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1.
Nutrients ; 13(1)2021 Jan 11.
Artigo em Inglês | MEDLINE | ID: mdl-33440675

RESUMO

The risk of recurrence of estrogen receptor-positive breast cancer remains constant, even 20 years after diagnosis. Recurrence may be more likely in patients pre-programmed for it already in the womb, such as in the daughters born to obese mothers. Maternal obesity persistently alters offspring's gut microbiota and impairs tumor immune responses. To investigate if the gut dysbiosis is linked to increased risk of mammary cancer recurrence in the offspring of obese rat dams, we fed adult offspring genistein which is known to have beneficial effects on the gut bacteria. However, the effects of genistein on breast cancer remain controversial. We found that genistein intake after tamoxifen response prevented the increased risk of local recurrence in the offspring of obese dams but had no effect on the control offspring. A significant increase in the abundance of inflammatory Prevotellaceae and Enterobacteriaceae, and a reduction in short-chain fatty acid producing Clostridiaceae was observed in the offspring of obese dams. Genistein supplementation reversed these changes as well as reversed increased gut metabolite N-acetylvaline levels which are linked to increased all-cause mortality. Genistein supplementation also reduced genotoxic tyramine levels, increased metabolites improving pro-resolving phase of inflammation, and reversed the elevated tumor mRNA expression of multiple immunosuppressive genes in the offspring of obese dams. If translatable to breast cancer patients, attempts to prevent breast cancer recurrences might need to focus on dietary modifications which beneficially modify the gut microbiota.


Assuntos
Microbioma Gastrointestinal/efeitos dos fármacos , Genisteína/farmacologia , Neoplasias Mamárias Animais/microbiologia , Obesidade/microbiologia , Efeitos Tardios da Exposição Pré-Natal/microbiologia , Animais , Feminino , Neoplasias Mamárias Animais/tratamento farmacológico , Obesidade/etiologia , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Ratos , Ratos Sprague-Dawley
2.
Allergol. immunopatol ; 48(6): 530-536, nov.-dic. 2020. tab
Artigo em Inglês | IBECS | ID: ibc-199239

RESUMO

BACKGROUND: There is limited evidence on the association between prenatal smoking exposure and the risk of asthma in children. The aim of this prebirth cohort study was to investigate the association between prenatal and postnatal tobacco smoke exposure and the risk of asthma in Japanese children. METHODS: Study subjects were 1304 mother-child pairs. Information on the variables under study was obtained using repeated questionnaires that were completed by mothers, first prior to delivery, then shortly after birth and subsequently around 4, 12, 24, and 36 months after delivery. Ever asthma was defined as a maternal report of physician-diagnosed asthma at any time since birth. Current asthma was defined as the use of asthma medication at the time of the sixth survey. RESULTS: Logistic regression models revealed that maternal active smoking, either before pregnancy or during pregnancy, was not associated with the risk of ever asthma or current asthma. Further, no association was observed between postnatally living with at least one household smoker and the risk of asthma. Among children whose mothers are never smokers, maternal second-hand smoke (SHS) exposure at work and/or at home during pregnancy increased the risk of ever asthma and current asthma in children; adjusted odds ratio (95% confidence intervals) for ever asthma and current asthma were 2.41 (1.13-5.05) and 4.82 (1.68-13.43), respectively. CONCLUSIONS: Our findings suggest that maternal SHS exposure during pregnancy might be associated with an increased risk of ever asthma and current asthma in young children whose mothers have never smoked


No disponible


Assuntos
Humanos , Masculino , Feminino , Gravidez , Lactente , Pré-Escolar , Efeitos Tardios da Exposição Pré-Natal/etiologia , Asma/etiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Exposição Materna/efeitos adversos , Estudos Prospectivos , Fatores de Risco , Idade Gestacional , Modelos Logísticos , Japão , Inquéritos e Questionários
3.
PLoS One ; 15(10): e0235877, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33091010

RESUMO

Congenital Zika virus (ZIKV) exposure results in a spectrum of disease ranging from severe birth defects to delayed onset neurodevelopmental deficits. ZIKV-related neuropathogenesis, predictors of birth defects, and neurodevelopmental deficits are not well defined in people. Here we assess the methodological and statistical feasibility of a congenital ZIKV exposure macaque model for identifying infant neurobehavior and brain abnormalities that may underlie neurodevelopmental deficits. We inoculated five pregnant macaques with ZIKV and mock-inoculated one macaque in the first trimester. Following birth, growth, ocular structure/function, brain structure, hearing, histopathology, and neurobehavior were quantitatively assessed during the first week of life. We identified the typical pregnancy outcomes of congenital ZIKV infection, with fetal demise and placental abnormalities. We estimated sample sizes needed to define differences between groups and demonstrated that future studies quantifying brain region volumes, retinal structure, hearing, and visual pathway function require a sample size of 14 animals per group (14 ZIKV, 14 control) to detect statistically significant differences in at least half of the infant exam parameters. Establishing the parameters for future studies of neurodevelopmental outcomes following congenital ZIKV exposure in macaques is essential for robust and rigorous experimental design.


Assuntos
Transtornos da Audição/patologia , Malformações do Sistema Nervoso/patologia , Complicações Infecciosas na Gravidez/patologia , Efeitos Tardios da Exposição Pré-Natal/patologia , Transtornos da Visão/patologia , Infecção por Zika virus/complicações , Zika virus/fisiologia , Animais , Animais Recém-Nascidos , Feminino , Transtornos da Audição/etiologia , Macaca mulatta , Malformações do Sistema Nervoso/etiologia , Gravidez , Complicações Infecciosas na Gravidez/etiologia , Resultado da Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Transtornos da Visão/etiologia , Infecção por Zika virus/virologia
4.
PLoS One ; 15(9): e0239738, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32976529

RESUMO

The levels and activity of the enzyme paraoxonase 1 affect the vulnerability to the teratogenic effects of organophosphate pesticides. Mutant mice lacking the gene for paraoxonase1 (PON1-/-) are more susceptible to the toxic effects of chlorpyrifos, and were hypothesized to be more vulnerable to social behavior deficits induced by exposure to chlorpyrifos during gestation. Three experiments were performed comparing PON1-/- mice to PON1+/+ mice born to dams treated with 0.5 mg/kg chlorpyrifos or cornoil vehicle on gestational days 12-15. Chlofpyrifos-exposed male PON1-/- mouse pups had delayed development of reflexes in in the first experiment. In the second experiment, adult male and female PON1-/- mice and the female PON1+/+ mice all displayed lower social preference than the male vehicle-treated PON1+/+ mice. The PON1-/- mice and the female PON1+/+ mice displayed lower social preference compared to the PON1+/+ male mice. Male adult mice that had been exposed in utero to chlorpyrifos showed less conditioned social preference regardless of genotype. In the third study, the delayed reflex development was replicated in male and female PON1-/- mice, but chlorpyrifos did not augment this effect. Nest Odor Preference, a test of early social attachment to dam and siblings, was lower in PON1-/- mouse pups compared to PON1+/+ pups. This study shows for the first time that PON1-/- mice have a behavioral phenotype that indicates impaired reflex development and social behavior. Chlorpyrifos exposure during gestation tended to augment some of these effects.


Assuntos
Arildialquilfosfatase/genética , Clorpirifos/toxicidade , Inibidores da Colinesterase/toxicidade , Deficiências do Desenvolvimento/genética , Efeitos Tardios da Exposição Pré-Natal/genética , Comportamento Social , Teratogênios/toxicidade , Animais , Arildialquilfosfatase/deficiência , Feminino , Masculino , Camundongos , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Reflexo
5.
PLoS Med ; 17(8): e1003158, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32810187

RESUMO

BACKGROUND: Most of the women who smoke before pregnancy continue smoking during pregnancy, and some start to quit smoking after being pregnant, although existing guidelines for pregnancy recommend that women who smoke should quit smoking before pregnancy. Findings about the timing and intensity of maternal smoking, especially low-intensity smoking (1-9 cigarettes per day), and preterm birth are still inconsistent and ambiguous. This study aimed to examine the association of the timing of smoking and doses of smoking before pregnancy and during the first or second trimester of pregnancy with preterm birth in a large-scale population-based retrospective cohort study. METHODS AND FINDINGS: We used nationwide birth certificate data from singleton mother-infant pairs in the United States National Vital Statistics System, 2011-2018. All adult women with live singleton births, without preexisting hypertension or diabetes, and with complete data on smoking and gestational age at delivery were included. Participants reported their smoking status (yes or no) and daily number of cigarettes consumed before and during each trimester of pregnancy. The outcome of interest was preterm birth, defined as a birth before 37 weeks of gestation. Logistic regression models were used to estimate the odds ratio (OR) with 95% confidence intervals (CIs) of preterm birth associated with smoking status and the number of cigarettes consumed, adjusting for maternal age, race/ethnicity, parity, education levels, prepregnancy BMI, previous history of preterm birth, marital status, infant sex, and initiation of prenatal care. This study included 25,623,479 women, with a mean age of 29 years (range 20-50 years); 13,742,486 (53.6%) participants were of non-Hispanic white ancestry, 5,971,598 (23.3%) of Hispanic ancestry, and 3,417,456 (13.34%) of non-Hispanic black ancestry. The prevalence of preterm birth was 9.3% (n = 2,378,398). We found that maternal smoking during pregnancy, even at a very low level of intensity, was associated with an increased risk of preterm delivery. The adjusted ORs (95% CI) of preterm birth for mothers who smoked 1-2, 3-5, 6-9, 10-19, and ≥20 cigarettes per day during the first trimester compared with mothers who did not smoke were 1.31 (1.29-1.33), 1.31 (1.30-1.32), 1.33 (1.31-1.35), 1.44 (1.43-1.45), and 1.53 (1.52-1.55), respectively (all P values < 0.001), whereas for those who smoked during the second trimester, the corresponding ORs were 1.37 (1.35-1.39), 1.36 (1.35-1.38), 1.36 (1.34-1.38), 1.48 (1.47-1.49), and 1.59 (1.58-1.61), respectively (all P values < 0.001). Furthermore, smokers who quit before pregnancy, regardless of smoking intensity, had a comparable risk of preterm birth with nonsmokers, although this was not the case when cessation occurred in the first or second trimester of pregnancy. The major limitation of this study is the self-reported information about smoking, which may be subject to information bias. In addition, we cannot rule out the possibility of residual confounding caused by unmeasured factors in an observational research design. CONCLUSIONS: In this study, we observed that low-intensity cigarette consumption during either the first or second trimester of pregnancy, even as low as 1-2 cigarettes per day, was associated with an increased risk of preterm birth. These findings suggest that there is no safe level or safe trimester for maternal smoking during pregnancy. Women of reproductive age who smoke should be strongly encouraged and supported to quit smoking before pregnancy.


Assuntos
Fumar Cigarros/efeitos adversos , Fumar Cigarros/epidemiologia , Comportamento Materno , Nascimento Prematuro/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Adulto , Fumar Cigarros/tendências , Relação Dose-Resposta a Droga , Feminino , Humanos , Pessoa de Meia-Idade , Gravidez , Nascimento Prematuro/diagnóstico , Nascimento Prematuro/etiologia , Efeitos Tardios da Exposição Pré-Natal/diagnóstico , Efeitos Tardios da Exposição Pré-Natal/etiologia , Fatores de Risco , Autorrelato , Estados Unidos/epidemiologia , Adulto Jovem
6.
Life Sci ; 260: 118309, 2020 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-32841664

RESUMO

AIMS: Oral cavity pathogens play an important systemic role, modulating the development of several diseases. Periodontitis is a very common oral disease associated with dental biofilm. It is characterized by gum inflammation, periodontal ligament degeneration, dental cementum and alveolar bone loss. Studies point to the association between maternal periodontitis and adverse outcomes during pregnancy. However, they did not evaluate the impact of maternal periodontitis in the offspring. Thus, our objective was to investigate the effects of maternal periodontitis in the immune system of offspring. MATERIAL AND METHODS: For this evaluation we induced acute lung injury in rat pups. Pregnant rats were submitted or not to periodontitis by ligature technique. Thirty days after the birth, offspring was submitted to acute lung inflammation by administration of lipopolysaccharide (LPS, Salmonella abortus equi, 5 mg/kg, ip). KEY FINDINGS: Our results showed that maternal periodontitis increased myeloperoxidase activity, the levels of TNF-alpha and IL-17A in the bronchoalveolar fluid, the gene expression of TNF-alpha, IL-17A, and cyclooxygenases 1 and 2. In addition, maternal periodontitis did not alter the number of leukocytes migrated into the lung, tracheal responsiveness, expression of TLR4 and NF-KB translocation. SIGNIFICANCE: This study showed prenatal programming of the immune response induced by maternal periodontitis, and reinforces the importance of oral health care during pregnancy.


Assuntos
Lesão Pulmonar Aguda/imunologia , Reprogramação Celular , Periodontite/fisiopatologia , Efeitos Tardios da Exposição Pré-Natal/imunologia , Lesão Pulmonar Aguda/etiologia , Lesão Pulmonar Aguda/patologia , Animais , Animais Recém-Nascidos , Feminino , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , Lipopolissacarídeos/toxicidade , Masculino , NF-kappa B/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/patologia , Ratos , Fator de Necrose Tumoral alfa/metabolismo
7.
Nat Commun ; 11(1): 3593, 2020 07 17.
Artigo em Inglês | MEDLINE | ID: mdl-32681096

RESUMO

During pregnancy, maternal endocrine signals drive fetal development and program the offspring's physiology. A disruption of maternal glucocorticoid (GC) homeostasis increases the child's risk of developing psychiatric disorders later in life. We here show in mice, that the time of day of antenatal GC exposure predicts the behavioral phenotype of the adult offspring. Offspring of mothers receiving GCs out-of-phase compared to their endogenous circadian GC rhythm show elevated anxiety, impaired stress coping, and dysfunctional stress-axis regulation. The fetal circadian clock determines the vulnerability of the stress axis to GC treatment by controlling GC receptor (GR) availability in the hypothalamus. Similarly, a retrospective observational study indicates poorer stress compensatory capacity in 5-year old preterm infants whose mothers received antenatal GCs towards the evening. Our findings offer insights into the circadian physiology of feto-maternal crosstalk and assign a role to the fetal clock as a temporal gatekeeper of GC sensitivity.


Assuntos
Relógios Circadianos/efeitos dos fármacos , Glucocorticoides/efeitos adversos , Exposição Materna/efeitos adversos , Transtornos Mentais/etiologia , Efeitos Tardios da Exposição Pré-Natal/psicologia , Ansiedade , Comportamento/efeitos dos fármacos , Feminino , Glucocorticoides/administração & dosagem , Humanos , Recém-Nascido Prematuro/psicologia , Masculino , Transtornos Mentais/metabolismo , Transtornos Mentais/fisiopatologia , Transtornos Mentais/psicologia , Gravidez , Complicações na Gravidez/tratamento farmacológico , Cuidado Pré-Natal , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Receptores de Glucocorticoides/genética , Receptores de Glucocorticoides/metabolismo
9.
J Pediatr ; 222: 35-44.e1, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32418814

RESUMO

OBJECTIVE: To assess factors impacting child-welfare involvement and child abuse and neglect outcomes among prenatally substance-exposed infants. STUDY DESIGN: This was a retrospective review of case registry data regarding substance-exposed infants tracked statewide in Delaware from 2014 to 2018. Differences in maternal, infant, and substance exposure factors by level of child-welfare involvement (screened-in vs screened-out case status) and child abuse and neglect outcomes were examined. Screened-in status was defined as case acceptance for investigation, family assessment, or treatment referral. Using logistic regression, associations between factors and screened-in status and between factors and child abuse and neglect outcomes were assessed. Cases involving child abuse and neglect were analyzed qualitatively. RESULTS: Among 1222 substance-exposed infants, 70% were screened-in by child welfare for ongoing involvement; 28 (2.3%) of substance-exposed infants were identified as child abuse and neglect victims sustaining serious physical or fatal injury before 1 year of age. Most substance-exposed infants remained with caregivers; few entered foster care. Polysubstance exposure and maternal mental health condition were factors associated with screened-in status. Neither substance exposure type nor maternal mental health condition reliably predicted future child abuse and neglect. CONCLUSIONS: Substance-exposed infants had a significant risk for child abuse and neglect. Although maternal and substance exposure factors were associated with screened-in case status, they unreliably predicted future risk of child abuse and neglect.


Assuntos
Maus-Tratos Infantis/estatística & dados numéricos , Bem-Estar do Lactente/estatística & dados numéricos , Complicações na Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Transtornos Relacionados ao Uso de Substâncias , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Gravidez , Estudos Retrospectivos , Fatores de Risco
10.
Nat Commun ; 11(1): 2555, 2020 05 22.
Artigo em Inglês | MEDLINE | ID: mdl-32444624

RESUMO

Fetal alcohol exposure (FAE) is the leading preventable developmental cause of cognitive dysfunction. Even in the absence of binge drinking, alcohol consumption during pregnancy can leave offspring deficient. However, the mechanisms underlying these deficiencies are unknown. Using a mouse model of gestational ethanol exposure (GEE), we show increased instrumental lever-pressing and disruption of efficient habitual actions in adults, indicative of disrupted cognitive function. In vivo electrophysiology reveals disrupted action encoding in dorsolateral striatum (DLS) associated with altered habit learning. GEE mice exhibit decreased GABAergic transmission onto DLS projection neurons, including inputs from parvalbumin interneurons, and increased endocannabinoid tone. Chemogenetic activation of DLS parvalbumin interneurons reduces the elevated lever pressing of GEE mice. Pharmacologically increasing endocannabinoid tone mimics GEE effects on cognition and synaptic transmission. These findings show GEE induces long-lasting deficits in cognitive function that may contribute to human FAE, and identify potential mechanisms for future therapeutic targeting.


Assuntos
Corpo Estriado/fisiopatologia , Etanol/efeitos adversos , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/psicologia , Animais , Cognição/efeitos dos fármacos , Corpo Estriado/metabolismo , Corpo Estriado/fisiologia , Etanol/metabolismo , Feminino , Desenvolvimento Fetal , Humanos , Masculino , Camundongos Endogâmicos C57BL , Linhagem , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia
11.
Sci Rep ; 10(1): 8567, 2020 05 22.
Artigo em Inglês | MEDLINE | ID: mdl-32444626

RESUMO

In 1973, the Velsicol Chemical Company, which manufactured FireMaster, a brominated flame retardant, and NutriMaster, a nutritional supplement, mistakenly shipped hundreds of pounds of FireMaster to grain mills around Michigan where it was incorporated into animal feed and then into the food chain across the state. An estimated 6.5 million Michigan residents consumed polybrominated biphenyl (PBB)-laced animal products leading to one of the largest agricultural accidents in U.S. history. To date, there have been no studies investigating the effects of PBB on epigenetic regulation in sperm, which could explain some of the endocrine-related health effects observed among children of PBB-exposed parents. Fusing epidemiological approaches with a novel in vitro model of human spermatogenesis, we demonstrate that exposure to PBB153, the primary component of FireMaster, alters the epigenome in human spermatogenic cells. Using our novel stem cell-based spermatogenesis model, we show that PBB153 exposure decreases DNA methylation at regulatory elements controlling imprinted genes. Furthermore, PBB153 affects DNA methylation by reducing de novo DNA methyltransferase activity at increasing PBB153 concentrations as well as reducing maintenance DNA methyltransferase activity at the lowest tested PBB153 concentration. Additionally, PBB153 exposure alters the expression of genes critical to proper human development. Taken together, these results suggest that PBB153 exposure alters the epigenome by disrupting methyltransferase activity leading to defects in imprint establishment causing altered gene expression, which could contribute to health concerns in the children of men exposed to PBB153. While this chemical is toxic to those directly exposed, the results from this study indicate that the epigenetic repercussions may be detrimental to future generations. Above all, this model may be expanded to model a multitude of environmental exposures to elucidate the effect of various chemicals on germline epigenetics and how paternal exposure may impact the health of future generations.


Assuntos
Retardadores de Chama/efeitos adversos , Regulação da Expressão Gênica no Desenvolvimento , Impressão Genômica , Bifenil Polibromatos/efeitos adversos , Espermatozoides/patologia , Criança , DNA (Citosina-5-)-Metiltransferase 1/genética , Epigênese Genética , Feminino , Gametogênese , Humanos , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/patologia , RNA Longo não Codificante/genética , Espermatozoides/efeitos dos fármacos , Espermatozoides/metabolismo
12.
J Clin Psychiatry ; 81(2)2020 03 31.
Artigo em Inglês | MEDLINE | ID: mdl-32237297

RESUMO

Many observational studies have found an association between antidepressant drug prescription during pregnancy and neurodevelopmental disorders such as autism spectrum disorder, attention-deficit/hyperactivity disorder, and intellectual disability. The results of such studies cannot be considered conclusive because of the possible presence of inadequately measured, unmeasured, and unknown confounds. In this context, maternal anemia before or at but not after 30 weeks of gestation was recently associated with an increased risk of all 3 of these neurodevelopmental disorders. Additionally, meta-analysis has shown that maternal anemia during pregnancy is associated with other adverse gestational outcomes, as well. Given that anemia is common during pregnancy, and that iron deficiency during pregnancy can compromise neurodevelopment in the offspring, it is clear that maternal anemia during pregnancy should be included as a confound that is adjusted for in analyses in studies of psychotropic drugs in pregnancy. However, many studies that significantly associated gestational exposure to antidepressants with adverse pregnancy outcomes did not adjust for maternal anemia during pregnancy. This issue is not merely academic because studies with such "significant" findings discourage depressed pregnant women from accepting antidepressants; therefore, women and their unborn children may risk experiencing the known harms associated with untreated depression during pregnancy. Additionally, such "significant" findings may provoke unjustified guilt in women who do use antidepressants during pregnancy, especially if the pregnancy is associated with an adverse outcome. Whereas this is not an endorsement of the unquestioning use of antidepressants during pregnancy, it does imply that those who argue against medication use during pregnancy should re-examine the science on which their views are based.


Assuntos
Anemia/complicações , Antidepressivos/efeitos adversos , Transtorno Depressivo/tratamento farmacológico , Transtornos do Neurodesenvolvimento/etiologia , Complicações Hematológicas na Gravidez/sangue , Efeitos Tardios da Exposição Pré-Natal/etiologia , Adolescente , Adulto , Anemia/epidemiologia , Criança , Transtorno Depressivo/epidemiologia , Feminino , Idade Gestacional , Humanos , Masculino , Transtornos do Neurodesenvolvimento/induzido quimicamente , Transtornos do Neurodesenvolvimento/epidemiologia , Gravidez , Complicações Hematológicas na Gravidez/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Adulto Jovem
13.
Br J Nutr ; 124(3): 286-295, 2020 08 14.
Artigo em Inglês | MEDLINE | ID: mdl-32234086

RESUMO

Maternal nutritional programming by a high-fat (HF) diet is related to hepatic lipid accumulation and steatosis in offspring. Conjugated linoleic acid (CLA) might ameliorate impaired hepatic lipid homoeostasis; therefore, the aim was to investigate the potential preventive effect of maternal CLA consumption on TAG metabolism alterations induced by HF diets in adult male rat offspring receiving or not receiving CLA. Female Wistar rats were fed a control (C) diet, HF diet or HF diet supplemented with CLA (HF+CLA) for 4 weeks before mating and throughout pregnancy and lactation. After weaning, for 9 weeks, male offspring of C or HF rats continued with the same diets as their mothers (C/C or HF/HF groups, respectively) and male offspring of HF+CLA rats were fed HF or HF+CLA diets (HF+CLA/HF or HF+CLA/HF+CLA groups, respectively). Nutritional parameters, serum and liver TAG levels, the TAG secretion rate (TAG-SR) and the activities as well as gene expression of key hepatic enzymes involved in TAG regulation were assessed. The most interesting results were that maternal CLA decreased epididymal white adipose tissue weight and prevented serum and liver TAG accumulation induced by a HF diet in adult male offspring receiving or not receiving CLA. The prevention of liver steatosis in HF+CLA/HF+CLA and HF+CLA/HF offspring was associated with an increased hepatic TAG-SR. Overall, this study provides evidence that maternal CLA consumption programmes TAG regulation and in this way contributes to lowering lipid levels in tissues and preventing liver steatosis in particular.


Assuntos
Dieta Hiperlipídica/efeitos adversos , Suplementos Nutricionais , Fígado Gorduroso/prevenção & controle , Ácidos Linoleicos Conjugados/administração & dosagem , Efeitos Tardios da Exposição Pré-Natal/prevenção & controle , Tecido Adiposo Branco/metabolismo , Animais , Fígado Gorduroso/etiologia , Feminino , Fígado/metabolismo , Masculino , Exposição Materna/efeitos adversos , Fenômenos Fisiológicos da Nutrição Materna , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Ratos , Ratos Wistar
14.
Pediatr Blood Cancer ; 67(6): e28269, 2020 06.
Artigo em Inglês | MEDLINE | ID: mdl-32196946

RESUMO

OBJECTIVE: Exploring the effect of maternal obesity during pregnancy on the long-term health of offspring is of great importance. The aim of this study was to evaluate the association between maternal pre-pregnancy obesity and future risk of childhood malignancies. STUDY DESIGN: A population-based cohort analysis comparing the risk for long-term childhood malignancies (up to the age of 18 years) in children born (1991-2014) to mothers with and without pre-pregnancy obesity (body mass index > 30) was conducted in July 2017. Childhood malignancies were predefined based on ICD-9 codes, as recorded in the hospital medical files. Children with congenital malformations and multiple gestations were excluded from the analysis. The Kaplan-Meier survival curve was constructed to compare cumulative oncological morbidity in both groups over time. The Cox proportional hazards model was used to control for confounders. RESULTS: During the study period, 241 273 infants met the inclusion criteria; 3268 were born to mothers with pre-pregnancy obesity. Children of obese women had significantly increased risk for several childhood malignancies (including brain tumors) as well as increased risk for total hospitalizations with malignancy diagnoses, even after controlling for several confounders (adjusted HR 1.90, 95% CI 1.07-3.37, P = 0.028). Cumulative incidence of oncological morbidity was also significantly increased over time in the studied group (log-rank P = 0.023). CONCLUSION: Maternal pre-pregnancy obesity is significantly associated with an increased long-term risk for general childhood malignancies, and specifically brain tumors in the offspring. These results are important when counseling mothers regarding potential future risks and recommended lifestyle modifications.


Assuntos
Neoplasias/epidemiologia , Obesidade Materna/complicações , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Adolescente , Adulto , Criança , Pré-Escolar , Feminino , Seguimentos , Hospitalização , Humanos , Incidência , Lactente , Recém-Nascido , Israel/epidemiologia , Masculino , Neoplasias/etiologia , Neoplasias/patologia , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/patologia , Prognóstico , Estudos Retrospectivos , Fatores de Risco
15.
Sci Rep ; 10(1): 4311, 2020 03 09.
Artigo em Inglês | MEDLINE | ID: mdl-32152374

RESUMO

The extensive literature has reported adverse effects on environmental tobacco smoke (ETS) on children's health. We aim to analyze associations of ETS with dry night cough, croup, pneumonia, and frequent common cold and to disentangle the effects of prenatal, infancy and childhood exposure by multilevel logistic regression. A cross-sectional study was conducted among 41,176 children aged 3-8 years in 8 major cities of China during 2010-2011, and obtained demographic information, smoke exposure information, and respiratory outcomes. Parents' smoking habit and indoor tobacco smoke odor were considered as two indicators of ETS. The prevalences of respiratory outcomes were 6.0% for croup, 9.5% for frequency common cold, 17.1% for dry night cough and 32.3% for pneumonia respectively in the study. The associations between respiratory outcomes and parental smoking were not obvious, while indoor tobacco smoke odor was clearly and strongly associated with most respiratory outcomes, with adjusted odds ratios ranging from 1.06 to 1.95. Both infancy and childhood exposure to tobacco smoke odor were independent risk factors, but infancy exposure had a higher risk. The results explore that ETS increased the risk of respiratory outcomes in children, highlighting the need for raising awareness about the detrimental effects of tobacco smoke exposure.


Assuntos
Poluição do Ar em Ambientes Fechados/efeitos adversos , Saúde da Criança/tendências , Exposição Ambiental/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/etiologia , Doenças Respiratórias/etiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Fumar Tabaco/efeitos adversos , Criança , Pré-Escolar , China/epidemiologia , Estudos Transversais , Feminino , Humanos , Lactente , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/patologia , Prevalência , Doenças Respiratórias/epidemiologia , Doenças Respiratórias/patologia , Fatores de Risco
16.
Sci Rep ; 10(1): 3905, 2020 03 03.
Artigo em Inglês | MEDLINE | ID: mdl-32127562

RESUMO

Nonhereditary factors play an important role in the occurrence of congenital heart disease (CHD). This study was to explore the possible parental nonhereditary exposure factors relevant to the occurrence of CHD in the northeastern Sichuan area. A total of 367 children with CHD and 367 children without congenital malformations aged 0 to 14 years old were recruited from the Affiliated Hospital of North Sichuan Medical College and Nanchong Central Hospital between March 2016 and November 2018. This study was designed as a case-control study with 1:1 frequency matching, in which the parents of cases and controls were interviewed with the same questionnaire according to the gestational age of the child, maternal age during pregnancy and the same maternal race/ethnicity. Then, 322 matched case-control pairs were analysed by SPSS 22. Thirty-one suspicious factors were entered into the binary logistic regression analysis after univariate regression analysis of 55 factors (alpha = 0.05). The analysis results showed that 7 factors were significantly associated with the occurrence of CHD. Thus, augmenting maternal mental healthcare, improving the quality of drinking water, obtaining adequate nutrition, maintaining a healthy physical condition during pregnancy, enhancing parents' level of knowledge and maintaining a healthy lifestyle may lower the occurrence of CHD.


Assuntos
Cardiopatias Congênitas/etiologia , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/etiologia , Teratogênios/toxicidade , Criança , Pré-Escolar , China , Feminino , Humanos , Lactente , Masculino , Gravidez , Fatores de Risco
17.
Int J Mol Sci ; 21(6)2020 Mar 13.
Artigo em Inglês | MEDLINE | ID: mdl-32183232

RESUMO

Exposure to certain environmental factors during the early stages of development was found to affect health in adulthood. Among other environmental factors, oxidative stress has been suggested to be involved in fetal programming, leading to elevated risk for metabolic disorders, including type 2 diabetes; however, the possibility that antioxidant consumption during early life may affect the development of diabetes has scarcely been studied. The aim of this study was to investigate the effects of N-acetyl-l-cysteine (NAC) given during pregnancy and lactation on the susceptibility of offspring to develop glucose intolerance at adulthood. C57bl6/J mice were given NAC during pregnancy and lactation. High fat diet (HFD) was given to offspring at an age of 6 weeks for an additional 9 weeks, till the end of the study. Isolated islets of NAC-treated offspring (6 weeks old, before HFD feeding) had an increased efficacy of glucose-stimulated insulin secretion and a higher resistance to oxidative damage. Following HFD feeding, glucose tolerance and insulin sensitivity of NAC-treated offspring were improved. In addition, islet diameter was lower in male offspring of NAC-treated mice compared to their HFD-fed littermates. NAC consumption during early life improves glucose tolerance in adulthood in mice.


Assuntos
Acetilcisteína/uso terapêutico , Antioxidantes/uso terapêutico , Intolerância à Glucose/prevenção & controle , Obesidade Materna/etiologia , Efeitos Tardios da Exposição Pré-Natal/prevenção & controle , Acetilcisteína/administração & dosagem , Acetilcisteína/farmacologia , Animais , Antioxidantes/administração & dosagem , Antioxidantes/farmacologia , Células Cultivadas , Dieta Hiperlipídica/efeitos adversos , Feminino , Intolerância à Glucose/tratamento farmacológico , Intolerância à Glucose/etiologia , Células Secretoras de Insulina/efeitos dos fármacos , Células Secretoras de Insulina/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Gravidez , Efeitos Tardios da Exposição Pré-Natal/tratamento farmacológico , Efeitos Tardios da Exposição Pré-Natal/etiologia
18.
JAMA Netw Open ; 3(3): e201417, 2020 03 02.
Artigo em Inglês | MEDLINE | ID: mdl-32207831

RESUMO

Importance: An association between maternal exposure to magnetic field (MF) nonionizing radiation during pregnancy and the risk of attention-deficit/hyperactivity disorder (ADHD) has been reported in both animal and human studies. Objectives: To determine whether maternal exposure to high levels of MF nonionizing radiation is associated with an increased risk of ADHD in offspring by using more accurate measurements of MF nonionizing radiation levels and physician-diagnosed ADHD, rather than self-reports, and to determine whether the association differs for the subtypes of ADHD with or without immune-related comorbidities. Design, Setting, and Participants: A longitudinal birth cohort study was conducted at Kaiser Permanente Northern California among 1482 mother-child pairs whose mothers were participants of an existing birth cohort and whose level of exposure to MF nonionizing radiation was captured during pregnancy in 2 studies conducted from October 1, 1996, to October 31, 1998, and from May 1, 2006, to February 29, 2012. The offspring were followed up from May 1, 1997, to December 31, 2017. Exposure: All participating women wore a monitoring meter for 24 hours during pregnancy to capture the level of exposure to MF nonionizing radiation from any sources. Main Outcomes and Measures: Physician-diagnosed ADHD and immune-related comorbidities of asthma or atopic dermatitis up to 20 years of age in offspring captured in the Kaiser Permanente Northern California electronic medical record from May 1, 1997, to December 31, 2017. Confounders were ascertained during in-person interviews during pregnancy. Results: Among the 1454 mother-child pairs (548 white [37.7%], 110 African American [7.6%], 325 Hispanic [22.4%], 376 Asian or Pacific Islander [25.9%], and 95 other or unknown [6.5%]; mean [SD] maternal age, 31.4 [5.4] years]), 61 children (4.2%) had physician-diagnosed ADHD. Using Cox proportional hazards regression to account for follow-up time and confounders, compared with children whose mothers had a low level of exposure to MF nonionizing radiation during pregnancy, children whose mothers were exposed to higher levels of MF nonionizing radiation had more than twice the risk of ADHD (adjusted hazard ratio [aHR], 2.01; 95% CI, 1.06-3.81). The association was stronger for ADHD that persisted into adolescence (≥12 years of age), with an aHR of 3.38 (95% CI, 1.43-8.02). When the subtypes of ADHD were examined, the association existed primarily for ADHD with immune-related comorbidities (asthma or atopic dermatitis), with an aHR of 4.57 (95% CI, 1.61-12.99) for all ADHD cases and an aHR of 8.27 (95% CI, 1.96-34.79) for persistent cases of ADHD. Conclusions and Relevance: Consistent with the emerging literature, this study suggests that in utero exposure to high levels of MF nonionizing radiation was associated with an increased risk of ADHD, especially ADHD with immune-related comorbidity. The findings should spur more research to examine the biological association of in utero MF exposure with risk of ADHD in offspring, given that almost everyone is exposed to it.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade/epidemiologia , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Exposição à Radiação/efeitos adversos , Radiação não Ionizante/efeitos adversos , Adulto , Transtorno do Deficit de Atenção com Hiperatividade/etiologia , California/epidemiologia , Criança , Pré-Escolar , Estudos de Coortes , Feminino , Humanos , Estudos Longitudinais , Campos Magnéticos , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/psicologia , Modelos de Riscos Proporcionais , Adulto Jovem
19.
Life Sci ; 246: 117432, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-32061867

RESUMO

Our previous studies have shown that prenatal cold stress leads to placental inflammatory response and induces anxiety-like behavior reduced in offspring rats. However, the role and mechanisms by which prenatal cold stress affects offspring remain unclear. The aim of this study was to determine the metabolic profiles from the maternal serum and helpful in understanding the role and mechanisms by which prenatal cold stress affects the offspring. In this study, liquid chromatography-mass spectrometry (LC/MS) was used to analyze serum metabolites, and PCA, PLS-DA, and OPLS-DA were performed to analyze changes in metabolites in the maternal serum after cold stress of 3 or 7 days. The results showed that 19 metabolites in the CS (cold stress 7 days)-NS (control) group and 23 metabolites in the CT (cold stress 3 days)-NT (control) group were significantly altered. These metabolites were mainly associated with unsaturated fatty acid synthesis, and arachidonic acid, linoleic acid, and glutamine and glutamate metabolism. The data indicated that prenatal cold stress not only affected the maternal neuroendocrine system, but also affected the immune system, and lipid and amino acid metabolism. These results further supported the findings of our previous studies on the effects of prenatal cold stress on the mother and offspring. A more comprehensive understanding of these data may lead to maternal intervention that can reverse the damage of prenatal stressors.


Assuntos
Resposta ao Choque Frio , Metabolômica , Efeitos Tardios da Exposição Pré-Natal/etiologia , Animais , Feminino , Cromatografia Gasosa-Espectrometria de Massas , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/sangue , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Ratos , Ratos Wistar
20.
PLoS One ; 15(2): e0229323, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32092095

RESUMO

Recent research using the Avon Longitudinal Study of Parents and Children (ALSPAC) demonstrated an association between maternal grandmother smoking in pregnancy and the autistic traits of impaired social communication and repetitive behaviour in granddaughters but not grandsons, but of paternal grandmother smoking and early development of myopia in the grandchild. Here we investigate whether grandmaternal smoking in pregnancy is associated with intolerance to loud sounds. ALSPAC collected information during the index pregnancy from the study parents on the smoking habits, social and other features of their own parents. Maternal report when the child was aged 6 and 13 included hating loud sounds; at age 11 the child was tested for volume preference for listening to music through headphones. Statistical analysis compared results for grandchildren in relation to whether a parent had been exposed in utero to maternal smoking, adjusted for their grandparents' social and demographic attributes. We hypothesised that there would be sex differences in the effects of grandmaternal prenatal smoking, based on previous intergenerational studies. For 6-year-old children maternal report of intolerance to loud noise was more likely in grandsons if the maternal grandmother had smoked [adjusted odds ratio (AOR) 1.27; 95% confidence interval (CI) 1.03,1.56; P = 0.025], but less likely in girls [AOR 0.82; 95%CI 0.63,1.07] Pinteraction <0.05. If the paternal grandmother had smoked the grandchildren were less likely to be intolerant, especially girls. The objective measure of choice of volume for music through headphones showed that grandsons of both maternal and paternal smoking grandmothers were less likely to choose high volumes compared with granddaughters (P<0.05). In line with our prior hypothesis of sex differences, we showed that grandsons were more intolerant of loud sounds than granddaughters particularly at age 6, and this was confirmed by objective measures at age 11.


Assuntos
Transtorno do Espectro Autista/etiologia , Doença Ambiental/etiologia , Avós , Relação entre Gerações , Som/efeitos adversos , Fumar Tabaco , Adolescente , Transtorno do Espectro Autista/epidemiologia , Criança , Inglaterra/epidemiologia , Doença Ambiental/epidemiologia , Feminino , Humanos , Estudos Longitudinais , Masculino , Ruído/efeitos adversos , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Fatores de Risco , Comportamento Social , Fumar Tabaco/efeitos adversos , Fumar Tabaco/epidemiologia
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