Epidemiological studies have shown that human papillomavirus (HPV) infection is the main cause of cervical cancers and cervical intraepithelial neoplasia(CIN).And different types of HPV have different carcinogenicity,different cervical cancer pathological types and prognoses of cervical cancer.The effective way to decrease the cervical cancer morbidity is to detect and classify the high-risk HPV infection in early time,and carry out intervention therapy in early time.Therefore,detecting HPV subtypes in clinic will have great significance in prevention and treatment of cervical cancer and cervical precancerous.

Objective To investigate the mechanism of myocardial ischemia and reperfusion-induced acute lung injury (ALl) and protective effect of ischemic postconditioning.Methods Forty SD rats were allocated to sham group,myocardial ischemia/reperfusion group (reperfusion group),ischemic postconditioning group (postconditioning group),and ischemic postconditioning + phosphatase and tensin homolog deleted on chromosome ten (PTEN) inhibiting group (inhibitor group) according to the random number table,with 10 rats per group.Myocardial ischemia/reperfusion was induced by left anterior descending coronary artery occlusion.Postconditioning was performed within 1 minute before reperfusion consisting of 3 10 s cycles of reperfusion followed by 10 s occlusion.Lung was immediately removed 120 minutes after reperfusion for HE stain,immunohistochemical detection of inflammatory factors and apoptosis factors,TUNEL assay of cell apoptosis,and Western blot of protein kinase B (Akt),phospho-Akt (p-Akt),glycogen synthase kinase-3β (GSK-3β),and phospho-GSK-3β (p-GSK-3β).Results Down-regulated B-cell lymphoma-2 (Bcl-2) and IL-10 and up-regulated Bcl-2 associated X protein (Bax),cysteinyl aspartate specific proteinase-3 (Caspase-3),IL-6 as well as IL-8 were observed in other 3 groups compared with sham group (P ＜0.01).Moreover,down-regulated Bax,Caspase-3,IL-6,IL-8 as well as TUNEL and up-regulated Bcl-2 as well as IL-10 were observed in reperfusion group compared to postconditioning group and tensor group (P ＜ 0.01).No statistical differences were found among the four groups in levels of Akt,p-Akt,and GSK-3β,but level of p-GSK-3β was significantly down-regulated in reperfusion group compared to other 3 groups(P ＜ 0.01).Conclusion Development of ALI may relate to down-regulation of p-GSK-3β evoked directly by the release of inflammation factors in early period of myocardial ischemia/reperfusion and ischemic postconditioning may attenuate the condition.

Objective To evaluate the effects of ischemic postconditioning on brain injury induced by myocardial ischemia-reperfusion (I/R) in diabetic rats.Methods Diabetes mellitus was induced by intraperitoneal streptozotocin 60 mg/kg and confirmed by blood glucose level ＞ 16.7 mmol/L.Thirty male Sprague-Dawley rats,weighing 220-280 g,in which diabetes mellitus was successfully induced,were randomly allocated into 3 groups (n =10 each) using a random number table:group sham operation (group S),group I/R and group ischemic postconditioning (group P).Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery in I/R and P groups.Group P received 3 cycles of 10 s reperfusion followed by 10 s ischemia at the end of myocardial ischemia.The rats were sacrificed at 120 min of reperfusion and the brains were removed for microscopic examination and for determination of cell apoptosis (by TUNEL) and expression of interleukin-6 (IL-6),IL-8,IL-10,glycogen synthase kinase-3 beta (GSK-3β) and phosphorylated GSK-3β (pGSK-3β) (by immuno-histochemistry).Apoptotic index was calculated.Results Compared with group S,apoptotic index was significantly increased,IL-6 and IL-8 expression was up-regulated,and IL-10 and pGSK-3β expression was downregulated in I/R and P groups (P ＜ 0.01).Compared with group I/R,apoptotic index was significantly decreased,IL-6 and IL-8 expression was down-regulated,and IL-10 and pGSK-3β expression was up-regulated in group P (P＜0.01).There was no significant difference in GSK-3β expression among the 3 groups (P ＞ 0.05).The pathologic changes were significantly attenuated in group P as compared with group I/R.Conclusion Ischemic postconditioning can attenuate brain injury induced by myocardial I/R in diabetic rats,and inhition of activity of GSK-3β may be involved in the mechanism.

OBJECTIVE:To evaluate the pharmacoeconomics of pantoprazole vs. ranitidine in the treatment of gastricesophagitis reflux disease(GERD). METHODS:Retrieved from PubMed,EMBase,The Cochrane Library,CNKI,VIP and Wanfang database, RCTs about pantoprazole vs. ranitidine in the treatment of GERD were selected until Sept. 2014. Two reviewers independently screened literature in accordance with the inclusion and exclusion criteria,and extracted the data of included studies. Stata 12.0 soft-ware was used to estimate therapeutic efficacy index and cost,and cost-effectiveness analysis was performed with the decision tree model. RESULTS:A total of 7 RCTs were included,involving 1 389 patients. Cost-effectiveness analysis showed that for gradeⅠ-Ⅲ(by Savary-Miller standard)GERD,cost-effectiveness ratios of ranitidine were all lower than those of pantoprazole(gradeⅠ:18.86 vs. 57.93;gradeⅡorⅢ:35.58 vs. 146.13);gradeⅠ,Ⅱ,Ⅲincremental cost-effectiveness ratio(ICER)were 335.53,349.85,349.85. Sensitivity analysis supported this conclusion. CONCLUSIONS:Ranitidine is more economic therapy plan for gradeⅠ-Ⅲ GERD, but its ICER fluctuates greatly. Individual therapy plan should be formulated according to disease condition and economic condition.

Objective To investigate the effects of ischemic pre- and postconditioning on cerebral glycogen synthase kinase-3 beta (GSK-3β) activity in a rat model of global cerebral ischemia-reperfusion (I/R).Methods Forty male Wistar rats weighing 200-230 g were randomly allocated into 4 groups (n =10 each) : Ⅰ group sham operation (group S); Ⅱ group I/R; Ⅲ group ischemic preconditioning (group IPR) and Ⅳ group ischemic postconditioning (group IPO). The animals were anesthetized with intraperitoneal 10% chloral hydrate 0.4 ml/100 g. Global cerebral ischemia was induced by four-vessel-occlusion in group Ⅱ , Ⅲ and Ⅳ. Bilateral vertebral arteries were cauterized and bilateral carotid arteries were occluded for 10 min. In group IPR cerebral ischemia was preceded by 3 cycles of 10 s ischemia followed by 30 s reperfusion. The group IPO received 3 cycles of 30 s reperfusion followed by 10 s ischemia at the end of 10 min cerebral ischemia. The animals were killed 2 days later. The brains were immediately removed for determination of neuronal apoptosis in the cortex (by TUNEL), the infarct size (by TTC), p-GSK-3β activity (by spectrum assay) and the expression of Bcl-2, Bax and Caspase-3 (by SP). Linear correlation of p-GSK-3β activity with the number of apoptotic neurons in the cortex and cerebral infarct size was analyzed. Results Cerebral I/R significantly increased the number of apoptotic neurons in the cortex and infarct size, decreased p-GSK-3β activity, down-regulated Bcl-2 expression and up-regulated Bax and Caspase-3 expression in group I/R as compared with group S. Ischemic pre- and postconditioning significantly attenuated these cerebral I/R-induced changes. The p-GSK-3β activity was negatively correlated with the number of apoptotic neurons in the cortex and cerebral infarct size. Conclusion Ischemic pre- and postconditioning reduces cerebral I/R injury through inhibiting the activity of GSK-3β.

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 investigate the effect of ischemic post-conditioning (IPO) on the level of Heme oxygenase-1 (HO-1) in acute ischemia - reperfusion (I/R) injury of lung in order to illuminate its protective mechanism.Methods Forty-eight adult SD rats were randomly divided (random number) into 6groups ( n =8 each):sham operation group ( S group) ; I/R group in which the hilum of left lung was clamped for 45 min followed by 105 min reperfusion; IPO group in which left lung hilum was clamped for 45min and post - conditioned by alternation of 30 s reperfusion with 30 s re-occlusion for three times before perfect perfusion for 102 min; Hemin (HM) + I/R group; ZnPPⅨ (zinc protoporphyrin Ⅸ) + IPO group and HM + S group.Arterial partial pressure of oxygen ( PaO2 ) and malondialdehyde (MDA) content in blood serum were assayed.The left lung was removed for determination of wet/dry (W/D) lung weight ratio and level of HO-1 protein was detected by immunohistochemical technique and pathohistological changes were observed under light microscopic examination. Comparisons among multiple groups were studied by using one-way analysis of variance (ANOVA). Statistical comparisons within groups were analyzed by using paired t -test.Results The level of HO-1 in lung tissue was significantly increased in the I/R group compared with the S group and the HM + S group (P ＜0.01,P ＜0.05).Compared to the I/R group,the IPO and the HM + I/R groups had significant higher level of HO-1 ( P ＜ 0.05,P ＜ 0.01 ).The PaO2 was significantly lower in all experimental groups than that in the S group (90 ± 11 ) mmHg.However,the values of PaO2 in the IPO and the HM + I/R groups were higher than that in the I/R group (P ＜ 0.01 ).In addition to severe lung tissue damage evidenced by pathohistological changes,the lung wet/dry (W/D) weight ratio and MDA level in blood serum were significantly higher in the I/R group than those in the S group (P ＜0.01 ),whereas the lung damage was attenuated either by IPO or by HM pretreatment (P ＜ 0.05,IPO or HM + I/R vs.I/R).Conclusions IPO can attenuate the lung ischemia - reperfusion injury through upregulating the level of HO-1 protein and inhibiting lipid peroxidation injury.

Objective To systematically review the efficacy of bispectral index (BIS) monitoring for prevention of intraoperative awareness in patients under general anesthesia.Methods The Cochrane Central Register of Controlled Trials (Central),PubMed,Medline,and EMBASE were searched for randomized controlled clinical trials involving detection of intraoperative awareness in patients in whom BIS was used or not under general anesthesia.The quality of the studies was evaluated by the method recommended by Cochrane Collaboration.Evaluation indexes included the incidence of intraoperative awareness.Meta-analysis was conducted using RevMan 5.1 software.Results Five randomized controlled clinical trials involving 34181 patients were included in this meta-analysis.There were 17432 cases in whom BIS was applied and the incidence of intraoperative awareness was 0.132％.There were 16749 cases in whom BIS was not used and the incidence of intraoperative awareness was 0.245％.There was no significant difference in the incidence of intraoperative awareness between the two groups (P ＞0.05).Further analysis was performed according to the method of anesthesia.In inhalational anesthesia,there were 13288 cases in whom BIS was applied and the incidence of intraoperative awareness was 0.128％,and there were 13202 cases in whom BIS was not applied and the incidence of intraoperative awareness was 0.113％.There was no significant difference in the incidence of intraoperative awareness between the two groups (P ＞ 0.05).In total intravenous anesthesia,there were 4144 cases in whom BIS was applied and the incidence of intraoperative awareness was 0.145％,and there were 3547 cases in whom BIS was not applied and the incidence of intraoperative awareness was 0.733 ％.The incidence of intraoperative awareness was significantly lower in the patients in whom BIS was applied than those in whom BIS was not applied (P ＜ 0.01).Conclusion BIS monitoring can effectively prevent the development of intraoperative awareness in patients under total intravenous anesthesia,but can not prevent the development of intraoperative awareness in patients under inhalational anesthesia.

Objective To study the anti-tumor effects of humulon on arylamine N-acetyltransferase-1(NAT1)activity.Methods Employing HPLC,using PABA as substrate,in intact SGC-7901 cells and their cytoplasm,making PABA being acetylated to Ac-PABA by NAT1 as the activity of NAT1.Reverse transcriptase polymerase chain reaction(RT-PCR)assay was used to study the expression of the NAT1 mRNA.Results The results show that humulon could inhibit the production of Ac-PABA in intact SGC-7901 cell and the cytoplasm,the production of Ac-PABA was gradually increased with the interaction time increasing.But comparing with corresponding negative control group's,the production of Ac-PABA was decreased evidently and the humulone could inhibit the expression of NAT1 mRNA.Conclusion Humulon could prevent the occurrence and deterioration of cancer.Its mechanisms can be attributed to its effect on decreasing the production of acetylation of carcinogenic aromatic amines,which is acetylated from aromatic amines,and inhibiting the NAT1 activity and expression of NAT1 mRNA.