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RATIONALE & OBJECTIVE: Case-mix adjusted hemodialysis mortality has decreased since 1998. Many factors that influence mortality may have contributed to this trend and these associations may differ by continental region. We studied changes in hemodialysis facility practices over time and their potential role in mediating changes in patient survival. STUDY DESIGN: Observational prospective cohort study. SETTING & PARTICIPANTS: Adult hemodialysis patients treated in hemodialysis 500 facilities participating in the Dialysis Outcomes Practice Patterns Study (DOPPS) between 1999 and 2015 in the US, Japan, and 4 four European countries: Germany, Italy, Spain, and UK. PREDICTORS: Four practice measures at each facility: the percentages of patients with Kt/V>1.2, interdialytic weight gain [IDWG]<5.7%, phosphorus<6 mg/dL, and using AV fistulae. OUTCOMES: Patient survival. ANALYTICAL APPROACH: Mediation analyses, adjusted for case mix, were conducted using 3-year study phase as the exposure and facility practice measures as potential mediators. RESULTS: In Europe, we observed a 13% improvement in overall case-mix adjusted survival per decade. Trends in facility practice measures, especially Kt/V and phosphorus, explained 10% improvement in case-mix survival per decade, representing 77% (10% explained of 13% improvement) of the observed improvement. In Japan, 73% of the observed 12%/decade improvement in case-mix adjusted survival could be attributed to facility practices, especially Kt/V and IDWG. In the US, 56% of the observed 47%/decade improvement in case-mix adjusted survival could be attributed to facility practices, especially AV fistula use and phosphorus control. LIMITATIONS: Unmeasured changes in the characteristics of the patient population over this period may confound the observed associations. CONCLUSION: The improvements in adjusted hemodialysis patient survival in Europe, Japan, and the US from 1999 to 2015 can be largely explained by improvements in specific facility practices. Future changes in patient survival may be responsive to further evolution in the implementation of common clinical practices.
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AIM: To investigate the association between fish oil supplementation and subsequent risk of chronic kidney disease (CKD) among patients with diabetes, and further evaluate the mediation effect of typical glycolipid and inflammatory biomarkers. METHODS: In total, 24 497 patients with diabetes from the UK Biobank were included. Cox proportional hazards regression models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for CKD risk, and the rate advancement period was calculated to quantify and communicate the impact of fish oil upon that risk. In addition, we also used mediation analysis to assess the mediating role of plasma biomarkers. RESULTS: Overall, 7122 patients reported taking fish oil supplements. During a mean of 11.3 years of follow-up, 3533 CKD cases occurred. In the fully adjusted model, fish oil use was inversely associated with the incidence of CKD (HR 0.90; 95% CI: 0.83, 0.97), which was mediated by serum levels of HbA1c (4.7%), C-reactive protein (CRP) (3.4%) and high-density lipoprotein cholesterol (HDL-C) (2.3%). Participants who took fish oil supplements displayed the same risk of CKD events, but that risk was delayed by approximately 2.79 years compared with non-users of fish oil. CONCLUSIONS: Our findings advocate the beneficial role of fish oil use in preventing CKD among patients with diabetes, which may be mediated by serum levels of HbA1c, CRP and HDL-C, and support public health policies aiming to promote fish oil supplementation for the prevention of diabetes complications.
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Background: Both diabetic kidney disease (DKD) and chronic kidney disease (CKD) are more prevalent among individuals with lower levels of education in observational studies. To quantify the mediation effect of recognized cardiometabolic traits, we obtain causal estimates between education and DKD as well as CKD. Materials and methods: We assessed the causal effect of education on DKD and CKD, separately estimated the causal effect of 26 cardiometabolic traits on DKD and CKD, and finally calculated the mediating effects and mediating proportions of each using two-step, two-sample multivariable Mendelian randomization (MVMR). Furthermore, the genetic association between exposure, mediators, and outcomes was investigated using linkage disequilibrium score (LDSC) regression analysis. Expression quantitative trait loci (eQTL) were retrieved from the Genotype-Tissue Expression Project (GTEx) v8 to serve as genetic instrumental variables. Transcriptome-wide association studies (TWAS), Bayesian colocalization analysis, and Summary-data-based Mendelian Randomization (SMR) analysis were performed to explore underlying susceptibility genes between education, mediators, and kidney diseases. Results: Higher education with a genetically predicted 1-SD (4.2 years) was linked to a 48.64% decreased risk of DKD and a 29.08% decreased risk of CKD. After extensive evaluation of 26 cardiometabolic traits, 7 and 6 causal mediators were identified as mediating the effects of education on DKD and CKD, respectively. The largest mediating factor between education and DKD was BMI, which was followed by WHR, T2D, fasting insulin, SBP, fasting glucose, and DBP. In contrast, candidate mediators in the education-to-CKD pathway included BMI, followed by cigarettes smoked per day, WHR, SBP, T2D, and DBP. MR analysis revealed that TP53INP1 was found to be a shared susceptibility gene for cardiometabolic traits and DKD, while L3MBTL3 was found to be a shared susceptibility gene for cardiometabolic traits and CKD. Conclusion: Our findings provide solid evidence that education has a causally protective effect on the development of DKD and CKD. We additionally reveal significant directions for intervention on cardiometabolic traits that mitigate the negative effects of educational inequities on the onset of DKD and CKD. Our work demonstrates a shared genetic basis between education, cardiometabolic traits, and kidney diseases. Future research aiming at lowering kidney risk may benefit from these findings.
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Disparities in socioeconomic status (SES) are associated with an increased risk of cardiovascular disease (CVD). Depression is a highly prevalent cardiovascular risk factor among individuals with low SES. The present study aimed to gain a better understanding of the association between SES and CVD by examining the mediating effects of depression. 30,127 participants, 50.77â¯% female, with a mean age of 47.37â¯years from the National Health and Nutrition Examination Survey (NHANES) 2005-2018, were included. Weighted multivariable logistic regression analyses estimated the association between SES and CVD. Mediation analyses tested the mediating effects of depression. The multivariable-adjusted odds ratio (OR) of high SES for CVD was 0.42 (95â¯% confidence interval (CI): 0.36, 0.50; Pâ¯<â¯0.001). In parallel, depression was negatively associated with SES, in which the multivariable-adjusted ß was -1.42 (95â¯% CI: -1.62, -1.22; Pâ¯<â¯0.001) in high SES compared to low SES. For the association between depression and CVD, the multivariable-adjusted OR per 1-point increase of PHQ-9 score for CVD was 1.08 (95â¯% CI: 1.07, 1.09; Pâ¯<â¯0.001). The mediation models indicated that depression mediated 10.92â¯% of the total association between SES and CVD when fully adjusted. Identifying individuals with depression for appropriate treatment is promising for reducing the CVD burden among populations with low SES.
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BACKGROUND: Complex interconnections are evident among gut microbiota, circulating metabolites, inflammatory cytokines, and the pathogenesis of abdominal aortic aneurysms (AAA), with the causal dynamics yet to be comprehensively elucidated. The primary objective of this study was to elucidate the potential causal relationships involving gut microbiota-mediated plasma metabolites, inflammatory cytokines, and AAA. METHODS: We utilized data from genome-wide association studies predominantly comprising individuals of European ancestry, encompassing four major gut microbiota signatures, 233 plasma metabolite signatures (N = 136,016), 91 inflammatory cytokine signatures (N = 14,824), and AAA signatures (N = 1,458,875). Mendelian randomization (MR), employed in a two-sample format, was utilized as a tool to investigate the potential causal pathways from gut microbiota to the development of AAA. Additionally, a two-step MR approach was employed to dissect the impact of plasma metabolites and inflammatory cytokines on the relationship between gut microbiota and AAA and to ascertain the mediated fractions. RESULTS: Our findings indicate that five phylum or family-identical bacteria, 175 plasma metabolites, and seven inflammatory factors are causally associated with AAA. Among them, five bacterial species from the same phylum or family, identified from different GWAS data, were strongly associated with AAA. Of these, two exhibited negative causality and three exhibited positive causality. We found that the phylum Firmicutes and the families Oscillospiraceae might reduce the risk of AAA, whereas the families Prevotellaceae, Sutterellaceae, and Aminobacteriaceae might increase the risk of AAA. Further screening indicated that phylum Firmicutes id.1672 (GCST90017114) may confer a protective effect against AAA by reducing triglyceride levels in medium/small high-density lipoprotein (HDL). CONCLUSION: MR analysis has delineated a causal pathway from gut microbiota, through plasma circulating metabolites and inflammatory cytokines, to the pathogenesis of AAA. The role of intestinal flora and certain biomarkers may provide a reference for the diagnosis of AAA, and contribute to the prevention, diagnosis, and treatment of AAA disease.
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Aneurisma da Aorta Abdominal , Citocinas , Microbioma Gastrointestinal , Estudo de Associação Genômica Ampla , Análise da Randomização Mendeliana , Aneurisma da Aorta Abdominal/microbiologia , Aneurisma da Aorta Abdominal/sangue , Aneurisma da Aorta Abdominal/genética , Humanos , Microbioma Gastrointestinal/fisiologia , Microbioma Gastrointestinal/genética , Citocinas/sangue , Masculino , Feminino , Inflamação/sangue , Inflamação/genéticaRESUMO
OBJECTIVE: Control beliefs have been found to influence adaption to a cancer diagnosis. This study explored interrelationships among education, control beliefs, and health-related quality of life (HRQoL) in patients with breast, prostate, colorectal, and lung cancer and tested weather control beliefs act as mediators. METHODS: Six hundred and five patients with breast (n = 205), prostate (n = 205), colorectal (n = 124), and lung (n = 71) cancer from two German cancer registries answered standardized questionnaires. Response rate was 54%. HRQoL was assessed with the EORTC QLQ-C30 core questionnaire and control beliefs (internal, external, and fatalistic) were evaluated using the IPC-questionnaire. Education was measured on a scale ranging from 1 to 8. Data were analyzed using multiple mediation models. RESULTS: There was a positive correlation between education and HRQoL. Internal beliefs were positive and external beliefs were negative correlated with HRQoL. Internal control beliefs mediated the relationship between education and global health-related quality of life (.299, CI .122, .531), physical functioning (.272, CI .110, .486), emotional functioning (.325, CI .120, .578), and pain (-.288, CI - .558, - .094). External and fatalistic control beliefs did not act as mediators. CONCLUSION: Patients with low education feel they have less control over their cancer disease and consequently a poorer health-related quality of life.
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Neoplasias da Mama , Escolaridade , Neoplasias Pulmonares , Neoplasias da Próstata , Qualidade de Vida , Sistema de Registros , Humanos , Qualidade de Vida/psicologia , Masculino , Feminino , Pessoa de Meia-Idade , Idoso , Neoplasias Pulmonares/psicologia , Neoplasias da Próstata/psicologia , Neoplasias da Mama/psicologia , Neoplasias Colorretais/psicologia , Alemanha , Inquéritos e Questionários , AdultoRESUMO
BACKGROUND: The current understandings of the relationship between air pollution (AP), greenspace exposure and Parkinson's Disease (PD) remain inconclusive. METHODS: We engaged 441,462 participants from the UK Biobank who were not diagnosed with PD. Utilizing Cox proportional hazard regression model, relationships between AP [nitrogen dioxide (NO2), and nitrogen oxides (NOX), particulate matter < 2.5 µm in aerodynamic diameter(PM2.5), coarse particulate matter between 2.5 µm and 10 µm in aerodynamic diameter(PM2.5-10), particulate matter < 10 µm in aerodynamic diameter(PM10)], greenspace exposure, and PD risk were determined independently. Our analyses comprised three models, adjusted for covariates, and affirmed through six sensitivity analyses to bolster the robustness of our findings. Moreover, mediation analysis was deployed to discern the mediating effect of AP between greenspaces and PD. RESULTS: During a median follow-up of 12.23 years (5,574,293 person-years), there were 3,293 PD events. Each interquartile (IQR) increment in NO2 and PM10 concentrations were associated with 10% and 8% increase in PD onset risk, while the increases in NOX, PM2.5 and PM2.5-10 were not associated with PD risk. Additionally, greenspace may safeguard by reducing NO2 and PM10 levels, with the effect mediated by NO2 and PM10 in greenspace-PD relationship. CONCLUSION: Our findings indicate that an IQR increase in ambient NO2 and PM10 concentrations was associated with risk of PD development, while other pollutants (NOX, PM2.5 and PM2.5-10) were not associated with PD risk. Firstly, we find that augmented exposure to greenspace was associated with the lower PD risk by reducing NO2 and PM10 levels.
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Poluição do Ar , Exposição Ambiental , Doença de Parkinson , Material Particulado , Humanos , Doença de Parkinson/epidemiologia , Doença de Parkinson/etiologia , Masculino , Feminino , Poluição do Ar/efeitos adversos , Pessoa de Meia-Idade , Idoso , Material Particulado/efeitos adversos , Estudos Prospectivos , Exposição Ambiental/efeitos adversos , Dióxido de Nitrogênio/efeitos adversos , Dióxido de Nitrogênio/análise , Reino Unido/epidemiologia , Adulto , Seguimentos , Parques Recreativos/estatística & dados numéricos , Fatores de RiscoRESUMO
AIM: To investigate the associations of metabolic score for insulin resistance (METS-IR) with all-cause and cardiovascular disease (CVD)-specific mortality and the potential mediating role of biological ageing. METHODS: A cohort of 19 204 participants from the National Health and Nutrition Examination Survey (NHANES) 1999-2018 was recruited for this study. Cox regression models, restricted cubic splines, and Kaplan-Meier survival curves were used to determine the relationships of METS-IR with all-cause and CVD-specific mortality. Mediation analyses were performed to explore the possible intermediary role of biological ageing markers, including phenotypic age (PhenoAge) and biological age (BioAge). RESULTS: During a median follow-up of 9.17 years, we observed 2818 deaths, of which 875 were CVD-specific. Multivariable Cox regression showed that the highest METS-IR level (Q4) was associated with increased all-cause (hazard ratio [HR] 1.38, 95% confidence interval [CI] 1.14-1.67) and CVD mortality (HR 1.52, 95% CI 1.10-2.12) compared with the Q1 level. Restricted cubic splines showed a nonlinear relationship between METS-IR and all-cause mortality. Only METS-IR above the threshold (41.02 µg/L) was positively correlated with all-cause death. METS-IR had a linear positive relationship with CVD mortality. In mediation analyses, we found that PhenoAge mediated 51.32% (p < 0.001) and 41.77% (p < 0.001) of the association between METS-IR and all-cause and CVD-specific mortality, respectively. For BioAge, the mediating proportions of PhenoAge were 21.33% (p < 0.001) and 15.88% (p < 0.001), respectively. CONCLUSIONS: This study highlights the detrimental effects of insulin resistance, as measured by METS-IR, on all-cause and CVD mortality. Moreover, it underscores the role of biological ageing in mediating these associations, emphasizing the need for interventions targeting both insulin resistance and ageing processes to mitigate mortality risks in metabolic disorders.
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Envelhecimento , Doenças Cardiovasculares , Resistência à Insulina , Inquéritos Nutricionais , Humanos , Doenças Cardiovasculares/mortalidade , Masculino , Feminino , Pessoa de Meia-Idade , Estados Unidos/epidemiologia , Adulto , Estudos de Coortes , Idoso , Síndrome Metabólica/mortalidade , Síndrome Metabólica/epidemiologia , Causas de Morte , Fatores de RiscoRESUMO
BACKGROUND: The triglyceride-glucose (TyG) index is a risk marker for arterial stiffness; however, the extent to which the TyG index is associated with arterial stiffness via lipids and inflammation remains unknown. The first aim was to probe the relationship between the TyG index and arterial stiffness in two surveys. The second aim was to clarify whether lipids and inflammation mediate this relationship. METHODS: The sample size of 13,726 U.S. individuals from the National Examination Survey (NHANES) and 3,964 Chinese individuals from the China Health and Retirement Longitudinal Study (CHARLS 2015) were enrolled. Weighted multivariate logistic and linear regression models, as well as restricted cubic spline (RCS) and mediation analyses, were utilized to estimate complex relationships between the TyG index, arterial stiffness, lipids (non-high-density lipoprotein cholesterol [non-HDL-C]) and inflammation (C-reactive protein [CRP]) biomarkers. RESULTS: A total of 3,420 U.S. patients and 992 Chinese patients were diagnosed with increased arterial stiffness. Regression analyses demonstrated that higher quartiles of the TyG index were associated with a greater incidence of increased arterial stiffness (NHANES: OR = 2.610, 95% CI = 2.043-3.334, P < 0.001; CHARLS: OR = 1.579, 95% CI = 1.057-2.360, P < 0.001). Participants with a higher TyG index/higher CRP level or with a higher TyG index/higher non-HDL-C level had the highest incidence of increased arterial stiffness in the two surveys. The results were still consistent when the sensitivity analysis was implemented with stricter clinical cut-off values of non-HDL-C. Mediation analysis verified that lipids (mediated effect: ß = 0.012, P < 0.001 in NHANES; ß = 0.020, P < 0.001 in CHARLS) and inflammation (mediated effect: ß = 0.003, P < 0.001 in NHANES; ß = 0.006, P < 0.001 in CHARLS) partially mediated this relationship. CONCLUSIONS: These results indicated a positive linear correlation between the TyG index, non-HDL-C level, CRP level and increased arterial stiffness in two surveys. Furthermore, lipids and inflammation could partly mediate the correlation of the TyG index with arterial stiffness in both surveys.
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Glicemia , Proteína C-Reativa , Inflamação , Triglicerídeos , Rigidez Vascular , Humanos , Triglicerídeos/sangue , Feminino , Masculino , Pessoa de Meia-Idade , Inflamação/sangue , Proteína C-Reativa/metabolismo , Proteína C-Reativa/análise , Glicemia/metabolismo , Idoso , China/epidemiologia , Biomarcadores/sangue , Fatores de Risco , AdultoRESUMO
Previous research has already examined the relationship between Future Anxiety, a construct recently introduced in Italy, and mental health in young adults, although possible mediating variables in this relationship have so far never been investigated. The present study attempts to fill this gap by exploring the incidence of Future Anxiety on psychological distress (i.e., Stress, Anxiety and Depression) in a group of 302 young Italian adults (18-30 years; M = 21.9; SD = 2.6; 49.0% males; 51.0% females), presenting and evaluating the simultaneous mediating effect of Intolerance of Uncertainty and Non-Pathological Worry. Findings highlighted how Future Anxiety had a positive and significant direct effect on Stress and Depression, but not on Anxiety. In the three serial mediation models proposed, Intolerance of Uncertainty and Non-Pathological Worry mediated the relationship between Future Anxiety and mental health outcomes. The results also confirmed the hypothesized serial mediation effect by highlighting how young adults with greater Future Anxiety experienced more Intolerance of Uncertainty, which positively affected Non-Pathological Worry levels and, in turn, exacerbated psychological distress. Finally, results indicated that female participants experienced more Stress, Anxiety, and Depression in relation to Future Anxiety compared to males. Starting from the review of main references on this subject, the results discussed provide new insights for understanding youth psychological distress. Finally, practical implications for the design of supportive interventions for this study's target group are proposed.
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The consumption of protein-rich foods stimulates satiety more than other macronutrient-rich foods; however, the underlying mechanisms-of-action are not well-characterized. The objective of this study was to identify the direct and indirect effects of postprandial amino acid (AA) responses on satiety. Seventeen women (mean ± SEM, age: 33 ± 1 year; BMI: 27.8 ± 0.1 kg/m2) consumed a eucaloric, plant-based diet containing two servings of lean beef/day (i.e., 7.5 oz (207 g)) for 7 days. During day 6, the participants completed a 12 h controlled-feeding, clinical testing day including repeated satiety questionnaires and blood sampling to assess pre- and postprandial plasma AAs, PYY, and GLP-1. Regression and mediation analyses were completed to assess AA predictors and hormonal mediators. Total plasma AAs explained 41.1% of the variance in perceived daily fullness (p < 0.001), 61.0% in PYY (p < 0.001), and 66.1% in GLP-1 (p < 0.001) concentrations, respectively. Several individual AAs significantly predicted fluctuations in daily fullness, PYY, and GLP-1. In completing mediation analyses, the effect of plasma leucine on daily fullness was fully mediated by circulating PYY concentrations (indirect effect = B: 0.09 [Boot 95% CI: 0.032, 0.17]) as no leucine-fullness direct effect was observed. No other mediators were identified. Although a number of circulating AAs predict satiety, leucine was found to do so through changes in PYY concentrations in middle-aged women.
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Aminoácidos , Sobrepeso , Peptídeo YY , Período Pós-Prandial , Carne Vermelha , Saciação , Humanos , Feminino , Adulto , Aminoácidos/sangue , Peptídeo YY/sangue , Saciação/efeitos dos fármacos , Sobrepeso/sangue , Peptídeo 1 Semelhante ao Glucagon/sangue , Biomarcadores/sangue , Refeições , Animais , Bovinos , Resposta de Saciedade/efeitos dos fármacosRESUMO
Background: Education, cognition, and intelligence are phenotypically and genetically related. Education has been shown to have a protective effect on the risk of developing cervical spondylosis. However, it is unclear whether cognition and intelligence have independent causal effects on cervical spondylosis, and whether health and lifestyle factors influence this association. Methods: We first assessed the independent effects of education, cognition, and intelligence on cervical spondylosis by two-sample Mendelian randomization and multivariable Mendelian randomization analysis, and evaluated 26 potential association mediators using two-step Mendelian randomization, and calculated the median proportion. Results: The results showed that only education had an independent causal effect on cervical spondylosis, and had a protective effect on the risk of cervical spondylosis (ß: 0.3395; se: 0.166; p < 0.05; OR:0.71; [95%CI: 0.481-0.943]. Of the 26 potential associated mediators, a factor was identified: SHBG (mediated proportion: 2.5%). Univariable Mendelian randomization results showed that the risk factors for cervical spondylosis were time spent watching TV (OR:1.96; [95%CI: 1.39-2.76]), smoking (OR:2.56; [95%CI: 1.061-1.486]), body mass index (OR:1.26; [95%CI: 1.124-1.418]), percentage of body fat (OR:1.32; [95%CI: 1.097-1.593]), major depression (OR:1.27; [95%CI: 1.017-1.587]) and sitting height (OR:1.15; [95%CI: 1.025-1.291]). Protective factors include computer using (OR:0.65; [95%CI: 0.418-0.995]), sex hormone binding globulin (OR:0.87; [95%CI: 0.7955-0.951]) and high-density lipoprotein (OR:0.90; [95%CI: 0.826-0.990]). Conclusion: Our findings demonstrate the causal and independent effects of education on cervical spondylosis and suggest that lifestyle media may be a priority target for the prevention of cervical spondylosis due to low educational attainment.
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BACKGROUND: Body mass index (BMI) and lipid disorders are both known to be strongly associated with the development of diabetes, however, the indirect effect of lipid parameters in the BMI-related diabetes risk is currently unknown. This study aimed to investigate the mediating role of lipid parameters in the association of BMI with diabetes risk. METHODS: We assessed the association of diabetes risk with BMI, as well as lipid parameters including high-density lipoprotein cholesterol(HDL-C), low-density lipoprotein cholesterol(LDL-CF and LDL-CS), triglycerides(TG), total cholesterol(TC), remnant cholesterol(RC), non-HDL-C, and combined indices of lipid parameters with HDL-C (RC/HDL-C ratio, TG/HDL-C ratio, TC/HDL-C ratio, non-HDL/HDL-C ratio, LDL/HDL-C ratio) using data from 15,453 subjects in the NAGALA project. Mediation models were used to explore the mediating role of lipid parameters in the association of BMI with diabetes risk, and mediation percentages were calculated for quantifying the strength of the indirect effects. Finally, receiver operating characteristic curve (ROC) analysis was used to compare the accuracy of BMI and BMI combined with lipid parameters in predicting incident diabetes. RESULTS: Multivariate regression models, adjusted for confounding factors, demonstrated robust associations of lipid parameters, BMI, with diabetes risk, with the exception of TC, LDL-CF, LDL-CS, and non-HDL-C. Mediation analysis showed that lipid parameters except TC, LDL-CF, LDL-CS, and Non-HDL-C were involved in and mediated the association of BMI with diabetes risk, with the largest mediation percentage being the RC/HDL-C ratio, which was as high as 40%; it is worth mentioning that HDL-C and HDL-C-related lipid ratio parameters also play an important mediating role in the association between BMI and diabetes, with the mediator proportion being greater than 30%. Finally, based on the ROC results, we found that the prediction performance of all lipid parameters in the current study except TC was significantly improved when combined with BMI. CONCLUSION: Our fresh findings suggested that lipid parameters partially mediated the association of BMI with diabetes risk; this result indicated that in the context of diabetes risk screening and disease management, it is important to not only monitor BMI but also pay attention to lipid parameters, particularly HDL-C and HDL-C-related lipid ratio parameters.
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Índice de Massa Corporal , Lipídeos , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Lipídeos/sangue , Análise de Mediação , Adulto , Estudos de Coortes , Fatores de Risco , Biomarcadores/sangue , Diabetes Mellitus/sangue , Diabetes Mellitus/epidemiologia , HDL-Colesterol/sangue , Idoso , Diabetes Mellitus Tipo 2/sangue , Triglicerídeos/sangue , Seguimentos , PrognósticoRESUMO
INTRODUCTION: Residential greenness may influence COPD mortality, but the causal links, risk trajectories, and mediation pathways between them remain poorly understood. OBJECTIVES: We aim to comprehensively identify the potential causal links, characterize the dynamic progression of hospitalization or posthospital risk, and quantify mediation effects between greenness and COPD. METHODS: This study was conducted using a community-based cohort enrolling individuals aged ≥ 18 years in southern China from January 1, 2009 to December 31, 2015. Greenness was characterized by normalized difference vegetation index (NDVI) around participants' residential addresses. We applied doubly robust Cox proportional hazards model, multi-state model, and multiple mediation method, to investigate the potential causal links, risk trajectories among baseline, COPD hospitalization, first readmission due to COPD or COPD-related complications, and all-cause death, as well as the multiple mediation pathways (particulate matter [PM], temperature, body mass index [BMI] and physical activity) connecting greenness exposure to COPD mortality. RESULTS: Our final analysis included 581,785 participants (52.52% female; average age: 48.36 [Standard Deviation (SD): 17.56]). Each interquartile range (IQR: 0.06) increase in NDVI was associated with a reduced COPD mortality risk, yielding a hazard ratio (HR) of 0.88 (95 % CI: 0.81, 0.96). Furthermore, we observed per IQR (0.04) increase in NDVI was inversely associated with the risk of multiple transitions (baseline - COPD hospitalization, baseline - death, and readmission - death risks), especially a declined risk of all-cause death after readmission (HR = 0.66 [95 %CI: 0.44, 0.99]). Within the observed association between greenness and COPD mortality, three mediators were identified, namely PM, temperature, and BMI (HR for the total indirect effect: 0.773 [95 % CI: 0.703, 0.851]), with PM showing the highest mediating effect. CONCLUSIONS: Our findings revealed greenness may be a beneficial factor for COPD morbidity, prognosis, and mortality. This protective effect is primarily attributed to the reduction in PM concentration.
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Researchers have increasingly considered approaches to learning (ATL) a key indicator of school readiness. Our study purposed to examine the impacts of parental warmth on children's approaches to learning, and the mediating role of self-efficacy, as well as the moderating role of teacher-child closeness in this relationship. Using a whole-group sampling method, 414 Chinese children aged 5-6 years participated this research together with their parents and teachers. Parents of those children were asked to fill out in person questionnaires on parental warmth, children's approaches to learning, and self-efficacy. Children's teachers completed the questionnaire regarding teacher-child closeness. Results indicated that children with high parental warmth were more likely to get high approaches to learning and their self-efficacy played a partial mediating role in this link. In addition, teacher-child closeness moderated the correlation between parental warmth and children's self-efficacy. Specifically, the association between parental warmth and children's self-efficacy was stronger for children with high teacher-child closeness than those with low teacher-child closeness. The results extend our understanding of how parental warmth affects children's approaches to learning, revealing that strategies that could enhance self-efficacy would be effective in improving children's approaches to learning.
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BACKGROUND: Socioeconomic status as measured by education, income, or occupation, has been associated with fibromyalgia but the underlying mechanism and the role of lifestyle factors are unclear. Thus, we examine the role of modifiable lifestyle factors (body mass index, physical activity, alcohol consumption and smoking) in the association between education and self-reported fibromyalgia. METHODS: We used data from 74,157 participants in the population-based prospective Norwegian Women and Cancer (NOWAC) study. Socioeconomic position, operationalized as years of educational attainment, and lifestyle factors were assessed via self-reported questionnaires. Multiple mediation analysis was used to decompose total effects into direct and indirect effects. Estimates were reported as hazard ratios (HRs) with 95% confidence intervals (CIs). RESULTS: The cumulative incidence of fibromyalgia was 3.2% after a median follow up time of 13 years. Fibromyalgia was inversely associated with years of educational attainment for ≤ 9 years (HR = 2.56; 95% CI 2.32-2.91) and for 10-12 years (HR = 1.84; 95% CI 1.72-2.02), compared with ≥ 13 years of education. Overall, all lifestyle factors together jointly mediated 17.3% (95% CI 14.3-21.6) and 14.1% (95% CI 11.3-18.9) of the total effect for ≤ 9 years and 10-12 years of education, respectively. Smoking and alcohol consumption contributed the most to the proportion mediated, for ≤ 9 years (5.0% and 7.0%) and 10-12 years (5.6% and 4.5%) of education. CONCLUSION: The association between education and self-reported fibromyalgia was partly explained through lifestyle factors, mainly smoking and alcohol consumption.
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Fibromialgia , Humanos , Feminino , Fatores de Risco , Autorrelato , Estudos Prospectivos , Análise de Mediação , Estilo de Vida , EscolaridadeRESUMO
BACKGROUND: Triage is the first step in providing prompt and appropriate emergency nursing and addressing diagnostic issues. Rapid clinical reasoning skills of emergency nurses are essential for prompt decision-making and emergency care. Nurses experience limitations in emergency nursing that begin with triage. This cross-sectional study explored the mediating effect of perceived triage competency and clinical reasoning skills on the association between Korean Triage and Acuity Scale (KTAS) proficiency and emergency nursing competency. METHODS: A web-based survey was conducted with 157 emergency nurses working in 20 hospitals in South Korea between mid-May and mid-July 2022. Data were collected utilizing self-administered questionnaires to measure KTAS proficiency (48 tasks), perceived triage competency (30 items), clinical reasoning skills (26 items), and emergency nursing competency (78 items). Data were analyzed using the PROCESS macro (Model 6). RESULTS: Perceived triage competency indirectly mediate the relationship between KTAS proficiency and emergency nursing competency. Perceived triage competency and clinical reasoning skills were significant predictors of emergency nursing competency with a multiple linear mediating effect. The model was found have a good fit (F = 8.990, P <.001) with, a statistical power of 15.0% (R² = 0.150). CONCLUSIONS: This study indicates that improving emergency nursing competency requires enhancing triage proficiency as well as perceived triage competency, which should be followed by developing clinical reasoning skills, starting with triage of emergency nurses.
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Identifying mechanisms of childhood abuse-adulthood psychopathology relations could facilitate preventive efforts, but most prior studies used cross-sectional or two-wave designs and did not test the effects of childhood maternal and paternal abuse separately. Our 18-year three-wave study thus determined if Wave 2 daily stress reactivity and risk appraisal severity mediated Wave 1 retrospectively-reported childhood maternal and paternal abuse on Wave 3 generalized anxiety disorder (GAD), major depressive disorder (MDD), panic disorder (PD), alcohol (AUD), and substance use disorder (SUD) self-rated symptom severity. Longitudinal structural equation modeling was employed, adjusting for Wave 1 psychopathology severity. Higher childhood maternal and paternal abuse consistently predicted greater future daily stress reactivity and risk appraisal, and these mediators subsequently predicted increased GAD, MDD, and PD, but not AUD and SUD severity. Daily stress reactivity and risk appraisal consistently mediated the pathways between childhood maternal and paternal abuse predicting heightened adulthood GAD, MDD, and PD (Cohen's d = 0.333-0.888) but not AUD and SUD severity. Mediation effect sizes were stronger for childhood maternal (24.5-83.0%) than paternal (19.5-56.0%) abuse as the predictor. The latent interaction between Wave 1 childhood maternal and paternal abuse did not moderate the effect of Wave 1 maternal or paternal abuse on any Wave 3 adulthood psychopathology severity through Wave 2 daily stress reactivity and risk appraisal. Our research emphasizes the urgent requirement for continuous evaluation and intervention initiatives in trauma-informed care, both in inpatient and outpatient treatment settings.
Assuntos
Transtornos de Ansiedade , Transtorno Depressivo Maior , Estresse Psicológico , Transtornos Relacionados ao Uso de Substâncias , Humanos , Feminino , Masculino , Adulto , Estudos Longitudinais , Transtorno Depressivo Maior/psicologia , Transtornos Relacionados ao Uso de Substâncias/psicologia , Estresse Psicológico/psicologia , Transtornos de Ansiedade/psicologia , Transtorno de Pânico/psicologia , Análise de Mediação , Alcoolismo/psicologia , Sobreviventes Adultos de Maus-Tratos Infantis/psicologia , Sobreviventes Adultos de Maus-Tratos Infantis/estatística & dados numéricos , Índice de Gravidade de Doença , Adolescente , Maus-Tratos Infantis/psicologia , Maus-Tratos Infantis/estatística & dados numéricos , Criança , Experiências Adversas da Infância/estatística & dados numéricos , Adulto Jovem , Fatores de Risco , Pessoa de Meia-IdadeRESUMO
The influence of brain atrophy on sleep microstructure in Spinocerebellar Ataxias (SCAs) has not been extensively explored limiting the use of these sleep traits as surrogate biomarkers of neurodegeneration and clinical phenotype. The objective of the study is to explore the relationship between sleep microstructure and brain atrophy in SCA2 and its role in the clinical phenotype. Fourteen SCA2 mutation carriers (7 pre-manifest and 7 manifest subjects) underwent polysomnographic, structural MRI, and clinical assessments. Particularly, markers of REM and non-REM sleep microstructure, measures of cerebellar and brainstem atrophy, and clinical scores were analyzed through correlation and mediation analyses. The sleep spindle activity exhibited a negative correlation with the number of trials required to complete the verbal memory test (VMT), and a positive correlation with the cerebellar volume, but the significance of the latter correlation did not survive multiple testing corrections. However, the causal mediation analyses unveiled that sleep spindle activity significantly mediates the association between cerebellar atrophy and VMT performance. Regarding REM sleep, both phasic EMG activity and REM sleep without atonia exhibited significant associations with pontine atrophy and disease severity measures. However, they did not demonstrate a causal mediation effect between the atrophy measures and disease severity. Our study provides evidence about the association of the pontocerebellar atrophy with sleep microstructure in SCA2 offering insights into the cerebellar involvement in cognition via the control of the sleep spindle activity. Therefore, our findings may help to understand the disease pathogenesis and to better characterize sleep microstructure parameters as disease biomarkers.Clinical trial registration number (TRN): No applicable.
RESUMO
BACKGROUND: Identifying moral behavior in complex situations is the key ability for children to develop prosocial behavior. The theory of mind (ToM) and empathy provide the cognition and emotional motivation required for the development of moral sensitivity. In this study, we investigated the associations among ToM, empathy, and moral sensitivity and explored the possible differences between Chinese preschool children aged 4 and 5 years. METHODS: One hundred and thirty children completed the unexpected-content and change-of-location tasks as well as questionnaires about empathy and moral sensitivity individually. A one-way analysis of variance and the multi-group mediation SEM were used to examine the associations of the three variables and age differences. RESULTS: The scores of 5-year-old children in the dimensions of care, fairness, authority, and sanctity and the total score were higher than those of 4-year-old children. Moral sensitivity was positively correlated with both ToM and empathy after we controlled for verbal IQ and gender. Multigroup mediation analyses showed age-based differences in the associations among moral sensitivity, ToM, and empathy. Empathy's mediation effect was partial among 4-year-old children and complete among 5-year-old children. CONCLUSIONS: These findings contribute to understanding the cognitive and emotional factors in the formation of children's moral sensitivity. They also point to a promising approach to promoting the development of moral sensitivity and evidence for educators to understand the process of children's socialization.