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1.
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
2.
BJOG ; 127(1): 8-16, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31529594

RESUMO

BACKGROUND: With expanding recreational cannabis legalisation, pregnant women and their offspring are at risk of potentially harmful consequences. OBJECTIVES: To assess the prevalence of recreational cannabis use among pregnant women, health outcomes associated with prenatal recreational cannabis use, and the potential impact of recreational cannabis legalisation on this population. SEARCH STRATEGY: Five databases and the grey literature were systematically searched (2000-2019). SELECTION CRITERIA: Human studies published in English or French reporting on the prevalence of prenatal recreational cannabis use in high-income countries. DATA COLLECTION AND ANALYSIS: Data on study characteristics, prenatal substance use, and health outcomes were extracted and qualitatively synthesised. MAIN RESULTS: Forty-one publications met our inclusion criteria. The overall prevalence of prenatal cannabis use varied substantially (min-max: 0.24-22.6%), with the greatest use in the first trimester. In the three studies with temporal data available, rates of prenatal cannabis use increased across years. Only 7/41 and 5/41 studies provided information on gestational age of exposure and frequency of use, respectively. The concomitant use of alcohol, illicit drugs, and tobacco was higher among cannabis users than nonusers. Prenatal cannabis use was associated with select neonatal, but not maternal, health outcomes. There were insufficient data to compare prenatal cannabis use between the pre- and post-legalisation periods. CONCLUSION: Cannabis use among pregnant women is prevalent and may be associated with adverse neonatal outcomes. Future studies should assess the gestational age and frequency of cannabis exposure, and usage patterns prior to and following legalisation. TWEETABLE ABSTRACT: Women who consume cannabis during pregnancy could risk predisposing their newborns to poor birth outcomes.


Assuntos
Uso da Maconha/efeitos adversos , Complicações na Gravidez/etiologia , Países Desenvolvidos , Métodos Epidemiológicos , Feminino , Idade Gestacional , Humanos , Renda , Recém-Nascido de Baixo Peso , Terapia Intensiva Neonatal/estatística & dados numéricos , Uso da Maconha/epidemiologia , Uso da Maconha/legislação & jurisprudência , Saúde Materna , Gravidez , Complicações na Gravidez/epidemiologia , Resultado da Gravidez/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia
3.
BMJ ; 367: l6398, 2019 12 04.
Artigo em Inglês | MEDLINE | ID: mdl-31801789

RESUMO

OBJECTIVE: To evaluate the associations between maternal diabetes diagnosed before or during pregnancy and early onset cardiovascular disease (CVD) in offspring during their first four decades of life. DESIGN: Population based cohort study. SETTING: Danish national health registries. PARTICIPANTS: All 2 432 000 liveborn children without congenital heart disease in Denmark during 1977-2016. Follow-up began at birth and continued until first time diagnosis of CVD, death, emigration, or 31 December 2016, whichever came first. EXPOSURES FOR OBSERVATIONAL STUDIES: Pregestational diabetes, including type 1 diabetes (n=22 055) and type 2 diabetes (n=6537), and gestational diabetes (n=26 272). MAIN OUTCOME MEASURES: The primary outcome was early onset CVD (excluding congenital heart diseases) defined by hospital diagnosis. Associations between maternal diabetes and risks of early onset CVD in offspring were studied. Cox regression was used to assess whether a maternal history of CVD or maternal diabetic complications affected these associations. Adjustments were made for calendar year, sex, singleton status, maternal factors (parity, age, smoking, education, cohabitation, residence at childbirth, history of CVD before childbirth), and paternal history of CVD before childbirth. The cumulative incidence was averaged across all individuals, and factors were adjusted while treating deaths from causes other than CVD as competing events. RESULTS: During up to 40 years of follow-up, 1153 offspring of mothers with diabetes and 91 311 offspring of mothers who did not have diabetes were diagnosed with CVD. Offspring of mothers with diabetes had a 29% increased overall rate of early onset CVD (hazard ratio 1.29 (95% confidence interval 1.21 to 1.37); cumulative incidence among offspring unexposed to maternal diabetes at 40 years of age 13.07% (12.92% to 13.21%), difference in cumulative incidence between exposed and unexposed offspring 4.72% (2.37% to 7.06%)). The sibship design yielded results similar to those of the unpaired design based on the whole cohort. Both pregestational diabetes (1.34 (1.25 to 1.43)) and gestational diabetes (1.19 (1.07 to 1.32)) were associated with increased rates of CVD in offspring. We also observed varied increased rates of specific early onset CVDs, particularly heart failure (1.45 (0.89 to 2.35)), hypertensive disease (1.78 (1.50 to 2.11)), deep vein thrombosis (1.82 (1.38 to 2.41)), and pulmonary embolism (1.91 (1.31 to 2.80)). Increased rates of CVD were seen in different age groups from childhood to early adulthood until age 40 years. The increased rates were more pronounced among offspring of mothers with diabetic complications (1.60 (1.25 to 2.05)). A higher incidence of early onset CVD in offspring of mothers with diabetes and comorbid CVD (1.73 (1.36 to 2.20)) was associated with the added influence of comorbid CVD but not due to the interaction between diabetes and CVD on the multiplicative scale (P value for interaction 0.94). CONCLUSIONS: Children of mothers with diabetes, especially those mothers with a history of CVD or diabetic complications, have increased rates of early onset CVD from childhood to early adulthood. If maternal diabetes does have a causal association with increased CVD rate in offspring, the prevention, screening, and treatment of diabetes in women of childbearing age could help to reduce the risk of CVD in the next generation.


Assuntos
Doenças Cardiovasculares/epidemiologia , Diabetes Mellitus/fisiopatologia , Diabetes Gestacional/fisiopatologia , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Adulto , Doenças Cardiovasculares/etiologia , Dinamarca/epidemiologia , Feminino , Seguimentos , Humanos , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Adulto Jovem
4.
Environ Health Prev Med ; 24(1): 74, 2019 Dec 07.
Artigo em Inglês | MEDLINE | ID: mdl-31812162

RESUMO

BACKGROUND: There have been inconsistent findings reported on maternal passive smoking during pregnancy and child risk of ADHD. In this study, ADHD symptoms at pre-school age children in association with prenatal passive and active tobacco smoke exposure determined by maternal plasma cotinine levels in the third trimester were investigated. METHODS: This was a follow-up study of the birth cohort: the Hokkaido Study on Environment and Children's Health. Children whose parents answered Strengths and Difficulties Questionnaire (SDQ) to identify child ADHD symptoms (hyperactivity/inattention and conduct problems) and total difficulties at age 5 years with available maternal plasma cotinine level at the third trimester were included (n = 3216). Cotinine levels were categorized into 4 groups; ≦ 0.21 ng/ml (non-smoker), 0.22-0.51 ng/ml (low-passive smoker), 0.52-11.48 ng/ml (high-passive smoker), and ≧ 11.49 ng/ml (active smoker). RESULTS: Maternal cotinine levels of active smokers were significantly associated with an increased risk of total difficulties (OR = 1.67) and maternal low- and high-passive smoking also increased the risk (OR = 1.11, 1.25, respectively) without statistical significance. Similarly, maternal cotinine levels of active smokers were associated with an increased risk of hyperactivity/inattention (OR = 1.49). Maternal low- and high-passive smoking and active smoking increased the risk of hyperactivity/inattention (OR = 1.45, 1.43, and OR = 1.59, respectively) only in boys. CONCLUSION: Our findings suggested that maternal active smoking during pregnancy may contribute to the increased risk of child total difficulties and hyperactivity/inattention at pre-school age. Pregnant women should be encouraged to quit smoking and avoid exposure to tobacco smoke.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade/etiologia , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/etiologia , Fumar Tabaco/efeitos adversos , Adulto , Transtorno do Deficit de Atenção com Hiperatividade/epidemiologia , Transtorno do Deficit de Atenção com Hiperatividade/fisiopatologia , Transtorno do Deficit de Atenção com Hiperatividade/psicologia , Pré-Escolar , Cotinina/sangue , Feminino , Seguimentos , Humanos , Japão/epidemiologia , Masculino , Mães , Gravidez , Terceiro Trimestre da Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Risco , Fatores Sexuais , Fumar Tabaco/epidemiologia
5.
PLoS Med ; 16(11): e1002972, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31721775

RESUMO

BACKGROUND: Maternal smoking during pregnancy is an established risk factor for low infant birth weight, but evidence on critical exposure windows and timing of fetal growth restriction is limited. Here we investigate the associations of maternal quitting, reducing, and continuing smoking during pregnancy with longitudinal fetal growth by triangulating evidence from 3 analytical approaches to strengthen causal inference. METHODS AND FINDINGS: We analysed data from 8,621 European liveborn singletons in 2 population-based pregnancy cohorts (the Generation R Study, the Netherlands 2002-2006 [n = 4,682]) and the Born in Bradford study, United Kingdom 2007-2010 [n = 3,939]) with fetal ultrasound and birth anthropometric measures, parental smoking during pregnancy, and maternal genetic data. Associations with trajectories of estimated fetal weight (EFW) and individual fetal parameters (head circumference, femur length [FL], and abdominal circumference [AC]) from 12-16 to 40 weeks' gestation were analysed using multilevel fractional polynomial models. We compared results from (1) confounder-adjusted multivariable analyses, (2) a Mendelian randomization (MR) analysis using maternal rs1051730 genotype as an instrument for smoking quantity and ease of quitting, and (3) a negative control analysis comparing maternal and mother's partner's smoking associations. In multivariable analyses, women who continued smoking during pregnancy had a smaller fetal size than non-smokers from early gestation (16-20 weeks) through to birth (p-value for each parameter < 0.001). Fetal size reductions in continuing smokers followed a dose-dependent pattern (compared to non-smokers, difference in mean EFW [95% CI] at 40 weeks' gestation was -144 g [-182 to -106], -215 g [-248 to -182], and -290 g [-334 to -247] for light, moderate, and heavy smoking, respectively). Overall, fetal size reductions were most pronounced for FL. The fetal growth trajectory in women who quit smoking in early pregnancy was similar to that of non-smokers, except for a shorter FL and greater AC around 36-40 weeks' gestation. In MR analyses, each genetically determined 1-cigarette-per-day increase was associated with a smaller EFW from 20 weeks' gestation to birth in smokers (p = 0.01, difference in mean EFW at 40 weeks = -45 g [95% CI -81 to -10]) and a greater EFW from 32 weeks' gestation onwards in non-smokers (p = 0.03, difference in mean EFW at 40 weeks = 26 g [95% CI 5 to 47]). There was no evidence that partner smoking was associated with fetal growth. Study limitations include measurement error due to maternal self-report of smoking and the modest sample size for MR analyses resulting in unconfounded estimates being less precise. The apparent positive association of the genetic instrument with fetal growth in non-smokers suggests that genetic pleiotropy may have masked a stronger association in smokers. CONCLUSIONS: A consistent linear dose-dependent association of maternal smoking with fetal growth was observed from the early second trimester onwards, while no major growth deficit was found in women who quit smoking early in pregnancy except for a shorter FL during late gestation. These findings reinforce the importance of smoking cessation advice in preconception and antenatal care and show that smoking reduction can lower the risk of impaired fetal growth in women who struggle to quit.


Assuntos
Peso ao Nascer/efeitos dos fármacos , Fumar Cigarros/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/etiologia , Adulto , Feminino , Desenvolvimento Fetal , Retardo do Crescimento Fetal/etiologia , Peso Fetal , Feto , Idade Gestacional , Humanos , Recém-Nascido , Recém-Nascido Pequeno para a Idade Gestacional , Exposição Materna/efeitos adversos , Análise da Randomização Mendeliana , Países Baixos/epidemiologia , Gravidez , Primeiro Trimestre da Gravidez/efeitos dos fármacos , Estudos Prospectivos , Abandono do Hábito de Fumar/psicologia , Reino Unido/epidemiologia
6.
Food Funct ; 10(11): 7216-7226, 2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31612177

RESUMO

Offspring of dams exposed to excess folic acid during the perigestational period have been shown by us to be predisposed to metabolic dysfunction revealed by hyperglycemia, glucose intolerance, increased insulin and decreased adiponectin in late adulthood. This work aims to characterize adipocyte phenotype and expression profile of genes in the regulation of lipid and glucose metabolism in visceral adipose tissue and in skeletal muscle. From mating until weaning, a recommended dose of folic acid for pregnancy (C, 2 mg of folic acid per kg of diet) or a high folic acid dose (HFA, 40 mg of folic acid per kg of diet) was administered to Sprague-Dawley females. At 10 months of age progeny were divided into groups fed the standard chow (C/STD and HFA/STD) and groups fed the standard chow plus drinking water with 10% fructose (C/FRU and HFA/FRU), as an additional metabolic challenge. Adipocyte morphology and quantification of key genes involved in lipid and glucose metabolism were studied in visceral adipose tissue and skeletal muscle of 13 months old offspring. HFA exposure led to an enlargement of visceral adipose cells most likely mediated by an upregulation of lipoprotein lipase, and it tended to downregulate Glut4 in visceral adipose tissue and skeletal muscle. Fructose exposure in a background of perigestational excess folic acid, but not in controls, induced an upregulation of lipogenesis pathway genes and it decreased jejunal expression of the proton-coupled folate transporter (Pcft1). In addition, fructose exposure led to a downregulation of jejunal Sglt1 in control animals. Our data suggest that high folic acid exposure during the perigestational period caused morphologic and genic alterations related to insulin resistant states indicating that this intervention may act as an effective programmer of long-term metabolic dysfunction.


Assuntos
Suplementos Nutricionais/efeitos adversos , Ácido Fólico/efeitos adversos , Doenças Metabólicas/etiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Animais , Suplementos Nutricionais/análise , Feminino , Ácido Fólico/administração & dosagem , Transportador de Glucose Tipo 4/genética , Transportador de Glucose Tipo 4/metabolismo , Resistência à Insulina , Gordura Intra-Abdominal/metabolismo , Masculino , Fenômenos Fisiológicos da Nutrição Materna , Doenças Metabólicas/genética , Doenças Metabólicas/metabolismo , Músculo Esquelético/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/genética , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Transportador de Folato Acoplado a Próton/genética , Transportador de Folato Acoplado a Próton/metabolismo , Ratos , Ratos Sprague-Dawley
7.
Artigo em Inglês | MEDLINE | ID: mdl-31623306

RESUMO

This study aimed to investigate the association between environmental exposure to tobacco smoke (ETS) during early life and astigmatism in Chinese preschool children. In this cross-sectional study, information concerning prenatal and postnatal ETS exposure at three stages of early life (during pregnancy, from birth to one year and from one to three years), visual problems of children and parents (including a confirmed diagnosis of astigmatism), socio-demographics and perinatal characteristics were obtained from 27,890 parent-reported questionnaires. Logistic regression analyses were undertaken to yield adjusted odds ratios (OR) for assessing their associations. After adjusting for the potential confounders, children were more likely to exhibit astigmatism when they were exposed to ETS during pregnancy + from one to three years [OR (95% CI) = 1.37 (1.02, 1.84)], or from birth to one year + from one to three years [OR (95% CI) = 1.36 (1.11, 1.66)], or during pregnancy + from birth to one year + from one to three years old [OR (95% CI) = 1.29 (1.16, 1.45)], compared to children without ETS exposure at any stage of early life. In Chinese preschool children, prenatal and postnatal astigmatism was associated with ETS exposure; the greater the ETS dose, the greater the astigmatism risk.


Assuntos
Astigmatismo/etiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Astigmatismo/epidemiologia , Astigmatismo/fisiopatologia , Pré-Escolar , China/epidemiologia , Estudos Transversais , Feminino , Humanos , Lactente , Recém-Nascido , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Poluição por Fumaça de Tabaco/estatística & dados numéricos
8.
Int J Gynaecol Obstet ; 147(3): 292-300, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31520411

RESUMO

BACKGROUND: Betel nut is the fourth most commonly abused substance worldwide and has been associated with significant adverse health outcomes. Little is known about its effects on the fetus. OBJECTIVE: To perform a systematic review of studies investigating prenatal betel nut use and adverse perinatal outcomes. SEARCH STRATEGY: Pubmed, Embase, and Cochrane databases were searched from inception until July 2018 using the terms areca, betel nut, pregnancy, pregnancy complications, and infection. SELECTION CRITERIA: Eligible studies included case-control, cohort, and randomized control studies involving pregnant women. DATA COLLECTION AND ANALYSIS: Where appropriate, bivariate meta-analysis was performed, and odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. MAIN RESULTS: In total, 28 studies were screened and eight studies (including 15 270 women) were included in the review and meta-analysis. Preterm birth, low birthweight, and anemia were most commonly investigated. Meta-analysis revealed a significant association between betel nut use and low birthweight, with a pooled OR of 1.75 (95% CI, 1.35-2.27). CONCLUSIONS: The review identified only eight eligible studies, all based in the Asia-Pacific region. There was a significant association between low birthweight and betel nut exposure in pregnancy. Further prospective studies are needed to confirm this association.


Assuntos
Areca/efeitos adversos , Nascimento Prematuro/induzido quimicamente , Efeitos Tardios da Exposição Pré-Natal/etiologia , Transtornos Relacionados ao Uso de Substâncias , Adulto , Feminino , Humanos , Recém-Nascido de Baixo Peso , Recém-Nascido , Gravidez , Complicações na Gravidez/etiologia , Resultado da Gravidez , Nascimento Prematuro/etiologia , Estudos Prospectivos
9.
Life Sci ; 233: 116741, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31398419

RESUMO

AIMS: Carbon black nanoparticles (CBNPs) are widely used in industrial field. Sensitive stages such as pregnancy are assumed to be more susceptible to stimulus, however whether pregnancy exposure to CBNPs (PrE-to-CBNPs) would cause long-term toxic effects in dams and the underlying mechanisms remain poorly addressed. The present study is aimed to determine the long-term toxic effects of PrE-to-CBNPs in dams. MATERIALS AND METHODS: The pregnant mice were randomly divided into control group, low (21 µg/animal), medium (103 µg/animal) and high (515 µg/animal) CBNPs-treated groups. From gestational day (GD) 9 to GD18, the pregnant mice were intranasal exposed. At 49 days after parturition, lung tissues and bronchoalveolar lavage fluid (BALF) were obtained. Weight change, lung histopathology, lung ultrastructural pathology, cell count in BALF, oxidative stress/inflammatory maker and autophagy/lysosome-related protein expression were determined. KEY FINDINGS: PrE-to-CBNPs caused a dose-dependent persistent lung injury in mice even 49 days after parturition, including the deteriorative lung histopathological changes, elevation of oxidative stress marker Nrf-2, HO-1 and CHOP, infiltration of macrophage and increased mRNA expression of inflammatory cytokines in the lung tissues and elevation of cells in BALF. However, PrE-to-CBNPs did not induce significant neutrophil infiltration and fibrosis. Moreover, we found that CBNPs could deposit in the lysosomes and decrease cathepsin D (an important hydrolase in lysosome), which might be associated with the dysfunction of lysosome and autophagy. SIGNIFICANCE: Our study demonstrated that PrE-to-CBNPs could result in long-term lung injury in dams, and lysosomal dysfunction was probably linked to this process.


Assuntos
Inflamação/complicações , Lesão Pulmonar/etiologia , Lisossomos/patologia , Nanopartículas/efeitos adversos , Estresse Oxidativo , Efeitos Tardios da Exposição Pré-Natal/etiologia , Fuligem/efeitos adversos , Animais , Autofagia , Citocinas/metabolismo , Feminino , Lesão Pulmonar/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Gravidez , Efeitos Tardios da Exposição Pré-Natal/patologia
10.
BMJ Case Rep ; 12(8)2019 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-31420423

RESUMO

Neonatal hypoparathyroidism is one of the rare causes of hypocalcaemia. Several cases of neonatal hypoparathyroidism secondary to maternal hyperparathyroidism have been reported. In this case report, we have a term neonate with normal birth history who presented with late onset hypocalcemic seizures. After excluding polyendocrinopathies and related syndromes, hypocalcaemia seizures were secondary to maternal asymptomatic hypoparathyroidism. Since this is one variety of unusual case of maternal and fetal hypoparathyroidism, further testing was mandatory to confirm familial origin. This focuses on the need for every clinician to test maternal metabolic status in case of neonatal manifestations.


Assuntos
Hipocalcemia/etiologia , Hipoparatireoidismo/complicações , Doenças do Recém-Nascido/etiologia , Complicações na Gravidez/etiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Convulsões/etiologia , Feminino , Humanos , Recém-Nascido , Gravidez
11.
Pediatrics ; 144(2)2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31266824

RESUMO

OBJECTIVE: In this study, we determined the prevalence of hearing loss in 157 children with proven congenital cytomegalovirus (cCMV) infection. We looked at possible risk determinants for developing hearing loss and proposed recommendations for screening and follow-up in the newborn. METHODS: In a prospective 22-year study, 157 children with proven cCMV infection were evaluated for sensorineural hearing loss (SNHL). The development of SNHL was correlated with the type of maternal infection (primary versus nonprimary), the gestational age of maternal primary infection, imaging findings at birth, and the presence of symptomatic or asymptomatic infection in the newborn. RESULTS: Of all children, 12.7% had SNHL, and 5.7% needed hearing amplification because of SNHL. Improvement, progression, and fluctuations of hearing thresholds were seen in 45%, 53.8%, and 5.7% of the children, respectively. Hearing loss was more common in the case of a symptomatic infection at birth (P = .017), after a maternal primary infection in the first trimester of pregnancy (P = .029), and in the presence of abnormalities on a neonatal brain ultrasound and/or MRI (P < .001). CONCLUSION: SNHL is a common sequela in children with cCMV infection. Risk factors for SNHL were primary maternal infections before the 14th week of pregnancy, the presence of a disseminated infection at birth, and imaging abnormalities in the newborn. These children may benefit from a more thorough investigation for SNHL than children who do not present with those risk factors.


Assuntos
Infecções por Citomegalovirus/complicações , Infecções por Citomegalovirus/diagnóstico por imagem , Perda Auditiva/diagnóstico por imagem , Perda Auditiva/etiologia , Efeitos Tardios da Exposição Pré-Natal/diagnóstico por imagem , Efeitos Tardios da Exposição Pré-Natal/etiologia , Pré-Escolar , Feminino , Seguimentos , Humanos , Lactente , Recém-Nascido , Masculino , Triagem Neonatal/métodos , Gravidez , Estudos Prospectivos
12.
Biomed Res Int ; 2019: 3426092, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31281833

RESUMO

Anxiety is one of the most frequent psychiatric disorders. Despite the fact that most studies describe an anxiolytic effect of testosterone, hyperandrogenemia in mothers is assumed to be related to an increased risk of mood disorders in their offspring. An increasing body of scientific evidence suggests that an altered expression of interneuronal markers of the hippocampus may be the cause of anxiety. The aim of this study was to examine the influence of maternal hyperandrogenemia on behavioral parameters of anxiety-like behavior, neuropeptide Y (NPY) and parvalbumin (PV) expression in the hippocampus, and the level of the brain-derived neurotrophic factor (BDNF) in the hippocampus and cerebral cortex. Pregnant female Wistar albino rats were treated with testosterone undecanoate on the 20th day of gestation. Anxiety-like behavior in adult female offspring was evaluated by the elevated plus maze test and the open field. The number of PV and NPY immunoreactive cells in the hippocampus was determined immunohistochemically. The level of BDNF expression in the hippocampus and cerebral cortex was analyzed with the Western blot test. Prenatal hyperandrogenization increased anxiety-like behavior in female offspring and decreased expression of NPY+ and PV+ in the CA1 region of the hippocampus as compared to the control group. BDNF expression in the hippocampus and cerebral cortex of prenatally androgenized female offspring was significantly increased in comparison with the controls. Prenatal hyperandrogenization may be the cause of anxiety-like behavior in female offspring. Decrease in NPY and PV expression in the hippocampus may explain the possible mechanism of hyperandrogenization induced anxiety.


Assuntos
Ansiedade/etiologia , Comportamento Animal , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Hipocampo/metabolismo , Interneurônios/fisiologia , Inibição Neural/fisiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Virilismo/complicações , Animais , Ansiedade/sangue , Ansiedade/fisiopatologia , Estradiol/sangue , Feminino , Hipocampo/fisiopatologia , Aprendizagem em Labirinto , Neuropeptídeo Y/metabolismo , Parvalbuminas/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/sangue , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Ratos Wistar , Testosterona/administração & dosagem , Testosterona/sangue , Testosterona/farmacologia , Virilismo/fisiopatologia
13.
Nat Rev Endocrinol ; 15(8): 456-478, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31270440

RESUMO

Maternal lifestyle during pregnancy, as well as early nutrition and the environment infants are raised in, are considered relevant factors for the prevention of childhood obesity. Several models are available for the prediction of childhood overweight and obesity, yet most have not been externally validated. Moreover, the factors considered in the models differ among studies as the outcomes manifest after birth and depend on maturation processes that vary between individuals. The current Review examines and interprets data on the early determinants of childhood obesity to provide relevant strategies for daily clinical work. We evaluate a selection of prenatal and postnatal factors associated with child adiposity. Actions to be considered for preventing childhood obesity include the promotion of healthy maternal nutrition and weight status at reproductive age and during pregnancy, as well as careful monitoring of infant growth to detect early excessive weight gain. Paediatricians and other health-care professionals should provide scientifically validated, individual nutritional advice to families to counteract excessive adiposity in children. Based on systematic reviews, original papers and scientific reports, we provide information to help with setting up public health strategies to prevent overweight and obesity in childhood.


Assuntos
Fertilização , Saúde Materna/tendências , Obesidade Pediátrica/etiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Aleitamento Materno/tendências , Criança , Feminino , Fertilização/fisiologia , Humanos , Lactente , Recém-Nascido , Obesidade Pediátrica/diagnóstico , Obesidade Pediátrica/prevenção & controle , Gravidez , Efeitos Tardios da Exposição Pré-Natal/diagnóstico , Efeitos Tardios da Exposição Pré-Natal/prevenção & controle , Fatores de Risco
14.
Food Funct ; 10(8): 5018-5031, 2019 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-31355385

RESUMO

Maternal restriction of dietary proteins during pregnancy and lactation is known to induce renal disease in later life. High fructose intake causes metabolic syndrome, which results in an increased risk of chronic kidney disease development. We investigated whether quercetin intake during lactation affects high-fructose-diet-induced inflammation and autophagy flux in the kidneys of high-fructose-diet-fed adult female offspring exposed to maternal normal-protein (NP) or low-protein (LP) diets. Pregnant Wistar rats received diets containing 20% (NP) or 8% (LP) casein, and 0 or 0.2% quercetin containing NP diets (NP/NP or NP/NPQ) in experiment (Expt.) 1 and 0 or 0.2% quercetin containing LP diets (LP/LP or LP/LPQ) in Expt. 2 during lactation. At weaning, pups that received a diet of distilled water (Wa) or 10% fructose solution (Fr) were divided into six groups: NP/NP/Wa, NP/NP/Fr, NP/NPQ/Fr in Expt. 1, and LP/LP/Wa, LP/LP/Fr, LP/LPQ/Fr in Expt. 2. At week 12, macrophage infiltration, mRNA levels of TNF-α and IL-6, and markers of autophagy flux in the kidneys of male offspring were examined. We found that macrophage number and, TNF-α and IL-6 mRNA levels increased in the kidneys of the NP/NP/Fr or LP/LP/Fr, respectively. Conversely, macrophage number and IL-6 levels in the NP/NPQ/Fr or LP/LPQ/Fr decreased. LC3B-II levels were downregulated in the NP/NP/Fr or LP/LP/Fr rats. In contrast, LC3B-II levels were upregulated, while p62 levels were downregulated in the NP/NPQ/Fr and LP/LPQ/Fr rats. In conclusion, maternal quercetin intake during lactation may cause long-term alterations in inflammation and autophagy flux in the kidneys of high-fructose-diet-fed adult female offspring.


Assuntos
Autofagia/efeitos dos fármacos , Frutose/efeitos adversos , Nefropatias/prevenção & controle , Desnutrição/complicações , Efeitos Tardios da Exposição Pré-Natal/prevenção & controle , Quercetina/administração & dosagem , Animais , Feminino , Frutose/metabolismo , Humanos , Interleucina-6/genética , Interleucina-6/imunologia , Rim/efeitos dos fármacos , Rim/imunologia , Rim/fisiopatologia , Nefropatias/etiologia , Nefropatias/imunologia , Nefropatias/fisiopatologia , Lactação , Masculino , Desnutrição/metabolismo , Fenômenos Fisiológicos da Nutrição Materna , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/imunologia , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Ratos , Ratos Wistar , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/imunologia
15.
Food Funct ; 10(8): 4505-4521, 2019 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-31348478

RESUMO

Adverse early-life exposures program an increased risk of chronic metabolic diseases in adulthood. However, the effects of genistein consumption in early life on metabolic health are unclear. Our objective was to investigate whether perinatal genistein intake could mitigate the deleterious effects of a high-fat diet (HF) on metabolism in dams and female offspring and to explore the role of the gut microbiota in mediating the transgenerational effects. C57BL/6 female mice were fed a HF, HF with genistein (0.6 g kg-1 diet) or normal control diet for 3 weeks before mating and throughout pregnancy and lactation. The offspring had free access to normal diet from weaning to 24 weeks of age. A glucose tolerance test was performed and the levels of serum insulin and lipid were measured. The cecal contents were collected for 16s rDNA sequencing. The results showed that perinatal genistein intake could not only significantly reduce blood glucose levels, insulin and free fatty acids (FFA) in dams, but also improve glucose tolerance, insulin sensitivity and serum lipid profiles in adult female offspring. Significant enrichment of short-chain fatty acid (mainly butyrate)-producing bacteria might play crucial roles in deciphering the metabolic benefits of perinatal genistein intake in dams. The obvious decrease in harmful microorganisms and increase in Erysipelotrichaceae_incertae_sedis were associated with the protective effects of maternal genistein intake on female offspring. In addition, Bifidobacterium might be an important factor for deciphering the metabolic improvement in both dams and female offspring by dietary genistein. Overall, perinatal genistein intake attenuated the harmful effects of HF on metabolism in both dams and female offspring, and the protective effects were associated with the alterations in the gut microbiota, which provides new evidence and targets for mitigating the poor effects of adverse early-life exposures on metabolic health in later life.


Assuntos
Microbioma Gastrointestinal , Genisteína/metabolismo , Doenças Metabólicas/prevenção & controle , Efeitos Tardios da Exposição Pré-Natal/prevenção & controle , Animais , Glicemia/metabolismo , Dieta Hiperlipídica/efeitos adversos , Feminino , Teste de Tolerância a Glucose , Humanos , Insulina/sangue , Masculino , Fenômenos Fisiológicos da Nutrição Materna , Doenças Metabólicas/etiologia , Doenças Metabólicas/metabolismo , Doenças Metabólicas/microbiologia , Camundongos , Camundongos Endogâmicos C57BL , Linhagem , Assistência Perinatal , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Efeitos Tardios da Exposição Pré-Natal/microbiologia
16.
Life Sci ; 233: 116689, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31348949

RESUMO

BACKGROUND: Maternal metabolic syndrome during gestation and lactation leads to several Se-status-related metabolic changes in offspring. MS leads to hepatomegaly, liver oxidation, resistance to insulin challenges and selenoptroteins expression upregulation, producing an energy imbalance in hepatocytes. As Se is necessary for correct heart function, Se deposits are depleted and selenoproteins expression downregulated in heart; this depletion being related to cardiovascular damage. Recently, selenoproteins have been directly implicated in the central endocrine regulation of appetite and energy homeostasis. METHODS: To obtain information about how Se is involved in regulating endocrine peripheral energy balance during MS process, two experimental groups of dam rats were used: control (Se: 0.1 ppm) and MS (Fructose 65% and Se: 0.1 ppm). At the end of lactation (21d old), the pups' appetite profile, tissular Se deposits and peptides from gastrointestinal tract (including pancreas), leptin, skeletal growth markers and cytokines in serum were measured. RESULTS: MS-exposed pups present changes in Se homeostasis, appetite profile and endocrine energy balance signals related to impaired insulin secretion and high leptin serum values. This profoundly affects the pups' growth profile since muscle and bones are in catabolic process and brown adipose tissue (BAT) mass decreases. CONCLUSION: These results indicate that the pups are suffering a process similar to diabetes type 1 which appeared when dams received low Se dietary supply and they point to Se as an important marker and key treatment for these disorders during gestation and lactation that affect future adult health.


Assuntos
Doenças do Sistema Endócrino/etiologia , Metabolismo Energético/efeitos dos fármacos , Desenvolvimento Fetal/efeitos dos fármacos , Síndrome Metabólica/complicações , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Selênio/administração & dosagem , Animais , Biomarcadores/sangue , Doenças do Sistema Endócrino/patologia , Feminino , Homeostase , Resistência à Insulina , Leptina/sangue , Masculino , Fenômenos Fisiológicos da Nutrição Materna , Síndrome Metabólica/tratamento farmacológico , Estresse Oxidativo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Ratos , Ratos Wistar , Selênio/efeitos adversos , Selênio/sangue
17.
BMC Res Notes ; 12(1): 423, 2019 Jul 16.
Artigo em Inglês | MEDLINE | ID: mdl-31311588

RESUMO

Epidemiologic and cross-sectional studies suggest that early life farming and animal exposures are associated with major health benefits, influencing immune development and modifying the subsequent risk of allergic diseases, including asthma. The Wisconsin Infant Study Cohort (WISC) study was established in central Wisconsin to test the hypothesis that early life animal farm exposures are associated with distinct innate immune cell maturation trajectories, decreased allergen sensitization and reduced respiratory viral illness burden during the first 2 years of life. Beginning in 2013, a total of 240 families have been enrolled, 16,522 biospecimens have been collected, and 4098 questionnaires have been administered and entered into a secure database. Study endpoints include nasal respiratory virus identification and respiratory illness burden score, allergic sensitization, expression of allergic disease, and anti-viral immune response maturation and profiles. The WISC study prospective design, broad biospecimen collections, and unique US rural community will provide insights into the role of environmental exposures on early life immune maturation profiles associated with protection from allergic sensitization and significant respiratory viral disease burden. The WISC study findings will ultimately inform development of new strategies to promote resistance to severe respiratory viral illnesses and design primary prevention approaches for allergic diseases for all infants.


Assuntos
Asma/diagnóstico , Exposição Ambiental/análise , Fazendas , Hipersensibilidade/diagnóstico , Adulto , Animais , Asma/epidemiologia , Asma/etiologia , Estudos Transversais , Exposição Ambiental/efeitos adversos , Feminino , Humanos , Hipersensibilidade/epidemiologia , Hipersensibilidade/etiologia , Lactente , Masculino , Idade Materna , Gravidez , Efeitos Tardios da Exposição Pré-Natal/diagnóstico , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Estudos Prospectivos , Projetos de Pesquisa , Wisconsin/epidemiologia
18.
PLoS One ; 14(6): e0218539, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31220154

RESUMO

Zika virus (ZIKV) is a mosquito-borne flavivirus associated with microcephaly and other neurological disorders in infants born to infected mothers. Despite being declared an international emergency by the World Health Organization, very little is known about the mechanisms of ZIKV pathogenesis or the long-term consequences of maternal ZIKV infection in the affected offspring, largely due to the lack of appropriate rodent models. To address this issue, our lab has developed a working model of prenatal ZIKV infection in rats. In this study, we infected immune competent pregnant female rats with 105-107 PFU of ZIKV (PRVABC59, Puerto Rico/Human/Dec 2015) in order to examine its pathogenesis in the dams and pups. We examined the febrile response and sickness behavior in the dams, in addition to neonatal mortality, microglia morphology, cortical organization, apoptosis, and brain region-specific volumes in the offspring. Here, we demonstrate that pregnant and non-pregnant female rats have a distinct febrile response to ZIKV infection. Moreover, prenatal ZIKV infection increased cell death and reduced tissue volume in the hippocampus and cortex in the neonatal offspring. For the first time, we demonstrate the efficacy and validity of an immunocompetent rat model for maternal ZIKV infection that results in significant brain malformations in the neonatal offspring.


Assuntos
Efeitos Tardios da Exposição Pré-Natal/patologia , Convulsões/patologia , Infecção por Zika virus/patologia , Animais , Apoptose , Córtex Cerebral/metabolismo , Córtex Cerebral/patologia , Feminino , Hipocampo/metabolismo , Hipocampo/patologia , Masculino , Microglia/metabolismo , Microglia/patologia , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Ratos , Ratos Sprague-Dawley , Convulsões/etiologia , Convulsões/fisiopatologia , Células Vero , Infecção por Zika virus/complicações , Infecção por Zika virus/fisiopatologia
19.
Environ Toxicol ; 34(10): 1105-1113, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31240815

RESUMO

The aim of the present study was to evaluate the effects of maternal exposure to triclosan (TCS) during pregnancy and lactation on the uterine morphology of rat offspring. For this, 32 Wistar rat dams were distributed into four dose groups (eight mothers per group), and gavage daily, throughout pregnancy and lactation, as follows: Group I-control (GI): corn oil; Group II (GII): TCS diluted in corn oil at a dose of 75 mg/kg/d; Group III (GIII): TCS diluted in corn oil at a dose of 150 mg/kg/d; Group IV (GIV): TCS diluted in corn oil at a dose of 300 mg/kg/d. A female pup of each mother was selected, and at 90 days the pups were euthanized for weighing and collection of the uterus for histomorphometric analysis. The results showed that the mean litter weight was minor in all the groups treated with TCS, when compared with control. The levels thyroid hormones thyroxine (T4) and triiodothyronine (T3) in TCS mother rats were reduced; however the levels of thyroid stimulating hormone (TSH) were increases. The offspring of all groups exposed to TCS presented deregulation of the estrous cycle, compared with control. Analysis of the uterine histological structure demonstrated that all layers of the uterus were affected by the administration of TCS, and the morphometric analysis showed increased uterine layers thickness in the treated groups. We concluded that maternal exposure to TCS during pregnancy and lactation causes intrauterine development restriction, deregulation of the oestrous cycle, and alters uterine tissue in rat offspring.


Assuntos
Anti-Infecciosos Locais/efeitos adversos , Retardo do Crescimento Fetal/etiologia , Exposição Materna/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Triclosan/efeitos adversos , Útero/crescimento & desenvolvimento , Animais , Ciclo Estral/efeitos dos fármacos , Feminino , Desenvolvimento Fetal/efeitos dos fármacos , Retardo do Crescimento Fetal/fisiopatologia , Humanos , Lactação/efeitos dos fármacos , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Ratos , Ratos Wistar , Hormônios Tireóideos/metabolismo , Útero/efeitos dos fármacos , Útero/fisiologia
20.
BMC Pregnancy Childbirth ; 19(1): 189, 2019 May 30.
Artigo em Inglês | MEDLINE | ID: mdl-31146718

RESUMO

BACKGROUND: The burden of childhood and adult obesity disproportionally affects Hispanic and African-American populations in the US, and these groups as well as populations with lower income and education levels are disproportionately affected by environmental pollution. Pregnancy is a critical developmental period where maternal exposures may have significant impacts on infant and childhood growth as well as the future health of the mother. We initiated the "Maternal And Developmental Risks from Environmental and Social Stressors (MADRES)" cohort study to address critical gaps in understanding the increased risk for childhood obesity and maternal obesity outcomes among minority and low-income women in urban Los Angeles. METHODS: The MADRES cohort is specifically examining whether pre- and postpartum environmental exposures, in addition to exposures to psychosocial and built environment stressors, lead to excessive gestational weight gain and postpartum weight retention in women and to perturbed infant growth trajectories and increased childhood obesity risk through altered psychological, behavioral and/or metabolic responses. The ongoing MADRES study is a prospective pregnancy cohort of 1000 predominantly lower-income, Hispanic women in Los Angeles, CA. Enrollment in the MADRES cohort is initiated prior to 30 weeks gestation from partner community health clinics in Los Angeles. Cohort participants are followed through their pregnancies, at birth, and during the infant's first year of life through a series of in-person visits with interviewer-administered questionnaires, anthropometric measurements and biospecimen collection as well as telephone interviews conducted with the mother. DISCUSSION: In this paper, we outline the study rationale and data collection protocol for the MADRES cohort, and we present a profile of demographic, health and exposure characteristics for 291 participants who have delivered their infants, out of 523 participants enrolled in the study from November 2015 to October 2018 from four community health clinics in Los Angeles. Results from the MADRES cohort could provide a powerful rationale for regulation of targeted chemical environmental components, better transportation and urban design policies, and clinical recommendations for stress-coping strategies and behavior to reduce lifelong obesity risk.


Assuntos
Exposição Ambiental/efeitos adversos , Hispano-Americanos/estatística & dados numéricos , Exposição Materna/efeitos adversos , Obesidade Pediátrica/etiologia , Efeitos Tardios da Exposição Pré-Natal/etiologia , Adulto , Feminino , Ganho de Peso na Gestação , Humanos , Recém-Nascido , Los Angeles , Obesidade Pediátrica/etnologia , Pobreza/estatística & dados numéricos , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etnologia , Estudos Prospectivos , Projetos de Pesquisa , Fatores de Risco , Determinantes Sociais da Saúde , População Urbana/estatística & dados numéricos
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