Venous thrombotic disease is a serious disease,which impact on health and life-threatening.Pulmonary embolism and deep-vein thrombosis are the two components of a single disease called venous thromboembolism in obstetrics and gynecology.but it can be difficult to diagnose because clinical symptoms and signs are non-specific or absent in early venous thrombus embolism (VTE).It has great value that how to use the most economic,simple,efficient method for screened high-risk groups,timely and accurate laboratory diagnosis of VTE.

With the development of genomics , bioinformation , engineering , computer science and other fields, it has witnessed explosive growth of molecular diagnostic technologies.More and more technologies are used in desease diagnosis , therapy and prevention , which have presented a huge opportunity and challenge for clinical laboratory.Each technology has corresponding field of application , so it is a crucial problem for clinical laboratory to select appropriate molecular diagnostic technology for personalized medicine.

European Society of Hypertension/European Society of Cardiology jointly published new guidelines on diagnosis and treatment of hypertension in 2007.It reflected the the latest developments on comprehensive assessment,treatment modalities and strategies,as well as therapeutic approach for special populations.In addition,the new guidelines updated evaluation.It also stressed the importance of an early,faster and more stringent treatment and aggressive combination therapy.More impartantly,it requested prevention and treatment earlier.It is of great importance for the guidelines to guide the current diagnosis and treatment of hypertension.

Brain ; metabolism ; pathology ; Child, Preschool ; Chromatography, High Pressure Liquid ; Diagnosis, Differential ; Folate Receptor 1 ; genetics ; metabolism ; Folic Acid ; blood ; cerebrospinal fluid ; metabolism ; Folic Acid Deficiency ; diagnosis ; drug therapy ; etiology ; Humans ; Infant ; Leucovorin ; therapeutic use ; Malnutrition ; complications ; diagnosis ; Tetrahydrofolates ; cerebrospinal fluid ; metabolism

ObjectiveTo explore the association of smoking to the Aspirin and Clopidogrel antiplatelet in patients with stable angina after percutaneous coronary intervention (PCI). Methods241 smoking patients and 252 non-smoking patients underwent PCI for stable coronary artery disease, all patients had taken aspirin 100 mg/d for 7 d or more. The arachidonic acid (AA)- and adenosine diphosphate (ADP)-induced platelet aggregation were tested as they got in hospital. Then, they accepted Clopidogrel 300 mg as loading dose, continued with 75 mg/d for 3 d. The ADP-induced platelet aggregation were re-tested. ResultsThe incidence of aspirin resistance (AR) and aspirin semiresponder (ASR) was 19.1% in all the cases, and was 25.5% in smoking group, 14.3% in non-smoking group (P=0.027). Age (OR=3.79，95%CI: 1.77～8.12) and smoking (OR=1.98，95%CI: 1.18～4.43) were the independent risk factors of AR and ASR. The incidence of Clopidogrel resistance was 19.5% in all the cases, and was 13.2% in smoking group, 24.3% in non-smoking group (P=0.03). Smoking (OR=0.22，95%CI: 0.09～0.54) may reduce the risk of Clopidogrel resistance. ConclusionSmoking increased the risk of AR and ASR, but reduced the risk of Clopidogrel resistance.

0.05).However,there were significant differences between group C and A,group C and B,respectively(Pa

Background Studies showed that inflammatory process participates in the pathogenesis anddevelopment of diabetic retinopathy targeting retinal vascular endothelial cells (RVECs).A growing body of evidence revealed that metformin reduces the risk of micro-and macro-vascular complications by protecting blood-brain barrier,however,whether it plays a protective effect on human retinal vascular by similar mechanism is still unelucidated.Objective This study was to investigate the effects of metformin on the proliferation,migration and secreting monocyte chemotactic protein-1 (MCP-1) and interleukin-8 (IL-8) of human retinal vascular endothelial cells (RVECs) under the stimulation of tumor necrosis factor-alpha (TNF-α).Methods RVECs were cultured and divided into normal control group,metformin (5 mmol/L) group,TNF-α 2.5 ng/ml group,and TNF-α+metformin (5,10,20 and 40 mmol/L,respectively) groups.Corresponding drugs were added into medium according to grouping for 24 hours.Cell numbers were calculated before and after treatment.The metabolic activity (absorbancy) of RVECs was measured with MTS assay.Cell migration of RVECs was assessed with transwell migration assay.The MCP-1 and IL-8 concentrations in the cell supernatant were detected by ELISA assay.Results The number of the cells was significantly different among the normal control group,metformin group,TNF-α group,and TNF-α+metformin (5,10,20 and 40 mmol/L,respectively) groups (F =189.31,P ＜ 0.01).The metabolic activities of RVECs were 0.32 + 0.02,0.32±0.03,0.97 ± 0.02,0.90 ± 0.05,0.76 ± 0.15,0.74 ± 0.05 and 0.41 ± 0.03;migrated cell numbers were (1 214±49),(1 200±45),(1 648±43),(1 309±48),(1 279±73),(961±60) and (942±106)/field;the concentrations of MCP-1 were (0.385 ±0.050),(0.362±0.060),(2.285 ±0.200),(1.131 ±0.180),(0.622 ± 0.120),(0.537±0.090) and (0.492±0.130) μg/ml,and those of IL-8 were (0.385±0.080),(0.390±0.120),(1.123±0.130),(0.899±0.180),(0.680±0.060),(0.417±0.090) and (0.335±0.100) μg/ml in the normal control group,metformin group,TNF-α group,and TNF-α + metformin (5,10,20 and 40 mmol/L,respectively) groups,showing significant differences among the groups (F =73.31,103.89,150.92,268.32,all at P＜ 0.01).The cell number,cell metabolic activity,migrated cell number,and MCP-1 and IL-8 levels in the cell supernatant were evidently increased in the TNF-α group compared with the normal control group,and those in the TNF-α+10 mmol/L metformin group,TNF-e +20 mmol/L metformin group and TNF-α+40 mmol/L metformin group were significantly decreased in comparison with the TNF-α group (all at P＜0.05).Conclusions Metformin can inhibit TNF-α-induced proliferation,migration and MCP-1 and IL-8 secretion of the cells,and therefore plays a protective role on RVECs in the inflammatory environment.

Objective To explore the expression of FOXM1 in non-small cell lung cancer(NSCLC) and the relationship between FOXM1 expression and the clinical pathological factors,clinical response to target-therapy in NSCLC remained unknown.Methods A total of 80 NSCLC patients were recruited into this study,FOXM1 expression was assessed by immunohistochemistry and analyzed with the clinical pathological factors and clinical response to target-therapy.Results The positive rate of FOXM1 expression was 41.25%.The positive expression of FOXM1 had no significant difference in patients with different age,gender,cancer staging,smoking history(P>0.05),but had significant difference in patients with different degree of differentiation,lymph node metastasis(P<0.05).Survival time in patients with positive FOXM1 expression was significant shorter than that with negative FOXM1 expression(P<0.05).Conclusion The expression of FOXM1 closely correlated with patients histological differentiation,lymph node metastasis,progress-free survival time in patients with positive FOXM1 expression was significantly shorter than those with negative FOXM1 expression.

ObjectiveTo analyze the autophagy of mouse melanoma B16 cells induced by TNF-ct.MethodsMouse melanoma B 16 cells treated with TNF-α were used in this study.The expression levels of LC3- Ⅱand Beclinl were measured by western blot and mRNA levels of autophagy related gene atg5,atg7 and atgl2 were measured by reverse transcription polymerase chain reaction (RT-PCR) after TNF-α treatment.ResultsThe viability of B16 cells were obviously inhibited after incubation with TNF-α.The expression levels of autophagy related protein LC3- Ⅱ and Beclinl were elevated in TNF-α treated B16 cells compared with in control B16 cells.The mRNA expression levels of autophagy related gene Atg5,atg7 and atg12 showed consistent up regulation in TNF-a treated B16 cells compared with in control B16 cells.ConclusionTNF-α can induce autophagic cell death in B16 cells.

Congresses as Topic ; Otorhinolaryngologic Surgical Procedures ; Rhinitis ; surgery ; Skull Base ; surgery