23 research outputs found
Effect of n-3 (Omega-3) polyunsaturated fatty acid supplementation on metabolic and inflammatory biomarkers and body weight in patients with Type 2 Diabetes Mellitus: a systematic review and meta-analysis of RCTs
Beneficial effects of n-3 fatty acids on metabolic biomarkers in patients with type 2 diabetes (T2DM) has been reported. The objectives of this current research were to investigate the effects of n-3 supplementation on metabolic factors, weight, and body mass index (BMI) in patients with type 2 diabetes mellitus (T2DM), using a meta-analysis of randomized, controlled trials (RCTs). Online databases PubMed, Embase, Web of Science, and Science Direct were searched until 2021 to identify eligible articles. Thirty-two trials were included. The results showed that n-3 consumption can significantly reduce glycemic factors including fasting blood sugar (FBS) (β0.36 (β0.71 to β0.01)), glycated hemoglobulin (HbA1c) (β0.74 (β1.13 to β0.35)), and homeostatic model assessment of insulin resistance (HOMA.IR) (β0.58 (β1.13 to β0.03)). Furthermore, significant improvement in lipid profile including triglycerides (TG) (β0.27 (β0.37 to β0.18)), total cholesterol (β0.60 (β0.88 to β0.32)), low density lipoprotein (LDL) (β0.54 (β0.85 to β0.23)), and high-density lipoprotein (HDL) (0.60 (0.23 to 0.96)) levels were found in the present meta-analysis. The reduction in the inflammatory markerβs tumor necrosis factor-alpha (TNF-Ξ±) (β0.13 (β0.75 to 0.48)) and c-reactive protein (CRP) (β0.72 (β1.70 to 0.27)), as well as weight (β0.09 (β0.24 to 0.07)) and BMI (β0.13 (β0.29 to 0.02)) were not statistically significant. Furthermore, the findings revealed that the optimal dose and duration of n-3 consumption for patients with T2DM is 1000β2000 mg/d for more than 8 weeks. The present meta-analysis and review reveals that n-3 supplementation can improve glycemic factors and lipid profile in patients with T2DM. Furthermore, n-3 supplementation may provide beneficial effects on inflammatory markers and body weight if used at the appropriate dose and duration
Physics-Informed Deep Learning to Reduce the Bias in Joint Prediction of Nitrogen Oxides
Atmospheric nitrogen oxides (NOx) primarily from fuel combustion have
recognized acute and chronic health and environmental effects. Machine learning
(ML) methods have significantly enhanced our capacity to predict NOx
concentrations at ground-level with high spatiotemporal resolution but may
suffer from high estimation bias since they lack physical and chemical
knowledge about air pollution dynamics. Chemical transport models (CTMs)
leverage this knowledge; however, accurate predictions of ground-level
concentrations typically necessitate extensive post-calibration. Here, we
present a physics-informed deep learning framework that encodes
advection-diffusion mechanisms and fluid dynamics constraints to jointly
predict NO2 and NOx and reduce ML model bias by 21-42%. Our approach captures
fine-scale transport of NO2 and NOx, generates robust spatial extrapolation,
and provides explicit uncertainty estimation. The framework fuses
knowledge-driven physicochemical principles of CTMs with the predictive power
of ML for air quality exposure, health, and policy applications. Our approach
offers significant improvements over purely data-driven ML methods and has
unprecedented bias reduction in joint NO2 and NOx prediction
Differential Cytotoxicity and Reactive Oxygen Species Generation in Pulmonary and Aortic Cells Exposed to Inorganic Arsenic and Monomethylarsonous Acid
Chronic ingestion of arsenic (As), a common ground water contaminant, has demonstrated to result in numerous deleterious health outcomes including black foot disease, various cancers, and hyperpigmentation. Chronic arsenic ingestion has also been associated with the development of atherosclerosis and hypertension, though the cellular mechanisms have not been well elucidated. Recent studies have shown that an arsenic metabolite, monomethylarsonous acid (MMAs), causes a higher degree of toxicity than inorganic arsenic (iAs) and may be linked to arsenic-induced vascular diseases. This study explores possible reactive oxygen species that may contribute to atherosclerosis and examines the different cytotoxic effects of iAs and MMAs on thoracic aorta smooth muscle cells (A7r5) and rat pulmonary arterial smooth muscle cells (rPASMC) in culture to look for the generation of malondialdehyde, hydrogen peroxide, and superoxide. Cytotoxicity was determined by cell counts and Trypan Blue exclusion, MTT assay, and light microscopy to study altered smooth muscle cell morphology, cell viability and cytotoxicity. Cells treated with various concentrations of either iAs and MMAs displayed cytotoxic effects and MMAs was significantly more toxic in both A7r5 and rPASMC. After a 24 hour exposure the LC50 in A7r5 treated with iAs was determined to be 11 Β΅M, and 700 nM when treated with MMAs. In rPASMC treated with iAs the LC50 was determined to be 26.5 Β΅M, and 4 Β΅M with MMAs treatment showing higher toxicity in A7r5 cells than in rPASMC. No significant difference in MDA formation or superoxide production was observed with treatment of iAs and MMAs in both A7r5 and rPASMC. Hydrogen peroxide was measured in the extracellular medium of rPASMC and displayed a 12% increase after a 2 hour treatment with 100 nM (p=0.006) iAs and 1 Β΅M iAs (p=0.0002) when compared to untreated cells, a 7% increase when treated with 1 Β΅M MMAs (p=0.03) and a 9% increase when treated with 10 Β΅M MMAs (p=0.0003). In A7r5 cells there was a significant increase in the release of hydrogen peroxide with exposure to 1 Β΅M MMAs displaying a 59% increase (p=0.0169) and 10 Β΅M MMAs displaying a 70% increase (p=0.003) when compared to untreated cells.These results suggest that the increased toxicity of MMAs could be due to increased hydrogen peroxide activity in A7r5 cells, but is not due solely due to oxidative stress when analyzed in vitro. Other mechanisms need to be further explored to understand the association between arsenic and cardiovascular disease
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Prenatal and Early-Life Environmental Exposures and Asthma Risk among Children
Asthma is a chronic lung disease in which the airways become inflamed and produce increased mucus making air flow in and out of the lungs difficult. With the prevalence of asthma higher among children compared to adults, possible environmental exposures that may lead to asthma exacerbations in children were investigated. In-utero exposures to environmental contaminants may increase the risk for asthma development and exacerbations in children and those living near a Superfund Site may be more susceptible. Additionally, early-life exposure to particulate matter with a diameter of 2.5 micrometers or less (PM2.5) may increase the risk of asthma exacerbations.Extensive exposure measurements available from a well-characterized longitudinal birth cohort study, the New Bedford Cohort (NBC), which consisted of mothers who were pregnant and living near the New Bedford Harbor (NBH) Superfund Site from 1993-1998, were used to develop prediction models for a much larger population-based dataset of relative sociodemographic risk factors available from the Pregnancy to Early Life Longitudinal (PELL) data system. Prediction models were created for cord-serum polychlorinated biphenyls (PCBs), Ο,Οβ²-dichlorodiphenyl dichloroethylene (DDE), hexachlorobenzene (HCB), cord blood lead (Pb), and maternal hair mercury (Hg). Combinations of these contaminants along with non-chemical exposures including distance to nearest roadway and distance to the NBH were analyzed to determine whether prenatal exposures were associated with asthma exacerbations in children. Findings suggest that certain prenatal joint exposures increase the risk of asthma exacerbations among children.The association between early-life exposure to PM2.5 and the risk of asthma or wheeze hospitalizations, emergency department visits or observational stays was also investigated among children in the PELL data system. Daily PM2.5 concentrations were estimated at a 4-km resolution using satellite remote sensing, land use, and meteorological data. Asthma or wheeze exacerbations among low birthweight children were associated with short-term increases in PM2.5 concentrations at low levels in Massachusetts in stratified analyses. Overall, results suggest that prenatal environmental exposures may increase the risk of asthma or wheeze among children
Recommended from our members
Prenatal and Early-Life Environmental Exposures and Asthma Risk among Children
Asthma is a chronic lung disease in which the airways become inflamed and produce increased mucus making air flow in and out of the lungs difficult. With the prevalence of asthma higher among children compared to adults, possible environmental exposures that may lead to asthma exacerbations in children were investigated. In-utero exposures to environmental contaminants may increase the risk for asthma development and exacerbations in children and those living near a Superfund Site may be more susceptible. Additionally, early-life exposure to particulate matter with a diameter of 2.5 micrometers or less (PM2.5) may increase the risk of asthma exacerbations.Extensive exposure measurements available from a well-characterized longitudinal birth cohort study, the New Bedford Cohort (NBC), which consisted of mothers who were pregnant and living near the New Bedford Harbor (NBH) Superfund Site from 1993-1998, were used to develop prediction models for a much larger population-based dataset of relative sociodemographic risk factors available from the Pregnancy to Early Life Longitudinal (PELL) data system. Prediction models were created for cord-serum polychlorinated biphenyls (PCBs), Ο,Οβ²-dichlorodiphenyl dichloroethylene (DDE), hexachlorobenzene (HCB), cord blood lead (Pb), and maternal hair mercury (Hg). Combinations of these contaminants along with non-chemical exposures including distance to nearest roadway and distance to the NBH were analyzed to determine whether prenatal exposures were associated with asthma exacerbations in children. Findings suggest that certain prenatal joint exposures increase the risk of asthma exacerbations among children.The association between early-life exposure to PM2.5 and the risk of asthma or wheeze hospitalizations, emergency department visits or observational stays was also investigated among children in the PELL data system. Daily PM2.5 concentrations were estimated at a 4-km resolution using satellite remote sensing, land use, and meteorological data. Asthma or wheeze exacerbations among low birthweight children were associated with short-term increases in PM2.5 concentrations at low levels in Massachusetts in stratified analyses. Overall, results suggest that prenatal environmental exposures may increase the risk of asthma or wheeze among children
Early-life exposure to PM2.5 and risk of acute asthma clinical encounters among children in Massachusetts: a case-crossover analysis.
Using Birth Cohort Data to Estimate Prenatal Chemical Exposures for All Births around the New Bedford Harbor Superfund Site in Massachusetts.
Correction to: Early-life exposure to PM2.5 and risk of acute asthma clinical encounters among children in Massachusetts: a case-crossover analysis.
Using Birth Cohort Data to Estimate Prenatal Chemical Exposures for All Births around the New Bedford Harbor Superfund Site in Massachusetts.
Effect of <i>n</i>-3 (Omega-3) Polyunsaturated Fatty Acid Supplementation on Metabolic and Inflammatory Biomarkers and Body Weight in Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis of RCTs
Beneficial effects of n-3 fatty acids on metabolic biomarkers in patients with type 2 diabetes (T2DM) has been reported. The objectives of this current research were to investigate the effects of n-3 supplementation on metabolic factors, weight, and body mass index (BMI) in patients with type 2 diabetes mellitus (T2DM), using a meta-analysis of randomized, controlled trials (RCTs). Online databases PubMed, Embase, Web of Science, and Science Direct were searched until 2021 to identify eligible articles. Thirty trials were included. The results showed that n-3 consumption can significantly reduce glycemic factors including fasting blood sugar (FBS) (β0.36 (β0.71 to β0.01)), glycated hemoglobulin (HbA1c) (β0.74 (β1.13 to β0.35)), and homeostatic model assessment of insulin resistance (HOMA.IR) (β0.58 (β1.13 to β0.03)). Furthermore, significant improvement in lipid profile including triglycerides (TG) (β0.27 (β0.37 to β0.18)), total cholesterol (β0.60 (β0.88 to β0.32)), low density lipoprotein (LDL) (β0.54 (β0.85 to β0.23)), and high-density lipoprotein (HDL) (0.60 (0.23 to 0.96)) levels were found in the present meta-analysis. The reduction in the inflammatory markerβs tumor necrosis factor-alpha (TNF-Ξ±) (β0.13 (β0.75 to 0.48)) and c-reactive protein (CRP) (β0.72 (β1.70 to 0.27)), as well as weight (β0.09 (β0.24 to 0.07)) and BMI (β0.13 (β0.29 to 0.02)) were not statistically significant. Furthermore, the findings revealed that the optimal dose and duration of n-3 consumption for patients with T2DM is 1000β2000 mg/d for more than 8 weeks. The present meta-analysis and review reveals that n-3 supplementation can improve glycemic factors and lipid profile in patients with T2DM. Furthermore, n-3 supplementation may provide beneficial effects on inflammatory markers and body weight if used at the appropriate dose and duration