoxygenase-1 and the pathologic construction changes were determined by HE staining in the lower right lung of rats in the 3 groups.@*RESULTS@#The respiration dysfunction caused by oil acid could be prominently improved by ulinastain. There was only a little expression of hemeoxygenase-1 in the lung of Group A, but the expression increased in Group B and significatively increased in Group C.@*CONCLUSION@#Ulinastatin may protect the rats from acute lung injury through increasing the expression of HO-1.