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 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 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 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.

Diagnosis, Differential ; Humans ; Meniere Disease ; diagnosis ; therapy ; Vertigo ; diagnosis ; therapy

Objective To investigate the effects of penehyclidine hydrochloride on activities of nuclear factor kappa B (NF-kB) and activator protein-1 (AP-1) during actue lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (group S),blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloride group (group PHCD).The model of actue lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.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 PHCD group,PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,blood samples were obtained for measurement of concentrations of tumor necrosis factor-alpha (TNF-α) in serum.The lungs were then removed for determination of lung water content,myeloperoxidase (MPO) activaty (by colorimetric assay),NF-κB and AP-1 activaties (using electrophoretic mobility shift assay) in lung tissues,and for microscopic examination of pathologic changes (under light microscope).The left lung was lavaged,and lung permeability index (LPI) was calculated.Results Compared with S group,lung water content,LPI,serum TNF-α level and activites of MPO,NF-κB and AP-1 were significantly increased in THSR and PHCD groups.Compared with THSR group,lung water content,LPI,serum TNF-α concentrations and activites of MPO,NF-κB and AP-1 were significantly decreased in PHCD group.The pathological damage to lung tissues was significantly reduced in PHCD group as compared with THSR group.Conclusion PHCD can inhibit activities of NF-κB and AP-1 in lung tissues,thus mitigating acute lung injury induced by blunt chest trauma-HSR in rats.

Objective To investigate the effects of penehyclidine hydrochloride on Fas/FasL expression during acute lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male SPF Sprague-Dawley rats, aged 8 weeks, weighing 245-275 g, were randomly assigned into 3 equal groups using a random number table: sham operation group (group Sham) , blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloric group (group PHCD).The model of acute lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until mean arterial pressure was decreased to 35-45 mmHg within 15 min, and maintained at this level for 60 min, followed by resuscitation.In PHCD group, PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established, the rats were sacrificed, the lungs were then removed for microscopic examination of pathologic changes and for determination of Fas, FasL and caspase-8 expression, and interleukin-6 (IL-6) and IL-1β contents in lung tissues.Apoptotic index was calculated.Results Compared with group Sham, the expression of Fas, FasL and caspase-8 was significantly up-regulated, and AI and contents of IL-6 and IL-1β were increased in THSR and PHCD groups (P＜O.05).Compared with group THSR, the expression of Fas, FasL and caspase-8 was significantly down-regulated,and AI and contents of IL-6 and IL-1β were decreased in group PHCD (P＜0.05).The pathologic changes of lungs were significantly reduced in group PHCD compared with group THSR.Conclusion The mechanism by which penehyclidine hydrochloride inhibits lung cell apoptosis induced by blunt chest trauma-HSR is associated with inhibition of Fas/FasL expression in 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.

One hundred and twenty five patients, who underwent cystoscopic examination, were randomly divided into two groups: the control group ( n = 62) received conventional cystoscopy, and the treatment group (n = 63) received rociverine 20 mg 1 h before cystoscpy.The pain levels were evaluated using numeric rating scale (NRS) in all patients.The average NRS during examination was 2.1 ±0.9 and 3.6 ± 1.8 in treatment group and control group respectively( P ＜0.01 ).The pain scores in control g roupwere still higher than those in treatment group 15 min and 1 d after procedure ( P ＜ 0.01 or 0.05,respectively).