Objective To observe the correlation between protein C activity-dependent clotting time-normalized ratio (PCAT-NR) and the related blood coagulation parameters,e.g.,fibrinogen (Fib),factor Ⅶ coagulant activity (Ⅶ:C),factor Ⅷcoagulant activity (F Ⅷ:C),antithrombin (AT),D-dimer (DD) in patients with acute cerebral infarction.Methods One hundred cases of patients who were diagnosed as acute cerebral infarction according to clinical manifestations and imaging examinations were taken as the test group and 75 healthy subjects were taken as control group.The values of Fib,FⅦ:C,FⅧ:C,AT,PCAT-NR,DD were tested and the difference between the two groups were compared.The differences of Fib,FⅦ:C,FⅧ:C,DD and AT between declined PCAT-NR group and normal PCAT-NR group in the patients with acute cerebral infarction were analyzed.The correlations of PCAT-NR with other coagulation parameters in acute cerebral infarction cases were compared.Results The values of Fib (3.38 ± 1.25) g/L,F Ⅶ:C (130.5 ± 15.9) ％,FⅧ:C (135.8 ± 43.1) ％ and DD (2.12:±:3.01) mg/L in the acute cerebral infarction group were significantly higher than those of control group,while the values of AT (83.94 ± 14.95) ％ and PCAT-NR (0.87 ± 0.23) in test group were significantly lower than those the control group (P＜0.05).The values of Fib (4.03 ± 1.25)g/L,FⅦ:C (138.2 ±6.9)％ and FⅧ:C (151.5 ± 54.9)％ of PCAT-NR declined group in the patients with acute cerebral infarction were significantly higher than those of PCAT-NR normal group (P ＜ 0.05),while the values of DD,AT were not statistically different between two groups (P ＞ 0.05).The values of PCAT-NR were significantly negatively correlated with Fib,FⅧ:C and DD in the patients with acute cerebral infarction (r =-0.484,-0.356 and-0.473,respectively (all P ＜ 0.05).There was no correlation of PCAT-NR with FⅦ:C and AT (P ＞ 0.05).Conclusion The PCAT-NR decline was associated with high coagulation state in patients with acute cerebral infarction.This decline has some correlation with high level of blood clotting factor Ⅷ and Fib.

0.05),but the proliferation rate(P

Objective To assess willingness to pay(wtp)for typhoid vi vaccine in typhoid epidemic area in Guangxi Zhuang Autonomous Region and to provide evidence for introduction of the vaccine.Methods Applying the method of wtp was investigated in typhoid epidemic area,the curve of "price-accept ratio model"was drawn up with Probit regression.Results The formula of "price-accept ratio model" was described as following:Probit(p)=0.88952-0.46296X.The WTP for typhoid vi vaccine was $10.41,with a 95% confidence interval of $6.67～16.24.Conclusions WTP for typhoid vi vaccine was around $10 in Guangxi typhoid epidemic area.The Contingent Valuation Method was applicable in the investigation of WTP.

Objective To observe the role of human hepatocarcinoma HepG2 cell culture supernatant on T lymphocyte of the activation, proliferation, IL-2 secretion and inducing apoptosis in vitro. To explore the mechanism of immune escape in tumor.Methods Peripheral blood mononuclear cells (PBMC) were cultured with different concentration of tumor cell culture supernatant. Cell proliferation was examined with standard cytometry and MTT. The apoptotic rate and immune phenotype were analyzed by FACS. The level of IL-2 was determined with ELISA.Results Adding HepG2 supernatant, there was no significant influence in activation of lymphocyte, but the proliferation rat and the secretion of IL-2 were obviously decreased. The lymphocyte apoptosis rate was raised.Conclusion The tumor cell may produce a certain soluble protein, thus escape from the immune surveillance of tumor-bearing host.

Objective:To explore the role of CD28 in the activation of human peripheral blood ?? +T cells by Mycobacterium tuberculosis (Mtb) low molecular peptide antigen in vitro Methods:Mtb antigen and anti CD28 monoclonal antibody (mAb) were used as signal 2 to stimulate the r? + T cell from PBMC the expression of CD28 molecule on ?? +T cells, proliferation rate of ?? +T cells and expression of CD69 molecule on activated ?? +T cells were analyzed by using flow cytometry Results:CD28 molecule was expressed on 50% of ?? +T cells Neither Anti CD28 nor Mtb antigen alone, but both presence, could stimulate ?? +T cells activation and proliferation CD69 molecule was expressed on activated ?? + T cells.Conclusion:The CD28 molecule could provide the costimulatory signal in the full activation of ?? +T cells by Mtb low molecular peptide antigen CD69 molecule was also an early activation marker of ?? +T cells

Objective To investigate the role of PKCθ signal pathway on regulation of L-selectin (CD62L) expression in human activated γδT cells. Methods Human peripheral blood mononuclear cells (PBMC) were stimulated with Mycobacterium tuberculosis antigen (Mtb-Ag) and cultured for 6-8 d to generate Mtb-Ag activated T cells(MtbAT) as γδT cells enrichment T cell line. The MtbAT were stimulated with PMA or PMA + IMN for 3, 6, 12 and 24 h, respectively, or MtbAT cultured for 8 d were stimulated with Mtb-Ag, or PMA, with or without PKC0 inhibitor Rottlerin for 4 h. After the treated cells stained with fluo-rescent labeled monoclonal antibodies, the expression of CD62L on γδT cells were measured by flow cytome-try (FCM ). Results The expression of CD62L on γδT cells cultured for 6-8 d were 75.0%-87.0%. Decrease of CD62L from the surface of γδT cells by 3 h to 12 h after exposure to PMA (42.3% to 23.5% ), but CD62L expression increased to 53.2% when γδT cells were exposed to PMA for 24 h. The expression of CD62L of γδT cells decreased to 52.1% and 39.3% respectively when γδT cells were exposed to PMA + IMN for 3 h and 6 h. After treated with PMA + IMN for 12 h and 24 h, the expression of CD62L were 52.9% and 35. 3% respectively. The CD62L expression of γδT cells treated with PMA and Rottlerin (47.9%) were higher than that treated with PMA alone (31.8%). After Mtb-Ag restimulated MtbAT for 4 h, the CD62L level of γδT cells decreased from 70.0% to 54.8%, Rottlerin could inhibite Mtb-Ag down regulation CD62L level of γδT cells (63.1%). Conclusion The CD62L expression of γδT cells could be ingibited partly by the inhibitor of PKCθ signal pathway may regulate L-selectin (CD62L) expression of activated human γδT cells.

BACKGROUND:Previous study has observed that the calf acellular dermal membrane exhibits slow repair efficiency, fast degradability speed and other shortcomings in the repair of cartilage defects. OBJECTIVE:To investigate the repair effect of the col agen type Ⅱ-modified acel ular dermal membrane on cartilage defects in rabbits. METHODS:The fetal rabbit chondrocytes were seeded onto the col agen type Ⅱ-modified acel ular dermal membrane, and the composite was then observed under scanning electron microscope at 3, 7 and 14 days. Cartilage defect models were established on the bilateral femoral condyles of 24 New Zealand white rabbits, and these model rabbits were randomly allocated to three groups. The cartilage-acellular dermal membrane and cartilage-collagen type Ⅱ-modified acellular dermal membrane were implanted into the defect regions of control and experimental groups, respectively. Those received no intervention were as blank control group. Collagen type Ⅱ immunohistochemical staining and Wakitani scoring system were performed at 6 and 12 weeks postoperatively. RESULTS AND CONCLUSION:Chondrocytes grew and adhered well in the scaffold. The Wakitani scores in the experimental group were significantly lower than those in the control and blank control groups at postoperative 6 and 12 weeks (P<0.05). At 6 and 12 weeks postoperatively, collagen type Ⅱ immunohistochemical staining was the strongest in the experimental group, with yellow and brown particles in the cytoplasm;the control group was positive for collagen type Ⅱ immunohistochemical staining, while the blank control group was negative for the staining. Our findings suggest that the collagen type Ⅱ-modified acellular dermal membrane is beneficial for the repair of cartilage defects.

85%. The concentrated MCS in different amount was added to the IFN-?(100 pg/mL) and LPS (10 ng/mL) enriched culture media. The IL-12 production by monocytes was determined by the enzyme- linked immunosorbent assay(ELISA).The expression of CD14 and CD1a was analyzed by flow cytometry 5 days after the monocytes were co-cultured with MCS. Results The production of monocytic IL-12 was down-regulated by MCS in a dose dependent manner. The amount of IL-12 from monocytes decreased along with an increased dose (25-100?L) of MCS applied in the reaction. It was also observed that the differentiation from CD14 expressing monocytes to CD1a dendritic cells was impaired by MCS. The ability of MCS to inhibit the production of IL-12 by monocytes and to suppress the differentiation of monocytes to dendritic cells in vitro could be disrupted by PD98059,an ERK specific inhibitor. Conclusions MCS appears to inhibit IL-12p40 production by monocytes and inhibit differentiation of monocytes in vitro via secretion of ERK stimulating factor. The inhibitory factors in MCS and their chemical natures need further research.

Objective To establishment a method for detection of multiple drug resistance gene of Yersina pestis using polymerase chain reaction(PCR), to provide a guidance for treatment of plague. Methods According to National Center for Biotechnology Information (NCBI) released sequences of aminoglycoside resistant genes of streptomycin resistant,strB,strA,beta lactam antibiotics resistant genes tem,shv,and ctx-m,sulfamilamide resistant genes sul1, sul2, and sul3, a pair of primers of each gene was designed. DNAs of 282 strains isolated from plague natural foci in Qinghai Province were amplified by PCR using every pair of primers. The products were separated using gel electrophoresis, and the results were visualized through a gel imaging system. The susceptibility of 282 Yersina pestis to streptomycin, sulfamethoxazole and ceftriaxone was tested by drug sensitivity test. Results The PCR amplification results of all samples were negative,and strains with streptomycin,sulfamilamide and beta lactam antimicrobial drug resistance genes were not found. Drug sensitivity test showed that 282 strains were highly sensitive to streptomycin,sulfamethoxazole and ceftriaxone sodium.The diameter of bacteriostasis ring>19,17,21 mm, respectively. Conclusions It is a feasible method to use PCR technology to detect the multiple drug resistance genes of Yersinia pestis. Using this method to systematically monitor the resistance gene of Yersinia pestis is an efficient, economical and practical experimental method, which can provide guidance for the treatment of plague disease.

Metastatic vascular calcification and calcinosis universalis, as severe complications of parathyroid hyperfunction and hyperparathyroidism, have attracted more attention in patients with renal secondary hyperparathyroidism and primary hyperparathyroidism. But, they are of little concern in patients with long-term negative calcium balance related parathyroid hyperfunction or hyperparathyroidism caused by calcium and/or vitamin D insufficiency (CVI). CVI is common in the population. Relatively low level of serum calcium and negative calcium balance caused by long-term CVI result in parathyroid hyperfunction or hyperparathyroidism, which may cause secretion of PTH beyond the physiological level, leading to bone absorption and release of a large amount of bone calcium into the blood. It may not only cause bone loss and osteoporosis, but also form metastatic vascular calcification or calcinosis universalis presented by cardiovascular diseases and other multi-organ lesions. Early calcium deposition can gradually fade after reasonable treatment, but middle arterial calcification is not easy to fade once it occurs. Therefore, vascular calcification and calcium deposition should be actively prevented and early screened and diagnosed. The early prevention, diagnosis and treatment of parathyroid hyperfunction or hyperparathyroidism can prevent, delay, or even reverse the occurrence and development of metastatic vascular calcification and calcinosis universalis, which is significant for disease prevention and protecting the patients' health influenced by these diseases.