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BACKGROUND: Bleeding risk brought by intensive lipid-lowering therapy and low low-density lipoprotein cholesterol is concerning, while evidence regarding the relationship between remnant cholesterol and bleeding is frightening. This study aimed to investigate the association between remnant cholesterol at admission and an in-hospital bleeding event after acute ischemic stroke or transient ischemic attack (TIA). METHODS AND RESULTS: A total of 3222 eligible patients admitted to Shanghai Huashan Hospital between 2015 and 2021 with complete lipid data were analyzed. Patients were classified into low (<20.0 mg/dL), moderate (20.0-29.9 mg/dL), and high (≥30 mg/dL) groups by remnant cholesterol. The mean age of patients was 63.0± 13.1 years, including 2301 (71.4%) men and 651 (20.2%) with TIA. The median (interquartile range) of remnant cholesterol was 18.6 (13.5-25.9) mg/dL. After adjustment for confounding variables, patients with low remnant cholesterol had a higher risk of bleeding events (odds ratio, 2.56 [95% CI, 1.12-6.67]) than those with moderate remnant cholesterol. The high remnant cholesterol group was not significantly associated with bleeding risk. Combined assessment of low-density lipoprotein cholesterol and remnant cholesterol further identified patients with the highest risk of bleeding events. CONCLUSIONS: Low remnant cholesterol levels were associated with bleeding events during the acute stage of ischemic stroke and TIA. The assessment of remnant cholesterol could inform the bleeding risk during hospitalization both for patients and physicians in clinical practice.
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Colesterol , Ataque Isquêmico Transitório , AVC Isquêmico , Humanos , Masculino , Ataque Isquêmico Transitório/epidemiologia , Ataque Isquêmico Transitório/sangue , Ataque Isquêmico Transitório/etiologia , Pessoa de Meia-Idade , AVC Isquêmico/epidemiologia , AVC Isquêmico/sangue , AVC Isquêmico/diagnóstico , Feminino , Colesterol/sangue , Idoso , Fatores de Risco , China/epidemiologia , Medição de Risco , Estudos Retrospectivos , Biomarcadores/sangue , Hemorragia/epidemiologia , Hemorragia/sangueRESUMO
BACKGROUND: Previous studies into relationship between high-density lipoprotein cholesterol (HDL-C) and cognitive decline were constrained to a single measurement, leaving the association between HDL-C variability and risk of cognitive decline unclear. METHODS: We identified 5930 participants from the China Health and Retirement Longitudinal Study (CHARLS) who were devoid for stroke, dementia, and memory-related diseases at baseline and underwent a minimum of 2 sequential health examinations during 2011-2015. Variability in HDL-C was defined as (1) variability independent of the mean (VIM), (2) average real variability (ARV), and (3) standard deviation (SD) of HDL-C change from baseline and follow-up visits. Cognitive function was evaluated in 2018 by Mini-mental state examination (MMSE) in the Chinese version. Logistic regression was employed to explore the association between HDL-C variability and cognitive decline. Odd ratios (OR) and 95 % confidence intervals (CI) were reported. RESULTS: The study included participants from CHARLS, mean age of 57.84±8.44 years and 44 % male. After adjustment for covariates, the highest quartile of VIM was associated with an increased risk of cognitive decline [OR:1.049, 95 %CI: 1.014-1.086] compared to the lowest quartile. For each SD increment of VIM, the OR was 1.015 (95 %CI:1.003-1.027). Strong dose-response relationships were identified (P for trend: 0.005). Consistent results were obtained for other measures of HDL-C variability (ARV and SD). Similar patterns were identified in different dimensions of cognition. CONCLUSIONS: Elevated HDL-C variability was associated with increased cognitive decline risk. Strategies to reducing HDL-C variability may lower the risks of cognitive decline among the general population.
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HDL-Colesterol , Disfunção Cognitiva , Humanos , Masculino , Feminino , HDL-Colesterol/sangue , Disfunção Cognitiva/sangue , Disfunção Cognitiva/epidemiologia , China/epidemiologia , Pessoa de Meia-Idade , Idoso , Estudos Longitudinais , Fatores de Risco , Estudos de Coortes , Testes de Estado Mental e DemênciaRESUMO
The acceleration of aging is a risk factor for numerous diseases, and diet has been identified as an especially effective anti-aging method. Currently, research on the relationship between dietary nutrient intake and accelerated aging remains limited, with existing studies focusing on the intake of a small number of individual dietary nutrients. Comprehensive research on the single and mixed anti-aging effects of dietary nutrients has not been conducted. This study aimed to comprehensively explore the effects of numerous dietary nutrient intakes, both singly and in combination, on the acceleration of aging. Data for this study were extracted from the 2015-2018 National Health and Nutrition Examination Surveys (NHANES). The acceleration of aging was measured by phenotypic age acceleration. Linear regression (linear), restricted cubic spline (RCS) (nonlinear), and weighted quantile sum (WQS) (mixed effect) models were used to explore the association between dietary nutrient intake and accelerated aging. A total of 4692 participants aged ≥ 20 were included in this study. In fully adjusted models, intakes of 16 nutrients were negatively associated with accelerated aging (protein, vitamin E, vitamin A, beta-carotene, vitamin B1, vitamin B2, vitamin B6, vitamin K, phosphorus, magnesium, iron, zinc, copper, potassium, dietary fiber, and alcohol). Intakes of total sugars, vitamin C, vitamin K, caffeine, and alcohol showed significant nonlinear associations with accelerated aging. Additionally, mixed dietary nutrient intakes were negatively associated with accelerated aging. Single dietary nutrients as well as mixed nutrient intake may mitigate accelerated aging. Moderately increasing the intake of specific dietary nutrients and maintaining dietary balance may be key strategies to prevent accelerated aging.
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Envelhecimento , Dieta , Nutrientes , Inquéritos Nutricionais , Humanos , Feminino , Masculino , Pessoa de Meia-Idade , Adulto , Dieta/estatística & dados numéricos , Dieta/métodos , Nutrientes/administração & dosagem , Idoso , Adulto Jovem , Ingestão de Alimentos/fisiologia , Modelos LinearesRESUMO
OBJECT: The relationship between sleep duration trajectories and cognitive decline remains uncertain. This study aims to examine the connections between various patterns of sleep duration and cognitive function. METHODS: Group-based trajectory modeling (GBTM) was employed to identify longitudinal trajectories of sleep duration over four-year follow-up period, while considering age, sex and nap duration as adjustments. Logistic regression was utilized to analyze the association between sleep trajectories and cognition, with odds ratios (OR) and 95 % confidence intervals (CI) reported. Subgroup analyses based on various demographic characteristics were conducted to explore potential differences in sleep trajectories and cognitive decline across different population subgroups. RESULTS: A total of 5061 participants were followed for four years, and three sleep duration trajectories were identified: high increasing (n = 2101, 41.6 %), stable increasing (n = 2087, 40.7 %), and low decreasing (n = 873, 17.7 %). After adjustment for basic demographic information, health status, and baseline cognition, the high increasing trajectory was found to be associated with cognitive decline in terms of global cognition (OR:1.52,95 %CI:1.18-1.96), mental intactness (OR:1.36,95 %CI:1.07-1.73) and episodic memory (OR:1.33, 95 %CI:1.05-1.67), as compared to stable increasing trajectory. These associations were particularly prominent among the non-elderly population (≤65 years) and those without depressive symptoms. CONCLUSION: This study suggests that both high increasing and low decreasing sleep duration trajectories are linked to cognitive decline, as compared to the stable increasing trajectory. Long-term attention to changes in sleep duration facilitates early prevention of cognitive decline.
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Disfunção Cognitiva , Sono , Humanos , Masculino , Feminino , Disfunção Cognitiva/epidemiologia , Estudos Longitudinais , China/epidemiologia , Idoso , Pessoa de Meia-Idade , Sono/fisiologia , Fatores de Tempo , Cognição/fisiologia , Duração do SonoRESUMO
Objectives. Current lung cancer screening protocols primarily evaluate pulmonary nodules, yet often neglect the malignancy risk associated with small nodules (≤10 mm). This study endeavors to optimize the management of pulmonary nodules in this population by devising and externally validating a Multimodal Integrated Feature Neural Network (MIFNN). We hypothesize that the fusion of deep learning algorithms with morphological nodule features will significantly enhance diagnostic accuracy.Materials and Methods. Data were retrospectively collected from the Lung Nodule Analysis 2016 (LUNA16) dataset and four local centers in Beijing, China. The study includes patients with small pulmonary nodules (≤10 mm). We developed a neural network, termed MIFNN, that synergistically combines computed tomography (CT) images and morphological characteristics of pulmonary nodules. The network is designed to acquire clinically relevant deep learning features, thereby elevating the diagnostic accuracy of existing models. Importantly, the network's simple architecture and use of standard screening variables enable seamless integration into standard lung cancer screening protocols.Results. In summary, the study analyzed a total of 382 small pulmonary nodules (85 malignant) from the LUNA16 dataset and 101 small pulmonary nodules (33 malignant) obtained from four specialized centers in Beijing, China, for model training and external validation. Both internal and external validation metrics indicate that the MIFNN significantly surpasses extant state-of-the-art models, achieving an internal area under the curve (AUC) of 0.890 (95% CI: 0.848-0.932) and an external AUC of 0.843 (95% CI: 0.784-0.891).Conclusion. The MIFNN model significantly enhances the diagnostic accuracy of small pulmonary nodules, outperforming existing benchmarks by Zhanget alwith a 6.34% improvement for nodules less than 10 mm. Leveraging advanced integration techniques for imaging and clinical data, MIFNN increases the efficiency of lung cancer screenings and optimizes nodule management, potentially reducing false positives and unnecessary biopsies.Clinical relevance statement. The MIFNN enhances lung cancer screening efficiency and patient management for small pulmonary nodules, while seamlessly integrating into existing workflows due to its reliance on standard screening variables.
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Algoritmos , Neoplasias Pulmonares , Redes Neurais de Computação , Tomografia Computadorizada por Raios X , Humanos , Neoplasias Pulmonares/diagnóstico por imagem , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/patologia , Tomografia Computadorizada por Raios X/métodos , Estudos Retrospectivos , Masculino , Aprendizado Profundo , Feminino , Nódulo Pulmonar Solitário/diagnóstico por imagem , Pessoa de Meia-Idade , Reprodutibilidade dos Testes , Idoso , Nódulos Pulmonares Múltiplos/diagnóstico por imagem , Nódulos Pulmonares Múltiplos/patologia , Detecção Precoce de Câncer/métodos , ChinaRESUMO
Observational epidemiological studies have reported a relationship between remnant cholesterol and stroke. However, the results are inconclusive, and causality remains unclear due to confounding or reverse causality. Our objective in this study was to investigate the causal relevance of remnant cholesterol and the risk of stroke and its subtypes using the Mendelian randomization (MR) approach. Genome-wide association studies (GWASs) including 115,082 European individuals (UK Biobank) were used to identify instruments for remnant cholesterol, including intermediate-density lipoprotein (IDL) cholesterol and very-low-density lipoprotein (VLDL) cholesterol. Summary-level data for total stroke, intracerebral hemorrhage, subarachnoid hemorrhage, ischemic stroke (IS), and IS subtypes were obtained from GWAS meta-analyses conducted by the MEGASTROKE consortium. Univariable and multivariable MR analyses were performed. The GWAS identified multiple single-nucleotide polymorphisms after clumping for remnant cholesterol (n = 52), IDL cholesterol (n = 62), and VLDL cholesterol (n = 67). Assessed individually using MR, remnant cholesterol (weighted median: odds ratio [OR] 1.32 per 1-SD higher trait; 95% CI: 1.04-1.67; P = 0.024) had effect estimates consistent with a higher risk of LAS-IS, driven by IDL cholesterol (OR 1.32; 95% CI: 1.04-1.68; P = 0.022). In multivariable MR, IDL cholesterol (OR 1.46; 95% CI: 1.10-1.93; P = 0.009) retained a robust effect on LAS-IS after controlling for VLDL cholesterol and high-density lipoprotein cholesterol. The MR analysis did not indicate causal associations between remnant cholesterol and other stroke subtypes. This study suggests that remnant cholesterol is causally associated with the risk of LAS-IS driven by IDL cholesterol.
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BACKGROUND AND AIM: Previous studies have demonstrated an association between SUA and dyslipidemia. This study aims to explore the temporal relationship between SUA and dyslipidemia. METHODS AND RESULTS: Based on the Beijing Health Management Cohort conducted from 2013 to 2018, the data of a physical examination population was collected, including a total of 6630 study subjects. Cross-lagged panel analysis was employed to examine the temporal relationship between elevated SUA levels and dyslipidemia, indicated by either elevated TG or decreased HDL-C. The path coefficient and the 95 % CI from baseline TG to follow-up SUA were as follows: in the general population, men, women, and people with BMI ≥25 kg/m2were 0.027 (0.008-0.045), 0.024 (0.001-0.048), 0.032 (0.001-0.063) and 0.033 (0.006-0.059) (P < 0.05); however, the path coefficient from baseline SUA to follow-up TG and the 95 % CI were not statistically significant. Furthermore, the path coefficients and 95 % CIs between elevated SUA and decreased HDL-C were not statistically significant, both in the general population and in populations stratified by gender and BMI. CONCLUSIONS: We found a temporal relationship from elevated TG to elevated SUA in the general population and the populations stratified by gender and BMI (≥25 kg/m2). However, we did not observe a reverse relationship from elevated SUA to elevated TG. Additionally, we did not find a temporal relationship between decreased HDL-C and elevated SUA in both the general population and the stratified populations.
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Dislipidemias , Ácido Úrico , Masculino , Humanos , Feminino , Estudos de Coortes , Pequim/epidemiologia , Dislipidemias/diagnóstico , Dislipidemias/epidemiologia , Estudos TransversaisRESUMO
BACKGROUND: Prior studies have reported the cross-sectional relationship between lung function and arterial stiffness, while the longitudinal association remains unclear to date. This study aimed to investigate whether abnormal lung function and its subtypes at baseline are associated with increased arterial stiffness using a cohort. METHODS AND RESULTS: This was a secondary analysis extracting 2461 participants from Beijing Health Management Cohort as baseline and annually followed for development of arterial stiffness. Abnormal lung function was defined by forced expiratory volume in 1s <80% of the predicted value, forced vital capacity of the predicted value, or forced expiratory volume in 1s/forced vital capacity ratio <70%. Increased arterial stiffness was determined by brachial-ankle pulse wave velocity ≥1400 cm/s. Cox proportional hazards model was used to calculate the hazard ratio and population attributable fraction. The mean age was 42.8±8.1 years, and 444 (18.0%) cases developed increased arterial stiffness during a median follow-up of 3.0 years. The adjusted hazard ratio (95% CI) of arterial stiffness was 1.47 (95% CI, 1.10-1.96) for abnormal lung function, with a population attributable fraction of 3.9% (95% CI, 0.8-7.1). Of subtypes, only obstructive ventilatory dysfunction was significantly associated with arterial stiffness (adjusted hazard ratio, 2.06 [95% CI, 1.27-3.36]), not restricted ventilatory dysfunction (adjusted hazard ratio, 0.95 [95% CI, 0.54-1.65]). Consistent results were observed on multiple sensitivity analyses. CONCLUSIONS: Our study indicated a longitudinal association of abnormal lung function with increased arterial stiffness using a large cohort, especially for the obstructive ventilatory dysfunction.
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Índice Tornozelo-Braço , Rigidez Vascular , Humanos , Adulto , Pessoa de Meia-Idade , Estudos Longitudinais , Índice Tornozelo-Braço/métodos , Análise de Onda de Pulso/métodos , Estudos de Coortes , PulmãoRESUMO
BACKGROUND: Intraindividual differences between estimated glomerular filtration rate (eGFR) based on cystatin C (eGFRcys) and creatinine (eGFRcr) can convey important clinical information regarding the health status. However, the clinical implications of these differences (eGFRdiff) for risk of cognitive decline and motoric cognitive risk syndrome (MCR) remains unclear. We aimed to investigate the longitudinal associations of eGFRdiff with cognitive trajectories and incident MCR. METHODS: Based on the China Health and Retirement Longitudinal Study, we identified two study sub-cohorts: one for cognitive trajectory follow-up (6423 participants; years:2011-2018) and another for incident MCR follow-up (2477 participants; years:2011-2015). The eGFRdiff was defined as eGFRcys minus eGFRcr. Adjusted ordinal and binary logistics regression models were separately used to assess the associations of eGFRdiff with cognitive trajectories and incident MCR. We also performed discordance analyses for eGFRdiff vs eGFRcys, eGFRcr or eGFR based on both creatinine and cystatin C (eGFRcys-cr). RESULTS: In the first sub-cohort, four distinct 7-year cognitive trajectories were identified. Each 1-SD higher eGFRdiff (value for eGFRcys minus eGFRcr) was associated with a lower risk of poorer cognitive trajectories (OR: 0.909, 95% CI: 0.877-0.942). In the second sub-cohort, 121 participants developed incident MCR after a 4-year follow-up. Each 1-SD higher eGFRdiff (value for eGFRcys minus eGFRcr) was linked with a 25.3% (95%CI: 16.6%-33.2%) decreased risk for MCR. The above associations persisted in individuals with normal kidney function. Additionally, the risk for cognitive decline and incident MCR was more strongly associated with eGFRcys than eGFRcr and eGFRcys-cr. For the discordance analyses, 'discordantly high eGFRdiff/low eGFR' group, but not 'discordantly low eGFRdiff/high eGFR', exhibited a significantly lower risk of poorer cognitive trajectories and MCR compared to the concordant group. CONCLUSIONS: A large negative difference between eGFRcys and eGFRcr (eGFRcys lower than eGFRcr) was associated with higher risk of cognitive decline and incident MCR. The eGFRdiff could capture additional valuable risk information beyond eGFRcys, eGFRcr, and eGFRcys-cr.
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OBJECTIVE: The aim of this study was to explore the mutually causal relationship between NAFLD and type 2 diabetes. METHODS: Based on the data obtained from GWAS, this study employed bidirectional two-sample MR analysis to investigate the causal relationship between NAFLD and type 2 diabetes, and also examined the causal relationship between liver fat accumulation and type 2 diabetes as well as the relationship between NAFLD and FPG, IR. RESULTS: In MR analysis of NAFLD and type 2 diabetes, when NAFLD as an exposure and type 2 diabetes as a result, the OR (95 % CI) was 1.10890 (1.00135-1.22801); in the reverse analysis, the OR value was not statistically significant. In MR analysis of NAFLD, FPG and IR, there was no statistical significance in both directions. In MR analysis of liver fat accumulation and type 2 diabetes, when liver fat as an exposure and type 2 diabetes as a result, the OR (95 % CI) was 1.17516 (1.02054-1.35321); in the reverse analysis, the OR value (95 % CI) was 1.06283 (1.02879-1.09799). CONCLUSION: There is a unidirectional causal relationship between NAFLD and type 2 diabetes. Furthermore, a bidirectional causal relationship exists between liver fat accumulation and type 2 diabetes.
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Diabetes Mellitus Tipo 2 , Hepatopatia Gordurosa não Alcoólica , Humanos , Hepatopatia Gordurosa não Alcoólica/complicações , Hepatopatia Gordurosa não Alcoólica/epidemiologia , Hepatopatia Gordurosa não Alcoólica/genética , Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/genética , Análise da Randomização Mendeliana , Estudo de Associação Genômica AmplaRESUMO
BACKGROUND: The early detection of benign and malignant lung tumors enabled patients to diagnose lesions and implement appropriate health measures earlier, dramatically improving lung cancer patients' quality of living. Machine learning methods performed admirably when recognizing small benign and malignant lung nodules. However, exploration and investigation are required to fully leverage the potential of machine learning in distinguishing between benign and malignant small lung nodules. OBJECTIVE: The aim of this study was to develop and evaluate the ResNet50-Ensemble Voting model for detecting the benign and malignant nature of small pulmonary nodules (<20 mm) based on CT images. METHODS: In this study, 834 CT imaging data from 396 patients with small pulmonary nodules were gathered and randomly assigned to the training and validation sets in an 8:2 ratio. ResNet50 and VGG16 algorithms were utilized to extract CT image features, followed by XGBoost, SVM, and Ensemble Voting techniques for classification, for a total of ten different classes of machine learning combinatorial classifiers. Indicators such as accuracy, sensitivity, and specificity were used to assess the models. The collected features are also shown to investigate the contrasts between them. RESULTS: The algorithm we presented, ResNet50-Ensemble Voting, performed best in the test set, with an accuracy of 0.943 (0.938, 0.948) and sensitivity and specificity of 0.964 and 0.911, respectively. VGG16-Ensemble Voting had an accuracy of 0.887 (0.880, 0.894), with a sensitivity and specificity of 0.952 and 0.784, respectively. CONCLUSION: Machine learning models that were implemented and integrated ResNet50-Ensemble Voting performed exceptionally well in identifying benign and malignant small pulmonary nodules (<20 mm) from various sites, which might help doctors in accurately diagnosing the nature of early-stage lung nodules in clinical practice.
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BACKGROUND AND AIM: Although an association between skeletal muscle mass index and nonalcoholic fatty liver disease (NAFLD) has previously been demonstrated, the causal direction remains unclear. Herein, we investigated the directional association between NAFLD and the serum creatinine-to-body weight ratio (sCr/bw), a surrogate marker of the muscle mass index, using longitudinal data. METHODS: We recruited 9662 participants in 2017 and performed follow-up over 4 years. We evaluated whether sCr/bw was related to NAFLD development (Analysis I) and whether NAFLD was associated with a low sCr/bw incidence (Analysis II) using logistic regression models. Furthermore, a random intercept cross-lagged panel model was applied to evaluate the bidirectional association between sCr/bw ratio and NAFLD (Analysis III). RESULTS: Analysis I demonstrated an association between sCr/bw and incident NAFLD (odds ratio [OR] = 0.160, 95% confidence interval [CI]:0.107-0.232). Analysis II indicated a relationship between NAFLD and subsequent low sCr/bw ratio (OR = 1.524, 95% CI: 1.258-1.846). Analysis III indicated that the standard regression coefficient from sCr/bw to subsequent hepatic steatosis (HS) was -0.053 for ßsCr/bw2017 â HS2019 and -0.060 for ßsCr/bw2019 â HS2021 and the coefficient from HS to subsequent sCr/bw was -0.093 for ßHS2017 â sCr/bw2019 and -0.112 for ßHS2019 â sCr/bw2021 (all P < 0.05). CONCLUSIONS: This study indicated mutual causality between sCr/bw and NAFLD. Considering that sCr/bw is a surrogate marker of muscle mass index, the findings emphasize that NAFLD and low muscle mass form a vicious cycle, which should be taken seriously in clinical practice.
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Hepatopatia Gordurosa não Alcoólica , Humanos , Hepatopatia Gordurosa não Alcoólica/etiologia , Creatinina , Músculo Esquelético , Biomarcadores , Peso CorporalRESUMO
BACKGROUND: Impaired sensitivity to thyroid hormones is a newly proposed clinical entity associated with hyperuricemia in the subclinical hypothyroid population. However, it is unknown whether the association exists in the euthyroid population. This study aimed to explore the association of impaired sensitivity to thyroid hormones (assessed by the thyroid feedback quantile-based index [TFQI], parametric thyroid feedback quantile-based index [PTFQI], thyrotrophic thyroxine resistance index [TT4RI] and thyroid-stimulating hormone index [TSHI]) with hyperuricemia and quantify the mediating effect of body mass index BMI in the euthyroid population. METHODS: This cross-sectional study enrolled Chinese adults aged ≥ 20 years who participated in the Beijing Health Management Cohort (2008-2019). Adjusted logistic regression models were used to explore the association between indices of sensitivity to thyroid hormones and hyperuricemia. Odds ratios [OR] and absolute risk differences [ARD] were calculated. Mediation analyses were performed to estimate direct and indirect effects through BMI. RESULTS: Of 30,857 participants, 19,031 (61.7%) were male; the mean (SD) age was 47.3 (13.3) years; and 6,515 (21.1%) had hyperuricemia. After adjusting for confounders, individuals in the highest group of thyroid hormone sensitivity indices were associated with an increased prevalence of hyperuricemia compared with the lowest group (TFQI: OR = 1.18, 95% CI 1.04-1.35; PTFQI: OR = 1.20, 95% CI 1.05-1.36; TT4RI: OR = 1.17, 95% CI 1.08-1.27; TSHI: OR = 1.12, 95% CI 1.04-1.21). BMI significantly mediated 32.35%, 32.29%, 39.63%, and 37.68% of the associations of TFQI, PTFQI, TT4RI and TSHI with hyperuricemia, respectively. CONCLUSIONS: Our research revealed that BMI mediated the association between impaired sensitivity to thyroid hormones and hyperuricemia in the euthyroid population. These findings could provide useful evidence for understanding the interaction between impaired sensitivity to thyroid hormone and hyperuricemia in euthyroid individuals and suggest the clinical implications of weight control in terms of impaired thyroid hormones sensitivity.
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Hiperuricemia , Adulto , Masculino , Humanos , Feminino , Hiperuricemia/complicações , Estudos Transversais , Hormônios Tireóideos , Obesidade/complicações , Obesidade/epidemiologia , Tiroxina , TireotropinaRESUMO
Few studies have explored the effects of fine particulate matter (PM2.5) and its constituents on the progression of cerebral blood flow velocity (BFV) and the potential modifying role of greenness. In this study, we investigated the association of PM2.5 and its constituents, including sulfate (SO4 2-), nitrate (NO3 -), ammonium (NH4 +), organic matter (OM), and black carbon (BC), with the progression of BFV in the middle cerebral artery. Participants from the Beijing Health Management Cohort who underwent at least two transcranial Doppler sonography examinations during 2015-2020 were recruited. BFV change and BFV change rate were used to define the progression of cerebral BFV. Linear mixed effects models were employed to analyze the data, and the weighted quantile sum regression assessed the contribution of PM2.5 constituents. Additionally, greenness was examined as a modifier. Among the examined constituents, OM exhibited the strongest association with BFV progression. An interquartile range increase in PM2.5 and OM exposure concentrations was associated with a decrease of -16.519 cm/s (95% CI: -17.837, -15.201) and -15.403 cm/s (95% CI: -16.681, -14.126) in BFV change, and -10.369 cm/s/year (95% CI: -11.387, -9.352) and -9.615 cm/s/year (95% CI: -10.599, -8.632) in BFV change rate, respectively. Furthermore, stronger associations between PM2.5 and BFV progression were observed in individuals working in areas with lower greenness, those aged under 45 years, and females. In conclusion, reducing PM2.5 levels in the air, particularly the OM constituent, and enhancing greenness could potentially contribute to the protection of cerebrovascular health.
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Background We aimed to examine separate and joint associations of remnant cholesterol (RC) accumulation and variability with the risk of carotid atherosclerosis (CAS) in the general population. Methods and Results A total of 6213 participants who underwent 3 sequential health examinations during 2010 to 2015 were enrolled and were followed up until December 31, 2021. Cumulative RC (cumRC) and RC variability among the 3 visits were the exposure of interest in our study. Adjusted Cox models were performed to calculate the hazard ratio (HR) and 95% CI. C-statistics, integrated discrimination improvement, and the net reclassification index were used to estimate the incremental predictive ability. During a median follow-up of 4.00 years, 2613 participants developed CAS. Higher cumRC (HR, 1.33 [95% CI, 1.17-1.52]) and greater RC variability (HR, 1.22 [95% CI, 1.08-1.39]) were significantly associated with elevated risk of CAS, independent of traditional cardiovascular risk factors and low-density lipoprotein cholesterol. Participants were divided into 4 groups according to the median of cumRC and RC variability to assess their joint associations. Compared with "low cumRC and low variability," "high cumRC and high variability" had the highest risk of CAS, followed by "high cumRC and low variability" and "low cumRC and high variability." Finally, joint assessment of RC accumulation and variability had the significantly highest incremental effect on the predictive value of CAS versus single-time-point measures of RC. Conclusions Excessive cumRC levels and greater RC variability were each independently associated with higher incidence of CAS, and their coexistence could further yield significantly higher risks.
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Doenças das Artérias Carótidas , Colesterol , Humanos , Fatores de Risco , Estudos Prospectivos , LDL-Colesterol , Doenças das Artérias Carótidas/diagnóstico por imagem , Doenças das Artérias Carótidas/epidemiologiaRESUMO
BACKGROUND: The causal relationship between blood pressure variability (BPV) and arterial stiffness remains debated. OBJECTIVE: This study aimed to explore the temporal and bidirectional associations between long-term BPV and arterial stiffness using a cohort design with multiple surveys. METHODS: Participants from the Beijing Health Management Cohort who underwent health examinations from visit 1 (2010-2011) to visit 5 (2018-2019) were enrolled in this study. Long-term BPV was defined as intraindividual variation using the coefficient of variation (CV) and SD. Arterial stiffness was measured by brachial-ankle pulse wave velocity (baPWV). The bidirectional relationship between BPV and arterial stiffness was explored using cross-lagged analysis and linear regression models, with records before and after visit 3 categorized as phase 1 and phase 2, respectively. RESULTS: Of the 1506 participants, who were a mean of 56.11 (SD 8.57) years old, 1148 (76.2%) were male. The cross-lagged analysis indicated that the standardized coefficients of BPV at phase 1 directing to the baPWV level at phase 2 were statistically significant but not vice-versa. The adjusted regression coefficients of the CV were 4.708 (95% CI 0.946-8.470) for systolic blood pressure, 3.119 (95% 0.166-6.073) for diastolic pressure, and 2.205 (95% CI 0.300-4.110) for pulse pressure. The coefficients of the SD were 4.208 (95% CI 0.177-8.239) for diastolic pressure and 4.247 (95% CI 0.448-8.046) for pulse pressure. The associations were predominant in the subgroup with hypertension, but we did not observe any significant association of baPWV level with subsequent BPV indices. CONCLUSIONS: The findings supported a temporal relationship between long-term BPV and arterial stiffness level, especially among people with hypertension.
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Hipertensão , Rigidez Vascular , Humanos , Masculino , Criança , Feminino , Pressão Sanguínea/fisiologia , Índice Tornozelo-Braço , Estudos de Coortes , Rigidez Vascular/fisiologia , Análise de Onda de Pulso , Hipertensão/epidemiologiaRESUMO
Background and Objectives: Lung cancer remains a leading cause of cancer mortality worldwide. Accurately classifying benign pulmonary nodules and malignant ones is crucial for early diagnosis and improved patient outcomes. The purpose of this study is to explore the deep-learning model of ResNet combined with a convolutional block attention module (CBAM) for the differentiation between benign and malignant lung cancer, based on computed tomography (CT) images, morphological features, and clinical information. Methods and materials: In this study, 8241 CT slices containing pulmonary nodules were retrospectively included. A random sample comprising 20% (n = 1647) of the images was used as the test set, and the remaining data were used as the training set. ResNet combined CBAM (ResNet-CBAM) was used to establish classifiers on the basis of images, morphological features, and clinical information. Nonsubsampled dual-tree complex contourlet transform (NSDTCT) combined with SVM classifier (NSDTCT-SVM) was used as a comparative model. Results: The AUC and the accuracy of the CBAM-ResNet model were 0.940 and 0.867, respectively, in test set when there were only images as inputs. By combining the morphological features and clinical information, CBAM-ResNet shows better performance (AUC: 0.957, accuracy: 0.898). In comparison, a radiomic analysis using NSDTCT-SVM achieved AUC and accuracy values of 0.807 and 0.779, respectively. Conclusions: Our findings demonstrate that deep-learning models, combined with additional information, can enhance the classification performance of pulmonary nodules. This model can assist clinicians in accurately diagnosing pulmonary nodules in clinical practice.
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Aprendizado Profundo , Neoplasias Pulmonares , Humanos , Estudos Retrospectivos , Neoplasias Pulmonares/diagnóstico por imagem , Tomografia Computadorizada por Raios X/métodosRESUMO
BACKGROUND: Time-location information (time spent on commuting, indoors and outdoors around residential and work places and physical activity) and infiltrated outdoor pollution was less considered estimating individual exposure to ambient air pollution. Studies investigating the association between individual exposure to particulate matter (PM) with aerodynamic diameter < 10 µm (PM10) and < 2.5 µm (PM2.5) and carotid atherosclerosis presented inconsistent results. Moreover, combined effect of pollutants on carotid atherosclerosis was not fully explored. We aimed to investigate the association between long-term individual time-weighted average exposure to PM2.5 and PM10 and the risk of carotid atherosclerosis, and further explore the overall effect of co-exposure to pollutants on carotid atherosclerosis. METHODS: The study population included 3069 participants derived from the Beijing Health Management Cohort (BHMC) study. Daily concentration of ambient air pollutants was estimated by land-use regression model at both residential and work addresses, and one- and two-year time-weighted average individual exposure was calculated by further considering personal activity pattern and infiltration of ambient air pollution indoors. We explored the association of PM2.5 and PM10 with carotid atherosclerosis and pooled the overall effect of co-exposure to ambient air pollutants by quantile g-computation. RESULTS: A significant association between time-weighted average exposure to PM2.5 and PM10 and carotid atherosclerosis was observed. Per interquartile range increase in two-year exposure to PM2.5 (Hazard ratio (HR): 1.322, 95% confidence interval (CI): 1.219-1.434) and PM10 (HR:1.213, 95% CI: 1.116-1.319) showed the strongest association with carotid atherosclerosis, respectively. Individuals in higher quartiles of pollutants were at higher risk for carotid atherosclerosis compared with those in the lowest quartile group. Concentration response functions documented the nearly linear and nonlinear relationship and interpreted the upward trends of the risk for carotid atherosclerosis with increasing level of pollutant concentrations. Moreover, effect estimates for the mixture of pollutants and carotid atherosclerosis were larger than any of the individual pollutants (HR (95% CI) was 1.510 (1.338-1.704) and 1.613 (1.428-1.822) per quartile increase for one-year and two-year time-weighted average exposure, respectively). CONCLUSIONS: Individual time-weighted average exposure to PM2.5 and PM10 was associated with carotid atherosclerosis. Co-exposure to ambient air pollution was also positively associated with carotid atherosclerosis.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Humanos , Material Particulado/efeitos adversos , Material Particulado/análise , Pequim/epidemiologia , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , China/epidemiologiaRESUMO
Background: Previous studies have reported the separate association of arterial stiffness (AS) and blood pressure with peripheral arterial disease (PAD). Objectives: The aim of this study was to investigate the risk stratification capacity of AS on incident PAD beyond blood pressure status. Methods: A total of 8,960 participants from Beijing Health Management Cohort were enrolled at the first health visit between 2008 and 2018 and then followed until the incidence of PAD or 2019. Elevated AS was defined as brachial-ankle pulse-wave velocity (baPWV) >1,400 cm/s, including moderate stiffness (1,400 ≤ baPWV <1,800 cm/s) and severe stiffness (baPWV ≥1,800 cm/s). PAD was defined as ankle-brachial index <0.9. A frailty Cox model was used to calculate the HR, integrated discrimination improvement, and net reclassification improvement. Results: During follow-up, 225 participants (2.5%) developed PAD. After adjusting for confounding factors, the highest risk for PAD was observed in the group with elevated AS and blood pressure (HR: 2.253; 95% CI: 1.472-3.448). Among participants with ideal blood pressure and those with well-controlled hypertension, PAD risk was still significant for severe AS. The results remained consistent in multiple sensitivity analyses. In addition, baPWV significantly improved the predictive capacity for PAD risk beyond systolic and diastolic blood pressures (integrated discrimination improvement 0.020 and 0.190, net reclassification improvement 0.037 and 0.303). Conclusions: This study suggests the clinical importance of combined evaluation and control of AS and blood pressure for the risk stratification and prevention of PAD.
RESUMO
BACKGROUND AND AIM: Conflicting results suggest a link between serum uric acid and diabetes and previous studies ignored the effect of continuous exposure of serum uric acid on diabetes risk. This study aims to characterize hyperuricemia trajectories in middle-aged adults and to examine its potential impact on diabetes risk, considering the role of obesity, dyslipidemia, and hypertension. METHODS AND RESULTS: The cohort included 9192 participants who were free of diabetes before 2013. The hyperuricemia trajectories during 2009-2013 were identified by latent class growth models. Incident diabetes during 2014-2018 was used as the outcome. Modified Poisson regression models were used to assess the association of trajectories with diabetes. Furthermore, marginal structural models were used to estimate the mediating effects of the relationship between hyperuricemia trajectories and diabetes. We identified three discrete hyperuricemia trajectories: high-increasing (n = 5794), moderate-stable (n = 2049), and low-stable (n = 1349). During 5 years of follow-up, we documented 379 incident diabetes cases. Compared with the low-stable pattern, the high-increasing pattern had a higher risk of developing diabetes (RR, 1.42; 95% CI: 1.09-1.84). In addition, the percentages of total effect between the high-increasing hyperuricemia pattern and diabetes mediated by obesity, dyslipidemia, and hypertension were 24.41%, 18.26%, and 6.29%. However, the moderate-stable pattern was not associated with an increased risk of diabetes. CONCLUSIONS: These results indicate that the high-increasing hyperuricemia trajectory is significantly associated with an increased risk of diabetes. Furthermore, obesity, dyslipidemia, and hypertension play mediating roles in the relationship between the high-increasing hyperuricemia pattern and increased diabetes risk.