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BACKGROUND: The soluble triggering receptor expressed on myeloid cells 2 (sTREM2) in cerebrospinal fluid (CSF) is considered a biomarker of microglia activity. The objective of this study was to investigate the trajectory of CSF sTREM2 levels over time and examine its association with sex. METHODS: A total of 1,017 participants from the Alzheimer's Disease Neuroimaging Initiative Study (ADNI) with at least one CSF sTREM2 record were included. The trajectory of CSF sTREM2 was analyzed using a growth curve model. The association between CSF sTREM2 levels and sex was assessed using linear mixed-effect models. RESULTS: CSF sTREM2 levels were increased with age over time (P < 0.0001). No significant sex difference was observed in sTREM2 levels across the entire sample; however, among the APOE ε4 allele carriers, women exhibited significantly higher sTREM2 levels than men (ß = 0.146, P = 0.002). CONCLUSION: Our findings highlight the association between CSF sTREM2 levels and age-related increments, underscoring the potential influence of aging on sTREM2 dynamics. Furthermore, our observations indicate a noteworthy association between sex and CSF sTREM2 levels, particularly in individuals carrying the APOE ε4 allele.
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Doença de Alzheimer , Biomarcadores , Glicoproteínas de Membrana , Neuroimagem , Receptores Imunológicos , Humanos , Doença de Alzheimer/líquido cefalorraquidiano , Doença de Alzheimer/diagnóstico por imagem , Feminino , Masculino , Glicoproteínas de Membrana/líquido cefalorraquidiano , Glicoproteínas de Membrana/genética , Receptores Imunológicos/genética , Idoso , Estudos Longitudinais , Neuroimagem/métodos , Biomarcadores/líquido cefalorraquidiano , Idoso de 80 Anos ou mais , Apolipoproteína E4/genética , Envelhecimento/líquido cefalorraquidiano , Caracteres Sexuais , Pessoa de Meia-IdadeRESUMO
BACKGROUND: Previous studies have suggested a connection between impaired olfactory function and an increased risk of rapid eye movement sleep behavior disorder (RBD) in individuals diagnosed with Parkinson's disease (PD). However, there is a gap in knowledge regarding the potential impact of olfactory dysfunction on the long-term patterns of sleep disorders among early PD patients. METHODS: Data from the Parkinson's Progression Markers Initiative program included 589 participants with assessments of sleep disorders using the Epworth Sleepiness Scale (ESS) and RBD Screening Questionnaire (RBDSQ). Olfactory dysfunction at baseline was measured using the University of Pennsylvania Smell Identification Test. Trajectories of sleep disorders over a 5-year follow-up were identified using group-based trajectory modeling, and the relationship between olfactory dysfunction and sleep disorder trajectories was examined through binomial logistic regression. RESULTS: Two distinct trajectories of sleep disorders over the 5-year follow-up period were identified, characterized by maintaining a low or high ESS score and a low or high RBDSQ score. An inversion association was observed between olfactory function measures and trajectories of excessive daytime sleepiness (odds ratio [OR] = 0.97, 95% confidence interval [CI] 0.95, 1.00, p = 0.038), after controlling for potential covariates. Similarly, olfactory function showed a significant association with lower trajectories of probable RBD (OR = 0.96, 95% CI 0.94, 0.98, p = 0.001) among early PD individuals. Consistent findings were replicated across alternative analytical models. CONCLUSIONS: Our findings indicated that olfactory dysfunction was associated with unfavorable long-term trajectories of sleep disorders among early PD.
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Background and Objective: While earlier studies have focused on the relationship between stress and obesity, there was a gap in understanding the potential impact of positive psychological factors, such as resilience, on obesity. By investigating the role of psychological resilience with obesity, this study aimed to address this gap and tackle obesity through a positive psychological framework. Methods: Participants consisted of 2445 community residents from Shenzhen, China, with a mean age of 41.09 ± 13.72 years, comprising 846 males and 1599 females. Psychological resilience was measured using the Brief Resilience Scale; gender, age, marital status, education level, smoking status, alcohol consumption, frequency of physical exercise, and perceived stress were considered potential confounding factors. The relationship between psychological resilience and body mass index (BMI) was examined through multiple linear regression and logistic regression analyses. Results: The participants had an average psychological resilience score of 3.46 (standard deviation [SD] = 0.62) and an average BMI of 22.59 (SD = 3.35), with 104 individuals (4.3%) identified with obesity. In the fully adjusted multiple linear regression model, a higher psychological resilience score was associated with a higher BMI (ß = 0.507, 95% CI:0.283, 0.731). In the logistic regression model, higher psychological resilience scores were linked to increased obesity risk, with a more significant association observed among males (odds ratio [OR] = 2.169, 95% CI:1.155, 4.073), while psychological resilience acted as a protective factor against underweight among females (OR = 0.528, 95% CI:0.376, 0.816). Conclusion: The study demonstrated a significant link between higher psychological resilience and elevated BMI, emphasizing the complex relationship between psychological fortitude and weight management. Interventions targeting socioeconomic status, education, lifestyle habits, and physiological well-being might offer a promising strategy for enhancing psychological resilience and promoting healthier weight. Emphasizing self-efficacy and coping skills at the individual level could contribute to balanced weight and comprehensive health outcomes, addressing the global challenge of obesity.
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BACKGROUND: The study aimed to find out the association between sleep duration and psychological resilience in a population-based survey. MATERIALS AND METHODS: A cross-sectional survey was conducted in August 2022, employing a cluster random sampling method to recruit community residents at Futian District in Shenzhen, China. A total of 2,445 participants aged 18 years and over were included in the study. The Brief Resilience Scale (BRS) was utilized to measure psychological resilience, and sleep duration was classified according to the American Heart Association's sleep duration categories. Multivariable linear regression was used to analyze the relationship between psychological resilience and sleep duration after adjusting for gender, age, smoking status, physical exercise frequency, body mass index (BMI), and education level. RESULTS: The participants displayed moderate levels of psychological resilience, with a mean resilience score of 3.46 (standard deviation [SD] = 0.62) and a mean sleep duration of 7.04 h (SD = 1.10). After adjusting for covariates, longer sleep duration was associated with higher psychological resilience (ß = 0.047, P < 0.05), indicating that participants with a long sleep duration had higher resilience scores than those with a short sleep duration. CONCLUSION: Longer sleep duration is positively associated with higher psychological resilience in community residents. These findings suggest that improving sleep duration may be a promising approach to enhancing psychological resilience, preventing psychological problems, and promoting overall physical and mental health development.
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OBJECTIVE: To examine the associations of excessive daytime sleepiness (EDS) and probable rapid eye movement sleep behavior disorder (pRBD), respectively, with impulsive-compulsive behaviors (ICBs) over a 5-year follow-up in patients with early Parkinson's disease (PD). METHODS: The Parkinson's Progression Markers Initiative is a multicenter cohort study based on an ongoing and open-ended registry. Longitudinal associations of sleep disorders with ICB over 5-year follow-up visits were estimated using generalized linear mixed-effects models among PD participants. RESULTS: A total of 825 PD participants were enrolled at baseline. The study sample had a median baseline age of 63.1 (interquartile range: 55.6-69.3) years and comprised 496 (61.5%) men. Among them, 201 (24.9%) had ICB at baseline. In the generalized mixed-effects models, EDS (odds ratio [OR] = 1.09, 95% confidence interval [CI] 1.05, 1.12) and RBD (OR = 1.07, 95% CI 1.03, 1.12) were substantially associated with higher odds of developing ICB over time in PD patients, after multivariate adjustment including age, gender, family history, GDS score, STAI-Y score, MDS-UPDRS part III score, LEDD, and disease duration. Consistent results were observed when stratifying by age at baseline, gender, and PD family history. CONCLUSIONS: The study findings suggest a longitudinal association between EDS and pRBD with an increased risk of developing ICB in patients with PD. The findings emphasize the significance of evaluating and addressing sleep disorders in PD patients as a potential approach to managing ICB.
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Doença de Parkinson , Humanos , Masculino , Feminino , Doença de Parkinson/epidemiologia , Doença de Parkinson/complicações , Doença de Parkinson/psicologia , Pessoa de Meia-Idade , Idoso , Estudos Prospectivos , Transtorno do Comportamento do Sono REM/epidemiologia , Transtorno do Comportamento do Sono REM/complicações , Transtornos do Sono-Vigília/epidemiologia , Comportamento Compulsivo/epidemiologia , Comportamento Impulsivo , Distúrbios do Sono por Sonolência Excessiva/epidemiologia , Estudos de CoortesRESUMO
The aim of this study was to evaluate the associations between psychological resilience and epigenetic clocks assessed by DNA methylation age predictions. We used data from 4018 participants in the Health and Retirement Study. Multivariable linear regression models were used to estimate the association between psychological resilience and epigenetic clocks adjusted for age, sex, race, body mass index, smoking status, and years of education. Thirteen epigenetic clocks were used in our analysis and were highly correlated with one another. A higher psychological resilience score was associated with slower DNA methylation age acceleration for the majority of epigenetic clocks after multivariable adjustment. These findings imply that people with a higher level of psychological resilience may experience slower DNA methylation age acceleration and biological aging.
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Epigênese Genética , Resiliência Psicológica , Humanos , Aposentadoria , Metilação de DNA , Envelhecimento/genéticaRESUMO
OBJECTIVES: To investigate whether shorter telomere length is a causal risk factor for systemic lupus erythematosus (SLE) in the Asian population. METHODS: We applied the two-sample Mendelian randomization (MR) method to the pooled statistics from a genome-wide association study (GWAS) of 6,707 SLE cases and 16,047 controls. We selected nine single-nucleotide polymorphisms (SNPs) with genome-wide significance as instrumental variables for telomere length. The main analysis was carried out by the random-effects inverse-variance weighted (IVW) method. Horizontal pleiotropy was evaluated by the intercept of MR-Egger regression. RESULTS: A potentially causal relationship between longer genetically predicted telomere length and increased risk of systemic lupus erythematosus (OR = 1.72, 95%CI: 1.21, 2.46, p = 0.01) was observed. The MR-Egger regression demonstrated an intercept proximal to zero (intercept = 0.017, p = 0.69), which does not provide evidence of the presence of horizontal pleiotropy. CONCLUSIONS: Our findings provided evidence supporting a potential causal relationship between longer telomere length and increased risk of systemic lupus erythematosus.
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Lúpus Eritematoso Sistêmico , Telômero , Humanos , Asiático , Estudo de Associação Genômica Ampla , Lúpus Eritematoso Sistêmico/genética , Análise da Randomização Mendeliana , Telômero/genética , Encurtamento do Telômero/genética , Predisposição Genética para DoençaRESUMO
Background: Telomere length (TL) has been recognized to be fundamental to the risk of autoimmune disorders. However, the role of leukocyte TL in Graves' disease has not yet been fully elucidated. In the study, we exploited the two-sample Mendelian randomization (MR) design to evaluate the causal effect of leukocyte TL on the risk of Graves' disease. Methods: Genome-wide association study (GWAS) data of leukocyte TL from the Singapore Chinese Health Study (SCHS) cohort and Graves' disease from Biobank Japan (BBJ, 2176 cases and 210,277 controls) were analyzed. Nine single nucleotide polymorphisms (SNPs) were selected as instrumental variables (IVs) for TL. We used the inverse variance weighted (IVW) approach as the main estimator and MR-Egger regression, weighted median, simple mode, and weighed mode methods as complementary estimators. Horizontal pleiotropy was assessed using the intercept from MR-Egger. Results: The analysis demonstrated that genetically predicted longer leukocyte TL was causally associated with a lower risk of Graves' disease using the IVW method (odds ratio [OR]: 1.64, 95% confidence interval [CI]: 1.23-2.17, P=2.27e-04, and other complementary MR approaches achieved similar results. The intercept from the MR-Egger analysis provided no noticeable evidence of horizontal pleiotropy (ß=0.02, P=0.641). MR-PRESSO method reported no outliers (P=0.266). Conclusions: Our results provided evidence to support a genetic predisposition to shorter leukocyte TL with an increased risk of Graves' disease. Further studies are warranted to explore the mechanism underlying the association.
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Doença de Graves , Análise da Randomização Mendeliana , Bancos de Espécimes Biológicos , Estudo de Associação Genômica Ampla , Doença de Graves/genética , Humanos , Japão/epidemiologia , Leucócitos , TelômeroRESUMO
BACKGROUND: Infection with viruses such as human papillomavirus (HPV) is known to induce carcinomas, including esophageal carcinoma (EC). However, the possible role of viruses other than HPV in EC carcinogenesis is unclear in many studies. Here, we aimed to explore the association between infection with viruses other than HPV and EC risk by integrating existing studies of epidemiology in a meta-analysis. METHODS: The PubMed, Web of Science, Cochrane Library and China National Knowledge Infrastructure databases were searched. The Newcastle-Ottawa scale was used to assess the quality of the included studies. Odds ratios (ORs) or relative risks (RRs) (with 95% confidence intervals [CIs]) were pooled to estimate the association between virus infection and risk of EC. RESULTS: We included 31 eligible studies involving nine different viruses. Overall, an increased risk of EC was associated with hepatitis B virus (HBV) infection (OR = 1.19, 95%CI 1.01-1.36) and hepatitis C virus (HCV) infection (OR = 1.77, 95%CI 1.17-2.36), but not human immunodeficiency virus (HIV) infection, according to the current evidence. The evidence for an association with Epstein-Barr virus (EBV), herpes simplex virus 1 (HSV-1), JC virus (JCV), cytomegalovirus (CMV), human T-lymphotropic virus 1 (HTLV-1) or Merkel cell polyomavirus (MCPyV) infection was insufficient. CONCLUSIONS: We confirmed the relationship between HBV and HCV infection and the risk of EC, but we found no association of EC risk with HIV and EBV infection. The roles of HSV-1, JCV, CMV, HTLV-1, and MCPyV were not clear because of the limited number of studies.
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Alphapapillomavirus , Carcinoma , Infecções por Vírus Epstein-Barr , Infecções por Polyomavirus , Herpesvirus Humano 4 , Humanos , Papillomaviridae/genéticaRESUMO
Cigarette smoking is a factor capable of inducing esophageal squamous cell carcinoma (ESCC). However, the biological pathways that are responsible for tumor development and are directly affected by cigarette smoking remain unknown. To explore the role of cigarette smoking in ESCC, we developed a long-term cigarette smoke extract (CSE) exposed cell model using the normal immortalized SHEE esophageal epithelial cell line, which would malignantly transform after long-term cultivation without carcinogens. CSE-exposed cells displayed higher malignancy and differently expressed several lncRNAs. Among them, H19, a lncRNA responsible for proliferation and invasion, was upregulated in CSE-exposed SHEE cells. In tumors from ESCC patients, H19 was significantly increased in smoking ESCC patients compared to non-smoking patients, and H19 was overexpressed and correlated with pathological tumor size in smokers. These results indicated that cigarette smoking lead to a different biological change from non-smoking induced ESCC and H19 related to cancer development during CSE-induced carcinogenesis.