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Results: 1 to 10 of 20

Publication Record


Photoperiod during maternal pregnancy and lifetime depression in offspring.
Devore EE, Chang SC, Okereke OI, McMahon DG, Schernhammer ES
(2018) J Psychiatr Res 104: 169-175
MeSH Terms: Adult, Antidepressive Agents, Cohort Studies, Depression, Female, Humans, Logistic Models, Maternal Exposure, Middle Aged, Nurses, Photoperiod, Pregnancy, Pregnancy Trimester, Second, Prenatal Exposure Delayed Effects, Psychiatric Status Rating Scales, Suicide, United States
Show Abstract · Added March 18, 2020
Experimental studies indicate that perinatal light exposure has enduring effects on affective behaviors in rodents; however, insufficient research has explored this hypothesis in humans. We examined photoperiod (i.e., day length) metrics during maternal pregnancy in relation to lifetime depression in the longitudinal Nurses' Health Study (NHS) and NHS II. 160,723 participants reported birth date and birth state (used to derive daily photoperiod based on published mathematical equations), and clinician-diagnosed depression and antidepressant use throughout adulthood. Logistic regression was used to estimate odds ratios (OR) (and 95% confidence intervals [CI]) for depression (defined as clinician diagnosis and antidepressant use) across quintiles of two exposures during maternal pregnancy: 1) total photoperiod (total number of daylight hours) and 2) differences between minimum/maximum photoperiod; each trimester of pregnancy was examined separately. Total photoperiod during maternal pregnancy was not associated with depression overall or by trimester of pregnancy. However, larger differences between minimum/maximum photoperiod during maternal pregnancy were related to lower odds of depression (multivariable [MV]-adjusted OR: 0.86, 95% CI: 0.83, 0.90 comparing extreme quintiles of exposure; p-trend<0.0001); this association appeared specific to the second trimester of pregnancy (MV-adjusted p-trends = 0.03, <0.0001, and 0.3 across the three trimesters, respectively). In addition, birth at higher latitude (where larger differences in minimum/maximum photoperiod exist) was associated with a significant reduction in the lifetime risk of depression. These findings are consistent with an emerging hypothesis in which perinatal light exposure may influence risk of depression, and they might be understood through the conceptual framework of adaptive developmental plasticity.
Copyright © 2018 Elsevier Ltd. All rights reserved.
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MeSH Terms
Effects of antenatal betamethasone on preterm human and mouse ductus arteriosus: comparison with baboon data.
Shelton EL, Waleh N, Plosa EJ, Benjamin JT, Milne GL, Hooper CW, Ehinger NJ, Poole S, Brown N, Seidner S, McCurnin D, Reese J, Clyman RI
(2018) Pediatr Res 84: 458-465
MeSH Terms: Animals, Betamethasone, Ductus Arteriosus, Ductus Arteriosus, Patent, Echocardiography, Female, Gene Expression Profiling, Gene Expression Regulation, Humans, Infant, Premature, Maternal Exposure, Mice, Oxygen, Papio, Polymerase Chain Reaction, Prostaglandins
Show Abstract · Added November 26, 2018
BACKGROUND - Although studies involving preterm infants ≤34 weeks gestation report a decreased incidence of patent ductus arteriosus after antenatal betamethasone, studies involving younger gestation infants report conflicting results.
METHODS - We used preterm baboons, mice, and humans (≤27 weeks gestation) to examine betamethasone's effects on ductus gene expression and constriction both in vitro and in vivo.
RESULTS - In mice, betamethasone increased the sensitivity of the premature ductus to the contractile effects of oxygen without altering the effects of other contractile or vasodilatory stimuli. Betamethasone's effects on oxygen sensitivity could be eliminated by inhibiting endogenous prostaglandin/nitric oxide signaling. In mice and baboons, betamethasone increased the expression of several developmentally regulated genes that mediate oxygen-induced constriction (K channels) and inhibit vasodilator signaling (phosphodiesterases). In human infants, betamethasone increased the rate of ductus constriction at all gestational ages. However, in infants born ≤25 weeks gestation, betamethasone's contractile effects were only apparent when prostaglandin signaling was inhibited, whereas at 26-27 weeks gestation, betamethasone's contractile effects were apparent even in the absence of prostaglandin inhibitors.
CONCLUSIONS - We speculate that betamethasone's contractile effects may be mediated through genes that are developmentally regulated. This could explain why betamethasone's effects vary according to the infant's developmental age at birth.
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16 MeSH Terms
Validation of maternal recall of early pregnancy medication exposure using prospective diary data.
Sundermann AC, Hartmann KE, Jones SH, Torstenson ES, Velez Edwards DR
(2017) Ann Epidemiol 27: 135-139.e2
MeSH Terms: Adolescent, Adult, Anti-Inflammatory Agents, Non-Steroidal, Data Collection, Female, Humans, Interviews as Topic, Maternal Exposure, Mental Recall, Middle Aged, Nonprescription Drugs, North Carolina, Pregnancy, Pregnancy Complications, Pregnancy Trimester, First, Prescription Drugs, Prospective Studies, Sensitivity and Specificity, Tennessee, Texas, Young Adult
Show Abstract · Added February 21, 2019
PURPOSE - Data about maternal recall accuracy for classifying early pregnancy medication exposure are meager. Nonetheless, studies often rely on recall to evaluate potential impact of pharmaceuticals on the developing fetus.
METHODS - Right from the Start is a community-based pregnancy cohort that enrolled women from North Carolina, Tennessee, and Texas. A subset of 318 women participated in daily medication diaries initiated before conception (2006-2012). We examined nonsteroidal anti-inflammatory drugs (NSAIDs) as an example of a drug type that is difficult to study due to its intermittent and primarily over-the-counter use as well as its incomplete documentation in medical and pharmaceutical records. Selective serotonin reuptake inhibitors (SSRI) were assessed as a prescription medication comparator. Maternal recall of NSAID and SSRI use in early pregnancy was examined by comparing diary data (gold standard) to first-trimester interview.
RESULTS - Sensitivity and specificity for recall of NSAID exposure were 78.6% and 62.3%, respectively (kappa statistic: 0.41), with 72.3% agreement for exposure classification. Sensitivity and specificity for recall of SSRI exposure were 77.8% and 99.0%, respectively (kappa statistic: 0.79), with 97.8% agreement.
CONCLUSIONS - Our findings suggest the validity of maternal recall varies with medication type and prospective data collection should be prioritized when studying early pregnancy drug exposures.
Copyright © 2016 Elsevier Inc. All rights reserved.
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GLI3 Links Environmental Arsenic Exposure and Human Fetal Growth.
Winterbottom EF, Fei DL, Koestler DC, Giambelli C, Wika E, Capobianco AJ, Lee E, Marsit CJ, Karagas MR, Robbins DJ
(2015) EBioMedicine 2: 536-43
MeSH Terms: Adolescent, Adult, Arsenic, Birth Weight, Child Health, Environmental Exposure, Female, Fetal Development, Gene Expression Profiling, Groundwater, Humans, Kruppel-Like Transcription Factors, Maternal Exposure, Middle Aged, Nerve Tissue Proteins, Octamer Transcription Factor-3, Placenta, Pregnancy, Prenatal Exposure Delayed Effects, Signal Transduction, Water Pollutants, Chemical, Water Pollution, Young Adult, Zinc Finger Protein Gli3
Show Abstract · Added November 2, 2015
Although considerable evidence suggests that in utero arsenic exposure affects children's health, these data are mainly from areas of the world where groundwater arsenic levels far exceed the World Health Organization limit of 10 μg/L. We, and others, have found that more common levels of in utero arsenic exposure may also impact children's health. However, the underlying molecular mechanisms are poorly understood. To address this issue, we analyzed the expression of key developmental genes in fetal placenta in a birth cohort of women using unregulated water supplies in a US region with elevated groundwater arsenic. We identified several genes whose expression associated with maternal arsenic exposure in a fetal sex-specific manner. In particular, expression of the HEDGEHOG pathway component, GLI3, in female placentae was both negatively associated with arsenic exposure and positively associated with infant birth weight. This suggests that modulation of GLI3 in the fetal placenta, and perhaps in other fetal tissues, contributes to arsenic's detrimental effects on fetal growth. We showed previously that arsenic-exposed NIH3T3 cells have reduced GLI3 repressor protein. Together, these studies identify GLI3 as a key signaling node that is affected by arsenic, mediating a subset of its effects on developmental signaling and fetal health.
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24 MeSH Terms
Maternal micronutrient deficiency leads to alteration in the kidney proteome in rat pups.
Ahmad S, Basak T, Anand Kumar K, Bhardwaj G, Lalitha A, Yadav DK, Chandak GR, Raghunath M, Sengupta S
(2015) J Proteomics 127: 178-84
MeSH Terms: Animals, Female, Kidney, Maternal Exposure, Micronutrients, Pregnancy, Prenatal Exposure Delayed Effects, Proteome, Rats, Rats, Wistar
Show Abstract · Added November 3, 2017
Maternal nutritional deficiency significantly perturbs the offspring's physiology predisposing them to metabolic diseases during adulthood. Vitamin B12 and folate are two such micronutrients, whose deficiency leads to elevated homocysteine levels. We earlier generated B12 and/or folate deficient rat models and using high-throughput proteomic approach, showed that maternal vitamin B12 deficiency modulates carbohydrate and lipid metabolism in the liver of pups through regulation of PPAR signaling pathway. In this study, using similar approach, we identified 26 differentially expressed proteins in the kidney of pups born to mothers fed with vitamin B12 deficient diet while only four proteins were identified in the folate deficient group. Importantly, proteins like calreticulin, cofilin 1 and nucleoside diphosphate kinase B that are involved in the functioning of the kidney were upregulated in B12 deficient group. Our results hint towards a larger effect of vitamin B12 deficiency compared to that of folate presumably due to greater elevation of homocysteine in vitamin B12 deficient group. In view of widespread vitamin B12 and folate deficiency and its association with several diseases like anemia, cardiovascular and renal diseases, our results may have large implications for kidney diseases in populations deficient in vitamin B12 especially in vegetarians and the elderly people.This article is part of a Special Issue entitled: Proteomics in India.
Copyright © 2015 Elsevier B.V. All rights reserved.
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10 MeSH Terms
First-trimester antihistamine exposure and risk of spontaneous abortion or preterm birth.
Aldridge TD, Hartmann KE, Michels KA, Velez Edwards DR
(2014) Pharmacoepidemiol Drug Saf 23: 1043-50
MeSH Terms: Abortion, Spontaneous, Adolescent, Adult, Female, Histamine Antagonists, Humans, Maternal Exposure, Pregnancy, Pregnancy Trimester, First, Prospective Studies, Risk, United States, Young Adult
Show Abstract · Added June 27, 2014
PURPOSE - We tested whether antihistamine exposure during early pregnancy is associated with spontaneous abortion (SAB) or preterm birth (PTB).
METHODS - Women were enrolled in Right from the Start (2004-2010), a prospective pregnancy cohort. Data about first-trimester antihistamine use were obtained from screening and first-trimester interviews. Self-reported outcomes included SAB and PTB and were verified by medical records. Cox proportional hazards models were used to test for an association between antihistamine use and each outcome, both performed adjusting for confounders.
RESULTS - Among the 2685 pregnancies analyzed, 14% (n = 377) reported use of antihistamines. Among antihistamine users, 12% (n = 44) experienced SABs, and 6% (n = 21) had PTBs. Antihistamine exposure was not associated with SAB (adjusted hazard ratio [aHR] = 0.88, 95% confidence interval [CI] 0.64, 1.21) or PTB, which was modified by maternal race (aHR = 1.03, 95%CI 0.61, 1.72 among White women and aHR = 0.43, 95%CI 0.14, 1.34 among Black women).
CONCLUSIONS - Despite the biologic plausibility that antihistamine use may influence pregnancy outcomes, we did not detect evidence of an association with SAB or PTB. These data demonstrate the utility of large prospective cohorts for evaluating drug safety in pregnancy when concerns are raised from animal models.
Copyright © 2014 John Wiley & Sons, Ltd.
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2 Members
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13 MeSH Terms
Mom knows best: the universality of maternal microbial transmission.
Funkhouser LJ, Bordenstein SR
(2013) PLoS Biol 11: e1001631
MeSH Terms: Animals, Breast Feeding, Female, Humans, Infant, Newborn, Infectious Disease Transmission, Vertical, Maternal Exposure, Microbiota, Pregnancy
Show Abstract · Added October 8, 2015
The sterile womb paradigm is an enduring premise in biology that human infants are born sterile. Recent studies suggest that infants incorporate an initial microbiome before birth and receive copious supplementation of maternal microbes through birth and breastfeeding. Moreover, evidence for microbial maternal transmission is increasingly widespread across animals. This collective knowledge compels a paradigm shift—one in which maternal transmission of microbes advances from a taxonomically specialized phenomenon to a universal one in animals. It also engenders fresh views on the assembly of the microbiome, its role in animal evolution, and applications to human health and disease.
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9 MeSH Terms
PPAR signaling pathway is a key modulator of liver proteome in pups born to vitamin B(12) deficient rats.
Ahmad S, Kumar KA, Basak T, Bhardwaj G, Yadav DK, Lalitha A, Chandak GR, Raghunath M, Sengupta S
(2013) J Proteomics 91: 297-308
MeSH Terms: Amino Acids, Animals, Animals, Newborn, Carbohydrates, Female, Gene Expression Profiling, Gene Expression Regulation, Lipids, Liver, Maternal Exposure, Micronutrients, Peroxisome Proliferator-Activated Receptors, Pregnancy, Proteome, Proteomics, Rats, Signal Transduction, Vitamin B 12, Vitamin B 12 Deficiency
Show Abstract · Added November 3, 2017
UNLABELLED - Maternal nutritional deficiency in-utero is known to predict risk of complex disorders like cardiovascular disease, diabetes and many neurological disorders in the offspring and vitamin B12 is one such critical micronutrient. Here we performed 2D-DIGE followed by MALDI TOF/TOF analysis to identify proteins that are differentially expressed in liver of pups born to mothers fed vitamin B12 deficient diet vis-à-vis control diet. To further establish causality, we analyzed the effect of B12 rehabilitation at parturition on the protein levels and the phenotype in pups. We identified 38 differentially expressed proteins that were enriched in pathways involved in the regulation of amino acid, lipid and carbohydrate metabolism. Further, three enzymes in the β-oxidation pathway (hydroxyacyl-coenzyme A dehydrogenase, medium-chain specific acyl-CoA dehydrogenase, 3-ketoacyl-CoA thiolase) were down-regulated in pups born to mothers fed vitamin B12 deficient diet. We observed age-dependent differential expression of peroxisome proliferator activated-receptor (PPAR) α and γ in the deficient pups. Interestingly, expression of 27 proteins that were differentially expressed was restored to the control levels after rehabilitation of female rats with vitamin B12 from parturition. Our study thus provides the first evidence that maternal vitamin B12 deficiency influences lipid and other micronutrient metabolism in pups through regulation of PPAR signaling pathway.
BIOLOGICAL SIGNIFICANCE - Maternal vitamin B12 deficiency has been shown to predict the onset of complex disorders like atherosclerosis, type II diabetes etc. in the next generation during their adulthood. We have shown earlier that pups born to female rats fed with vitamin B12 deficient diet were obese and developed high levels of other intermediate traits such as triglycerides, cholesterol etc. that are related to the risk of diabetes and cardiovascular disorders. In this piece of work using differential proteomic approach we have identified the altered metabolic processes in the liver of vitamin B12 deficient pups. We have also documented that the proteins involved in β-oxidation pathway are down-regulated. Further, differential expression of PPARα and PPARγ was evidently documented as the master regulator for the alteration of lipid, amino acid and carbohydrate metabolism during maternal vitamin B12 deficiency.
© 2013. Published by Elsevier B.V. All rights reserved.
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1 Members
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19 MeSH Terms
Immune system disturbances in schizophrenia.
Horváth S, Mirnics K
(2014) Biol Psychiatry 75: 316-23
MeSH Terms: Animals, Anti-Inflammatory Agents, Brain, Female, Genetic Predisposition to Disease, Humans, Maternal Exposure, Membrane Proteins, Pregnancy, Pregnancy Complications, Infectious, RNA-Binding Proteins, Schizophrenia, Serpins, Transcriptome
Show Abstract · Added May 19, 2014
Epidemiological, genetic, transcriptome, postmortem, peripheral biomarker, and therapeutic studies of schizophrenia all point to a dysregulation of both innate and adaptive immune systems in the disease, and it is likely that these immune changes actively contribute to disease symptoms. Gene expression disturbances in the brain of subjects with schizophrenia show complex, region-specific changes with consistently replicated and potentially interdependent induction of serpin peptidase inhibitor, clade A member 3 (SERPINA3) and interferon inducible transmembrane protein (IFITM) family transcripts in the prefrontal cortex. Recent data suggest that IFITM3 expression is a critical mediator of maternal immune activation. Because the IFITM gene family is primarily expressed in the endothelial cells and meninges, and because the meninges play a critical role in interneuron development, we suggest that these two non-neuronal cell populations might play an important role in the disease pathophysiology. Finally, we propose that IFITM3 in particular might be a novel, appealing, knowledge-based drug target for treatment of schizophrenia.
Copyright © 2014 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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14 MeSH Terms
Influence of maternal asthma on the cause and severity of infant acute respiratory tract infections.
Carroll KN, Gebretsadik T, Minton P, Woodward K, Liu Z, Miller EK, Williams JV, Dupont WD, Hartert TV
(2012) J Allergy Clin Immunol 129: 1236-42
MeSH Terms: Adult, Asthma, Child, Child, Preschool, Female, Follow-Up Studies, Humans, Infant, Male, Maternal Exposure, Picornaviridae Infections, RNA, Viral, Respiratory Syncytial Virus Infections, Respiratory Syncytial Viruses, Rhinovirus, Skin Tests, Young Adult
Show Abstract · Added March 21, 2014
BACKGROUND - Respiratory syncytial virus (RSV) and rhinovirus infections are the most common significant infant respiratory tract illnesses and are associated with increased but differential risks of childhood asthma.
OBJECTIVE - We sought to determine whether maternal asthma is associated with higher odds of infant respiratory tract infection with rhinovirus versus RSV and increased infection severity.
METHODS - Mother-infant dyads were enrolled from 2004-2008 during an infant respiratory tract infection (104 with rhinovirus and 279 with RSV). Mothers were classified into mutually exclusive groups (atopic asthma, nonatopic asthma, and no asthma). We determined viral cause using PCR and the severity of the infant's respiratory tract infection using the bronchiolitis severity score. Adjusted relative odds of maternal asthma with viral cause were calculated by using logistic regression. Proportional odds models assessed the association of maternal asthma and infant infection severity.
RESULTS - Infants with a mother with atopic asthma compared with infants whose mothers did not have asthma were more likely to have rhinovirus versus RSV infection (adjusted odds ratio, 2.42; 95% CI, 1.19-4.90). Similarly, among infants with rhinovirus, having a mother with atopic asthma was associated with increased infection severity (adjusted odds ratio, 3.10; 95% CI, 1.21-7.98). This relationship was not seen among infants with RSV.
CONCLUSIONS - Clinically significant rhinovirus infection during infancy was more strongly associated with having a mother with atopic asthma than clinically significant RSV infection. Having a mother with atopic asthma was associated with increased severity of infant rhinovirus but not RSV infections. Infants with rhinovirus were more likely to have a familial atopic predisposition, which might partly explain the subsequent increased asthma risk.
Copyright © 2012 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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17 MeSH Terms