Objective To investigate the relationship of the1675A/G polymorphism of AT2 gene with the therapeutic effect of indapamide sustained release tablets in female patients with primary hypertension.Methods Two hundred and twenty female patients with primary hypertension were treated with Indapamide Sustained Release Tablets ( 1.5 mg · qd) for 8 weeks.The blood samples from the patients were collect to determine AT2 gene polymorphism by PCR combined with HRM and sequencing.Results Two hundred and five patients completed the test.In female patients,the therapeutic efficacy of indapamide sustained telease tablets among different AT2R genotypes( AA:70.6％,AG:71.6％,GG:71.4％ ) showed no significant difference ( x2=2.53,P=0.49 ),neither do the decline of BP after therapy ( F=0.39 and 0.19 respecrively,P ＞ 0.05).Conclusion The AT2 genotype was assumed to be not correlated to the blood pressure lowering response to Indapamide Sustained Release Tablets in female primary hypertension patients.

Objective:To investigate the clinical characteristics and outcome of novel coronavirus pneumonia (COVID-19)patients with different body mass index (BMI), and to provide the basis for disease assessment and prognosis.Methods:The clinical data of 541 patients with COVID-19 diagnosed in Xiaogan Hospital Affiliated to Wuhan University of Science and Technology from January 16 to March 28, 2020 were collected. The patients were divided into normal weight group, overweight group, and obesity group according to BMI. The clinical characteristics and outcomes of the three groups were compared. The correlation between BMI and clinical classification was analyzed by ordinal logistic regression.Results:There were 288 cases (53.23%) in normal weight group, 193 cases (35.67%) in overweight group, and 60 cases (11.09%) in obesity group. Compared with normal weight group, overweight and obesity groups displayed higher proportion of hypertension, with increased levels of white blood cells, neutrophils, C reactive protein, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and triglyceride in laboratory test results, and higher proportion of severe and critical illness ( P<0.05 or P<0.01). After adjusting for age, gender, and underlying diseases, regression analysis showed that higher BMI predicted more severe clinical classification ( OR=1.079, 95% CI 1.010-1.154). Conclusion:In COVID-19 patients, overweight and obese patients are more likely to develop into severe and critical illness, suggesting that obesity may be an important risk factor affecting the clinical outcome of COVID-19.

Objective:To explore the effects of online and offline peer support on the quality of life in middle-aged and elderly patients with type 2 diabetes mellitus (T2DM) in the community.Methods:Two sub-communities were selected from a community health service center in Hengyang, Hunan province, and randomly divided into the control community and the intervention community by coin tossing. From November 2018 to March 2019, totally 40 middle-aged and elderly T2DM patients who met inclusion criteria were enrolled from the control and intervention communities and included into the control group and the intervention group, respectively. Patients in the control group received routine community care, while patients in the intervention group received online and offline peer support for 6 months on the basis of routine care. The quality of life, body mass index (BMI) and fasting blood glucose (FBG) were compared between the two groups before intervention, 3 months and 6 months after intervention.Results:After 3 months of intervention, the psychological function, social relationship, quality of life scores of the intervention group were lower than those of the control group, and the differences were statistically significant ( P< 0.05) ; after 6 months of intervention, the psychological function, social relationship, quality of life, BMI and FBG of the intervention group were lower than those of the control group, and the differences were statistically significant ( P< 0.01) . Conclusions:Online and offline peer support can decrease the FBG, improve psychological function and social relationship of middle-aged and elderly T2DM patients in the community, and improve their quality of life.

Objective? To explore the current situation of health empowerment of elderly fragility fracture patients and to analyze its influencing factors. Methods? We selected four Class Ⅲ Grade A hospitals randomly in Hengyang. From October 2017 to February 2018, a total of 176 elderly fragility fracture inpatients were investigated with the self-designed general information questionnaire, Elderly Frailty Assessment Scale, Osteoporosis Self-Efficacy Scale (OSES), Health Empowerment Scale for Elderly Patients with Chronic Disease. Multiple linear regression analysis was used to explore the influencing factors of health empowerment of patients. Results? The score of health empowerment of elderly fragility fracture patients was (89.00±14.31) and responsibility belief dimension was with the highest score (3.74±0.88). Patients' health empowerment had a negative correlation with the frailty (r=-0.576, P＜0.01) and had a positive correlation with the self-efficacy (r=0.496, P＜ 0.01). Multiple linear regression analysis showed that the main influencing factors of health empowerment of patients included ages, education levels, medical payment methods, frailty and self-efficacy (P＜0.05). Conclusions? Nurses should pay attention to patients' health empowerment ability and provide the individualized nursing to strengthen the health empowerment ability of elderly fragility fracture patients.

Objective:To explore the epileptic phenotype spectrum of SLC6A1 gene mutations and their genotype-phenotype correlation. Methods:Four hundred patients with epilepsy of unknown etiology admitted to Epilepsy Center, Department of Neurology, Second Affiliated Hospital of Guangzhou Medical University from July 2019 to July 2024 were enrolled to screen the SLC6A1 gene mutations; the clinical characteristics, mutation pathogenicity, and changes of hydrogen bond between amino acids, stability and amino acid hydrophobicity of SLC6A1 gene encoded proteins caused by missense mutations in patients with SLC6A1 gene mutations were analyzed. At the same time, a comprehensive search was conducted in PubMed, HGMD and CNKI databases to collect the publicly reported SLC6A1 gene mutations related to epilepsy up to September 8, 2024; differences in proportion of missense mutations between the two most common and featured epileptic phenotypes and proportion of missense mutations in loops of SLC6A1 gene coding proteins were analyzed. Results:Five patients carried SLC6A1 gene mutations in 400 patients with epilepsy of unknown etiology: 2 had de novo heterozygous canonical splice site mutations (c.850-1G>A and c.1324-1G>A), with phenotypes as partial epilepsy combined with severe development delay and childhood absence epilepsy combined with mild developmental delay; 2 had de novo heterozygous missense mutations (c.187G>A/p.Gly63Ser and c.1081C>A/p.Pro361Thr), with phenotypes as partial epilepsy combined with mild development delay and generalized epilepsy combined with severe development delay; and one had heterozygous missense mutation of unknown origin (c.700G>A/p.Gly234Ser), with phenotype as Lennox-Gastaut syndrome. Four de novo mutations were evaluated as having pathogenic or likely pathogenic features, and one mutation of unknown origin was evaluated as of uncertain significance. In addition, 3 missense mutations caused significant changes in number or bonding form of hydrogen bonds between amino acids of the encoded proteins, with obviously decreased stability and hydrophobicity of the encoded proteins. (2) Results of literature analysis showed that 84 SLC6A1 mutations have been reported to be associated with epilepsy; combined with the genetic results in this study, a total of 89 SLC6A1 mutations were identified, including 53 missense mutations, 33 nonsense mutations, and 3 in-frame/in-del mutations; 7 epilepsy phenotypes were involved, including 38 patients with myoclonic atonic epilepsy (MAE), 16 with epilepsy, 12 with epileptic encephalopathy, 8 with childhood absence epilepsy, 6 with childhood-onset epilepsy, 6 with generalized epilepsy, and 3 with focal epilepsy. No significant difference in proportion of missense mutations was noted between MAE and epileptic encephalopathy patients ( P>0.05); however, the proportion of missense mutations in loops of the epileptic encephalopathy patients was significantly higher than that of the MAE patients ( P<0.05). Conclusion:SLC6A1 gene mutations can cause complex and diverse epilepsy phenotype spectrum, and most patients are accompanied by developmental delay; subregional effect of the encoded protein molecules may be a potential mechanism for different clinical phenotypes between MAE and epileptic encephalopathy caused by SLC6A1 gene mutations.