Objective To investigate relativity between the epidemiology of HPV and cervical carcinoma in Dali region,Yunnan province,through detecting the 13 high-risk human papillomavirus infection and Thinprep cytologic test in 2153 cases.Methods Real-time PCR was used to detect the 13 high-risk HPV (16,18,31,33,35,39,45,51,52,56,58,59,68) in2153 cases and 1604 cases were checked with Thinprep cytologic test.Results In 2153 samples,260 cases were infected with HPV,with the positive rate of 12.08％.The highest positive rates were ＞60 years old (18.18％),then ＞20 and ≤30 years old (14.41％);there was no significant difference in the positive rate among the various age groups (P =0.384).There were 1465 negative for intraepithelial lesion ormalignancy (NILM) cases (91.33％),86 atypical squamous cells of undetermined significance (ASC-US) and atypical squamous cells cannot exclude HSIL (ASC-H) cases (5.36％),32 low-grade squamous intraepithelial lesion cases (LSIL) cases (2.00％),21 high-grade squamous intraepithelial lesion cases (1.31％) through Thinprep cytologic test.The correlation coefficient is 0.893.Conclusions The infection rate of HPV in Dali region,Yunnan Province,has no significant difference among the various age groups.Application of 13 high-risk HPV infection test combined with Thinprep cytologic test could be more effective in screening cervical carcinoma.

Objective: : The present study aimed to identify the function of ischemic stroke (IS) patients’ peripheral blood and its role in IS, explore the pathogenesis, and provide direction for clinical research progress by comprehensive bioinformatics analysis. Methods: : Two datasets, including GSE58294 and GSE22255, were downloaded from Gene Expression Omnibus database. GEO2R was utilized to obtain differentially expressed genes (DEGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs were performed using the database annotation, visualization and integrated discovery database. The protein-protein interaction (PPI) network of DEGs was constructed by search tool of searching interactive gene and visualized by Cytoscape software, and then the Hub gene was identified by degree analysis. The microRNA (miRNA) and miRNA target genes closely related to the onset of stroke were obtained through the miRNA gene regulatory network. Results: : In total, 36 DEGs, containing 27 up-regulated and nine down-regulated DEGs, were identified. GO functional analysis showed that these DEGs were involved in regulation of apoptotic process, cytoplasm, protein binding and other biological processes. KEGG enrichment analysis showed that these DEGs mediated signaling pathways, including HTLV-I infection and microRNAs in cancer. The results of PPI network and cytohubba showed that there was a relationship between DEGs, and five hub genes related to stroke were obtained : SOCS3, KRAS, PTGS2, EGR1, and DUSP1. Combined with the visualization of DEG-miRNAs, hsa-mir-16-5p, hsa-mir-181a-5p and hsa-mir-124-3p were predicted to be the key miRNAs in stroke, and three miRNAs were related to hub gene. Conclusion : Thirty-six DEGs, five Hub genes, and three miRNA were obtained from bioinformatics analysis of IS microarray data, which might provide potential targets for diagnosis and treatment of IS.

To perform a systematic review of the data collected from case-control studies conducted earlier to investigate the correlation between E-selectin S128R polymorphism and ischemic stroke (IS) risk among the Chinese population. The PubMed, Web of Science, Chinese biomedical literature database (CBM), Chinese databases China National Knowledge Infrastructure (CNKI), WanfangData knowledge service platform (Wanfang Data), and information resource integration service platform (VIP) Databases were searched to retrieve case-control studies on the correlation between E-selectin gene S128R polymorphism and IS from the inception of the database till June 2019. The literature was screened, data were extracted, the risk of bias was reviewed, and the studies included were assessed independently by two reviewers. Stata ver. 12.0 software (Stata Corp LLC, College Station, TX, USA) was used to perform the meta-analysis. A total of 2907 cases from eight case-control studies involving 1478 IS patients and 1429 controls were included in this study. The R allele and RS genotype in E-selectin were found to be associated with the risk of IS as per the results of the meta-analysis (R vs. S : odds ratio [OR], 2.75; 95% confidence interval [CI], 2.15-3.51; p<0.00001; RS vs. SS : OR, 2.50; 95% CI, 1.95-3.19; p<0.00001; RR+RS vs. SS : OR, 2.85, 95% CI, 2.21-3.67; p<0.00001). The E-selectin gene S128R polymorphism is likely related to IS based on the results of a meta-analysis in the Chinese population, and the R allele and RS genotype of E-selectin may be IS risk factors.

Objective To investigate the neuroprotective effects of Fasudil in cerebral I/R injury in mice.Methods 51 C57BL/6J mice was divided into two groups,CMC treated group (n=26) and Fasudil treated group (n=25),randomly.The mice were treated with Fasudil (10 mg/kg) or CMC (0.5％ CMC 10 ml/kg) separately.Then the treated mice were subjected to 60 min of focal ischemia and 18 h reperfusion.The infarct volume of brain was analyzed by TTC staining with MCID image system.BBB permeability was assessed by Evans blue extravasation and albumin leakage which was detected by immuno-blotting assay.The activity of MMP9 was analyzed by zymography.Results The infarct volume in CMC group ((99.07±6.53) mm3) was larger than that in Fasudil group ((57.02±8.93) mm3),the difference was statistically significant (P＜0.01).The activity of MMP9 in the mice treated with Fasudil was lower than that in CMC group.Compared with the CMC group(albumin (2.95±0.77),Evans blue (5.15±0.24)),the albumin and Evans blue content in the Fasudil treated group (albumin (1.04±0.18),Evans blue (1.96±0.31))reduced significanctly(all P＜0.01).Conclusion Fasudil protects I/R damage by inhibiting the activity of MMP9 to maintain blood-brain barrier permeability.

Objective: : To explore the correlation between the polymorphism of histone deacetylase 9 gene (rs1060499865, rs723296, rs957960) and ischemic stroke (IS) in Chinese Han population in Dali region. Methods: : This study included 155 IS patients and 128 healthy physical examinees. TaqMan-polymerase chain reaction technology and multivariate logistic regression were performed. Results: : In the case group, there was no polymorphism of rs1060499865 observed in the two groups; whereas on the rs723296 locus the frequencies of C allele and TC genotype were significantly higher than that in the control group, alleles C and T were associated with a 2.158-fold increase in IS risk, and genotypes TC and TT were associated with a 2.269-fold increase in IS risk. The locus rs957960 exhibited no significant difference between the two groups. Conclusion : An association between rs723296 and the risk of IS was found in the Chinese Han population in Dali region. No significant association was found between rs1060499865, rs957960 and IS in the Chinese Han population in Dali region.

BACKGROUND:Oxidative injury is considered to be one of the important factors of cerebral ischemia-reperfusion injury.Superoxide dismutase 2(SOD2)is a key mitochondrial antioxidant molecule,and fenofibrate can regulate the expression of SOD2 by activating peroxisome proliferator-activated receptor α. OBJECTIVE:To explore whether the mechanism of fenofibrate in the treatment of cerebral ischemia-reperfusion injury depends on the expression of SOD2. METHODS:The TALENs system was used to construct SOD2 transgenic mice.The transgenic mice were genotyped by PCR and DNA sequencing techniques.The expression of SOD2 protein in transgenic mice was detected by western blot assay.Wild-type and SOD2 transgenic mice were randomly divided into four groups:wild-type control group(n=6),wild-type fenofibrate group(n=6),SOD2 transgenic control group(n=5)and SOD2 transgenic fenofibrate group(n=5).A mouse model of middle cerebral artery occlusion was prepared using the suture-occlusion method.After 90 minutes of ischemia,the thread was removed to reperfuse cerebral blood flow for 30 minutes.A cerebral blood flow monitor was used to monitor local cerebral blood flow.Brain tissue slices were taken for 2,3,5-triphenyltetrazolium chloride staining to analyze the situation of cerebral infarction in each group. RESULTS AND CONCLUSION:After PCR and DNA sequencing analysis,nine SOD2+/+ transgenic mice were successfully constructed.After cerebral ischemia-reperfusion,the wild-type fenofibrate group showed partial recovery of cerebral blood flow and significantly reduced cerebral infarction volume compared with the wild-type control group(P<0.001).There was no significant difference in cerebral blood flow and cerebral infarction volume between the SOD2 transgenic fenofibrate group and the SOD2 transgenic control group.The SOD2 transgenic control was superior to the wild-type control group in terms of improving cerebral blood flow and cerebral infarction(P<0.001).There were also no significant differences in cerebral blood flow and cerebral infarction volume between the wild-type fenofibrate group and the SOD2 transgenic control group and between the wild-type fenofibrate group and the SOD2 transgenic fenofibrate group.To conclude,the expression of SOD2 is one of the mechanisms of fenofibrate in the treatment of cerebral ischemia-reperfusion injury.

ObjectiveTo study the inhibitory effect of aloe-emodin （AE） on aluminum ion （Al³⁺）-induced β-amyloid protein 42 （Aβ₄₂） aggregation and its depolymerization on formed Aβ₄₂-Al³⁺ aggregates in vitro， and to investigate the effect of AE on the cytotoxicity of Aβ₄₂ aggregation in the presence of Al³⁺. MethodThe Aβ₄₂ group， Aβ₄₂+Al³⁺ group， Aβ₄₂+AE group， Aβ₄₂+Al³⁺+AE group and the depolymerization test group were set up in the experiment. The aggregation fibrosis process， aggregation morphology， aggregation size and cytotoxicity of Aβ₄₂ in each group were detected by thioflavin T （ThT） fluorescence assay， transmission electron microscopy （TEM）， dynamic light scattering （DLS） experiment and thiazolyl blue （MTT） cytotoxicity assay. ResultCompared with the Aβ₄₂ group， Al³⁺ could promote Aβ₄₂ aggregation， increase the fluorescence intensity of ThT by 124.48%， induce the aggregation of Aβ₄₂ to form fiber bundles with larger particle size， and significantly reduce the cell viability of human neuroblastoma SH-SY5Y cells （P<0.01）， thus reducing the cell survival rate to 51.05%. AE not only inhibited Aβ₄₂ aggregation， but also inhibited Al³⁺-induced Aβ₄₂ aggregation in a concentration-dependent manner. Compared with the Aβ₄₂+Al³⁺ group， high concentration of AE could reduce the ThT fluorescence intensity to 41.66%， and change the polypeptide aggregation pathway to form amorphous aggregates with small particle size. Besides， it significantly inhibited the cytotoxicity of Aβ₄₂ induced by Al³⁺ （P<0.01）， and restored the cell survival rate to 84.87%. Further depolymerization was conducted， AE could depolymerize Aβ₄₂-Al³⁺ aggregates to make the formed aggregates disappear and form some small-particle short fibers and amorphous structure aggregates with low toxicity. ConclusionAE can inhibit Aβ₄₂ aggregation and cytotoxicity in the presence of Al³⁺， depolymerize the formed Aβ₄₂-Al³⁺ aggregates and alleviate the cytotoxicity， thus laying the foundation for exploring the mechanism of AE in the treatment of Alzheimer's disease.