Purpose: To determine the protective effect of ginkgolide B (GB) against isoproterenol (ISO)-induced chronic heart failure in a rat model. Methods: A total of 32 male Wistar rats were randomly divided into 4 groups. Rats in control group received only saline, while rats in GB alone group were injected with GB at a dose of 20 mg/kg body weight (bwt) intraperitoneally (i.p). Another group of rats was injected with ISO subcutaneously (s.c.) at a dose of 85 mg/kg for 2 days (ISO group). Rats in the GB+ISO group were administered GB at a dose of 20 mg/kg, i.p., for 7 days prior to exposure to ISO s.c. at a dose of 85 mg/kg. Results: Rats pre-treated with GB for 7 days prior to ISO exposure showed a significant decrease in cardiac infarct size, and marked decreases in the levels of cardiac biomarkers, inflammatory and apoptotic biomarkers, and lipid peroxidation (p < 0.05), but significant improvement in the levels ofendogenous antioxidants (p < 0.05). In addition, GB administration resulted in marked increases in the protein expression levels of heme oxygenase-1 (HO-1) and Nrf2 in cardiac tissue (p < 0.05). Conclusion: These results indicate that pre-treatment of chronic heart failure rats with GB for 7 consecutive days considerably lowered inflammatory and apoptotic markers via upregulation of Nrf2/HO-1 signaling pathway. Thus, GB has cardioprotective potential in humans. Keywords: Ginkgolide B, Nrf2/HO-1, Inflammatory markers, Apoptotic markers, Antioxidants

BACKGROUND:There are no reliable risk factors to accurately predict progression to cervical cancer in patients with chronic cervicitis infected with human papillomavirus (HPV). The aim of this study was to create a validated predictive model based on the risk factors for cervical cancer. A model to estimate the risk of cervical cancer may help select patients for intervention therapy in order to reduce the occurrence of cervical cancer after HPV infection. METHODS:This retrospective analysis included 68 patients with cervical cancer and 202 healthy female controls. HPV infection and human leukocyte antigen (HLA) class II alleles in HLA-DRB1, 3-7, and 9 were detected. Other information was collected, including level of education and age at first parturition. Multiple regression analysis and an artificial neural network (ANN) were performed to identify the independent risk factors for cervical cancer, and based on these, an evaluation model for the prediction of the incidence of cervical cancer was formed. RESULTS:This model showed HPV to be a pivotal player in cervical cancer that increased the risk by 7.6-fold. The presence of the HLA-DRB1*13-2 and HLA-DRB1*3(17) alleles was associated with an increased risk of developing cervical cancer. Conversely, the HLA-DRB1*09012 and HLA-DRB1*1201 alleles were found to be associated with a reduced cervical cancer risk. In addition, other factors, such as age at first parturition and education level, had significant effects on cervical cancer risk. The model was applied to conduct a risk assessment of women in the mountain area of Wufeng County, Hubei Province in China. The sensitivity and specificity of our model both exceeded 95%. CONCLUSIONS:This model, based on etiology and HLA allele susceptibility, can estimate the risk of cervical cancer in chronic cervicitis patients after HPV infection. It combines genetic and environmental factors and significantly enhances the accuracy of risk evaluation for cervical cancer. This model could be used to select patients for intervention therapy and to guide patient classification management.

Based on the load forecast with fuzzy period and the improved niche genetic algorithm,the peak load regulation considering the wind power transmitted by UHV network in 2015’ wet season mode is researched for Hubei Power Grid according to its power consumption.With the minimum power loss as its goal and the unit ramp rate and system security as its constraints,an optimal dispatch model is established and a peak load regulation scheme of Hubei Power Grid is planed for different proportions of wind power transmitted by UHV network.Simulative result shows that,in case of wind power transmitted by UHV network in 2015’ wet season mode,the peak load regulation ability of Hubei Power Grid is not sufficient and the UHV network should take part in it.Compared with traditional ones,the proposed peak load regulation scheme,on the premise of safe system operation,fully utilizes the peak load regulation capability of thermal and pumped storage units and effectively reduces the net loss.

目的:探讨湖北省五峰县宫颈癌高发区人群宫颈癌发生的高危因素。方法:对1 010例健康人群及59例宫颈癌患者进行巴氏细胞学及人乳头瘤病毒（HPV）16/18DNA的检测,并采用问卷形成获取相关的个人资料,在此基础上按年龄进行病例-对照（1∶4）研究。结果:健康人群与宫颈癌患者HPV的感染率分别为23.4%、88.1%（P＜0.001）,健康人群中30-34岁,＞50岁出现两个HPV感染峰值,HPV16、HPV18感染及第一次性行为年龄＜18岁是宫颈癌发生的高危因素,相对危险度分别为OR=27.227（95%CI 12.489-59.335）,OR=47.959（95%CI 6.000-383.330）,OR=32.2（95%CI 7.87-131.75）。结论:HPV感染的高峰病毒的再度活化,HPV16、HPV16+HPV18的感染是该地区宫颈癌发生的关键因素,避免性行为年龄过早,定期追踪高危人群,研制高发区型别特异性疫苗是预防高发区宫颈癌的有效措施。

Uneven distribution characteristics of economic and wind energy decide that large scale wind power should be delivered to northern or eastem load centers in China. It＇s a complicated multiple objective decision making problem to select an appropriate wind access point. This paper introduced a selection method of optimal access point for large scale wind power through the ultra-high voltage （UHV） lines and analyzed its decision process based on decision theory of entropy weight. A comprehensive index system to evaluate the access point of large scale wind power was established which took into account the power demand, network frame structure, level of safety and stability, economy of the receiving end and etc. This method was used to select an access point for one province receiving large scale wind power from northem part in China through UHV channel. The result indicates that this method can evaluate the influences of large scale wind power on the receiving system and provide reference to the selection of optimal access point for wind power UHV channel

Objective: To screen neuronal sortilin-related receptor SORL1 gene SNP between late-onset familial Alzheimer disease(FAD) and healthy population without familial diseases.Methods: The clinical data and blood samples from 41 samples of FAD patients in three generations were collected.The numbers of healthy controls are 50.Using SNaPshot genetying system,at the 5′ end and the 3′ end of SORL1 gene,SNPs 8,9,10(rs668387,rs689021,rs641120) and 19,23(rs2070045,rs3824968) respectively were analyzed.Results: At the 3′ end of SORL1 gene,SNP 23 A alleles(TA,AA) were significant different(P=0.001,P0.001) between the two groups.Conclusion: SORL1 gene SNP 23 is a posible gene marker for FAD.Further study should be processed to increase the sample size.

AIMThe purpose of this study was to investigate 50 women from eight families with familial cervical cancer in Wufeng County, Hubei Province, China, a region with a high incidence of cervical cancer. Eighty-nine healthy women, of similar age, location and ethnicity, were selected as a control group.METHODSBlood samples were collected from both groups, and HLA-A, HLA-B, and HLA-DRB1 genotypes were profiled with the Multi-Analyte Profiling system (xMAP) (Luminex HLA-SSO) using a WAKFlow HLA typing kit. Results were analyzed with Luminex HLA typing software and showed good stability, reproducibility and specificity.RESULTSWe found several high risk alleles in women with familial cervical cancer, that associated with the highest risk being HLA-B*07 (OR = 8.7, 95% CI = 1.8-41.1).CONCLUSIONSHLA-B*07 is a high risk allele for cervical cancer, and has strong potential for use as a molecular biomarker.

In order to study the function of superconducting magnetic energy storage system in improving the output of wind farm,wind farm model and SMES model are made and four-machine 12-bus benchmark power system is built on the platform of PSCAD.The paper also studies 3 kinds of wind speed in the multi-generator model,and the function of superconducting magnetic energy storage device in the wind farms in the condition of short circuit.The simulation result indicate that the SMES device perfects well in controlling wind farm power flow under the circumstances of different wind speed,shot circuit.

湖北省五峰县是中国宫颈癌的高发区,是开展宫颈癌病因学研究的现场.本研究对该地区健康妇女及宫颈癌患者进行了包括人乳头瘤病毒感染、性生活、性伴侣、孕次、产次、初产年龄、社会经济地位、吸烟、营养、避孕方式、遗传易感性(HLA)等宫颈癌相关危险因素的调查及检测,并利用该调查资料构建湖北省五峰县宫颈癌判别模型,以用于该地区宫颈癌高危人群的筛选.现将结果报告如下.

A method of sequence-based typing (SBT) has been adopted to assort types of exons 2 and 3, which have the most polymorphism, of HLA-B locus of the Tujia nation group in Hubei province. The correlation among the HLA-B alleles, human papillomavirus (HPV) infection and cervical cancer risk has also been investigated. Under the condition of resident location and age, race unified, 100 specimens of cancer patients were sampled as a case group, of which 86 were HPV positive and were screened for HLA-B alleles; while 187 specimens were taken from healthy people, of which 92 were HPV negative as a control group. The result shows that by comparing the above mentioned 86 HPV positive cervical cancer group and 92 HPV negative normal group, it was concluded that HLA-B*6701 was only found in the cervical cancer group ( p < 0.034), which shows that HLA-B*6701 can be used as an important candidate biological marking gene for generation of cervical cancer in Wufeng county of Hubei province.

Herpes Simplex Virus type 2 (HSV-2) is one of the most common sexually transmitted pathogen worldwide. The host immune response induced by viral infection is cell-type specific. Little is known about the innate immune response to this virus in its natural host cells. In this study, we established an in vitro HSV-2 infection model with human cervical epithelial (HCE) cells. The viral infection was sufficient to induce expression of Toll-like receptors (TLRs), and western blot and reporter assays suggest that HSV-2 infection leads to dramatic activation of the NF-κB signaling pathway. The two critical cytokines,IL-6 and IFN-beta,were also induced after HSV-2 infection and maintained high levels during the course of experiment. The presence of NF-κB inhibitor, Isohelenin significantly blocked the production of both IL-6 and IFN-beta in response to HSV-2. Thus, our data provide direct evidence that the activation of NF-κB is required for the production of both IL-6 and IFN-beta induced by HSV-2 in HCE cells. Taken together, our results suggest the potential contributions of TLRs and a critical role of NF-κB in the innate immune response to HSV-2 infection in its natural host cells. This work was supported by grants from the National Natural Science Foundation of China (No. 30500465,30810103052)

Objective To study the relationship among HLA-A alleles,supertype,HPV infection and cervical cancer in Tu Nationality of Hubei province.Methods As a case-control surevy. The comparisons included the comparison between HPV positive cases and HPV positive women in control group,and the comparison between HPV positive cases and HPV negative women in control group. Number of cases was 100(HPV positive in 86),and control was 187 (HPV positive in 95 and HPV negative in 92). The most polymorphism of 2 and 3 exons of the HLA-A alleles were analyzed by the high-resolution typing method-sequence-based typing(SBT).Results Comparison between HPV positive cases and HPV positive control women. Supertype HLA-A3(Pcorrected=0.005,OR=2.36,95% CI=1.45～3.85) was risk factors. Comparison between HPV positive cases and HPV negative control women,HLA-A*0206 alleles (Pcorrected=0.025,OR=0.20,95% CI=0.07～0.58)supertype HLA-A2 (Pcorrected=0.005,OR=0.57,95% CI=0.37～0.88)was protective factor. Supertype HLA-A3 (Pcorrected=0.005,OR=2.36,95% CI=1.45～3.85) was also related to the susceptibility of cervical carcinoma.Conclusion Supertype HLA-A3 is a risk factor of cervical cancer.

Herpes simplex virus type 2 (HSV-2) is one of the most common sexually transmitted pathogens worldwide. The host immune response induced by viral infection is cell-type specific. Little is known about the innate immune response to this virus in its natural host cells. In this study, we established an in vitro HSV-2 infection model with human cervical epithelial (HCE) cells. The viral infection was sufficient to induce expression of Toll-like receptors (TLRs), and Western blot and reporter assays suggest that HSV-2 infection leads to dramatic activation of the NF-kappaB signaling pathway. More importantly, our data provide direct evidence that the activation of NF-kappaB is required for the production of both IL-6 and IFN-beta induced by HSV-2 in HCE cells. Taken together, our results suggest the potential contributions of TLRs and a critical role of NF-kappaB in the innate immune response to HSV-2 in HCE cells.

Herpes Simplex Virus type 2 (HSV‐2) is one of the most common sexually transmitted pathogen and can establish lifelong latency infection. Our previously studies have shown that HSV‐2 infection up‐regulates TLRs expression and activates NF‐kB signaling in human cervical epithelia (HCE) cells. In this study, we examined the cytokines production of HCE cells in response to HSV‐2. HCE cells were infected with HSV‐2 at 3 MOI and cultured for the certain period of times. The result showed that the secretion of IL‐6 and IFN‐beta increased dramatically after HSV‐2 infection and maintained high levels during the course of experiment . We asked whether or not the induction of cytokines requires NF‐¿B activity. To this end, we treated cells with Isohelenin and harvested the supernatants for ELISA assay. The presence of NF‐¿B inhibitor, Isohelenin significantly blocked the production of both IL‐6 and IFN‐beta in response to HSV‐2 compared to the untreated control. Thus, our data provide the direct evidence that the production of both IL‐6 and IFN‐beta induced by HSV‐2 in HCE cells was NF‐¿B dependent suggesting a critical role of NF‐¿B as a key regulator of cytokine production in response to HSV‐2 infection in its natural host cells. This work was supported by grant from the National Natural Science Foundation of China (No. 30500465, No. 30810103052)

Toll‐like receptors (TLRs) play a crucial role in the innate immune response against microbial infections, engaging differential signaling pathways, leading to activation of T cell and therefore triggering acquired immunity. Herpes Simplex Virus type 2 (HSV‐2) is one of the most common sexually transmitted pathogen and can establish lifelong latency infection. HSV‐2 is a significant co‐factor in the transmission and acquisition of HIV‐1. To determine the effect of HSV‐2 infection on TLRs expression pattern and to investigate the TLR‐mediated innate immune reponse to HSV‐2 in human cervical cells, we infected immortalized human cervical epithelial cells (HECs) with HSV‐2 (G strain) as a model in this study. The results showed that normal HECs expressed TLR1, 2, 3, 4,5, 6,9 and HSV‐2 infection up‐regulated TLRs expression at mRNA and protein level. TLR9 was dramatically elevated at late phage 36hr post‐infection by Real‐time RT‐PCR analysis. The NF‐kB and MAP Kinase p38 were rapidly activated as early as 1hr post‐infection. Different proinflammatory cytokines and interferons were also determined during the course of HSV‐2 infection. Thus, HECs possess the ability to sensor HSV‐2 infection and activate the host innate immune response through TLRs.This work was supported by grants from the National Natural Science Foundation of China (No. 30500465) and China Wuhan Chenguang Science Foundation.

Objective:To detect the expression levels of CDC 25A and CDC 25B and their clinical significance and analyze the distribution pattern of the expressions of their splicing variants CDC 25A1-2 and CDC 25B1-4 in cervical tissues. Methods:The mRNA and protein expressions of CDC 25s were detected in 61 cases of cervical cancer tissues and 18 cases of benign cervical disease by RT-PCR and Western blotting, respectively. The relationship between the expression of CDC 25s and the clinicopathological features of cervical cancer was analyzed by the statistical method. Results:The difference in the expression levels of CDC 25A and CDC 25B between cervical cancer tissues and benign cervical diseases was significant (P0.05). The expression level of CDC 25s splicing variants had significant correlation with age of cervical cancer patients, histological classification, clinicopathological staging, and differentiation of cervical cancer cells (P0.05), but had no correlation with lymph node metastasis in cervical cancer (P0.05). Conclusion:The CDC 25A and CDC 25 B are highly expressed in cervical cancer tissues compared with normal cervical tissues. The abnormal expressions of CDC 25s and the splicing variants may be one of the important intracellular regulating mechanisms for the tumorigenesis and development of cervical cancer.

The Myc has been characterized to be a key regulator of cell growth, proliferation, differentiation, and apoptosis for years. Myc is essential for embryonic development and dysregulation of Myc is observed in most of human cancers. Survivin, a member of the IAP family, inhibits activation of downstream effectors of apoptosis, caspase‐3 and ‐7, in cells exposed to apoptotic stimuli. An elevated survivin is also observed in human cancers. In this study, we found that knockdown of Myc expression with siRNA duplexes dramatically decreased the level of survivin in HeLa (a cervical cancer cell line) and MCF‐7 (a breast cancer cell line). RT‐PCR analysis demonstrated that the decease was due to reduction of survivin transcription in siRNA treated cells. In the other hand, overexpression of Myc led an increase of both survivin mRNA and protein. Finally, Our luciferase reporter assays confirmed that Myc was able to induce the survivin promoter in both cancer and normal cells. Further mutagenesis data suggested that Myc upregulated survivin transcription through a non‐canonical E‐box site (CACGCG) and Sp1 sites at the promoter. Thus, survivin is a Myc target and may contribute some functions of Myc in cancer cells. They both are potential targets for cancer therapy.This work was supported by grants from the National Natural Science Foundation of China (No. 30500465) and China Hubei Natural Science Foundation.