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.

Objective To evaluate the value of mini-thoracotomy for open heart surgery.Methods From December 1995 to January 2008,810 patients including 660 cases of congenital heart diseases,129 cases of valvular heart diseases and 21 cases of heart myxoma,underwent open heart surgery by mini-thoracotomy through cardiopulmonary bypass in our hospital.Among the cases,superior median sternotomy was performed on 36 patients,inferior median sternotomy was made on 59,right parasternal mini-thoracotomy was carried out in 3,right anterolateral thoracotomy was done on 658,and right axillary mini-thoracotomy was used in 54.A total of 382 patients received beating-heart surgery.Results The postoperative mortality in our patients was 1.5%(12 cases).In this series,the mean postoperative mechanical ventilation time,drainage volume,and hospital stay were(6.7?4.2) hours,(210?165) ml,and(7.4?4.9) days respectively.421 of the patients received no blood transfusion.None of the patients developed sternal dehiscence or mediastinal infection.Follow-up was available in 690(85%) of the patients up to a mean of(48.2?25.3) months,none of them died during the period.The cardiac function of the patients was significantly improved after the operation(preparation vs postoperation: 310 cases vs 478 cases for grade Ⅰ,438 vs 212 for grades Ⅱ-Ⅲ,and 62 vs 0 for grade Ⅳ,Z=-13.21,P=0.000).The mean cardiothoracic ratio was decreased significantly after the operation(0.51?0.11 vs 0.53?0.08,t=4.065,P=0.000),while the left ventricular ejection fraction was increased markedly(0.63?0.11 vs 0.57?0.11,t=-10.529,P=0.000).Conclusions The mini-thoracotomy is superior in cosmetic results and the postoperative morbidity rates of sternal malformation and infection.Proper selection of patients,good exposure of the surgical field,and skillful surgical procedures are crucial for the outcomes of the operation.

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.

Objective To investigate the correlation between interleukin-1β(IL-1β),interleukin-1 receptor antagonist(IL-1 ra)and the obesity of polycystic ovary syndrome(PCOS).Methods(1)From Oct.2006 to Jan.2007,118 PCOS patients were enrolled in this study in Peking University Third Hospital,which were divided into 56 patients in obese PCOS group and 62 patients in non-obese PCOS group according to the WHO International Obesity Task Force Asia-Pacific criteria[body mass index(BMI)25 kg/m2].The polymorphism of IL-1β gene promoter region,exon-5 and intron 2 of IL-1 ra gene were detected by PCR.(2)Twenty-nine obese PCOS patients and 31 non-obese PCOS patients were selected randomizedly serum levels of IL-1β,IL-1 ra were measured by ELISA,in the mean time,serum levels of fasting glucose,fasting insulin and the total white blood cell,hypersensitive C-reactive protein levels were measured.Results(1)Genetic test:the frequency of TT genotype and T allele of IL-1β promoter region(-511)in obese PCOS patients were significantly higher than those in non-obese patients(44.6％ vs.11.3％,63.4％ vs.39.5％,all P ＜0.05).The frequency of IL-1 ra Ⅰ / Ⅴ genotype and Ⅴ allele of IL-1 ra gene were 19.6％ and 9.8％ in obese PCOS patients,which were significantly higher than those in non-obese group(3.2％ and 1.6％,P ＜0.05).(2)Serological test:serum level of IL-1β and IL-1ra of(149 ±36)and(284 ±97)ng/L in obese PCOS group which were significantly higher than those in non-obese PCOS group[(96 ± 42)and(208 ± 84)ng/L,P ＜ 0.05].Fasting blood glucose,fasting insulin and hypersensitive C-reactive protein and white blood cell count were(5.1 ± 0.7)mmol/L,(17 ± 9)mU/L,(1.5 ± 0.6)mg/L and(7.0 ± 2.3)× 109/L in obese PCOS group,which were significantly higher than in non-obese PCOS group[(4.9 ±0.5)mmol/L,(11 ±8)mU/L,(0.9 ±0.4)mg/L and(5.9 ±1.3)× 109/L,P＜0.05].(3)The correlation between interleukin and BMI: serum levels of IL-1β(r =0.673)and IL-1 ra(r =0.557)were positively correlated with BMI in PCOS patients(P ＜ 0.05).Conclusions Inflammatory factors IL-1β and IL-1ra had correlation with obesity of PCOS patients,PCOS patients who carried T allele of IL-1β gene promoter region(-511)and Ⅴ allele of IL-1ra gene were high risk of obesity.

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.

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