Human tissue factor pathway inhibitor (TFPI) is a member of the Kunitz-type serine protease inhibitor family, which is divided into TFPI-1 and TFPI-2. The key function of TFPI-1 is anticoagulate, while TFPI-2 is a broad-spectrum serine protease inhibiter. Both of them are composed of three repeated Kunitz-type domains. Even though sharing some structural homology, they are quite different from each other in terms of the coding sequences, tissue origins and distribution, the functions and the mechanisms involved. These differences between TFPI-1 and TFPI-2 lead to the discrepancies in the roles they played in a variety of physiological and pathological processes. The recent progress in the related research is reviewed in this article.

OBJECTIVE:To study the effects of podophyllotoxin derivative QW-83 on human cervical cancer HeLa cell apopto-sis and its mechanism. METHODS:After treated with 0(negative control),0.01,0.1,1 and 10 μmol/L QW-83 and positive drug etoposide(VP-16)for 48 h,proliferation inhibition rate and IC50 of HeLa cell were determined by MTT assay. The morphological changes of HeLa cell were observed by Hochest 33342 staining after treated with QW-83 [0(negative control),2.5,5,10μmol/L] for 48 h;flow cytometry was used to detect apoptosis rate;semi quantitative RT-PCR was adopted to detect the expression of apop-tosis related gene P53,Bax,Casepase-3,Casepase-8,Casepase-9 and Bcl-2 mRNA. RESULTS:Compared with negative control, 1,10 μmol/L VP-16 and QW-83 had obvious proliferation inhibition effect on HeLa cells (P<0.05 or P<0.01),and IC50 were (5.11±0.43)μmol/L and(4.96±0.54)μmol/L. Hochest 33342 staining results showed QW-83 could obviously induce cells apopto-sis and nuclear pyknosis. Flow cytometry showed QW-83 could increase apoptosis rate in concentration-dependent manner,being 16.89%-62.56%. RT-PCR showed mRNA expression of P53,Bax,Caspase-3,Casepase-8 and Casepase-9,Bcl-2/Bax increased, while mRNA expression of Bcl-2 decreased after treated with QW-83(P<0.05). CONCLUSIONS:Podophyllotoxin derivative QW-83 can induce HeLa cell apoptosis,and its mechanism may be associated with regulate mRNA expression of apoptosis related gene.

Objective To explore whether intravenous injection of hydrogen‐rich saline having the protective effect on sodium taurocholate induced severe acute pancreatitis(SAP) associated lung injury(APALI) in rats and its possible mechanisms .Methods Fifty‐four healthy male SD rats were randomly divided into sham‐operation group (Sham group) ,model group (SAP+ NS group) and hydrogen water treatment group (SAP + HRS group) ,and each group was subdivided into 6 ,12 ,24 h subgroups .Six rats were killed at each time point for collecting serum ,lung tissue and pancreas tissue .Serum TNF‐αand IL‐1βlevels ,lung wet /dry weight ratio ,expression of TNF‐αmRNA and IL‐1βmRNA in the lung tissue were detected .The pathological evaluation of pancreas and lung tissue injury was performed .Results (1)The levels of TNF‐α and IL‐1β in serum ,pancreas and lung tissue pathological scores ,TNF‐αmRNA and IL‐1βmRNA expression levels in the lung tissue and lung wet dry weight ratio at the time points of 6 , 12 ,24 h in the SAP+NS group and the SAP+ HRS group were higher than those in the sham group (P<0 .05) .(2) Compared with the SAP+NS group ,the levels of serum TNF‐α,TNF‐αmRNA expression level in the lung tissue and lung wet dry weight ra‐tio at all time points in the SAP+ HRS group were lower(P<0 .05);the levels of serum IL‐1β,pancreas and lung tissue pathologi‐cal score and IL‐1β‐mRNA expression at 6 h in the lung tissue had no statistical difference between the SAP+NS group and SAP+HRS group ,but which at time points of 12 ,24 h in the SAP+ HRS group were lower than those in the SAP+NS group(P<0 .05) . Conclusion HRS realize the protection on APALI possibly via its elective anti‐oxidation action for inhibiting oxidative stress injury related cytokines expression .

Objective:To explore therapeutic effect of atorvastatin on aged patients with mild to moderate hyperten-sion.Methods:A total of 427 aged patients with mild to moderate hypertension treated in our hospital from Jul 2011 to Jul 2013 were randomly divided into routine treatment group (n=210)and atorvastatin group (n=217,received atorvastatin additionally based on routine treatment)according to number table.All patients were treated with a continuous 24 months.Therapeutic effect of controlling blood pressure,changes of blood pressure level and high sensitive C reactive protein (hsCRP)level and occurrence of adverse reactions during treatment were compared be-tween two groups.Results:Compared with routine treatment group,there was significant rise in total effective rate of long-term (24 months)controlling blood pressure (76.8% vs.85.9%),and significant reductions in blood pres-sure [(145.3±10.1/88.6±6.7)mmHg vs.(136.9±6.8/83.0±5.2)mmHg]and hsCRP [(2.02±0.29)mg/L vs. (1.60±0.18)mg/L]level in atorvastatin group,P<0.05 or <0.01. There was no significant difference in inci-dence rate of adverse reactions during treatment between two groups (P>0.05).Conclusion:Atorvastatin combined antihypertensive drugs can well control blood pressure and reduce inflammatory reactions,which is suitable for long term use in aged patients with hypertension.

Objective To investigate the clinical presentations, pathologic features, and the di-agnosis and treatment of prostate sarcomatoid carcinoma. Methods Two cases of prostate sarcoma-told carcinoma were analyzed with review of the relevant literature. Case 1, a 51-year-old man com-plained of dysuria and perineal discomfort for 2 months, was admitted because of acute urinary reten-tion. His serum PSA was 2.31 ng/ml. Heterogeneous density of the prostate left lobe and bladder neck involvement was shown on CT scan. Prostate sarcomatoid carcinoma was confirmed by transrec-tal prostate biopsy, and patient accepted radical cystoprostatectomy and ideal conduit followed with lo-cal radiotherapy and hormonal therapy. Case 2 was a 54-year-old male. This ease was admitted with a history of dysuria and intermittent gross hematuria for 1 month. Hypoechoic lesion was found by ul-trasonography,and heterogeneous density of the prostate was shown on CT scan. His serum PSA was 2.61 ng/ml. The prostate biopsy result showed prostate sarcoma. Radical cystoprostatectomy and ide-al conduit was performed on this case. Results The diagnosis of prostate sarcomatoid carcinoma in the 2 cases was confirmed by postoperative pathology. Under microscope, the neoplasm was mainly composed of epithelial and sarcomatoid mesenchymal cells,with a transitional region of these cells. Im-munohistochemical staining showed that the cells were positive for cytokeratin and epithelial membrane antigen. Vimentin was negative in the epithelial cells, but was positive in the majority of sarcomatoid cell. Both patients died of multi-metastasis at 43 and 19 months after surgery respectively. Conclu-sions Sarcomatoid carcinoma of the prostate is extremely rare with a high grade of malignancy,and its prognosis is poor. The diagnosis depends on pathological features and immunohistochemical studies. Radical resection combined with endocrine therapy and radiotherapy is considered to be the most relia-ble treatment so far.

Objective To evaluate the effects of ulinastatin on perioperative inflammatory response during cardiopulmonary bypass. Methods Comprehensive search of PubMed,EMbase,the Cochrane Library,CECDB,CQVIP,CNKI databases was conducted for randomized controlled trials(RCTs) published from January 1994 to June 2014.The included studies were evaluated strictly and the extracted data were analyzed by RevMan 5.2. Results A total of 7 RCTs including 335 patients were included,and 154 patients were in the experimental group,while 181 patients were in the control group.In the experimental group, patients were given Ulinastatin during surgery. System evaluation results show that, the concentration of TNF-α [ SMD (95%CI) were -3.48(-4.64,-2.31)] and IL-6 [SMD(95%CI) were -3.04(-4.54,-1.54)] in experimental group at 1 h after weaning from CPB were significantly lower than those in control group. Conclusion Ulinastatin used perioperatively in cardiopulmonary bypass can significantly reduce postoperative inflammation.

Objective To evaluate the effects of Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) signaling pathway on the brain injury induced by myocardial ischemia-reperfusion (I/R) in diabetic rats.Methods Pathogen-free male Sprague-Dawley rats,weighing 200-220 g,were used in this study.Diabetes mellitus was induced by intraperitoneal 1％ streptozotocin 60 mg/kg and confirmed by blood glucose level ≥ 16.7 mmol/L 3 days later.Twenty-four rats with diabetes mellitus were randomly allocated into 3 groups (n =8 each) using a random number table:sham operation group (group S),I/R group,and myocardial I/R + AG490 (JAK inhibitor) group (group ⅠA).Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery for 30 min,followed by 120 min of reperfusion in the rats anesthetized with pentobarbital sodium.AG490 3 mg/kg was injected intravenously at 20 min before reperfusion in group IA.The rats were sacrificed at 120 min of reperfusion,and the brains were removed for determination of caspase-3 and nuclear factor kappa B (NF-κB) activities (using colorimetric method),cell apoptosis (by TUNEL),and expression of interleukin-1 (IL-1),IL-6,IL-8,Bax,Bcl-2,cytochrome C (Cyt c),phosphorylated JAK2 (p-JAK2),and phosphorylated STAT3 (p-STAT3) (by Western blot).Apoptosis index was calculated.Results Compared with group S,the expression of Bax,Cyt c,IL-1,IL-6,IL-8,p-JAK2 and p-STAT3 was significantly up-regulated,the expression of Bcl-2 was down-regulated,and NF-κB and caspase-3 activities and apoptosis index were increased in I/R and IA groups (P＜0.05).Compared with group I/R,the expression of Bax,Cyt c,IL-1,IL-6,IL-8,p-JAK2 and p-STAT3 was significantly down-regulated,the expression of Bcl-2 was up-regulated,and NF-κB and caspase-3 activities and apoptosis index were decreased in group IA (P＜0.05).Conclusion Inflammatory responses mediated by JAK2/STAT3 signaling pathway are involved in the brain injury induced by myocardial I/R in diabetic rats.

Objective To evaluate the relationship between DJ?1 and diabetes mellitus ( DM )?caused influence on cardioprotection induced by ischemic postconditioning in rats. Methods Adult male Sprague?Dawley rats, aged 3 months, weighing 220-250 g, were used in the study. DM was induced by intraperitoneal injection of 1% streptozotocin 60 mg∕kg and confirmed by blood glucose≥16.7 mmol∕L. Forty?eight rats with DM were randomly divided into 3 groups ( n=16 each) using a random number table:sham operation group ( group DM?S ) , myocardial ischemia?reperfusion ( I∕R ) group ( DM?IR ) and ischemic postconditioning group (DM?IPO group). Another 48 normal rats received the equal volume of citrate buffer solution instead and served as control. Those rats were randomly divided into 3 groups ( n=16 each) using a random number table: sham operation group ( S group) , myocardial I∕R group ( IR group) and ischemic postconditioning group (IPO group). At 12 weeks after streptozotocin injection, myocardial I∕R was produced by 30 min occlusion of the left anterior descending branch of the coronary artery followed by 120 min reperfusion. Ischemic postconditioning was induced by 3 cycles of 10 s reperfusion followed by 10 s limb ischemia at the end of 30 min limb ischemia. At 120 min of reperfusion, the animals were sacrificed, and hearts were removed for determination of myocardial infarction size ( using TTC ) , and expression of DJ?1, phosphatase and tensin homologue ( PTEN) protein, and phosphorylated Akt ( p?Akt) in myocardial tissues ( by Western blot) . Results The infarction size was significantly increased in diabetic and nondiabetic rats during myocardial I∕R. The expression of DJ?1, PTEN protein and p?Akt was significantly higher during myocardial I∕R in nondiabetic rats, and the expression of PTEN protein and p?Akt was up?regulated, and no significant change was found in DJ?1 expression during myocardial I∕R in diabetic rats. Ischemic postconditioning reduced infarction size during myocardial I∕R and up?regulated the expression of DJ?1 and p?Akt, and down?regulated the expression of PTEN protein in nondiabetic rats, but not in diabetic rats. Compared with nondiabetic rats, the expression of DJ?1 and p?Akt was down?regulated, and the expression of PTEN protein was up?regulated after ischemic postconditioning in diabetic rats. Conclusion The mechanism by which DM abolishes cardioprotection induced by ischemic postconditioning is associated with down?regulation of DJ?1 expression in rats.

Objective To investigate clinical distribution and drug sensitivity of infectious pathogens in our wards for hematology malignancies. Methods Drug sensitivity tests of bacteria were performed by Kirby-Bauer method, 56 strains of pathogens were isolated from all detected samples. Results The results showed that the composition ratio of Gram-negtive bacteria, Gram-positive bacteria was 69.64%, 30.36%. In decreasing frequency, Escherichia coli (37.50%), Klebsiella pneumoniae (10.71%). All of staphylococcies were resistant to meticillin, and sensitive to vancomycin. Conclusion This study indicates that Gramnegative bacteria remain the predominant pathogens in microorganisms causing bloodstream infections for hematological malignancies at Huashan Hospital. The incidence of Escherichia coli is the highest. All of staphylococcies were resistant to meticillin.

Objective To investigate the effects of penehyclidine hydrochloride (PHC) on acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation in rats.Methods Forty male SpragueDawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 4 equal groups (n =10 each) using a random number table:sham operation group (S group),blunt chest trauma combined with hemorrhagic shock and resuscitation group (group THSR),PHC for prevention group (group P1)and PHC for treatment group (group P2).ALI was induced by dropping a 300 g weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs in anesthetized rats in THSR,P1 and P2 groups.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In P1 group,PHC 2 mg/kg was injected intravenously at 30 min before blunt chest trauma.In P2 group,PHC 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,arterial blood samples were obtained for blood gas analysis and for measurement of concentrations of interleukin-6 (IL-6) and interleukin-1β (IL-1β) in serum by ELISA.Oxygenation index (OI) was calculated.The animals were sacrificed and bronchoalveolar lavage fluid (BALF) was collected for determination of white blood cell count and protein concentrations.Lungs were removed for examination of pathological changes and ultrastructure and for determination of Toll-like receptor (TLR4) and phosphor-p38 mitogen activated protein kinase (p-p38MAPK) expression (by Western blot).Results Compared with group S,PaO2 and OI were significantly decreased,PaCO2,protein concentrations in BALF,white blood cell count,and IL-6 and IL-1β concentrations in serum were increased,and TLR4 and p-p38MAPK expression was up-regulated in THSR,P1 and P2 groups.Compared with group THSR,PaO2 and OI were significantly increased,PaCO2,protein concentrations in BALF,white blood cell count,and IL-6 and IL-lβ concentrations in serum were decreased,TLR4 and p-p38MAPK expression was down-regulated in P1 and P2 groups.No significant differences were found in the parameters mentioned above between P1 and P2 groups.Conclusion PHC can mitigate acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation in rats,and inhibited activation of TLR4/ p38MAPK signaling pathway and attenuated inflammatory responses are involved in the mechanism.