Association between socioeconomic status and post-stroke depression in middle-aged and older adults: results from the China health and retirement longitudinal study.

INTRODUCTION: Post-stroke depression (PSD) is a common neuropsychiatric complication that affects approximately one-third of stroke patients. The treatment and prognosis of this disease are poor. Socioeconomic status (SES) is closely related to health outcomes; however, only a few previous studies have focused on the association between SES and PSD. Given the substantial population of stroke patients in China, it is crucial to examine the potential risk factors associated with PSD. Conducting studies on this population and investigating the influence of economic conditions can provide valuable guiding theoretical insights into PSD prevention and management. METHODS: We used data from the 2018 China Health and Retirement Longitudinal Study and selected appropriate samples for analysis. Depression was estimated using the Center of Epidemiologic Studies Depression Scale-10, a validated tool for assessing depression in the general population. Multiple logistic regression analysis was employed to assess the association between SES and PSD and to evaluate any urban-rural differences. RESULTS: Of the 749 respondents, 370 (49.4%) had depression. Stroke patients with a middle school education demonstrated a greater risk of developing depression than those with a primary school education or below after adjusting for all control variables (odds ratio (OR) = 1.60, 95% confidence interval (CI): 1.03-2.51, P = 0.036). However, stroke patients with a high school education or above had a lower risk of developing depression than those with a primary school education or below (OR = 0.50, 95% CI: 0.28-0.88, P = 0.016). In rural areas, stroke patients with a high school or above education level had lower rates of depression than those with a primary school education or below (OR = 0.44, 95% CI: 0.21-0.91, P = 0.027). This difference was not significant in urban areas. CONCLUSIONS: SES significantly influences the occurrence of PSD, which is reflected by education attainment and annual household expenditures. Education attainment was an independent influence on PSD, with a more pronounced effect in rural versus urban areas. We hope to reduce the prevalence of PSD and enhance the comprehensive management of this disease by modifying the influencing factors. Sex, self-reported health status, activities of daily living, night-time sleep duration, and life satisfaction also influenced the occurrence of PSD.

Detection of Escherichia coli, Pseudomonas aeruginosa, Salmonella paratyphoid B, and Shigella dysentery in live Bacillus licheniformis products using propidium monoazide-real-time-quantitative polymerase chain reaction.

To eliminate the influences of excipients and interference of dead bacterial DNA on the detection of Escherichia coli, Pseudomonas aeruginosa, Salmonella paratyphoid B, and Shigella dysentery in live Bacillus licheniformis capsules, a polymerase chain reaction (PCR) method with high sensitivity and specificity was established. By combining bromide with propidium monoazide (PMA) -real-time quantitative PCR (qPCR) with microporous membrane filtration, excipients were removed, the filtrate was collected, and the bacteria were enriched using the centrifugal method. The optimal PMA working concentration, dark incubation time, and exposure time were determined. Specific E. coli, P. aeruginosa, S. paratyphoid B, and S. dysentery primers were selected to design different probes and a multiplex qPCR reaction system was established. The PMA-qPCR method was verified using different concentrations of dead and live bacteria. This method is efficient and accurate and can be widely applied to the detection of aforementioned pathogenic bacterial strains in live Bacillus licheniformis products.

Effect of ABCG1 gene DNA methylations on the lipid-lowering efficacy of simvastatin.

Aim: We investigated the effect of ABCG1 gene DNA methylation in the lipid-lowering efficacy of simvastatin. Materials & methods: An extreme sampling approach was used to select 211 individuals from the top and bottom 15% of adjusted lipid-lowering response residuals to simvastatin after eight consecutive weeks. DNA methylation was measured before treatment by the MethylTarget bisulfite sequencing method. Results:ABCG1_A DNA methylations were negatively associated with baseline high-density lipoprotein cholesterol (HDL-C) and the change in HDL-C after treatment. ABCG1_C methylations were also related to the change in triglyceride and HDL-C. Moreover, mean ABCG1_A and ABCG1_C methylations explain 7.2% of the ΔTC (total cholesterol) and 17.5% of the ΔHDL-C level variability, respectively. Conclusion: DNA methylations at the ABCG1 gene play significant inhibitory effects in the lipid-lowering therapy of simvastatin.

The effect of ABCA1 gene DNA methylation on blood pressure levels in a Chinese hyperlipidemic population.

Hypertension is an important public health challenge worldwide. Epigenetic studies are providing novel insight into the underlying mechanisms of hypertension. We investigated the effect of DNA methylation in ATP-binding cassette transporter 1 (ABCA1) gene on blood pressure levels in a Chinese hyperlipidemic population. We randomly selected 211 individuals with hyperlipidemia who had not received any lipid-lowering treatment at baseline from our previous statin pharmacogenetics study (n = 734). DNA methylation loci at the ABCA1 gene were measured by MethylTarget, a next generation bisulfite sequencing-based multiple targeted cytosine-guanine dinucleotide methylation analysis method. Mean DNA methylation level was used in statistical analysis. In all subjects, higher mean ABCA1_B methylation was positively associated with systolic blood pressure (SBP) (ß = 8.27, P = 0.008; ß = 8.78, P = 0.005) and explained 2.7% and 5.8% of SBP variation before and after adjustment for lipids, respectively. We further divided all patients into three groups based on the tertile of body mass index (BMI) distribution. In the middle tertile of BMI, there was a significantly positive relationship between mean ABCA1_A methylation and SBP (ß = 0.89, P = 0.003) and DBP (ß = 0.32, P = 0.030). Mean ABCA1_A methylation explained 11.0% of SBP variation and 5.3% of DBP variation, respectively. Furthermore, mean ABCA1_A methylation (ß = 0.79; P = 0.007) together with age and gender explained up to 24.1% of SBP variation. Our study provides new evidence that the ABCA1 DNA methylation profile is associated with blood pressure levels, which highlights that DNA methylation might be a significant molecular mechanism involved in the pathophysiological process of hypertension.

PHOSPHO1 Gene DNA Methylations are Associated with a Change in HDL-C Response to Simvastatin Treatment.

OBJECTIVE: Our aim was to detect the effects of DNA methylations in the phosphoethanolamine/ phosphocholine phosphatase (PHOSPHO1) gene on the therapeutic efficacy of simvastatin. METHODS: We used an extreme sampling approach by selecting 211 individuals from approximately the top and bottom 15% of adjusted lipid-lowering response residuals to simvastatin (n=104 for the high response group and n=107 for the low response group) from a total of 734 subjects with hyperlipidemia. They received a daily oral dose of 20 mg simvastatin for eight consecutive weeks. DNA methylation loci at the PHOSPHO1 gene were measured using high-throughput next-generation sequencing-based sequencing technology. Fasting serum lipids were measured at baseline and after eight weeks of simvastatin treatment. RESULTS: Mean PHOSPHO1 DNA methylation had a significant negative correlation with high-density lipoprotein cholesterol (HDL-C) variation (ß=-0.014, P=0.045) in the high response group. After stratifying by body mass index (BMI), the associations between the PHOSPHO1 DNA methylations and the change in HDL-C in response to simvastatin were more significant in obese subjects with a BMI of 25 kg/m2 or higher (ß=-0.027, P=0.002). Mean PHOSPHO1 methylation and traditional predictors could explain up to 24.7% (adjusted R2) of the change in HDL-C response in obese patients. There was a statistically significant additive interaction term (P=0.028) between BMI and mean PHOSPHO1 methylation in the model of the change in HDL-C in response to simvastatin. CONCLUSION: Our findings suggest that PHOSPHO1 DNA methylations are associated with a change in HDL-C in response to simvastatin treatment, and this association is especially dependent on the extent of patient obesity.