3R Nursing Combined with Dietary and Nutritional Interventions Enhances Self-care Ability in Elderly Patients with Vascular Dementia.

BACKGROUND: Vascular dementia (VD) is an extremely common neurological dysfunction in the elderly population, and greatly affects the patient's ability to take care of themselves. Recent research suggests that VD patients need more targeted and individualized nursing during treatment, so as to enhance cognitive function and therapeutic efficacy. The objective of this study is to observe the effect of reminiscence, reality, and remotivation (3R) nursing combined with dietary and nutritional interventions on elderly patients with VD, so as to provide clinical evidence for the management of VD in older adults. METHODS: 120 elderly VD patients admitted between December 2022 and December 2023 were selected, including 64 cases receiving 3R nursing combined with dietary and nutritional interventions (the research group) and 56 cases receiving routine nursing (the control group). The two groups were compared in terms of neurological function, self-care ability, and nutritional status before and after nursing, as well as nursing compliance. After the completion of the care, patients' quality of life and family satisfaction were investigated. RESULTS: In comparison with the control group, the research group displayed higher scores on the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA), greater self-care ability, and higher levels of nutritional proteins and grip strength (p < 0.05). In addition, patients in the research group displayed greater nursing compliance and quality of life of patients, as well as higher family satisfaction (p < 0.05). CONCLUSIONS: 3R nursing combined with dietary and nutritional interventions can effectively improve the neurological function of VD patients and enhance their self-care ability.

Effects of the enhanced public health intervention during the COVID-19 epidemic on respiratory and gastrointestinal infectious diseases in China.

The public health interventions to mitigate coronavirus disease 2019 (COVID-19) could also potentially reduce the global activity of influenza. However, this strategy's impact on other common infectious diseases is unknown. We collected data of 10 respiratory infectious (RI) diseases, influenza-like illnesses (ILIs), and seven gastrointestinal infectious (GI) diseases during 2015-2020 in China and applied two proportional tests to check the differences in the yearly incidence and mortality, and case-fatality rates (CFRs) over the years 2015-2020. The results showed that the overall RI activity decreased by 7.47%, from 181.64 in 2015-2019 to 168.08 per 100 000 in 2020 (p < 0.001); however, the incidence of influenza was seen to have a 16.08% escalation (p < 0.001). In contrast, the average weekly ILI percentage and positive influenza virus rate decreased by 6.25% and 61.94%, respectively, in 2020 compared to the previous 5 years (all p < 0.001). The overall incidence of GI decreased by 45.28%, from 253.73 in 2015-2019 to 138.84 in 2020 per 100 000 (p < 0.001), and with the greatest decline seen in hand, foot, and mouth disease (HFMD) (64.66%; p < 0.001). The mortality and CFRs from RI increased by 128.49% and 146.95%, respectively, in 2020, compared to 2015-2019 (p < 0.001). However, the mortality rates and CFRs of seven GI decreased by 70.56% and 46.12%, respectively (p < 0.001). In conclusion, China's COVID-19 elimination/containment strategy is very effective in reducing the incidence rates of RI and GI, and ILI activity, as well as the mortality and CFRs of GI diseases.

CBS gene polymorphism and promoter methylation-mediating effects on the efficacy of folate therapy in patients with hyperhomocysteinemia.

BACKGROUND: A decrease in cystathionine beta-synthase (CBS) enzyme activity could lead to hyperhomocysteinemia (HHcy). Studies have revealed that DNA methylation has a mediating effect on the development of diseases. The present study aimed to explore CBS promoter methylation-mediating effects on the efficacy of folate treatment for HHcy. METHODS: HHcy patients were treated with folate (5 mg/day) for 90 days and then divided into a failure group (Hcy ≥ 15 µmol/l) and a success group (Hcy < 15 µmol/l) according to post-treatment plasma Hcy levels. Genotyping of CBS gene (rs2851391 and rs706209) in patients (n = 638) was detected using a MassArray system (Sequenom, San Diego, CA, USA). The baseline DNA methylation levels of patients (n = 299) were detected using MethylTarget™ technology (Genesky Biotechnologies Inc., Shanghai, China). RESULTS: The CBS rs2851391 TC + CC genotype was related to a 57% reduction of failure risk in HHcy treatment compared to the TT genotype (95% confidence interval [CI] = 0.19-0.97). The CBS rs706209 CT + TT genotype had a 2.97-fold increased risk of failure to treatment compared to the CC genotype (95% CI = 1.52-5.80). After adjustment for confounding factors, the odds ratio (95% CI) for the risk of failure in HHcy treatment in total and male patients was 0.55 (0.32-0.93) and 0.34 (0.16-0.69), respectively, for patients with higher methylation levels (≥ methylation median). Additionally, baseline CBS promoter methylation mediated 33.39% of the effect of rs2851391 on the efficacy of folate treatment for HHcy (ACME [average causal mediation effects]: -0.05, 95% CI = -0.11 to 0.00, p = 0.046). CONCLUSIONS: The present study indicates that CBS gene polymorphism and promoter methylation could affect the efficacy of HHcy. There were potentially causal effects of genetic, epigenetic variations at the CBS rs2851391 locus on the efficacy of HHcy therapy with folate.

Prevalence and heritability of benign prostatic hyperplasia and LUTS in men aged 40 years or older in Zhengzhou rural areas.

BACKGROUND: Benign prostate hyperplasia (BPH) is the most common disease among aging males, but no reports have addressed the prevalence of BPH in Zhengzhou. Therefore, we aimed to understand the prevalence of BPH in men aged 40 years or older in Zhengzhou's rural areas through a cross-sectional study and analyzed the correlation with epidemiologic factors and the heritability of the disease. MATERIALS AND METHODS: A multistage sampling method was used to randomly select male respondents in Zhengzhou's rural areas. Men who were 40 years of age or older and their first-degree relatives were subjected to the International Prostate Symptom Score (IPSS) and related examinations. Heritability was calculated according to the prevalence of the first-degree relatives in the case and control groups. RESULTS: The prevalence of BPH was 10.04%. Its prevalence increased with age, from 2.17% in men aged 40-44 years to 31.11% in men aged 80 years or older. The average volume of the prostate was 17.16 ± 7.96 mL, and the average IPSS was 5.89 ± 5.91. The analysis of the correlation between the associated risk factors and BPH revealed that prostatitis and a history of prostatic hyperplasia were significant factors. Obesity, smoking, drinking, diabetes, and hypertension were not correlated with BPH. Of the 94 first-degree relatives of the cases, 53 had BPH (56.38%); of the 106 first-degree relatives of the controls, five had BPH (4.72%). Heritability appeared to account for 40.48% of BPH cases. The heritability of incomplete emptying, frequency, intermittency, urgency, weak stream, straining, and nocturia was 43.28, 71.37, 9.67, 5.67, 2.70, 53.36, and 19.12%, respectively. CONCLUSION: The total prevalence of BPH in men aged 40 years or older in Zhengzhou's rural areas was 10.04%, and the heritability of prostatic hyperplasia was 40.48%.

Association between BHMT and CBS gene promoter methylation with the efficacy of folic acid therapy in patients with hyperhomocysteinemia.

Both betaine homocysteine methyltransferase (BHMT) and cystathionine ß-synthase (CBS) are major enzymes in the metabolism of plasma homocysteine (Hcy). Abnormal methylation levels of BHMT and CBS are positively associated with Hcy levels. The present study is performed to explore the association between the methylation levels in the promoter regions of the BHMT and CBS genes and the efficacy of folic acid therapy in patient with hyperhomocysteinemia (HHcy). A prospective cohort study recruiting HHcy (Hcy ≥ 15 µmol/L) patients was performed. The subjects were treated with oral folic acid (5 mg/d) for 90 days, and the patients were divided into the success group (Hcy < 15 µmol/L) and the failure group (Hcy ≥ 15 µmol/L) according to their Hcy levels after treatment. In the logistic regression model with adjusted covariates, the patients with lower total methylation levels in the BHMT and CBS promoter regions exhibited 1.627-fold and 1.671-fold increased risk of treatment failure compared with higher methylation individuals, respectively. Similarly, subjects who had lower methylation levels (

Prediction model for the efficacy of folic acid therapy on hyperhomocysteinaemia based on genetic risk score methods.

No risk assessment tools for the efficacy of folic acid treatment for hyperhomocysteinaemia (HHcy) have been developed. We aimed to use two common genetic risk score (GRS) methods to construct prediction models for the efficacy of folic acid therapy on HHcy, and the best gene-environment prediction model was screened out. A prospective cohort study enrolling 638 HHcy patients was performed. We used a logistic regression model to estimate the associations of two GRS methods with the efficacy. Performances were compared using area under the receiver operating characteristic curve (AUC). The simple count genetic risk score (SC-GRS) and weighted genetic risk score (wGRS) were found to be independently associated with the efficacy of folic acid treatment for HHcy. Using the SC-GRS, per risk allele increased with a 1·46-fold increased failure risk (P < 0·001) after adjustment for traditional risk factors, including age, sex, BMI, smoking, alcohol consumption, history of diabetes, history of hypertension, history of hyperlipidaemia, history of stroke and history of CHD. When used the wGRS, the association was strengthened (OR = 2·08, P < 0·001). Addition of the SC-GRS and wGRS to the traditional risk model significantly improved the predictive ability by AUC (0·859). A precise gene-environment predictive model with good performance was developed for predicting the treatment failure rate of folic acid therapy for HHcy.

Genetic and epigenetic regulation of BHMT is associated with folate therapy efficacy in hyperhomocysteinaemia.

BACKGROUND AND OBJECTIVES: Hyperhomocysteinaemia (HHcy) is an independent risk factors for several disorders, including cardiovascular disease. The understanding of the relationship among genetic, epigenetic and the efficacy of folate therapy for HHcy remain unclear. This study aim to investigate whether betaine-homocysteine methyltransferase (BHMT) single-nucleotide polymorphisms (SNPs) and DNA methylation are related to the efficacy of folate therapy for HHcy and whether BHMT DNA methylation mediates the SNP-folate therapy efficacy association. METHODS AND STUDY DESIGN: A total of 638 patients with HHcy were involved in this prospective cohort study. Logistic and linear regression was used to explore associations among SNPs, DNA methylation, and folate therapy efficacy. Finally, mediation analysis was performed to investigate whether DNA methylation of BHMT mediates the association between SNPs and folate therapy efficacy. RESULTS: BHMT rs3733890 was significantly associated with folate therapy efficacy (p<0.05). BHMT and BHMT_1 DNA methylation level was significantly associated with folate therapy efficacy (p=0.017 and p=0.028). DNA methylation of BHMT and BHMT_1 mediated 34.84% and 33.06% of the effect of rs3733890 on folate therapy efficacy, respectively. CONCLUSIONS: There has a consistent interrelationship among BHMT genetic variants, methylation levels of BHMT, and folate therapy efficacy. BHMT and BHMT_1 DNA methylation proportionally mediated the effects of rs3733890 SNPs on the efficacy of folate therapy for HHcy.

Genetic polymorphisms of key enzymes in folate metabolism affect the efficacy of folate therapy in patients with hyperhomocysteinaemia.

The aim of this study is to analyse the efficacy rate of folate for the treatment of hyperhomocysteinaemia (HHcy) and to explore how folate metabolism-related gene polymorphisms change its efficacy. This study also explored the effects of gene-gene and gene-environment interactions on the efficacy of folate. A prospective cohort study enrolling HHcy patients was performed. The subjects were treated with oral folate (5 mg/d) for 90 d. We analysed the efficacy rate of folate for the treatment of HHcy by measuring homocysteine (Hcy) levels after treatment. Unconditioned logistic regression was conducted to analyse the association between SNP and the efficacy of folic acid therapy for HHcy. The efficacy rate of folate therapy for HHcy was 56·41 %. The MTHFR rs1801133 CT genotype, TT genotype and T allele; the MTHFR rs1801131 AC genotype, CC genotype and C allele; the MTRR rs1801394 GA genotype, GG genotype and G allele; and the MTRR rs162036 AG genotype and AG+GG genotypes were associated with the efficacy of folic acid therapy for HHcy (P<0·05). No association was seen between other SNP and the efficacy of folic acid. The optimal model of gene-gene interactions was a two-factor interaction model including rs1801133 and rs1801394. The optimal model of gene-environment interaction was a three-factor interaction model including history of hypertension, history of CHD and rs1801133. Folate supplementation can effectively decrease Hcy level. However, almost half of HHcy patients failed to reach the normal range. The efficacy of folate therapy may be genetically regulated.

Long non-coding RNA MALAT1 suppresses the proliferation and migration of endothelial progenitor cells in deep vein thrombosis by regulating the Wnt/ß-catenin pathway.

Deep vein thrombosis (DVT) is one of the most common circulating vascular diseases with an incidence of ~0.1% worldwide. Although anticoagulant medication remains to be the main therapeutic approach for patients with DVT, existing thrombus and pulmonary embolisms still pose as a threat to patient life. Therefore, effective targeted therapies need to be developed and studies are required to improve understanding of this condition. Endothelial progenitor cells (EPCs) originate from the bone marrow, are located in the peripheral blood and are involved in thrombus resolution. Long non-coding RNAs (lncRNAs) are non-coding RNAs that are >200 nucleotides in length. LncRNAs are associated with the development of numerous vascular diseases. Among these lncRNAs, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is downregulated in human atherosclerotic plaques. Furthermore, MALAT1 polymorphism resulted in vascular disease in Chinese populations. In the present study, the expression profile and potential functions of MALAT1 in DVT were investigated. The results revealed that MALAT1 was upregulated in DVT tissues. Furthermore, MALAT1 was able to regulate the biological behaviors of EPCs, including proliferation, migration, cell cycle arrest and apoptosis. In addition, the Wnt/ß-catenin signaling pathway is a promising downstream target of MALAT1 in DVT. The changes in biological behaviors in EPCs caused by silenced MALAT1 were reversed by inhibition of the Wnt/ß-catenin signaling pathway. In summary, the data indicated the roles of MALAT1 in the pathogenesis of DVT, and the MALAT1/Wnt/ß-catenin axis could be a novel therapeutic target for the treatment of DVT.

Identifying gene-environment interactions on the efficacy of folic acid therapy for hyperhomocysteinemia based on prediction model.

Various genetic and environmental factors or their interactions may result in the failure of folic acid therapy for hyperhomocysteinemia (HHcy). We hypothesized that an optimal predictive model of gene-environment interactions could be constructed to predict the efficacy of folic acid therapy in HHcy. A prospective cohort study of 638 HHcy patients was performed. The patients were treated with oral folic acid (5 mg/d) for 90 days. We used conditional inference tree model to stratify the failure risk of folic acid therapy synthesizing information from a weighted genetic risk score (wGRS) and environmental exposures, simultaneously interpreting the gene-environment interaction network in predicting the efficacy of HHcy. We detected high-order interactions between medical history of stroke, coronary heart disease (CHD), wGRS, and baseline total homocysteine (tHcy) on the failure risk of folic acid therapy. The wGRS in fourth quartile had 3.73-fold increased failure risk of folic acid treatment (odds ratio = 3.73, 95% confidence interval: 1.47-9.45). Stroke was identified as the key discriminator among the variables examined. A total of 3.3% of participants in failure group were at the lowest failure risk of folic acid therapy (nonstroke, non-CHD, baseline tHcy ≤ 31.1 µmol/L, wGRS ≤ 1.05). Individuals with stroke but with wGRS > 1.05 were at the highest failure risk of folic acid therapy (91.0% of participants in failure group). Medical history of stroke, CHD, wGRS, and baseline tHcy were consistently identified as significant risk factors for the failure risk of folic acid therapy. The multiple interactions between genetic and environmental factors can be visually presented via the conditional inference tree model.

TRIM32 overexpression improves chemoresistance through regulation of mitochondrial function in non-small-cell lung cancers.

BACKGROUND: TRIM32 is overexpressed in several human cancers. However, its expression pattern, biological characteristics and mechanisms in human non-small cell lung cancer (NSCLC) have not been reported. METHODS: We examined TRIM32 protein in 115 cases of NSCLC specimens. TRIM32 plasmid transfection and siRNA knockdown was carried out in NSCLC cell lines. AnnexinV/PI and JC-1 staining were performed to examine the change of apoptosis and mitochondrial membrane potential. Western blot was used to detect change of downstream proteins. RESULTS: We found that TRIM32 protein was upregulated in 69 cases and positively correlated with advanced TNM stage. TRIM32 overexpression also correlated with poor survival of NSCLC patients. Biological assays demonstrated that TRIM32 overexpression promoted while it depletion inhibited cell growth, colony formation and invasion. In addition, TRIM32 maintained NSCLC cell viability and reduced apoptosis when treated with cisplatin. JC-1 and CellRox staining demonstrated that TRIM32 could maintain mitochondrial membrane potential and reduce Reactive Oxygen Species (ROS) production after cisplatin treatment. Western blot analysis showed that TRIM32 overexpression downregulated caspase 3 cleavage and cytochrome c release. TRIM32 also positively regulated Bcl-2 protein expression and NF-κB signaling. Inhibition of NF-κB abolished the effects of TRIM32 on Bcl-2. CONCLUSION: Taken together, our results indicated that TRIM32 is overexpressed in NSCLC and regulates cisplatin resistance, possibly through NF-κB and Bcl-2.