Autoimmune Diseases ; immunology ; Gene Expression Regulation ; immunology ; Humans ; Immunoglobulin G ; genetics ; immunology ; Sclerosis ; genetics ; immunology ; pathology

Antigens, Neoplasm ; metabolism ; Carbonic Anhydrase IX ; Carbonic Anhydrases ; metabolism ; Carcinoma, Renal Cell ; diagnosis ; metabolism ; pathology ; Humans ; Kidney Neoplasms ; diagnosis ; metabolism ; pathology ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Neoplasm Grading ; Prognosis ; RNA-Binding Proteins ; metabolism ; Tumor Burden ; Vascular Endothelial Growth Factor A ; metabolism ; Von Hippel-Lindau Tumor Suppressor Protein ; metabolism

Hepatitis, Viral, Human ; pathology ; Humans ; Liver ; pathology ; Liver Cirrhosis ; pathology ; Liver Neoplasms ; genetics ; pathology ; Loss of Heterozygosity ; Microsatellite Instability ; Polymorphism, Single Nucleotide

Objective To analyze the change of disease spectrum and the direct cause of death in Xi'an Children's Hospital emergency patients in the past 2 years.Methods The cases of death in 130 emergency cases from 2009 to 2010 were retrospectively analyzed.Results The main causes of death in 2009 were pneumonia,congenital heart disease,asphyxia,neonatal pulmonary hemorrhage and intracranial hemorrhage.Meanwhile,The main cause of death in 2010 were pneumonia,asphyxia,viral encephalitis,congenital heart disease and neonatal pulmonary hemorrhage,which significantly changed compared with 2009.Major direct causes of death were found:respiratory failure in 25 cases (27.5％),heart failure in 17 patients ( 18.7％ ),shock in 17patients ( 18.7％ ),asphyxia in 16 cases ( 17.5％ ),and hernia in 16 cases ( 17.5％ ),Conclusion In order to reduce the mortality rate of emergency patients,we should strengthen health care,actively manage pulmonary infection,systemic infection,and shock,control heart failure,and prevent aspiration.

This paper developed a calculation method to acquire the yield load P of bone plate during four-point bending test. This method is based on the displacement--force (δ-F) curve function f(M)(δ) obtained from the test, each slope of the curve was calculated using piecewise smooth function and the line segment in f(M)(δ) elastic deformation area was searched by setting the minimum slope T. Slope S was obtained through linear fit so as to build parallel displacement function f(L)(δ). Then, approximating intersection point of f(M)(δ) and f(L)(δ) was obtained through linear interpolation. Thus, yield load P was acquired. The method in the paper was loyal to YY/T 0342-2002 regulation and was liable to program calculation. The calculating process was nothing to do with whether the initial point during the test was preloaded or unloaded, and there was no need to correct the original point. In addition, T was set in an ideal fitting level guaranteed by the fitting coefficient of determination R2, and thus S was very close to the real value, and P was with a high accuracy.
Biomechanical Phenomena ; Bone Plates ; Humans ; Models, Theoretical ; Posture ; Weight-Bearing

Disease Progression ; Hepatitis B, Chronic ; physiopathology ; Hepatitis, Chronic ; physiopathology ; Humans

Objective To compare the effect of traditional open surgery and laparoscopic repair of gastric perforation on postoperative pulmonary function.Methods Fifty patients were divided into two groups according to therapeutic method.Group A underwent traditional open gastric perforation repair(n=25).Group B underwent laparoscopic repair of gastric perforation(n=25).The pulmonary functions were examined at 1 day,3 days and 7 days postoperatively.Results All patients had different degrees of postoperative pulmonary function decline.After operation,the forced vital capacity(FVC)and forced expiratory volume in 1 second(FEV1)and vital capacity(VC)in group A were significantly lower than those in preoperation(P<0.05).The patients in laparoscopic operation group decreased significantly only on the first day postoperative.The postoperative pulmonary function of patients undergoing open surgery was significantly lower than that of patients undergoing laparoscopic surgery(P<0.05).Conclusion Laparoscopic repair of gastric perforation has less damage to the lung function than traditional open gastric perforation repair.Laparoscopic surgery plays an important role in the recovery of postoperative pulmonary function.

In order to meet the needs of training high-quality medical persons, combining teaching reform theory with foundational courses teaching practice, we summarize some successful experience in many respects such as construction and reformation of foundational educational system, grasping subject construction goal, bringing up and cultivating scientific researchers, improving experimental conditions. All we have done reveal that the combination of medicine and engineering is the characteristic form of development.

Objective To investigate the dynamic changes of endothelial progenitor cells (EPCs) in peripheral blood of patients with hypertensive cerebral hemorrhage.Methods Flow cytometry was used to detect the dynamic changes of EPCs in 79 cases of hypertensive cerebral hemorrhages as the experimental group and 70 cases of normal healthy people as the control group.Results In the acute phase after hemorrhage (3 days),EPCs in experimental group [(51.3 ±9.3) × 103/ml,(52.0 ±6.3) × 103/ml,(53.1 ±9.3) × 103/ml] were significantly lower than the control group [(75.4 ± 15.6) × 103/ml] (P ＜0.05).However,after that the level of EPCs in experimental group [(110.9 ± 12.0) × 103/ml,(132.8 ± 11.8)× 103/ml,(115.3 ±9.9) × 103/ml] increased rapidly and was significantly higher than the control group (P ＜0.05),and approximately two weeks later it reduced to normal levels [(83.1 ±7.9) × 103/ml].Conclusions In patients with hypertensive cerebral hemorrhage,the levels of EPCs in peripheral blood were closely related with the disease and might become a prognostic marker.

Objective To set up the molecular cytobiological model of endogenous coagulation factor Ⅷ (FⅧ) re-expressing in human liver cells L02,and to study the regulation pathway and molecular basis of the re-expression of FⅧ in L02 cells activated by NO signal.Methods The L02 cells at logarithm growth phase were selected and randomly divided into blank control group and experimental group, inhibitor group and inhibitor control group;they were cultured for 0,12,24,36,48,and 60 h.Flow cytometry was used to detect the expression of human FⅧ protein in L02 cells after treated for 48 h.Griess experiment was performed to detect the levels of NO in L02 cells at different time points;the transcription levels of human FⅧ gene,iNOS gene,NF-κB1 gene and I-κB alpha gene were detected by RT-PCR method.Western blotting method was used to detect the expression levels of human phosphorylated I-kappaB (phosphorylated I-κB)in L02 cells.Results The results of flow cytometry showed that the expression of human L02 FⅧ protein was found after treated with L-arginine for 48 h. The Griess results showed that the levels of NO in L02 cells in experimental group were significantly increased at 3,6,12,and 24 h (P<0.05)and the levels of NO in blank control group,inhibitor group and inhibitor control group had no changes. The RT-PCR results showed that the transcription of human FⅧ mRNA in L02 cells was found in experimental group,but there was no transcription of human FⅧ mRNA in blank control group,inhibitor group and inhibitor control group;the transcription levels of iNOS,NF-κB1 and I-κB alphain experiment group were increased(P<0.05)and the transcription levels of these genes in blank control group,inhibitor group and inhibitor control group had no changes. The Western blotting results showed that after adding L-arginine the expression level of phosphorylated I-κB was significantly increased (P < 0.05 ), other groups had no such change. Conclusion L-arginine can activate the phosphorylation of I-κB by NO signal pathway to lead to the changes in the expression of human FⅧ gene promoter upstream regulatory-related transcription factors NF-κB to activate the expression of human FⅧ in human liver cells L02.