Presenter: Fan Wu
Paper: Influence of Environment and Lifestyle on Incidence and Progress of Amyotrophic Lateral Sclerosis in A German ALS Population
Authors: Sonja Korner, Johanna Kammeyer, Antonia Zapf, Magdalena Kuzma-Kozakiewicz, Maria
Piotrkiewicz, Bożenna Kuraszkiewicz, Hanna Goszczynska, Marta Gromicho, Julian
Grosskreutz, Peter M. Andersen, Mamede de Carvalho, Susanne Petri
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease mainly affecting upper and
lower motor neurons in the brain and spinal cord. Pathogenesis of ALS is still unclear, and a multifactorial etiology is presumed. The remarkable clinical heterogeneity between different phenotypes of ALS patients suggests that environmental and lifestyle factors could play a role in onset and progression of ALS. We analyzed a cohort of 117 ALS patients and 93 controls. ALS patients and controls were compared regarding physical activity, dietary habits, smoking, residential environment, potentially toxic environmental factors and profession before symptom onset and throughout the disease course. Data were collected by a personal interview. For statistical analysis descriptive statistics, statistical tests and analysis of variance were used. ALS patients and controls did not differ regarding smoking, diet and extent of physical training. No higher frequency of toxic influences could be detected in the ALS group. ALS patients lived in rural environment considerably more often than the control persons, but this was not associated with a higher percentage of occupation in agriculture. There was also a higher percentage of university graduates in the ALS group. Patients with bulbar onset were considerably more often born in an urban environment as compared to spinal onset. Apart from education and environment, ALS phenotypes did not differ in any investigated environmental or life-style factor. The rate of disease progression was not influenced by any of the investigated environmental and life-style factors. The present study could not identify any dietary habit, smoking, physical activity, occupational factor as well as toxic influences as risk factor or protective factor for onset or progression of ALS. Living in rural environment and higher education might be associated with higher incidence of ALS.
The Department of Environmental and Occupational Health presents:
“Zinc homeostasis in the lung in health and disease”
Bruce R. Pitt, PhD
Professor, Environmental and Occupational Health
Professor, Pharmacology and Chemical Biology
Department of Environmental and Occupational Health
Graduate School of Public Health
University of Pittsburgh
Friday, January 31, 2020
1:00 pm – 2:00 pm
Conference Room 1155 - Public Health
Presented by Beth L. Roman, associate professor of human genetics, member of the Heart, Lung, and Blood Vascular Medicine Institute, and basic research director, HHT Center.
Presenter: Jenna Kuhn
Paper: Organophosphorus pesticide chlorpyrifos intake promotes obesity and insulin resistance through impacting gut and gut microbiota
Authors: Yiran Liang, Jing Zhan, Donghui Liu, Mai Luo, Jiajun Han, Xueke Liu, Chang Liu, Zheng Cheng, Zhiqiang Zhou, and Peng Wang
Disruption of the gut microbiota homeostasis may induce low-grade inflammation leading to obesity-associated diseases. A major protective mechanism is to use the multi-layered mucus structures to keep a safe distance between gut epithelial cells and microbiota. To investigate whether pesticides would induce insulin resistance/obesity through interfering with mucus-bacterial interactions, we conducted a study to determine how long-term exposure to chlorpyrifos affected C57Bl/6 and CD-1 (ICR) mice fed high- or normal-fat diets. To further investigate the effects of chlorpyrifos-altered microbiota, antibiotic treatment and microbiota transplantation experiments were conducted.
The results showed that chlorpyrifos caused broken integrity of the gut barrier, leading to increased lipopolysaccharide entry into the body and finally low-grade inflammation, while genetic background and diet pattern have limited influence on the chlorpyrifos-induced results. Moreover, the mice given chlorpyrifos-altered microbiota had gained more fat and lower insulin sensitivity.
Our results suggest that widespread use of pesticides may contribute to the worldwide epidemic of inflammation-related diseases.
Presenter: Grace Tengziyi Ge
Paper: Marine n−3 Fatty Acids and Prevention of Cardiovascular Disease and Cancer
Authors: JoAnn E. Manson, M.D., Dr.P.H., Nancy R. Cook, Sc.D., I‑Min Lee, M.B., B.S., Sc.D., William Christen, Sc.D., Shari S. Bassuk, Sc.D., Samia Mora, M.D., M.H.S.,Heike Gibson, Ph.D., Christine M. Albert, M.D.,M.P.H., David Gordon, M.A.T.,Trisha Copeland, M.S., R.D., Denise D’Agostino, B.S., Georgina Friedenberg, M.P.H., Claire Ridge, M.P.H., Vadim Bubes, Ph.D., Edward L. Giovannucci, M.D., Sc.D., Walter C. Willet, M.D., Dr.P.H., and Julie E. Buring, Sc.D.,
Higher intake of marine n−3 (also called omega-3) fatty acids has been associated with reduced risks of cardiovascular disease and cancer in several observational studies. Whether supplementation with n−3 fatty acids has such effects in general populations at usual risk for these end points is unclear.
We conducted a randomized, placebo-controlled trial, with a two-by-two factorial design, of vitamin D3 (at a dose of 2000 IU per day) and marine n−3 fatty acids (at a dose of 1 g per day) in the primary prevention of cardiovascular disease and cancer among men 50 years of age or older and women 55 years of age or older in the United States. Primary end points were major cardiovascular events (a composite of myocardial infarction, stroke, or death from cardiovascular causes) and invasive cancer of any type. Secondary end points included individual components of the composite cardiovascular end point, the composite end point plus coronary revascularization (expanded composite of cardiovascular events), site-specific cancers, and death from cancer. Safety was also assessed. This article reports the results of the comparison of n−3 fatty acids with placebo.
A total of 25,871 participants, including 5106 black participants, underwent randomization. During a median follow-up of 5.3 years, a major cardiovascular event occurred in 386 participants in the n−3 group and in 419 in the placebo group (hazard ratio, 0.92; 95% confidence interval [CI], 0.80 to 1.06; P = 0.24). Invasive cancer was diagnosed in 820 participants in the n−3 group and in 797 in the placebo group (hazard ratio, 1.03; 95% CI, 0.93 to 1.13; P = 0.56). In the analyses of key secondary end points, the hazard ratios were as follows: for the expanded composite end point of cardiovascular events, 0.93 (95% CI, 0.82 to 1.04); for total myocardial infarction, 0.72 (95% CI, 0.59 to 0.90); for total stroke, 1.04 (95% CI, 0.83 to 1.31); for death from cardiovascular causes, 0.96 (95% CI, 0.76 to 1.21); and for death from cancer (341 deaths from cancer), 0.97 (95% CI, 0.79 to 1.20). In the analysis of death from any
cause (978 deaths overall), the hazard ratio was 1.02 (95% CI, 0.90 to 1.15). No excess risks of bleeding or other serious adverse events were observed.
Supplementation with n−3 fatty acids did not result in a lower incidence of major cardiovascular events or cancer than placebo. (Funded by the National Institutes of Health and others; VITAL ClinicalTrials.gov number, NCT01169259.)
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Last Updated On Tuesday, January 22, 2019 by Orbell, Adam W
Created On Tuesday, January 22, 2019
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