Objective To explore the dynamic change and clinical signiticance of plasma D-damer level in patients with cerebral hemorrhage and acute craniocerebral injury.Methods 50 patients with cerebral hemorrhage and 40 patients with acute craniocerebral injury were selected,The enzyme-linked immunosorbent assay (ELISA) was used to measure plasma D-dimer level in two groups of patients after onset,and the results were compared with 40 healthy controls.Results The levels of plasma D-dimer in the patients with cerebral hemorrhage were 1.59mg/L,2.10mg/L,1.03 mg/L,0.82mg/L at 3 h,6h,12h,2d after onset,which in the patients with acute craniocerebral injury were 1.61mg/L,2.02mg/L,1.01mg/L and 0.67mg/L,respectively.And the plasma D-dimer levels were 0.50mg/L,0.49mg/L,0.47mg/L,0.48mg/L in the control group at 3h,6h,12h and 2d after onset.The levels of plasma D-dimer in the patients with acute craniocerebral injury were significantly higher than those in the control group,and the differences were statistically significant (t =9.35,12.17,4.03,3.05,all P ＜ O.05).At 7d after onset,the D-dimer levels in the cerebral hemorrhage group and acute craniocerebral injury group were 0.53mg/L,0.55mg/L,respectively,which of the control group was 0.47mg/L,there was no statistically significant difference among the three groups(P ＞ 0.05).Conclusion Cerebral hemorrhage patients and acute craniocerebral injury patients have high coagulation and fibrinolytic activity in brief increase trend,dynamic observation of plasma D-dimer level in patients with cerebral hemorrhage and acute craniocerebral injury is helpful to determine courses,condition and evaluate prognosis.

Objective To study the effects of abnormal blood flow on the secretion of ET-1/NO and the expression of the mRNA and the protein of ET-1, eNOS, VCAM-1, ICAM-1 and MCP-1 in human umbilical vein endothelial cells (HUVECs), so as to explore the mechanism of atherosclerosis （AS） caused by abnormal hemodynamics. MethodsThe HUVECs were divided into stress group, wall pressure group and normal group according to the different stress. The HUVECs were cultured under the corresponding stress for 24 hours and then collected. The secretion levels of NO and ET-1 were detected by enzyme method and radioimmunoassay method. The mRNA expression levels of eNOS and ET-1 were detected by qPCR. The expression levels of the mRNA and the protein of VCAM-1, ICAM-1, MCP-1 were detected by qPCR and Western blot. Results Compared with normal group, the secretion level and the mRNA expression level of ET-1 in wall pressure group increased significantly (P＜0.01), and the secretion level of NO and the mRNA expression level of eNOS in stress group also increased significantly (P＜0.01), The expressions level of the mRNA and the protein of VCAM-1, ICAM-1 and MCP-1 obviously increased in stress group and wall pressure group (P＜0.01). Conclusions Stress or wall pressure acting on HUVECs alone could lead to its dysfunction of the secretion and the expression of gene and protein. The mechanism of AS caused by abnormal blood flow was related to these dysfunction of HUVEC.

The historical surveillance results showed, there were 10 schistosomiasis cases in Huangshan City from 1994 to 2006. The survey in 2007 showed, the positive rates of blood examination for schistosomiasis in migrant workers and immigrant workers were 0.49% and 0.47% , respectively, but no schistosome-infected patients were detected by using the stool examination. An area with snails of 3 000 m~2 was found in the residence of the immigrant workers, but no infected snails were found. It is indicated that the mobile population has some impact on the transmission of schistosomiasis in the transmission-interrupted area. The surveillance and health education for the mobile population should be strengthened, and the imported infectious source should be prevented.

OBJECTIVE: High-fat diet is one of the main risk factors that disrupt the balance of gut microbiota, which eventually will induce colorectal cancer (CRC). Evodiamine (EVO) is a wildly used multifunctional traditional Chinese medicine extract. In this study, we investigated the role of gut microbiota in high-fat diet-propelled CRC and the potential of EVO for CRC chemoprevention. METHODS: Gut microbiota, serum d-lactic acid and endotoxin from 38 patients with colon cancer and 18 healthy subjects were detected by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA). In addition, body mass index, phospho-signal transducer and activator of transcription 3 (p-STAT3) expression in cancer tissues and paracancerous tissues were detected by immunohistochemistry. A mouse intestinal inflammatory tumor model was established by azomethane/sodium dextran sulfate, followed by treatment with EVO and 5-aminosalicylic acid (ASA). Gut microbiota and inflammatory factors were detected by quantitative polymerase chain reaction, while serum d-lactic acid and endotoxin were detected by ELISA. Furthermore, cell proliferation, cell apoptosis, and interleukin (IL)-6/STAT3/P65 pathway were evaluated by 5-ethynyl-2'-deoxyuridine, terminal-deoxynucleotidyl transferase-mediated nick-end labeling, and Western blot assays. RESULTS: In patients with colon cancer, the numbers of Enterococcus faecalis and Escherichia coli were increased, while those of Bifidobacterium, Campylobacter and Lactobacillus were decreased. Serum endotoxin and d-lactic acid levels and p-STAT3 levels were significantly increased. In the mouse model, both EVO and ASA inhibited tumor formation, decreased the proliferation of tumor cells, and induced apoptosis of tumor cells. Compared with the control group, the numbers of E. faecalis and E. coli were decreased, while Bifidobacterium, Campylobacter and Lactobacillus numbers were increased. In the EVO group, serum endotoxin and d-lactic acid levels and inflammatory factors were significantly decreased. Further, the IL6/STAT3/P65 signaling pathway was inhibited in the EVO group. CONCLUSION EVO may inhibit the occurrence of colon cancer by regulating gut microbiota and inhibiting intestinal inflammation. The potential mechanism involves inhibition of the IL6/STAT3/P65 signaling pathway, revealing its potential therapeutic significance in clinical applications.