RESUMO
OBJECTIVE: This study aimed to examine the temporal relationship between body mass index (BMI) and uric acid (UA), and their joint effect on blood pressure (BP) in children and adults. METHODS: The longitudinal cohorts for temporal relationship analyses consisted of 564 and 911 subjects examined twice 5-14 years apart from childhood to adulthood. The cross-sectional cohorts for mediation analyses consisted of 3102 children and 3402 nondiabetic adults. Cross-lagged panel analysis models were used to examine the temporal relationship between BMI and UA, and mediation analysis models the mediation effect of UA on the BMI-BP association. RESULTS: After adjusting for age, race, sex and follow-up years in children, and additionally smoking and alcohol drinking in adults, the path coefficients (standardized regression coefficients) from baseline BMI to follow-up UA (0.145 in children and 0.068 in adults) were significant, but the path coefficients from baseline UA to follow-up BMI (0.011 in children and 0.016 in adults) were not. In mediation analyses, indirect effects through UA on the BMI-systolic BP association were estimated at 0.028 (mediation effect = 8.8%) in children and 0.033 (mediation effect = 13.5%) in adults (P < 0.001 for both). Direct effects of BMI on systolic BP (0.289 in children and 0.212 in adults) were significant. The mediation effect parameters did not differ significantly between Blacks and Whites. CONCLUSIONS: Changes in BMI precede alterations in UA, and the BMI-BP association is in part mediated through BMI-related increase in UA both in children and in adults. These findings have implications for addressing mechanisms of obesity hypertension beginning in early life.
Assuntos
Pressão Sanguínea/fisiologia , Índice de Massa Corporal , Hipertensão/epidemiologia , Ácido Úrico/sangue , Adolescente , Adulto , Criança , Pré-Escolar , Feminino , Humanos , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Obesidade Infantil/epidemiologia , Adulto JovemRESUMO
The removal of excessive amounts of nitrate and phosphate from water sources, especially agricultural wastewater, has been of high significance to control eutrophication in aquatic systems. Here, a new method is reported for the removal of nitrate and phosphate simultaneously from wastewater based on the combination of the solution-phased adsorption (ADS) and dielectrophoresis (DEP) techniques. The plant ash was first selected as the adsorbent by screening tests, followed by a systematic investigation of using the adsorbent to remove nitrate and phosphate from wastewater under various experimental conditions, including the testing of adsorbent dosage, pretreatment time, water flow rate, and electrode voltage. The analysis of the adsorbent particles was also performed by scanning electron microscope (SEM) analysis, the energy dispersive X-ray spectroscopy (EDX) test, and the measurement of Zeta potentials. Compared with the ADS method alone, the introduction of DEP into the purification process has greatly increased the removal rate by 66.06% for nitrate and 43.04% for phosphate, respectively. In the meantime, it is observed that the processing time has been greatly reduced by 92% with the assistance of DEP.
Assuntos
Nitratos , Poluentes Químicos da Água , Adsorção , Eutrofização , Concentração de Íons de Hidrogênio , Cinética , Nitratos/análise , Fosfatos/química , Poluentes Químicos da Água/análiseRESUMO
The neurotoxicity caused by cadmium (Cd) is well known in humans and experimental animals. However, there is no effective treatment for its toxicity. In this study, we established Cd toxicity models in cultured cells or mice to investigate the detoxification effect of edaravone (Eda). We found that Eda protected GL261 cells from Cd toxicity and prevented the loss of cell viability. In Cd-exposed mice, liver, kidney and testicular damage, as well as cognitive dysfunction were observed. Oxidative stress and inflammatory responses, such as decreased SOD and CAT, increased LDH and MDA, and abnormal changes in the inflammatory factors TNF-α, IL-1ß, IL-6 and IL-10 were detected in serum and brain tissue. Eda protected mice from Cd-induced toxicity and abrogated oxidative stress and inflammatory responses. Also, Eda prevented inflammatory activation of microglia and astrocytes and was accompanied by restoration of the neuronal marker protein MAP2, indicating restoration of neuronal function. In addition, the BDNF-TrkB/Akt and Notch/HES-1 signaling axes were involved in the response of Eda to the elimination of Cd toxicity. In conclusion, Eda does contribute to the clearance of Cd-induced toxicity.
Assuntos
Encéfalo/efeitos dos fármacos , Cádmio/toxicidade , Edaravone/farmacologia , Sequestradores de Radicais Livres/farmacologia , Mediadores da Inflamação/antagonistas & inibidores , Estresse Oxidativo/efeitos dos fármacos , Animais , Encéfalo/metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/fisiologia , Disfunção Cognitiva/induzido quimicamente , Disfunção Cognitiva/tratamento farmacológico , Disfunção Cognitiva/metabolismo , Relação Dose-Resposta a Droga , Edaravone/uso terapêutico , Sequestradores de Radicais Livres/uso terapêutico , Mediadores da Inflamação/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos ICR , Estresse Oxidativo/fisiologiaRESUMO
[Figure: see text].
Assuntos
Pressão Sanguínea/fisiologia , Hemodinâmica/fisiologia , Hipertensão/fisiopatologia , Hipertrofia Ventricular Esquerda/fisiopatologia , Adulto , Estudos de Coortes , Feminino , Ventrículos do Coração/patologia , Ventrículos do Coração/fisiopatologia , Humanos , Hipertensão/diagnóstico , Hipertrofia Ventricular Esquerda/diagnóstico , Masculino , Pessoa de Meia-Idade , Medição de Risco/métodos , Medição de Risco/estatística & dados numéricos , Fatores de Risco , Adulto JovemRESUMO
BACKGROUND: It has been controversial whether to adjust for current body weight while examining the relationship between birthweight and blood pressure (BP). OBJECTIVE: The present study aims to partition the total effect of birthweight on BP into its direct effect and indirect effect through current body mass index (BMI). METHODS: The study cohort consisted of 6251 participants who had birthweight information with 13 443 observations on BMI and BP in pre-adolescence (4-11 years), adolescence (12-19 years), young adulthood (20-30 years) and mid-adulthood (31-58 years). General third-variable models were used to distinguish the mediation and suppression effects of current BMI on the birthweight-BP association at different ages. RESULTS: The total effect of birthweight on systolic BP measured as standardized regression coefficient (ß) without current BMI included in the model was 0.003 (P = .810) in pre-adolescents, -0.032 (P = .029) in adolescents, -0.066 (P = .002) in young adults and -0.051 (P = .023) in midlife adults. With additional adjustment for BMI, the direct effect of birthweight on systolic BP was strengthened to ß = -0.066 (P = .013), ß = -0.058 (P = .014), ß = -0.094 (P = .020), ß = -0.066 (P = .023); the suppression effects of BMI were calculated at 0.070, 0.027, 0.028 and 0.015 in the respective age groups. The decreasing trend of suppression effects with increasing age mimicked the trends of birthweight-BMI and BMI-BP correlations. CONCLUSIONS: Current body weight has a suppression effect, not a mediation effect, on the birthweight-BP association, with pre-adolescents having the greatest suppression effect. The suppression effect is predominantly determined by birthweight-BMI and BMI-BP correlations.
Assuntos
Peso ao Nascer/fisiologia , Pressão Sanguínea/fisiologia , Índice de Massa Corporal , Adolescente , Adulto , Distribuição por Idade , Criança , Pré-Escolar , Feminino , Humanos , Hipertensão/epidemiologia , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Adulto JovemRESUMO
This study aimed to dissect the direct effect of smoking and its indirect effect through body mass index (BMI) on leukocyte telomere length (LTL) and to distinguish the mediation and suppression effects of BMI. The study cohort included 1,037 adults (729 Whites and 308 African Americans; 42.1% males; mean age: 40.3 years) with LTL measurements by Southern blotting. General third variable models were used to distinguish the mediation and suppression effects of BMI on the smoking-LTL association. After adjusting for age, race, sex and alcohol drinking, the total effect of smoking on LTL was significant (standardized regression coefficient, ß= -0.061, p=0.034) without BMI included in the model. With additional adjustment for BMI, the indirect effect of smoking on LTL through BMI was estimated at ß= 0.011 (p=0.023), and the direct effect of smoking on LTL was strengthened to ß= -0.072 (p=0.012). The results were similar when pack-years of smoking was used. The effect parameters did not differ significantly between race and sex groups. These results suggest that BMI has a suppression effect, not a mediation effect, on the smoking-LTL association, which potentially contributes to previous inconsistencies in the effect of smoking on LTL.
Assuntos
Peso Corporal/genética , Peso Corporal/fisiologia , Fumar Cigarros/efeitos adversos , Fumar Cigarros/genética , Telômero/patologia , Adulto , Negro ou Afro-Americano/genética , Índice de Massa Corporal , Estudos de Coortes , Feminino , Humanos , Leucócitos/patologia , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Fatores Sexuais , Homeostase do Telômero/genética , Homeostase do Telômero/fisiologia , Encurtamento do Telômero/genética , Encurtamento do Telômero/fisiologia , População Branca/genéticaRESUMO
OBJECTIVES: The study assessed the hypothesis that smoking strengthens the association of adult arterial stiffness with long-term cumulative burden of blood pressure (BP) from childhood to adulthood. BACKGROUNDS: Tobacco smoking and elevated BPs are important risk factors of vascular stiffness. However, the synergistic effect of these two risk factors is not well established, especially for the long-term burden of elevated BP since childhood. METHODS: The study cohort consisted of 945 adults (661 whites and 284 blacks, aged 24-43 years) who have BP measured 4-15 times since childhood (aged 4-17 years) in Bogalusa, Louisiana. The adult arterial stiffness was measured as aorta-femoral pulse wave velocity (afPWV); the total area under the curve (AUC) and incremental AUC were used as a measure of long-term burden and trends of BP, respectively. RESULTS: Increased adult afPWV was significantly associated with higher adulthood (Pâ<â0.001), total AUC (Pâ<â0.001) and incremental AUC (Pâ<â0.001) values of SBP and DBP, but not with childhood BP, after adjusting for age, race, sex, BMI and heart rate. Furthermore, smoking was a significant predictor of increased adult afPWV and BP levels. In the interaction analyses, the increasing trend of afPWV with increasing adult SBP (Pâ=â0.009) and its incremental AUC (Pâ=â0.007) were significantly greater among the current smokers than among the nonsmokers. DBP showed a similar pattern regarding the smoking-BP interaction on afPWV. CONCLUSION: These results, by showing the synergistic effect of tobacco smoking and long-term BP measures from childhood to adulthood on arterial stiffening process, underscore the importance of undertaking preventive strategies early in life and smoking behavior control.
Assuntos
Pressão Sanguínea , Fumar/efeitos adversos , Rigidez Vascular , Adolescente , Adulto , Aorta/fisiopatologia , Área Sob a Curva , Artérias/fisiologia , População Negra , Criança , Pré-Escolar , Estudos de Coortes , Feminino , Frequência Cardíaca , Humanos , Hipertensão/fisiopatologia , Louisiana/epidemiologia , Masculino , Análise de Onda de Pulso , Fatores de Risco , População Branca , Adulto JovemRESUMO
BACKGROUND: Secondhand smoke (SHS) exposure increases cardiovascular disease risk. The objective of this study was to examine the association of SHS exposure in childhood and adulthood with adult arterial thickness. METHODS: The study cohort consisted of 415 nonsmoking adults (301 whites and 114 blacks; ages 26.2-48.0 years) enrolled in 2004-2010. The arterial wall thickness was measured as common, bulb and internal carotid artery intima-media thickness (IMT). SHS exposure data in childhood and adulthood were obtained by a questionnaire survey. RESULTS: Increased adult composite carotid IMT was significantly associated with SHS exposure (regression coefficient, ß = 53.1 µm, p < 0.001) after adjusting for race, age, gender, education, income, body mass index, systolic blood pressure, LDL cholesterol and triglycerides/HDL cholesterol ratio, with blacks (ß = 81.2 µm, p = 0.005) and whites (ß = 38.9 µm, p = 0.017) showing the same direction of the association. Furthermore, the SHS exposure in childhood showed a relatively stronger association with increased carotid IMT than the exposure in adulthood based on standardized ßs (0.180 vs. 0.106); the same trend in the difference between childhood and adulthood exposure was noted for duration of SHS exposure (0.186 vs. 0.145). The covariates-adjusted composite carotid IMT showed a significant increasing trend by the order of exposure status of none, adulthood only, childhood only and both (p for trend<0.001). CONCLUSIONS: If the relationship is causal, the associations observed in this study suggest that more awareness should be raised on the dangers of SHS exposure during childhood so that its effect may be mitigated and controlled early in the cardiovascular disease process.
Assuntos
Doenças das Artérias Carótidas/diagnóstico por imagem , Doenças das Artérias Carótidas/epidemiologia , Artéria Carótida Primitiva/diagnóstico por imagem , Espessura Intima-Media Carotídea , Exposição Ambiental/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Adulto , Negro ou Afro-Americano , Fatores Etários , Doenças das Artérias Carótidas/etnologia , Artéria Carótida Interna/diagnóstico por imagem , Feminino , Humanos , Louisiana/epidemiologia , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Estudos Retrospectivos , Medição de Risco , Fatores de Risco , Inquéritos e Questionários , Fatores de Tempo , População BrancaRESUMO
Age and metabolic syndrome are major risk factors for atherosclerosis. However, limited information is available regarding whether cigarette smoking, another major, modifiable risk factor, has synergistic effects with age and metabolic syndrome on subclinical atherosclerosis, particularly in young adults. This aspect was examined in 1,051 adults (747 whites and 304 blacks; aged 24-43 years) from the Bogalusa Heart Study. General linear models were used to examine the effects of cigarette smoking and its interactive effects with age and metabolic syndrome on carotid intima-media thickness (CIMT). After adjusting for age, race, and sex, current smokers had lower BMI (mean ± SE: 27.4 ± 0.4, 29.3 ± 0.5, and 29.9 ± 0.3 kg/m2 in current, former, and never smokers, respectively; p<0.0001) and lower levels of fasting glucose (82.8 ± 0.9, 89.5 ± 2.3, and 87.1 ± 1.1 mg/dL, respectively; p = 0.001) and insulin (10.6 ± 0.4, 14.2 ± 1.0, 13.6 ± 0. 6 µU/ml, respectively; p<0.0001). Despite being lean and having favorable levels of glucose and insulin, current smokers had greater CIMT (0.850 ± 0.012, 0.808 ± 0.011, and 0.801 ± 0.006 mm, respectively; p = 0.0004). Importantly, cigarette smoking showed significant interactions with age and metabolic syndrome on CIMT: Age-related change in CIMT in current smokers was significantly greater (0.013 ± 0.002 mm/year) than in nonsmokers (former and never smokers combined) (0.008 ± 0.001 mm/year) (p for interaction = 0.005); the difference in CIMT between those with and without metabolic syndrome was significantly greater in current smokers (0.154 ± 0.030 mm, p<0.0001) than in nonsmokers (0.031 ± 0.014 mm, p = 0.03) (p for interaction<0.0001). In conclusion, cigarette smoking significantly exacerbates the adverse effects of age and metabolic syndrome on subclinical atherosclerosis in young adults, which underscores the importance of prevention and cessation of cigarette smoking behavior in the young.
Assuntos
Envelhecimento , Aterosclerose/patologia , Síndrome Metabólica/complicações , Fumar/efeitos adversos , Adulto , Fatores Etários , Aterosclerose/sangue , Aterosclerose/etiologia , Glicemia/metabolismo , Índice de Massa Corporal , Artérias Carótidas/diagnóstico por imagem , Espessura Intima-Media Carotídea , Distribuição de Qui-Quadrado , HDL-Colesterol/sangue , LDL-Colesterol/sangue , Jejum/sangue , Feminino , Humanos , Insulina/sangue , Modelos Lineares , Masculino , Fatores de Risco , Triglicerídeos/sangue , Adulto JovemRESUMO
BACKGROUND: Cardiovascular risk factors in childhood are predictive of adulthood arterial stiffness. However, it is unknown whether this relationship varies by race or sex. METHODS: Six hundred and eighty adults aged 24 to 43 had been followed for an average of 26.3 years, from the Bogalusa Heart Study. Brachial to ankle pulse wave velocity (baPWV) measured by an automatic oscillometric technique was used as the outcome variable for arterial stiffness during adulthood. Body mass index (BMI), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), glucose, and systolic blood pressure (SBP), all measured in childhood, were used as predictors. The average values of childhood measurements at multiple time points were used, standardized to age, race, and sex-specific z-scores. RESULTS: In the total sample, childhood SBP was the only significant predictor (P < 0.001) for adult baPWV. Significant interactions between sex and BMI (P = 0.001), between sex and LDL-C (P = 0.035), and between race and HDL-C (P = 0.002) on adult baPWV were identified. Childhood predictors of adult baPWV were BMI (30.9 cm/s reduction in baPWV per standard deviation increase, 95% confidence interval [CI]: -55.0, -6.9 cm/s), LDL-C (30.8 cm/s increase, 95% CI: 2.9, 59.5 cm/s), and HDL-C (46.8 cm/s reduction, 95% CI: -76.2, -17.4 cm/s) in white males; SBP (38.2 cm/s increase, 95% CI: 11.0, 65.4 cm/s) in white females; BMI (71.3 cm/s reduction, 95% CI: -119.9, -22.7 cm/s) in black males; and none in black females. CONCLUSIONS: The associations of childhood cardiovascular risk factors with adult arterial stiffness varied by race and sex.