Objective Through two nationwide sero-epidemiological survey programs on hepatitis B virus (HBV),hepatitis B markers in Yunnan province were compared between the findings in 2014 and in 2006.Results were used to understand the HBV epidemic status in Yunnan province and to estimate the efficiency of measures on prevention and control of the disease.Methods People at the age of 1-29 years were sampled from 6 counties of the National Disease Surveillance sites in Yunnan province,by multi-stage random sampling method.Demographic information was collected by questionnaire,and 2-4 ml serum sample was taken to detect HBsAg,anti-HBs,anti-HBc,HBeAg and anti-HBe,by ELISA method.Results were logged-in the database and analyzed by SPSS 17.0.Results Between the two studies,no statistically significant differences were observed on the overall HBV infection rates and the positive rates of HBsAg,HBeAg,anti-HBe,anti-HBc.Positive rate of anti-HBs in 2014 was significantly higher than that in 2006.The main two combination profiles of hepatitis B markers were through the fifth model which was positive only for anti-HBs and the sixth model which was negative for all markers in 2006,and the same in 2014.Detection rate through the fifth profile in 2014 was significantly higher than the rate in 2006,while the detection rate of the sixth profile in 2014 was significantly lower than the one in 2006.When analyzing the differences in the same age group,between the two surveys,results showed that the positive rate of anti-HBs in 2014 was significantly higher than that in 2006,in both the10-14 and the 15-19 years-old groups.Positive rate of anti-HBc in the 20-29 year-olds in 2014 was significantly lower than the one of 2006.The positive rates of HBsAg in the age groups of 1-4,5-14 and 15-29 were 1.12％,1.61％ and 1.25％ respectively,in 2014.Conclusion Prevention and control measures on HBV seemed in great progres.However,more effective prevention and control measures should be taken continually among people under the age of 15,in Yunnan province.

Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in activation of astrocytes in midbrain periaqueductal gray (PAG) of rats with neuropathic pain.Methods A total of 72 pathogen-free male Sprague-Dawley rats,aged 9 weeks,weighing 160-200 g,were divided into 4 groups using a random number table:control group (group C,n =8),neuropathic pain group (group NP,n =40),dimethyl sulfoxide control group (group DS,n =12) and JNK inhibitor SP600125 group (group SP,n=12).Neuropathic pain was produced by chronic constriction injury (CCI).At 14 days after CCI,10 nmol JNK inhibitor SP600125 0.5 μl was intraperitoneally injected into the PAG in group SP,and 10％ dimethyl sulfoxide 0.5 μl was given instead in group DS.Eight rats were selected in group C,before CCI and at 3,7,14 and 21 days after CCI in group NP,and in DS and SP groups,and the mechanical pain threshold was measured before CCI,before administration on 14 days after CCI and at 30,45,60,75 and 90 min after administration.The rats in group C were sacrificed after the end of measurement of the mechanical pain threshold,and brains were removed for determination of phosphorylated JNK (p-JNK) and glial fibrillary acidic protein expression (by Western blot) in PAG region.The rats in group NP were sacrificed after the end of measurement of the mechanical pain threshold at each time point,and brains were removed for detection of p-JNK expression in PAG region.Four rats in DS and SP groups were sacrificed after the last measurement of the mechanical pain threshold at 45 min after administration,and brains were removed for determination of glial fibrillary acidic protein expression in PAG region.Results Compared with group C,the mechanical pain threshold was significantly decreased at each time point after CCI,and the expression of p-JNK was up-regulated at 7-21 days after CCI in group NP (P＜0.01).Compared with group DS,the mechanical pain threshold was significantly increased at 30 min after administration,and GFAP expression was down-regulated at 45 min after administration in group SP (P＜ 0.01).The mechanical pain threshold was significantly higher at 30-75 min after administration than before administration in group SP (P＜0.01).Conclusion The mechanism underlying activation of astrocytes in PAG is related to activating JNK in the rats with neuropathic pain.

Objective:To explore the relationship between psychological distress and intimacy in stroke patients and the mediating effect of different dyadic coping style, to provide theoretical guidance for improving the intimate relationship of stroke patients.Methods:A convenient sampling method was used to select 203 patients with stroke who visited the General Hospital of Ningxia Medical University, the People's Hospital of Ningxia Hui Autonomous Region and the Department of Neurology of Yinchuan First People's Hospital from December 2020 to July 2021 as the survey objects. The general information questionnaire, Kessler Psychological Distress Scale, Quality of Relationship Index and Dyadic Coping Inventory were used to investigate patients.Results:The scores of psychological distress, intimate relationship, positive dyadic coping and negative dyadic coping were 19.33 ± 7.46, 32.75 ± 6.79, 86.25 ± 13.22, and 16.46 ± 4.08, respectively. Correlation analysis showed that psychological distress was negatively correlated with intimate relationship and positive dyadic coping ( r=-0.195, -0.204, both P<0.01), psychological distress was positively correlated with negative dyadic coping ( r=0.229, P<0.01). The mediating effect of positive dyadic coping and negative dyadic coping on psychological distress and intimate relationship was 35.87% and 53.26%, respectively. Conclusions:The psychological distress indirectly affects the intimate relationship of stroke patients through positive dyadic coping and negative dyadic coping. Health care workers can guide patients to actively cope with the disease and encourage couples to strengthen communication, so as to enhance the intimacy of couples and promote their physical and mental health development.

Objective:To explore the effect of perceived stress on fatigue and its mechanism, so as to provide theoretical support for relieving the fatigue of the main caregivers of stroke patients.Methods:From December 2020 to August 2021, 311 main caregivers of stroke patients hospitalized in the Department of Neurology of Class Ⅲ Grade A hospitals in Yinchuan were selected by convenient sampling. The caregivers were investigated with the General Information Questionnaire, Perceived Stress Scale, Resourcefulness Scale, Social Support Rating Scale and Fatigue Scale.Results:In this study, a total of 311 questionnaires were distributed, and 308 valid questionnaires were recovered, with an effective recovery rate of 99.04%. The total scores of perceived stress, fatigue, resourcefulness and social support of the main caregivers of stroke patients were (24.98±6.36) , (5.31±2.86) , (83.98±12.85) and (39.76±6.21) respectively. Perceived stress were negatively correlated with resourcefulness and social support ( r=-0.313, -0.274, P<0.01) , and positively correlated with fatigue ( r=0.261, P<0.01) . Fatigue were negatively correlated with resourcefulness and social support ( r=-0.305, -0.268; P<0.01) . There was a positive correlation between resourcefulness and social support ( r=0.210, P<0.01) . The results of intermediary test showed that the direct effect of perceived stress on fatigue was valid, and the respective intermediary effect of resourcefulness and social support between perceived stress and fatigue, and the chain intermediary effect of resourcefulness and social support were also valid, with the amount of intermediary effect being 26.92%, 15.38% and 3.85% respectively. Conclusions:The chain mediation between perceived stress and fatigue is established between the resourcefulness and social support of the main caregivers of stroke patients. In the future, the mental and physical pressure of stroke patients can be alleviated by improving the resourcefulness of their main caregivers and providing social support.

Objective:To provide experimental evidence for genetic counseling and prenatal diagnosis by analyzing the clinical characteristics, screening and identification of the function of suspicious variants in a X-1inked spondyloepiphyseal dysplasia tarda (SEDT) family.Methods:The family members' medical history, general physical examination, femur, spine X-ray examination were collected. Peripheral blood samples of the family members were collected and DNA was extracted from these samples. Sequencing clinical whole exons of proband DNA by targeted gene high-throughput sequencing method, then analysis sequencing data. The suspicious mutation was confirmed in pedigree members by PCR and Sanger sequencing. Reverse transcription polymerase chain reaction (RT-PCR) experiments of total RNA from blood lymphocytes were performed. The amplification of exons 3 and 4 of the pathogenic gene were amplified and identified by agarose gel. The expression of the pathogenic gene was also detected.Results:Three affected males of the family were diagnosed with SEDT according to their clinical and radiological features. A nonsense mutation in the transport protein particle complex subunit 2 ( TRAPPC2) gene NM_001011658: c.91A>T (p.K31*) was found in the proband using whole exome sequencing. This variation was also detected in his cousin, but not in non-phenotypic members of the family. The RT-PCR result for amplification of exon 3 and 4 of peripheral blood lymphocytes was the same as those of normal controls, indicating that the mutation did not affect the splicing of transcripts. qPCR results showed that the transcriptional expression of TRAPPC2 in patients was significantly lower than that in family normal controls and normal people controls. Conclusion:Identification of the novel nonsense mutation (c.91A>T) in the SEDT family enables early patients screening, carrier detection, genetic counseling, prenatal diagnosis, and clinical prevention and treatment. The detailed genotype/phenotype descriptions contribute to the SEDT mutation spectrum. The study of the function of TRAPPC2 mutation will help to further elucidate the role of sedlin in cartilage.

Objective:To explore the influencing factors of AIDS-related deaths among HIV-infected patients in Shandong Province, to help reduce the risk of death and prolong survival time.Methods:The study population was HIV-infected patients in Shandong Province from 2017-2021, and Cox proportional hazards regression model was used to analyze the influencing factors of AIDS-related deaths and deaths within one year of confirmation.Results:Among 14 700 HIV- infected patients reported in Shandong Province in 2017-2021, 351 AIDS-related deaths occurred, accounting for 2.4% (351/14 700). The results of multifactorial Cox proportional hazards regression model analysis showed that the risk factors for AIDS-related deaths among HIV-infected patients included education level of junior high school, high school, and secondary school (a HR=1.37, 95% CI:1.01-1.84), sample source from healthcare institutions (a HR=1.61, 95% CI:1.22-2.12), duration of disease in AIDS stage (a HR=9.86,95% CI:6.86-14.19), baseline CD4 +T lymphocytes (CD4) undetected (a HR=3.93, 95% CI:2.69-5.75), duration of antiviral treatment (ART) <6 months (a HR=3.46, 95% CI:2.42-4.93) and no ART (a HR=1.45, 95% CI:1.02-2.07), final CD4 <200 cells/μl (a HR=3.51, 95% CI:2.18-5.65) and final CD4 undetected (a HR=10.58, 95% CI:6.15-18.19), and final viral load (VL) values of 50-999 copies/ml,≥1 000 copies/ml and undetected (a HR=2.59, 95% CI:1.07-6.26; a HR=9.50, 95% CI:5.60-16.12; a HR=15.33, 95% CI:8.91-26.36). Factors with higher risk of AIDS-related deaths within one year of confirmation of HIV-infected patients included samples originating from healthcare facilities (a HR=1.68, 95% CI: 1.19-2.36), AIDS stage of disease (a HR=10.60, 95% CI:7.13-15.75), baseline CD4 undetected (a HR=3.71, 95% CI:2.34-5.90), duration of ART <6 months (a HR=4.30, 95% CI:2.85-6.49) and no ART (a HR=2.05, 95% CI:1.35-3.13), final CD4 <200 cells/μl (a HR=5.45,95% CI:2.04-14.60) and final CD4 undetected (a HR=20.95, 95% CI: 7.69- 57.04), and final VL values of 50-999 copies/ml, ≥1 000 copies/ml and undetected (a HR=15.21, 95% CI: 2.54-91.21; a HR=42.93, 95% CI:9.64-191.20; a HR=61.35, 95% CI:13.85-271.77). Conclusions:Expanding the coverage of testing, promoting early detection and treatment, strengthening regular follow-up and the test of HIV-infected patients, grasping the progress of the disease to provide accurate management and treatment are important for reducing the disease mortality rate and prolonging the survival time of HIV-infected patients.

Objective: To investigate PLOD2 expression in esophageal squamous cell carcinoma, and to explore the potential mechanism by which PLOD2 promotes tumor metastasis. Methods: The expression of PLOD2 in 60 cases of esophageal squamous cell carcinoma (the patients were collected at the first Affiliated Hospital of Xinxiang Medical University, from January 2016 to December 2017) was investigated by immunohistochemistry. Fibrillar collagen formation and collagen deposition were detected by picrosirius red staining. Correlation of PLOD2 expression with clinical pathologic features of the patients was performed using χ² test and Kaplan-Meier analysis. After EC-109 cells were transfected with LV-vector and LV-over/PLOD2, the expression of PLOD2 was detected by real time PCR and the impact of POLD2 on invasion in EC-109 cells was determined by transwell migration and invasion assays. The expression of PLOD2/AKT epithelial-to-mesenchymal transition signal pathway related proteins was detected by Western blot. Results: The expression level of PLOD2 in esophageal squamous cell carcinoma was 81.7% (49/60 cases),higher than their paired noncancerous tissues(8.3%, 5/60; P<0.01), and correlated significantly with tumor depth of invasion and nodal metastasis (P<0.01). Picrosirius red staining showed that collagen deposition was increased and the degree of fibrillar organization was enhanced in carcinoma tissues that had higher PLOD2 expression. Transwell migration and invasion assays showed that PLOD2 significantly promoted the migration and invasion ability of EC-109 cells. Western blot showed that PLOD2 significantly increased the expression levels of p-FAK, p-AKT and vimentin in EC-109 cells. Conclusions Esophageal squamous cell carcinoma has a high expression of PLOD2 that correlates with tumor invasion and lymph node metastasis. PLOD2 promotes invasion and metastasis of esophageal squamous cell carcinoma through epithelial-to-mesenchymal transition via FAK/AKT signal pathway.