ObjectiveTo investigate the value for the clinical application of urokinase combined with Sodium Tanshion ⅡA in the treatment of cerebral thrombosis.Methods160 cases with cerebral thrombosis in our hospital were chosen.They were randomly divided into A group with 80 cases and B group with 80 cases.A group was the observation group (Tanshion ⅡA Urokinase combined treatment group),B group was the control group (urine kinase treatment group).2 weeks treatment was a course.The efficacy of treatment in the two groups at the end was taken for statistical analysis.ResultsThe neurological deficits were significantly improved in A and B group before and after treatment (P ＜ 0.05,there was statistically significant).The neurological deficit scores in A group after treatment was significantly lower than group B ( P ＜ 0.05,there was statistically significant).The total effective rate was 95 ％ by the treatment of urokinase and Tanshion Ⅱa in A group which was higher than group B ( P ＜ 0.05,there was statistically significant difference).ConclusionThe treatment of urokinase combined with Sodium Tanshion Ⅱa could improve neurological deficits and improve the clinical therapeutic effect.

Objective To study the relationship between the polymorphism of interleukin-12B (IL-12B)gene and coronary heart disease.Methods We recruited 256 patients with coronary heart disease admitted to our department as the study group and 256 normal subjects as the control group.The polymorphism of IL-12B gene was detected by polymerase chain reaction and single nucleotide polymorphism.Coronary artery stenosis,visfatin,high sensitive C reactive protein and cardiac function were determined.Results The difference in rs15677380 and rs14050311 allele frequencies between the study group and the control group was significant (χ2 =6.19,7.24,P=0.045,0.021).The G allele of rs15677380 and C allele of rs14050311 were risk factors for coronary heart disease (OR=1.32,1.49).Conclusion IL-12B gene is associated with the occurrence and development of carotid atherosclerosis and participates in the development of coronary heart disease.

Objective:To investigate the effects and underlying mechanisms of XRCC3 on esophageal squamous-cell carcinoma (ESCC) radiotherapy response. Methods:Expression levels of XRCC3 were detected by reverse transcription PCR, Western blot, and immunohistochemistry. We knocked down XRCC3 with lentiviral infection in ESCC cells. Cell apoptosis was examined by flow cytom-etry. DNA damage and telomere dysfunction-induced foci were determined by immunofluorescence. Results:The expression levels of XRCC3 in ESCC cells and tissues were higher than those in normal esophageal epithelial cells and corresponding adjacent noncancer-ous esophageal tissues. Knockdown of XRCC3 in ESCC cells substantially increased the therapeutic efficacy of radiation. We demon-strated that the radiation resistance of XRCC3 was attributed to the XRCC3-maintaining telomere stability, which reduced ESCC cell death through radiation-induced apoptosis. Conclusion: Our data suggested that XRCC3 protects ESCC cells from ionizing radia-tion-induced DNA damage and death by enhancing telomere stability. Thus, XRCC3 can be used as a promising therapeutic target for ESCCs.

Objective To investigate the impacts of pyruvate kinase M2 isoform (PKM2) silencing on the radiosensitivity of lung adenocarcinoma cell line (A549 cells) and the radiation synergy of xenografts, and to explore their mechanisms. Methods Plasmid pshRNA?PKM2 for interference with PKM2 expression was transfected into A549 cells, and empty vector?transfected cells and untransfected cells were set as con?trols. The silencing efficiency of pshRNA?PKM2 and the expression level of microtubule?associated protein 1 light chain 3(LC3) were measured by Western blot assay. The radiosensitizing effects in A549 cells and xen?ografts after PKM2 silencing were determined by colony?forming assay and xenografts growth curves. Autoph?agy formation in A549 cells and xenografts was analyzed by transmission electron microscopy, and the ex?pression level of PKM2 in xenografts was measured by immunohistochemistry. Comparison between groups was made by Student′s t?test, and the body weights of nude mice and xenograft volumes were subjected to a?nalysis of variance for continuous variables. Results Stable A549 cell lines transfected with pshRNA?PKM2 were successfully produced. Transfection with pshRNA?PKM2 significantly down?regulated PKM2 expression in A549 cells and xenografts (P= 0?? 001;P= 0?? 000). The sensitizer enhancement ratios for A549 cells and xenografts were 1?? 47 and 2?? 00, respectively. Interference with PKM2 expression enhanced radiation?in duced autophagy formation and significantly increased the ratio of LC 3 ? II / I ( P= 0.000 1 ) . Conclusions Silencing of PKM2 expression may enhance the radiosensitivity of A549 cells and xenografts by regulation of autophagy, which holds promise for becoming an effective radiosensitizing target for non?small cell lung canc?er, but still needs to be confirmed by further studies.

Objective:To investigate the relationship between the changes in inflammatory markers levels and the onset of post-traumatic stress disorder (PTSD) in the early stage of acute trauma..Methods:From January 2018 to June 2020, patients with acute trauma who were admitted to the Affiliated Hospital of Xuzhou Medical University were selected as subjects. Peripheral venous blood was collected on admission, on the 3rd and 7th day after trauma for routine blood test, C-reactive protein (CRP) and procalcitonin (PCT). The neutrophil to lymphocyte ratio (NLR) was calculated. The PCL-5 scale was used to evaluate PTSD symptoms one month later. The patients were divided into the PTSD group and non-PTSD group with the score of 38 as the boundary. The change rule of NLR in the PTSD group and the non-PTSD group were analyzed.Results:Ninety-one trauma patients were enrolled, including 23 patients in the PTSD group and 68 patients in the non-PTSD group. Compared with the healthy control group, the NLR of 91 trauma patients on admission, on the 3rd and 7th day were significantly higher (all P< 0.01). The NLR of the PTSD group was increased on the 7th day after trauma, which was significantly higher than that of the non-PTSD group ( P= 0.025). The non-PTSD group showed a decreasing trend, of which NLR on the 7th day was significantly lower than that on admission ( P= 0.001). In addition, high level of NLR on the 7th day after trauma (β= 0.206, P= 0.01) was a risk factor for PTSD onset. Conclusions:Dynamic monitoring of the changes in NLR after acute trauma would be of great clinical value to early warning of PTSD.

Objective To determine the risk factors associated with early allograft dysfunction (EAD) after liver transplantation. Methods We retrospectively analyzed the records of 138 patients who underwent liver transplantation from January 2006 to October 2016 in our department. Transplant recipients were divided into two groups:those who met the diagnostic criteria of EAD (EAD group) and those who did not (non-EAD group). We compared blood flow into the transplanted livers and other clinical features between the two groups using univariate and multivariate analysis. Results Intraoperative portal vein flow (PVF) maximum was significantly different between the two groups. Multivariate analysis revealed that intraoperative PVF maximum ＜1 600 mL/min was the only independent risk factor for the occurrence of EAD after liver transplantation in this cohort. Conclusion Intraoperative PVF maximum ＜1 600 mL/min is an independent risk factor for the occurrence of EAD after liver transplantation. Measuring intraoperative blood flow into the transplanted liver in liver transplant recipients may help identify patients at risk for developing EAD.

Objective:To investigate the effect of post-traumatic pain on post-traumatic stress disorder (PTSD).Methods:A prospective trial was conducted with the recruitment of patients referred to the Emergency Center of Affiliated Hospital of Xuzhou Medical University for acute trauma from January 2018 to June 2019, with the exclusion criteria: age < 18 years, severe eye injury, severe craniocerebral injury and other critical conditions. The clinical data and written informed consent were collected at admission, the post-traumatic pain was assessed by VAS scores and the trauma severity was assessed by ISS score. APACHEⅡ score were evaluated within 24 h after admission. One month after trauma, patients with history of mental illness, or history of major psychogenic trauma within one year or drug addiction were further excluded. Accordingly, 64 eligible patients were evaluated by VAS, and the PCL-5 scale was used to evaluated their PTSD symptoms. The patients were divided into the PTSD group and non-PTSD group according to PCL-5 score≥ 38, and the difference between the two groups in post-traumatic VAS scores was compared. Logistic regression analysis was used to analyze the risk factors of PTSD. Spearman correlation analysis was adopted to establish the correlation between VAS score at admission and PCL-5 score at one month after trauma. The receiver operator characteristic (ROC) curve was used to analyze the predictive value of traumatic pain intensity for PTSD onset.Results:Sixty-four patients were selected and defined as the PTSD group ( n=19) and non-PTSD group ( n=45). The VAS score at admission was significantly higher in the PTSD group than that in the non-PTSD group ( P=0.006). There was no significant difference in VAS scores and VAS variations at 1 month, and in ISS scores at admission and APACHEⅡ scores within 24 h after admission between the two groups. Traumatic pain was an independent risk factor for PTSD ( P=0.043). VAS score at admission was positively correlated with PCL-5 score at 1 month post-traumatically ( r=0.355, P=0.004). In addition, ROC curve analysis showed that VAS score > 8 at admission had predictive value for PTSD (sensitivity=100%, specificity=33%, P=0.000 2). Conclusions:Post-traumatic severe pain is an independent risk factor for PTSD, which requires prompt medical intervention.