TY - CHAP. T1 - Influence of prenatal nicotine exposure on development of neurotransmission in central respiratory neurons. AU - Fregosi, Ralph F.. PY - 2008/1/1. Y1 - 2008/1/1. N2 - This chapter considers the influence of prenatal nicotine exposure on the development of neurotransmission in central respiratory neurons. Neonatal mammals that are nicotine exposed in utero show abnormalities in central ventilatory control, such as reduced ventilatory output (1,2), altered breathing pattern (2-4), increased apnea frequency (2,4) and duration (5), delayed arousal in response to hypoxia (6,7), decreased sensitivity to hypoxia (1,4,5,8-11), and diminished capacity for autoresuscitation following severe hypoxic exposure (12,13). Although these findings provide substantial evidence that development of central ventilatory control is altered by prenatal nicotine exposure, the mechanism of nicotines action on respiratory-related neurons has not been identified. Identifying these mechanisms is important ...

Effects of Prenatal Alcohol Exposure on Central Nervous System DevelopmentPrenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD).

Choline is a crucial nutrient that contributes to several biological functions and serves as a precursor molecule to the neurotransmitter acetylcholine. Choline is integral to the development and function of the central nervous system, and its availability during the prenatal period has lasting and protective effects on neural function. Researchers have found that prenatal choline supplementation in the rat enhances learning and memory processes later in life, especially those involving spatial memory. Researchers have also demonstrated that choline protects against a number of physical stressors to the neural environment, such as prenatal alcohol exposure, induced seizures, and chronic stress-induced exposure to corticosteroids. Compared to the study of these types of physical stressors, relatively little research has examined the influence of prenatal choline exposure on psychological stress later in life. In an attempt to contribute to this field, the present study examined the effects of prenatal

Maternal Immune Activation Leads to Activated Inflammatory Macrophages in Offspring. http://www.ncbi.nlm.nih.gov/pubmed/24566386 Several epidemiological studies have shown an association between infection or inflammation during pregnancy and increased risk of autism in the child. In addition, animal models have illustrated that maternal inflammation during gestation can cause autism-relevant behaviors in the offspring; so called maternal immune activation…

The foregoing section provides a foundation from which to speculate on the possible role of estrogen and testosterone in both schizophrenia and autism. The authors current paper describes the increased susceptibility to acute infection by T. gondii caused by estrogen. Some human studies suggest that latent toxoplasmosis results from high prenatal testosterone rather than estrogen due to finding low second to fourth finger digit ratios in T. gondii infected subjects . Second to fourth finger digit ratios, or so-called 2D:4D ratios, are proposed markers of prenatal androgen exposure.. Low 2D:4D ratios reflect higher prenatal testosterone exposure and high ratios indicate low testosterone compared to estrogen exposure. Low ratios or high prenatal testosterone are often associated with autism and high ratios or relatively higher prenatal estrogen with schizophrenia. Recent research has cast doubt on the reliability of digit ratio to predict individual prenatal androgen exposure although a modest ...

Schizophrenia patients typically exhibit cognitive impairments that directly affect their daily functioning, but are not effectively treated by current antipsychotics. Maternal immune activation (MIA) during pregnancy, which can be triggered by a variety of infectious agents, has been associated with the development of schizophrenia in adult offspring. Epidemiological evidence indicates that elevated maternal levels of the chemokine interleukin- 8 (IL-8) during MIA contribute to the neurodevelopmental alterations underlying the disorder. The present experiments used an animal model of neurodevelopmental disorders to study the effects of MIA and chemokine receptor antagonism on the behavior of rat offspring, with behavioral tests chosen to examine cognitive functions that are typically impaired in human schizophrenia patients. The viral mimetic polyinosinic-polycytidylic acid (polyI:C) (4.0 mg/kg, i.v.) was injected into pregnant Long-Evans (LE) dams on gestational day (GD) 15. Dams were also ...

University of North Carolina researchers studied the effects of prenatal cocaine exposure on newborn brains. See what they found.

TY - JOUR. T1 - Prenatal exposure to fever is associated with autism spectrum disorder in the boston birth cohort. AU - Brucato, Martha. AU - Ladd-Acosta, Christine Marie. AU - Li, Mengying. AU - Caruso, Deanna. AU - Hong, Xiumei. AU - Kaczaniuk, Jamie. AU - Stuart, Elizabeth. AU - Fallin, Daniele Daniele. AU - Wang, Xiaobin. PY - 2017/11/1. Y1 - 2017/11/1. N2 - Autism spectrum disorder (ASD) is phenotypically and etiologically heterogeneous, with evidence for genetic and environmental contributions to disease risk. Research has focused on the prenatal period as a time where environmental exposures are likely to influence risk for ASD. Epidemiological studies have shown significant associations between prenatal exposure to maternal immune activation (MIA), caused by infections and fever, and ASD. However, due to differences in study design and exposure measurements no consistent patterns have emerged revealing specific times or type of MIA exposure that are most important to ASD risk. No prior ...

Water maze experience and prenatal choline supplementation differentially promote long-term hippocampal recovery from seizures in adulthood.

Maternal smoking during pregnancy increases the risk of Sudden Infant Death. A defect in cardiorespiratory control has been suggested. Chronic exposure to nicotine during fetal development of rat induced postnatal developmental disorders on central neural pathways [1], autonomic function [2], carotid body chemorecep-tors [3], ventilatory response to hyperoxia [4]. The interrelation between all these sparse data has to be investigated. We hypothesized that exposure to nicotine might impair or delay the development of respiratory control pathways, ie, of the carotid body chemoafferent pathway, causing an abnormal response to ventila-tory challenges. On the 5th day of gestation, pregnant Sprague-Dawley rats received a transdermal patch delivering, either 50 mg of nicotine free base over 21 days, or excipient. At birth, male pups were selected and analysed at postnatal day 3, 7, 11, 14, 21 and 68. The in vivo tyrosine hydroxylase activity was determined in offspring carotid bodies and brainstem ...

We previously showed that maternal cocaine administration resulted in a decrease in fetal rat body weight [9]. The present study demonstrated that the maternal cocaine treatment caused a significant decrease in fetal brain weight, as compared with the saline control group. This finding is consistent with the previous report in pregnant C57BL/6 mice, in which maternal subcutaneous administration of cocaine from gestation days 12-18 produced significant decreases in fetal body and brain weight [27]. The pair-fed studies demonstrated that maternal undernutrition was not a likely mediator of the effects caused by cocaine [27, 28]. Moreover, our data indicate that cocaine decreases fetal brain/body weight ratio, suggesting that cocaine have higher affinity toxic effects on the fetal brain than the body. Dow-Edwards [29] reported that fetal brain had between 26-42% more concentration of cocaine than fetal plasma after 90 min following either 30 or 60 mg/kg cocaine given via intragastric intubation to ...

Abstract. Chronic psychological stress is a risk factor for osteoporosis. Maternal active mastication during prenatal stress attenuates stress response. The aim of this study is to test the hypothesis that maternal active mastication influences the effect of prenatal stress on bone mass and bone microstructure in adult offspring. Pregnant ddY mice were randomly divided into control, stress, and stress/chewing groups. Mice in the stress and stress/chewing groups were placed in a ventilated restraint tube for 45 minutes, 3 times a day, and was initiated on day 12 of gestation and continued until delivery. Mice in the stress/chewing group were allowed to chew a wooden stick during the restraint stress period. The bone response of 5-month-old male offspring was evaluated using quantitative micro-CT, bone histomorphometry, and biochemical markers. Prenatal stress resulted in significant decrease of trabecular bone mass in both vertebra and distal femur of the offspring. Maternal active mastication ...

Objective: Determine the effectiveness of an intervention to reduce prenatal alcohol exposure in the Congo. Methods: We utilized a screening tool validated in the Congo to identify women who were drinking during pregnancy. The intervention was implemented by prenatal care providers comparing 162 women receiving the intervention with 58 (controls) who did not. The study endpoints were proportion of women who quit drinking, drinking days per week, drinks per drinking day, most drinks on any day, and number of binge episodes per week. Results: In the control group 36% of the women quit drinking compared to 54% in the intervention group (Chi-square 5.61; p = 0.02). The number of drinking days per week for the controls decreased by 50.1% compared to 68% for the intervention group (p = 0.008); drinks per drinking day for the controls decreased by 37% compared to 60.1% for the intervention group (p = 0.001); and most drinks on any occasion in the controls decreased by 38% compared to 61% for the ...

Background Prenatal substance use screening is recommended. The 4 Ps Plus screener includes questions on perceived problematic substance use in parents and partner that are not considered in risk stratification. Objectives This research examined the: (1) prevalence of self-reported problematic parental and partner substance use and associations with biochemically-verified prenatal substance use; (2) utility of self-reported perceptions of parent/partner substance use as proxies for prenatal substance use; and (3) degree to which the sensitivity of the 4Ps Plus can be augmented with consideration of parent/partner questions in risk stratification. Methods A convenience sample of 500 pregnant women was recruited between January 2017 and January 2018. Participants completed the 4Ps Plus and provided urine for drug testing. Diagnostic utility of problematic parent/partner substance use questions was assessed, then compared to the 4Ps Plus used as designed, and to the 4Ps Plus used with these 2 ...

A social- skills intervention called Childrens Friendship Training can lead to a decrease in hostile attributions or perceptions of children with prenatal alcohol exposure (PAE)

Canadian researchers have identified several specific white matter regions and deep grey matter regions in the brain that seem to be sensitive to prenatal alcohol exposure.

The persistence of neurobehavioral effects in female rats (Mol:WIST) exposed to 500 ppm technical xylene (dimethylbenzene, GAS-no 1330-20-7) for 6 hours per day on days 7-20 of prenatal development was studied. The dose level was selected so as not to induce maternal toxicity or decreased viability of offspring. Investigations of learning and memory abilities were performed using a Morris water maze. This task requires rats to spatially navigate, using distal extramaze cues to locate a small platform under the surface of the water in a large pool. At the age of 16 weeks, the exposed offspring showed impairments when the platform was relocated in the pool. Impaired performances after platform relocation were also observed in exposed offspring at 28 and 55 weeks of age, although the difference was not statistically significant at 55 weeks. These data could indicate that the effect was partly reversible, although over a long time period. However, another explanation could be that the animals became ...

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Here, we show that male, but not female, offspring that were exposed to prenatal hypoxia develop altered circulatory and vascular function that implicates the ET-1 system. To summarize, we found the following: (1) IUGR males had increased conversion of bET-1 to active ET-1 compared with controls, and this effect was partially normalized with L-NAME treatment; (2) no differences in bET-1 conversion to active ET-1 were observed between aged control and IUGR female offspring; (3) no differences in ET-1 interaction with its receptors were observed between control and IUGR offspring in either male or female offspring; (4) male IUGR offspring were hypertensive, and this increase in BP was partially mitigated by treatment with the dual ETA/B receptor antagonist tezosentan; (5) female IUGR offspring were not hypertensive compared with control offspring, and tezosentan treatment had little effect in either female treatment group. These results suggest that the ET-1 system, and possibly the conversion of ...

Ahmed S, Atlas E. 2016. Bisphenol S- and bisphenol A-induced adipogenesis of murine preadipocytes occurs through direct peroxisome proliferator activated receptor gamma activation. Int J Obes Relat Metab Disord 40(10):1566-1573, PMID: 27273607, 10.1038/ijo.2016.95. Alonso-Magdalena P, Quesada I, Nadal Á. 2015. Prenatal exposure to BPA and offspring outcomes. Dose Response 13(2):1559325815590395, PMID: 26676280, 10.1177/1559325815590395. Alonso-Magdalena P, Vieira E, Soriano S, Menes L, Burks D, Quesada I, et al. 2010. Bisphenol A exposure during pregnancy disrupts glucose homeostasis in mothers and adult male offspring. Environ Health Perspect 118(9):1243-1250, PMID: 20488778, 10.1289/ehp.1001993. Anderson OS, Peterson KE, Sanchez BN, Zhang Z, Mancuso P, Dolinoy DC. 2013. Perinatal bisphenol A exposure promotes hyperactivity, lean body composition, and hormonal responses across the murine life course. FASEB J 27(4):1784-1792, PMID: 23345456, 10.1096/fj.12-223545. Angle BM, Do RP, Ponzi D, ...

Methods We conducted a Mendelian randomization study to examine the association between maternal iron status with offspring adiposity and BP in adulthood. Instrumental variable (IV) analysis, using maternal C282Y as a genetic instrument for mothers ferritin, was performed. IV analysis uses the proportion of the variation in maternal ferritin that is explained by C282Y to provide an unconfounded estimate of the relationship with offspring outcomes. The results were compared to the results of multivariable ordinary least squares (OLS) regression examining the same relationship. Male and female offspring of mothers from the UK Women Cohort Study (UKWCS) were approached, of whom 348 with mean age of 41 years completed the study. About half were offspring of C282Y carriers. Offsprings BP, height and weight were measured at their local medical practice. Participants were also asked to self-measure their WC at home.. ...

Fingerprint Dive into the research topics of Prenatal nicotine exposure alters medullary nicotinic and AMPA-mediated control of respiratory frequency in vitro. Together they form a unique fingerprint. ...

Prenatal exposure to androgens as a factor of fetal programming. Sergio E. Both epidemiological and clinical evidence suggest a relationship between the prenatal environment and the risk of developing diseases during adulthood. The first observations about this relationship showed that prenatal growth retardation or stress conditions during fetal life were associated to cardiovascular, metabolic and other diseases in later life. However, not only those conditions may have lasting effects after birth.. Growing evidence suggests that prenatal exposure to steroids either of fetal or maternal origin could be another source of prenatal programming with detrimental consequences during adulthood. We have recently demonstrated that pregnant women with polycystic ovary syndrome exhibit elevated androgen levels compared to normal pregnant women, which could provide an androgen excess for both female or male fetuses.. We have further tested this hypothesis in an animal model of prenatal androgenization, ...

Whether intrauterine cocaine exposure (IUCE) explains unique variance in psychiatric functioning among school age children, even after controlling

Since the opioid epidemic was officially declared a federal public health emergency in October 2017, states have undertaken a wide range of activities to address opioid-related harms. In February 2019, ASTHO surveyed its members to understand how data is being utilized to address these harms in their jurisdictions. This brief summarizes the results of this survey and highlights data-based approaches used to address four types of opioid-related harms: prenatal substance exposure, neonatal abstinence syndrome, adverse childhood experiences, and injection drug use-associated infections.Read More ». ...

More than 17 percent of pregnant women between the ages of 15 and 44 smoke, according to the 2002 National Survey on Drug Use and Health.

(Medical Xpress)-Prenatal exposure to alcohol severely disrupts major features of brain development that potentially lead to increased anxiety and poor motor function, conditions typical in humans with Fetal Alcohol Spectrum ...

TY - JOUR. T1 - Anxiety-like behaviour and associated neurochemical and endocrinological alterations in male pups exposed to prenatal stress. AU - Laloux, Charlotte. AU - Mairesse, Jérôme. AU - Van Camp, Gilles. AU - Giovine, Angela. AU - Branchi, Igor. AU - Bouret, Sebastien. AU - Morley-Fletcher, Sara. AU - Bergonzelli, Gabriela. AU - Malagodi, Marithé. AU - Gradini, Roberto. AU - Nicoletti, Ferdinando. AU - Darnaudéry, Muriel. AU - Maccari, Stefania. PY - 2012/10. Y1 - 2012/10. N2 - Epidemiological studies suggest that emotional liability in infancy could be a predictor of anxiety-related disorders in the adulthood. Rats exposed to prenatal restraint stress ( PRS rats ) represent a valuable model for the study of the interplay between environmental triggers and neurodevelopment in the pathogenesis of anxious/depressive like behaviours. Repeated episodes of restraint stress were delivered to female Sprague-Dawley rats during pregnancy and male offspring were studied. Ultrasonic ...

In a prospective study (Morrow, Bandstra, Anthony, Ofir et al., 2001), a range of subtle deficits across the spectrum of neurobehavioural functioning were observed within the first postnatal week in infants with cocaine exposure. These deficits were partly correlated with reduced foetal growth. The deficits in functioning were larger as the number of trimesters of exposure increased. The authors suggest that prenatal cocaine exposure may produce more problematic effects in infants born prematurely and that cocaine exposed full-term infants may be more resilient. Other authors also suggest that any effect of cocaine on longer-term development is an indirect association, mediated by reduced birth weight, head circumference, other drug use or other prenatal issues (Behnke, Eyler, Garvan, Wobie & Hou, 2002; Bendersky & Lewis, 1999). In addition, one controlled study reports that mothers in a cocaine-exposed group had less frequent emotional contact with their infant and tended to have maladaptive ...

Researchers have known for years: what happens to mom in pregnancy affects the baby. That holds true with prenatal exposure to air pollution, which has lingering cardiovascular effects, such as birth defects and a higher risk of obesity, explained Jeanette Stingone, PhD, of Mount Sinai Health System.

The low activity allele of the maternal polymorphism, 5HTTLPR, in the serotonin transporter, SLC6A4, coupled with prenatal stress is reported to increase the risk for children to develop autism spectrum disorder (ASD). Similarly, maternal Slc6a4 knock-out and prenatal stress in rodents results in offspring demonstrating ASD-like characteristics. The present study uses an integrative genomics approach to explore mechanistic changes in early brain development in mouse embryos exposed to this maternal gene-environment phenomenon. Restraint stress was applied to pregnant Slc6a4 +/+ and Slc6a4 +/− mice and post-stress embryonic brains were assessed for whole genome level profiling of methylome, transcriptome and miRNA using Next Generation Sequencing. Embryos of stressed Slc6a4 +/+ dams exhibited significantly altered methylation profiles and differential expression of 157 miRNAs and 1009 genes affecting neuron development and cellular

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Prenatal alcohol exposure affects up to 2 to 5 percent of the US population. Children and adults with fetal alcohol spectrum disorders (FASD) struggle with life-long learning and behavioral problems. Without appropriate supports, individuals with FASD are at high risk for secondary conditions, such as mental health problems, trouble with the law, school disruption, and substance abuse. An early diagnosis and appropriate services can help prevent these secondary problems.. The FASD Diagnostic and Evaluation Clinic is a multidisciplinary clinic created in partnership through Mt. Hope Family Center and Developmental and Behavioral Pediatrics at Golisano Childrens Hospital within the University of Rochester Medical Center. The Clinic currently serves children and adolescents from infancy through age 16 years old. Services available include FASD diagnostic evaluations and neuropsychological assessments to identify the child or adolescents strengths and weaknesses to aid in treatment ...

TY - JOUR. T1 - Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders. AU - Lewis, Sarah J.. AU - Relton, Caroline. AU - Zammit, Stanley. AU - Smith, George Davey. PY - 2013/10. Y1 - 2013/10. N2 - BackgroundThe risk of childhood behavioural and psychiatric diseases could be substantially reduced if modifiable risk factors for these disorders were identified. The critical period for many of these exposures is likely to be in utero as this is the time when brain development is most rapid. However, due to confounding and other limitations of traditional epidemiological studies, identification of causal risk factors has proved challenging and on the whole research in this area has not been fruitful.ScopeIn this review, we highlight several alternative approaches including; comparisons across settings, the use of negative controls and natural experiments, which includes migration studies, studies of individuals conceived ...

This investigation was undertaken in order to know whether the postnatal tactile/kinesthetic stimulation is effective in reversing the Prenatal Stress, in the cytoarchitecture of the CA3 region of the hippocampus, in female pups. 12 pups of female rats from the Sprague-Dawley strain were distributed to Control Group (GC), the Prenatal Maternal Stress by restriction group (EP) and Prenatal Maternal Stress with postnatal tactile/ kinesthetic stimulation Group (EP-ETK). The Prenatal Maternal Stress in female pups increased neuronal density in CA3b and CA3c areas (p,0.001). When compared to Prenatal Maternal Stress, pups prenatal stress who received early tactile/kinesthetic stimulation showed a decrease in neuronal density in CA3b and CA3c areas (p , 0,001). Postnatal tactile/kinesthetic stimulation was shown to successfully reverse the Prenatal Maternal Stress effects by decreasing neuronal density in CA3b and CA3c hippocampal areas. ...

The details of bibliography - Exploring the potential to use data linkage for investigating the relationship between birth defects and prenatal alcohol exposure

Teens whose mothers drank alcohol regularly throughout the first trimester of pregnancy have a threefold increased risk of developing severe behavior problems,

Background: New measures of exposure prevention activity were used to evaluate the effectiveness of a 16 month management focused intervention addressing hazardous substance exposures in manufacturing work settings. Methods: Exposure prevention efforts were assessed using a previously published rating scheme developed for this study.1 The rating scheme yields a set of measures of exposure potentia

Results for hazardous substances exposure equipment from BreathSpec, Depth-Clear, Honeywell NORTH and other leading brands. Compare and contact a supplier near ...

TY - JOUR. T1 - Acute in utero exposure to lipopolysaccharide induces inflammation in the pre- and postnatal brain and alters the glial cytoarchitecture in the developing amygdala. AU - OLoughlin, Elaine. AU - Pakan, Janelle M.P.. AU - Yilmazer-Hanke, Deniz. AU - McDermott, Kieran W.. N1 - Funding Information: This project was funded by the Health Research Board (HRB), Ireland (Project HRA_POR/2010/159). Publisher Copyright: © 2017 The Author(s).. PY - 2017/11/2. Y1 - 2017/11/2. N2 - Background: Maternal immune activation (MIA) is a risk factor for neurodevelopmental disorders such as autism and schizophrenia, as well as seizure development. The amygdala is a brain region involved in the regulation of emotions, and amygdalar maldevelopment due to infection-induced MIA may lead to amygdala-related disorders. MIA priming of glial cells during development has been linked to abnormalities seen in later life; however, little is known about its effects on amygdalar biochemical and cytoarchitecture ...

In 2001, researchers Leonie Welberg and Jonathan Seckl published the literature review Prenatal Stress, Glucocorticoids, and the Programming of the Brain, in which they report on the effects of prenatal stress on the development of the fetal brain. The fetus experiences prenatal stress while in the womb, or in utero. In discussing the effects of prenatal stress, the authors describe prenatal programming, which is when early environmental experiences permanently alter biological structure and function throughout life.. Format: Articles Subject: Publications, Theories ...

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Two experiments examined the psychological and biological antecedents of hierarchical differentiation and the resulting consequences for productivity and conflict within small groups. In Experiment 1, which used a priming manipulation, hierarchically differentiated groups (i.e., groups comprising 1 high-power-primed, 1 low-power-primed, and 1 baseline individual) performed better on a procedurally interdependent task than did groups comprising exclusively either all high-power-primed or all low-power-primed individuals. There were no effects of hierarchical differentiation on performance on a procedurally independent task. Experiment 2 used a biological marker of dominance motivation (prenatal testosterone exposure as measured by a digit-length ratio) to manipulate hierarchical differentiation. The pattern of results from Experiment 1 was replicated; mixed-testosterone groups achieved greater productivity than did groups comprising all high-testosterone or all low-testosterone individuals. ...

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... Washington DC Sons of male mice exposed to prenatal stress ar...Tracy Bale PhD of the University of Pennsylvania and colleagues pre... This study shows that the effects of maternal stress in mice are pass...In general female mice tend to respond more to stress than do males. ...,Effects,of,prenatal,stress,passed,across,generations,in,mice,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters

For my course project, I have chosen the challenge area of prenatal risk factors with the subtopic of health. Prenatal health is a factor in a childs development and affects their school readiness and their learning. American babies, compared with those from other developed nations, are receiving inadequate prenatal care and less time at home with their parents during the first year of life (Lally, 2010). I am interested in assisting the women in my community receive quality prenatal care so that they have a safe pregnancy and so that their child has the best opportunity to be healthy, happy, and successful. In addition, I believe early childhood education is the foundation to a childs overall education and a mom who has quality prenatal care and has assistance for their childs development and learning from age birth to three, their child will be successful and ready to enter Pre-K or K. It is during the first few years of life that early experience starts shaping the foundational learning ...

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Researchers looked at internalizing and externalizing behaviors in children at 0.5, 1.5, and 3 years of age, comparing children exposed to benzodiazepines and sedative-hypnotics during pregnancy to unexposed children.

Prenatal and early childhood exposure to the chemical solvent tetrachloroethylene (PCE) found in drinking water may be associated with long-term visual impairments, particularly in the area of colour discrimination, according to a new study.

N-methyl-D-aspartate receptor dysfunction has been strongly suggested to link with the abnormalities seen in fetal alcohol syndrome. Thus, the effects of prenatal ethanol exposure on the total expression of NR1 splice variants and the cell surface expression of both NR1 and NR2 subunits in brain were investigated in rats. Western blot studies of membrane homogenates from cerebral cortices at postnatal days 1 through 21 indicate that prenatal ethanol treatment does not alter total NR1 expression or differential expression of NR1 splice variants during development. However, immunoprecipitation studies using PSD95 suggest that both C2-terminal variants and NR2A subunits at the cortical postsynaptic membrane of postnatal day 21 were significantly reduced after prenatal ethanol treatment. Moreover, C1-terminal variants were decreased in both pair-fed and ethanol-treated groups, while no significant differences in the levels of total NR1 subunits, NR1 splice variants containing the N- or C2-terminal

BACKGROUND: There is a lack of evidence regarding the effect of dose, pattern and timing of prenatal alcohol exposure and behaviour problems in children aged 2 years and older. METHODS: A 10% random sample of women delivering a live infant in Western Australia (1995-96) were invited to participate in an 8-year longitudinal survey (78% response rate n = 2224); 85% were followed-up at 2 years, 73% at 5 years and 61% at 8 years. Alcohol consumption was classified by combining the overall dose, dose per occasion and frequency to reflect realistic drinking patterns. Longitudinal analysis was conducted using generalized estimating equations (GEE) to investigate the association between child behaviour as measured by the Child Behaviour Checklist at 2, 5 and 8 years of age and prenatal alcohol exposure collected 3 months postpartum for each trimester separately, adjusting for a wide range of confounding factors. RESULTS: Low levels of prenatal alcohol were not associated with child behaviour problems. There

The goal of this study was to address the controversy over evidence of prenatal androgen exposure reflected in the digit ratios of women with PCOS. Recently our group showed that when 2D:4D were measured with Vernier calipers, women with PCOS did not demonstrate finger length patterns consistent with increased levels of in utero androgen exposure [12]. This was in contrast to a previous report that had also used Vernier calipers to measure 2D:4D in women with PCOS [9]. Since observed differences in 2D:4D are generally small, there is growing support that studies investigating potential effects of prenatal androgens use the most consistent and reliable technique available to measure finger lengths [13-15, 18-20]. In this study, we imaged the hands of women with four clinical phenotypes of PCOS, healthy female controls and men, and used computer-based calipers to measure their finger lengths since this method was recently validated to be the most reliable [14, 15]. Consistent with this being the ...

Ethanol is known as a potent teratogen responsible for the fetal alcohol syndrome characterized by cognitive deficits especially pronounced in juveniles but ameliorating in adults. Since the mechanisms of these deficits and following partial recovery are not fully elucidated, the aim of the present study was to investigate the process of synaptogenesis in the hippocampus over the first two months of life in control and fetal-alcohol rats. Ethanol was delivered to the pregnant dams by intragastric intubation throughout 7-21 gestation days at the daily dose of 6g/kg generating a mean blood alcohol level of 246.6±40.9mg/dl on gestation day 20. The spine densities as well as the expression of pre- and postsynaptic proteins, synaptophysin (SYP) and PSD-95 protein, were evaluated for three distinct hippocampal regions: CA1, CA2+3, and DG and four postnatal days: PD1, PD10, PD30 and PD60, independently. Our results confirmed an intensive synaptogenesis within the brain spurt period (first 10 postnatal days),

(Prenatal Cocaine Exposure and Cognitive Development) Research funded by the National Institute on Drug Abuse (NIDA) and the Albert Einstein Medical Center in Philadelphia states: Although numerous animal experiments and some human data show potent effects of cocaine on the central nervous system, we were unable to detect any difference in Performance, Verbal or Full Scale IQ

This study investigated infant neurobehavioral functioning during the newborn period in 334 full-term, African American neonates (187 cocaine exposed, 147 non-cocaine exposed) enrolled prospectively at birth, with documentation of drug exposure statu

Prenatal cocaine exposure (PCE), theorized in the 1970s, occurs when a pregnant woman uses cocaine and thereby exposes her fetus to the drug. Crack baby was a term coined to describe children who were exposed to crack (freebase cocaine in smokable form) as fetuses; the concept of the crack baby emerged in the US during the 1980s and 1990s in the midst of a crack epidemic. Other terms are cocaine baby and crack kid. Early studies reported that people who had been exposed to crack in utero would be severely emotionally, mentally, and physically disabled; this belief became common in the scientific and lay communities. Fears were widespread that a generation of crack babies were going to put severe strain on society and social services as they grew up. Later studies failed to substantiate the findings of earlier ones that PCE has severe disabling consequences; these earlier studies had been methodologically flawed (e.g. with small sample sizes and confounding factors). Scientists have come to ...

Prenatal exposure to alcohol has adverse effects on offspring neuroendocrine and behavioural functions. Alcohol readily crosses the placenta, thus directly affecting developing foetal endocrine organs. In addition, alcohol-induced changes in maternal endocrine function can disrupt the normal hormonal interactions between the pregnant female and foetal systems, altering the normal hormone balance and, indirectly, affecting the development of foetal metabolic, physiological and endocrine functions. The present review focuses on the adverse effects of prenatal alcohol exposure on offspring neuroendocrine function, with particular emphasis on the hypothalamic-pituitary-adrenal (HPA) axis, a key player in the stress response. The HPA axis is highly susceptible to programming during foetal and neonatal development. Here, we review data demonstrating that alcohol exposure in utero programmes the foetal HPA axis such that HPA tone is increased throughout life. Importantly, we show that, although ...

Background: In Fetal Alcohol Spectrum Disorder (FASD), structural and functional abnormalities in the cerebellum persist through adolescence and beyond. We hypothesize th..

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Meconium: Babys first stool may provide clues to fetal alcohol exposure * Fetal alcohol exposure is usually determined through self-reported maternal consumption. * New research shows that...

Date: June 2017 (Online). Source: JAMA Pediatrics, doi:10.1001/jamapediatrics.2017.0778. Question: Is there an association between different levels of prenatal alcohol exposure and child craniofacial shape at 12 months? Findings: This cohort study conducted an objective and sensitive craniofacial phenotype analysis of 415 children, which showed an association between prenatal alcohol exposure and craniofacial shape at almost […]. Read More ...

A new IU study examining effects of low-level developmental lead exposure in mice could explain why some people dependent on alcohol return to using.

2Department of Psychiatry, Emory University, Atlanta GA USA. A better understanding of potential mediators or moderators of fetal, infant and subsequent lifelong consequences of heavy prenatal alcohol exposure can help both to identify infants at highest risk and to inform prevention and intervention activities. Of particular interest are those potentially modifiable factors that seem to confer resilience despite exposure to risky levels of alcohol. As part of the Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD) consortium, a longitudinal cohort of pregnant women and their offspring have been followed at two sites in Ukraine from 2009-2015. A total of 285 women were recruited into a risky alcohol exposure group based on frequent heavy episodic drinking in the month around conception and/or in the most recent month of pregnancy. Demographic, social, health and lifestyle characteristics were collected on the mothers, and their nutritional status was measured at the time of ...

Excessive alcohol consumption has been shown to increase serum plasma levels of numerous immune cytokines. Maternal immune activation and elevated cytokines have been implicated in certain neurological disorders (e.g., autism and schizophrenia) in the offspring. We investigated the hypothesis that elevated cytokines during pregnancy are a risk factor in women who gave birth to a child with Fetal Alcohol Spectrum Disorder (FASD) or a child with neurobehavioral impairment, regardless of prenatal alcohol exposure. Moderate to heavy alcohol-exposed (AE) (N = 149) and low or no alcohol-exposed (LNA) (N = 92) women were recruited into the study during mid pregnancy (mean of 19.8 ± 5.8 weeks gestation) in two regions of Ukraine: Khmelnytsky and Rivne. Maternal blood samples were obtained at enrollment into the study at early to mid-pregnancy and during a third-trimester follow-up visit and analyzed for plasma cytokines. Children were examined at 6 and/or 12 months of age and were classified as having ...

Excessive alcohol consumption has been shown to increase serum plasma levels of numerous immune cytokines. Maternal immune activation and elevated cytokines have been implicated in certain neurological disorders (e.g., autism and schizophrenia) in the offspring. We investigated the hypothesis that elevated cytokines during pregnancy are a risk factor in women who gave birth to a child with Fetal Alcohol Spectrum Disorder (FASD) or a child with neurobehavioral impairment, regardless of prenatal alcohol exposure. Moderate to heavy alcohol-exposed (AE) (N = 149) and low or no alcohol-exposed (LNA) (N = 92) women were recruited into the study during mid pregnancy (mean of 19.8 ± 5.8 weeks gestation) in two regions of Ukraine: Khmelnytsky and Rivne. Maternal blood samples were obtained at enrollment into the study at early to mid-pregnancy and during a third-trimester follow-up visit and analyzed for plasma cytokines. Children were examined at 6 and/or 12 months of age and were classified as having ...

Importance Early-life exposures, such as prenatal maternal lifestyle, illnesses, nutritional deficiencies, toxin levels, and adverse birth events, have long been considered potential risk factors for neurodevelopmental disorders in offspring. However, maternal genetic factors could be confounding the association between early-life exposures and neurodevelopmental outcomes in offspring, which makes inferring a causal relationship problematic.Objective To test whether maternal polygenic risk scores (PRSs) for neurodevelopmental disorders were associated with early-life exposures previously linked to the disorders.Design, Setting, and Participants In this UK population-based cohort study, 7921 mothers with genotype data from the Avon Longitudinal Study of Parents and Children (ALSPAC) underwent testing for association of maternal PRS for attention-deficit/hyperactivity disorder (ADHD PRS), autism spectrum disorder (ASD PRS), and schizophrenia (SCZ PRS) with 32 early-life exposures. ALSPAC data ...

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CAH is a genetic steroidogenesis disorder. The most common form, 21OHD, leads to cortisol deficiency and, in turn, an excess of androgen, a hormone that promotes the development and maintenance of male sex characteristics. As a result of this androgen excess, prepubescent males and newborn, prepubescent, and grown females exhibit mature masculine characteristics. Prenatal treatment with dexamethasone, a corticosteroid that decreases androgen levels, has been shown to prevent the development of abnormal genitalia in female infants. The long-term effects of this treatment, however, have not been evaluated. This study will determine whether prenatal dexamethasone treatment causes any long-term side effects by examining children and young adults who received dexamethasone as fetuses and their mothers, who were exposed to dexamethasone while pregnant.. This study has three parts. In Part 1 of the study, participants will provide written consent for release of their medical records from their ...

CAH is a genetic steroidogenesis disorder. The most common form, 21OHD, leads to cortisol deficiency and, in turn, an excess of androgen, a hormone that promotes the development and maintenance of male sex characteristics. As a result of this androgen excess, prepubescent males and newborn, prepubescent, and grown females exhibit mature masculine characteristics. Prenatal treatment with dexamethasone, a corticosteroid that decreases androgen levels, has been shown to prevent the development of abnormal genitalia in female infants. The long-term effects of this treatment, however, have not been evaluated. This study will determine whether prenatal dexamethasone treatment causes any long-term side effects by examining children and young adults who received dexamethasone as fetuses and their mothers, who were exposed to dexamethasone while pregnant.. This study has three parts. In Part 1 of the study, participants will provide written consent for release of their medical records from their ...

We investigated the hypothesis that prenatal exposure to the synthetic estrogen, diethylstilbestrol (DES), similarly masculinizes or defeminizes cognitive development in women.. Forty-two DES-exposed women and 26 of their unexposed sisters were studied. No group differences were seen for abilities at which females excel on average (verbal fluency, perceptual speed and accuracy, and associative memory), for abilities at which males excel on average (visuospatial abilities), or for abilities that do not show sex differences (vocabulary, nonverbal intelligence). The time of prenatal exposure to DES correlated with visuospatial performance with later exposure associated with better performance. However, the subgroup of women exposed to DES late in gestation did not differ from unexposed women on these measures.. Results support the conclusion that prenatal exposure to DES has little or no influence on cognitive development in women. However, they do not preclude other types of early hormonal ...

Maternal stress can impair foetal development and program sex-specific disease outcomes in offspring through the actions of maternally produced glucocorticoids, predominantly corticosterone (Cort) in rodents. We have demonstrated in mice that male but not female offspring prenatally exposed to Cort (33 µg/kg/h for 60 h beginning at E12.5) develop cardiovascular/renal dysfunction at 12 months. At 6 months of age, renal function was normal but male offspring had increased plasma aldosterone concentrations, suggesting that altered adrenal function may precede disease. This study investigated the long-term impact of prenatal exposure to Cort on adrenal growth, morphology and steroidogenic capacity as well as plasma Cort concentrations in offspring at postnatal day 30 (PN30), 6 months and 12 months of age. Prenatal Cort exposure decreased adrenal volume, particularly of the zona fasciculata, in male offspring at PN30 but increased both relative and absolute adrenal weight at 6 months of age. By 12 ...

Research reports have documented a range of cognitive and behavioural outcomes associated with prenatal alcohol exposure. Contemporary studies have reported some of these outcomes in the absence of FAS physical features. Currently, no modal profile of abilities has been found to be unique to alcohol exposure, is observed in all those with prenatal alcohol exposure, or can be distinguished from that observed with some other neurobehavioural disorders. Furthermore, not every deficit that we may identify in a child with prenatal exposure to alcohol may be solely the result of alcohol exposure. An expert analysis of neurodevelopmental deficits caused by a range of teratogens and congenital disorders failed to result in a consensus on core deficits associated only with FASD.4. Research and experience has shown that features of FASD are complex and multifaceted, originating with organic brain damage caused by alcohol, but interacting with genetic and other influences. Over the lifespan of the affected ...

The objective of this study was to investigate cellular apoptosis in prenatal glucocorticoid overexposure and a postnatal high fat diet in rats. Pregnant Sprague-Dawley rats at gestational days 14 to 21 were administered saline (vehicle) or dexamethasone and weaned onto either a normal fat diet or a high fat diet for 180 days; in total four experimental groups were designated, i.e., vehicle treated group (VEH), dexamethasone treated group (DEX), vehicle treated plus high-fat diet (VHF), and dexamethasone treated plus high-fat diet (DHF). Chronic effects of prenatal liver programming were assessed at postnatal day 180. The apoptotic pathways involved proteins were analyzed by Western blotting for their expressions. Apoptosis and liver steatosis were also examined by histology. We found that liver steatosis and apoptosis were increased in the DHF, DEX, and VHF treated groups, and that the DHF treated group was increased at higher levels than the DEX and VHF treated groups. The expression of leptin was

INTRODUCTION: The effects of tobacco exposure are typically examined by comparing groups based on a cut-score of self-reported number of cigarettes or bioassays collected in cross-sectional studies. This study introduces a new fuzzy clustering method that facilitates detection of subtle exposure effects by objectively deriving subgroups from modeling multidimensional exposure measures. We test the new method on a known exposure effect (fetal growth) and report on the graded exposure effect detected in a pregnancy cohort. METHODS: 978 pregnant women were enrolled from 1986 to 1992 in the Maternal Infant Smoking Study of East Boston (MISSEB). Four kinds of exposure data were used to generate exposure groups: self-reported smoking, cotinine levels, nicotine levels, and nicotine dependence scores. Subgroups were identified via a comprehensive validation procedure. The results from MISSEB (number of exposure clusters, exposure effects on birth weight, body length, and head circumference) were compared with

In this review, we provide a synopsis of work on the epidemiologic evidence for prenatal infection in the etiology of schizophrenia and autism. In birth cohort studies conducted by our group and others, in utero exposure to infectious agents, prospectively obtained following biomarker assays of archived maternal sera and by obstetric records was related to an elevated risk of schizophrenia. Thus far, it has been demonstrated that prenatal exposure to influenza, elevated toxoplasma antibody, genital/reproductive infections, rubella, and other pathogens are associated with schizophrenia. Anomalies of the immune system, including enhanced maternal cytokine levels are also related to schizophrenia. Some evidence also suggests that maternal infection and immune dysfunction may be associated with autism. Although replication is required, these findings suggest that public health interventions targeting infectious exposures have the potential for preventing cases of schizophrenia and autism. Moreover, ...

The NICU Network Neurobehavioral Scales (NNNS) is a tool for the comprehensive examination of normal full-term infants, preterm infants, and infants at risk because of prenatal substance exposure. NICU stands for neonatal intensive care unit. The NNNS can be used with infants through 6 weeks of age - and as early as 32 weeks gestational age for preterm infants - to guide assessment, evaluation, and early intervention. It is designed to evaluate neurobehavioral and neurological profiles, adaptations to stress, and the withdrawal status of neonates exposed to drugs in utero. The NNNS is useful for assessment of all at-risk infants and can serve as a basis for consultation with families and a guide for intervention. The test takes about 20 minutes (plus 10-15 minutes for scoring) and can be administered by experiences clinicians after certification training, available internationally through video conferences.

During the 1970s and 1980s an increased amount of public and scientific attention was paid to the health and medical problems of individuals whose mothers were prescribed diethylstilbestrol (DES). A potent synthetic nonsteroidal estrogen, DES was first developed in 1938 and initially became available in the U.S. for treating a range of gynecologic conditions in 1941 (Apfel and Fisher, 1984). A few years later its approval by the FDA was broadened to include treatment of pregnant women for the purpose of preventing miscarriages. Though its efficacy had long been questioned by some in the medical community (Bambigboye and Morris, 2003; Dieckmann, 1953), DES remained popular with doctors until discovery in the early 1970s of an apparent association between prenatal exposure to DES and a rare form of vaginal cancer in females whose mothers used DES (Heinonen, 1973; Herbst and Bern, 1981). Subsequent research confirmed the transplacental mechanism of DES transmission (Maydl, et al., 1983) and ...

Prenatal stress could have great influence on development of offspring and might alter cognitive function and other physiological processes of children. The current study was conducted to study the effect of physical or psychological prenatal stress on addictive and anxiety-like behavior of male and female offspring during their adolescence period (postnatal day (PND) 40). Adult female rats were exposed to physical (swimming) or psychological (observing another female rat swimming) stress from day six of gestation for 10 days. Male and female offspring were assayed for anxiety-like behavior, motor and balance function and morphine conditioned place preference using the open field, elevated plus maze (EPM), rotarod and wire grip assay and conditioned place preference. Offspring in both physical and psychological prenatal stress groups demonstrated significant increase in anxiety-like behavior in EPM paradigm, but no alterations were observed in motor and balance function of animals. Offspring in ...

Effects on preterm delivery, gestational age and birth weight High doses of lead have been reported to cause spontaneous abortion in women. Data relating maternal blood lead to increased incidence of preterm delivery, gestational age and/or reduced birth weight have provided conflicting results but weight of evidence suggests that such effects are not likely below blood lead levels of 30 µg/dL. Prenatal Effects Effects of prenatal lead exposure upon neurobehavioural performance measures have been demonstrated in studies of experimental animals and presumably will occur in humans. However, available data are inadequate to establish the dose-effect relationships that characterize this endpoint. While effects have been observed upon early measures of mental and physical development, attenuation of effects typically occurs over time and, in most studies, are not associated with impacts upon measures such as IQ. However, effects of prenatal lead exposure upon IQ can be difficult to dissociate from ...

Fetal alcohol syndrome (FAS), a disorder that is indicated by distinct facial characteristics, growth retardation, and poor intellectual and attentional function, can occur when mothers drink alcohol heavily during pregnancy. A new study in the October issue of The Journal of Pediatrics shows that prenatal alcohol exposure can also affect an infants visual acuity or sharpness of vision.

At the NIEHS, researchers from the Epidemiology Branch are using biologic samples collected from pregnant Norwegian women to investigate how early-life exposure to environmental contaminants may affect adult health. The samples were collected from women enrolled in the Norwegian Mother and Child Cohort Study, or MoBa, an ongoing long-term prospective cohort study of pregnant Norwegian women and their children. NIEHS epidemiologists are analyzing these samples to measure the level of exposure to environmental contaminants in relation to a range of health endpoints, such as obesity and asthma, among the pregnant women and their children.

Read about a new study conducted by the Norwegian Institute of Public Health has confirmed a link between prenatal exposure to acetaminophen and an increased risk of developing asthma in early childhood.

(Maternal Cocaine Use and Birth Defects) Our data are from one of the first population-based studies in which trends for defects potentially caused by maternal cocaine use are examined; the results of our study show no significant change in the prevalence of multiple vascular disruption defects over time. We suspect that if cocaine is a teratogen, its teratogenicity is weak or is associated with a small subset of birth defects that are yet to be identified.

Fetal alcohol spectrum disorder (FASD) is a leading form of neurodevelopmental delay in Canada, affecting an estimated 3000 babies per year. FASD involves a range of disabilities that entail significant costs to affected individuals, families, and society. Exposure to alcohol in utero is a necessary factor for FASD development, and this has led to FASD being described as completely preventable. However, there are significant ethical challenges associated with FASD prevention. These challenges revolve around 1) what should be communicated about the risks of alcohol consumption during pregnancy, given some ongoing scientific uncertainty about the effects of prenatal alcohol exposure, and 2) how to communicate these risks, given the potential for stigma against women who give birth to children with FASD as well as against children and adults with FASD ...

This 8-year longitudinal study of mothers who drank alcohol during their pregnancy looked at the impact on behaviours in children over two years old

In the United States, prenatal alcohol exposure (PAE) is the most common preventable cause of developmental delay. Animal studies have shown some of the adverse effects of PAE on placental development, but few studies have examined these effects in humans. This is the first study to examine the effects of prenatal exposure to methamphetamine, marijuana, and cigarette smoking on human placental dev...

Early-life exposure to lipopolysaccharide reduces the severity of experimental autoimmune encephalomyelitis in adulthood and correlated with increased urine corticosterone and apoptotic CD4+ T cells

The practice of risk assessment with respect to accounting for early-life exposures to toxicants continues to develop, and specific components of this Supplemental Guidance may become outdated or may otherwise require modification in individual settings. It is EPAs intent to use, to the extent practicable and consistent with Agency statutes and regulations, the best available science in its risk assessments and regulatory actions and this Supplemental Guidance is not intended to provide any substantive or procedural obstacle in achieving that goal.. Therefore, the Supplemental Guidance has no binding effect on EPA or on any regulated entity. Where EPA does use the approaches in the Supplemental Guidance in developing risk assessments, it will be because EPA has decided in the context of that risk assessment that the approaches from the Supplemental Guidance are suitable and appropriate. This judgment will be tested through peer review, and the risk assessment will be modified to use different ...

The additional Supplemental Guidance describes possible approaches that EPA could use in assessing cancer risks exposures to children from 0 to 16 years of age. This marks the first time that Supplemental Guidance specifically related to children has been issued. It includes a review of existing scientific literature on chemical effects in animals and humans. The Supplemental Guidance also summarizes the results of the cancer studies that investigated early-life exposure, EPAs analysis of those studies, and analysis to strengthen the scientific basis for adjusting from studies conducted in adults to children. This document is consistent with the National Research Councils 1994 recommendation that EPA assess risks to infants and children whenever it appears that their risks might be greater than those of adults. ...

To examine whether prenatal exposure to glucocorticoids could adversely affect subsequent cellular development of the lung, we administered 0.2 mg/kg of dexamethasone to pregnant rats on gestational days 17, 18, and 19. Lungs of the offspring were then examined for patterns of cell acquisition (DNA) and growth (protein). DNA concentration (a marker of cell packing density) and DNA content (a measure of total cell numbers) were reduced during gestation, and the shortfalls in concentration persisted past weaning.

Greetings from the editors as we bring forth the third issue of this year. The month of February is observed as the International Prenatal Infections Prevention month. This is to create worldwide awareness of the burden and impact of prenatal infections and to promote measures to improve maternal and neonatal outcome. Prenatal infections are infections that are transmitted to the fetus or newborn during the antenatal period or during delivery. Prenatal infections of obstetric and neonatal significance are viral infections like Human immunodeficiency virus (HIV), Hepatitis B, Hepatitis E, Toxoplasmosis, Rubella, Cytomegalovirus, Herpes, Parvovirus, Varicella Zoster, bacterial infections like Syphilis, Group B Streptococcus, Listeria, tropical diseases like malaria and chronic diseases like tuberculosis to list a few. Around 2 to 3% of congenital anomalies are accountable to prenatal infections. HIV is a sexually transmitted or blood borne virus that affects the T lymphocytes in the body leading ...

Animal studies find that prenatal stress is associated with increased physiological and emotional reactivity later in life, mediated via fetal programming of the HPA axis through decreased glucocorticoid receptor (GR) gene expression. Post-natal behaviours, notably licking and grooming in rats, cause decreased behavioural indices of fear and reduced HPA axis reactivity mediated via increased GR gene expression. Post-natal maternal behaviours may therefore be expected to modify prenatal effects, but this has not previously been examined in humans. We examined whether, according to self-report, maternal stroking over the first weeks of life modified associations between prenatal depression and physiological and behavioral outcomes in infancy, hence mimicking effects of rodent licking and grooming. From a general population sample of 1233 first time mothers recruited at 20 weeks gestation we drew a stratified random sample of 316 for assessment at 32 weeks based on reported inter-partner psychological

NIH Funding Opportunities and Notices in the NIH Guide for Grants and Contracts: Effects of In Utero Alcohol Exposure on Adult Health and Disease (R21 - Clinical Trial Optional) PA-18-508. NIAAA

The Human Early Learning Partnership. University of British Columbia. Suite 440, 2206 East Mall. Vancouver, BC, V6T 1Z3, Canada. Phone: 604-822-1278. Fax: 604-822-0640. Email: [email protected]. ...

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Results Sixty subjects were included. The mean gestational age (GA) and birth weight (BW) were 36.8±3.03 weeks and 2.79±0.63kg. All exhibited NAS within 72 hours of life. 59/60 (98.3%) initiated treatment according to protocol. There was significant deviation from the protocol at 48 and 72 hours of treatment with 33% and 12% of the patients requiring more than the prescribed amount of methadone to control NAS. The mean (SD) total methadone exposure was 1.96±1.63 mg/kg, LOT 11.66±9 days and LOS 22.4±29.3 days suggesting significant variability in response. No significant correlation was found between BW or GA and LOT.. ...

1.. Holmes LB, Baldwin EJ, Smith CR, Habecker E, Glassman L, Wong SL, Wyszynski DF.Increased frequency of isolated cleft palate in infants exposed to lamotrigine during pregnancy. Neurology 70: 2152-2158, No. 22, Part 2, 27 May 2008 ...

Ensuring that you receive proper prenatal care is critical to your unborn childs health. In fact, undiagnosed prenatal infections may lead to permanent, debilitating birth injuries.

Prenatal contact with corticosteroids has long-term postnatal neurodevelopmental and somatic consequences. of spasms indicates that prenatal betamethasone publicity down-regulates genes encoding a number of important protein taking part in GABAergic and glutamatergic transmission. Interestingly, there have been significant sex-specific modifications after prenatal betamethasone in synapse-related gene manifestation but no such sex variations were within prenatally saline-injected settings. A pair-wise relevance evaluation revealed that, even though synapse gene manifestation in settings was 3rd party of sex, these genes type topologically specific gene materials in men and women and these materials are modified by betamethasone inside a sex-specific way. These findings may explain the sex differences in both regular occurrence and behavior and severity of infantile spasms. Adjustments in transcript manifestation and their coordination may donate to a molecular PA-824 substrate of long term ...