المؤلفون: Williams, Jennifer Anne¹, Romero, Vivian C.^2,3, Clinton, Chelsea M.⁴, Vazquez, Delia M.⁵, Marcus, Sheila M.⁶, Chilimigras, Julie L.⁴, Hamilton, Susan E.⁶, Allbaugh, Lucy J.⁶, Vahratian, Anjel M.⁴, Schrader, Ronald M.⁷, Mozurkewich, Ellen L.^4,8 emozurkewich@salud.unm.edu

المصدر: BMC Pregnancy & Childbirth. 8/3/2016, Vol. 16, p1-9. 9p.

مصطلحات موضوعية: *OMEGA-3 fatty acids, *VITAMIN D in human nutrition, *DEPRESSION in women, *POSTPARTUM depression diagnosis, *EDINBURGH Postnatal Depression Scale, *BECK Depression Inventory, *PSYCHIATRIC rating scales, *REGRESSION analysis, *PREVENTION, *PREVENTION of mental depression, *COMPARATIVE studies, *MENTAL depression, *DIETARY supplements, *RESEARCH methodology, *MEDICAL cooperation, *POSTPARTUM depression, *DURATION of pregnancy, *PREGNANCY complications, *PRENATAL diagnosis, *PSYCHOLOGICAL tests, *PUERPERIUM, *QUESTIONNAIRES, *RESEARCH, *RESEARCH funding, *VITAMIN D, *EVALUATION research, *RANDOMIZED controlled trials, *BLIND experiment, *PSYCHOLOGY, PHYSIOLOGICAL effect, PREVENTION of pregnancy complications

مستخلص: Background: Vitamin D insufficiency may be associated with depressive symptoms in non-pregnant adults. We performed this study to evaluate whether low maternal vitamin D levels are associated with depressive symptoms in pregnancy.Methods: This study was a secondary analysis of a randomized trial designed to assess whether prenatal omega-3 fatty acid supplementation would prevent depressive symptoms. Pregnant women from Michigan who were at risk for depression based on Edinburgh Postnatal Depression Scale Score or history of depression were enrolled. Participants completed the Beck Depression Inventory (BDI) and Mini International Neuropsychiatric Interview at 12-20 weeks, 26-28 weeks, 34-36 weeks, and 6-8 weeks postpartum. Vitamin D levels were measured at 12-20 weeks (N = 117) and 34-36 weeks (N = 112). Complete datasets were available on 105 subjects. Using regression analyses, we evaluated the relationship between vitamin D levels with BDI scores as well as with MINI diagnoses of major depressive disorder and generalized anxiety disorder. Our primary outcome measure was the association of maternal vitamin D levels with BDI scores during early and late pregnancy and postpartum.Results: We found that vitamin D levels at 12-20 weeks were inversely associated with BDI scores both at 12-20 and at 34-36 weeks' gestation (P < 0.05, both). For every one unit increase in vitamin D in early pregnancy, the average decrease in the mean BDI score was .14 units. Vitamin D levels were not associated with diagnoses of major depressive disorder or generalized anxiety disorder.Conclusions: In women at risk for depression, early pregnancy low vitamin D levels are associated with higher depressive symptom scores in early and late pregnancy. Future investigations should study whether vitamin D supplementation in early pregnancy may prevent perinatal depressive symptoms.Trial Registration: https://clinicaltrials.govTest/Registration Number: NCT00711971. [ABSTRACT FROM AUTHOR]

المؤلفون: Jang, Jun-Ho^1,2, Bruse, Shannon², Huneidi, Salam³, Schrader, Ronald M.¹, Monick, Martha M.³, Lin, Yong², Carter, A. Brent³, Klingelhutz, Aloysius J.⁴, Nyunoya, Toru^1,2 tnyunoya@lrri.org

المصدر: Environmental Health Perspectives. Sep2014, Vol. 122 Issue 9, p955-962. 8p. 4 Graphs.

مصطلحات موضوعية: *ALDEHYDES, *ANALYSIS of variance, *CELL culture, *CELLULAR aging, *CHROMOSOMES, *ENZYMES, *FIBROBLASTS, *IMMUNOBLOTTING, *LUNGS, *POLYMERASE chain reaction, *RESEARCH funding, *STATISTICS, *WERNER'S syndrome, *DATA analysis, *REVERSE transcriptase polymerase chain reaction, *DESCRIPTIVE statistics, *IN vitro studies

مستخلص: Background: Acrolein is a ubiquitous environmental hazard to human health. Acrolein has been reported to activate the DNA damage response and induce apoptosis. However, little is known about the effects of acrolein on cellular senescence. Objectives: We examined whether acrolein induces cellular senescence in cultured normal human lung fibroblasts (NHLF). Methods: We cultured NHLF in the presence or absence of acrolein and determined the effects of acrolein on cell proliferative capacity, senescence-associated β-galactosidase activity, the known senescence-inducing pathways (e.g., p53, p21), and telomere length. Results: We found that acrolein induced cellular senescence by increasing both p53 and p21. The knockdown of p53 mediated by small interfering RNA (siRNA) attenuated acrolein-induced cellular senescence. Acrolein decreased Werner’s syndrome protein (WRN), a member of the RecQ helicase family involved in DNA repair and telomere maintenance. Acrolein-induced down-regulation of WRN protein was rescued by p53 knockdown or proteasome inhibition. Finally, we found that acrolein accelerated p53-mediated telomere shortening. Conclusions: These results suggest that acrolein induces p53-mediated cellular senescence accompanied by enhanced telomere attrition and WRN protein down-regulation. [ABSTRACT FROM AUTHOR]