As curvas ponderais, propostas por SIQUEIRA para diagnóstico de desnutrição materna em gestantes normais, foram aplicadas a duas populações de gestantes que frequentaram o Serviço de Obstetrícia (pré-natal e clínica obstétrica) do Hospital das clínicas da Universidade Federal de Goiás (U.F.Go): um grupo foi constituído por gestantes que não apresentaram patologias próprias ou associadas à gestação (Grupo Normais) e o outro foi composto por gestantes que apresentaram processos patológicos (Grupo Patológicas). Foram estudadas variáveis relacionadas à gestação (peso habitual, ganho de peso na gestação, peso ao final da gravidez, estatura da gestante, perímetro cefálico materno, idade da gestante, peso da placenta e idade gestacional pelos métodos de Capurro e Último Período Menstrual Normal (UPMN) e ao recém-nascido (peso, comprimento, perímetro cefálico e perímetro torácico) para ambos os grupos de acordo com o estado nutricional da gestante (desnutridas, nutridas e obesas). Os resultados permitiram concluir que as curvas ponderais propostas por SIQUEIRA são aplicáveis a outros tipos de populações, quer se trate de gestantes normais ou de gestantes patológicas. Foram verificadas as medidas antropométricas (peso, comprimento, perímetro cefálico e perímetro torácico) de 42 crianças que constituíram o grupo Normais e de 23 crianças que formaram o grupo Patológicas, por ocasião do nascimento e ao completarem 1, 3, 6, 9 e 12 meses de idade segundo o estado nutricional materno (desnutridas, nutridas e obesas); foi ainda estudada a idade gestacional dessas 65 crianças pelos métodos de Capurro e do UPMN. Os resultados permitiram concluir que a desnutrição materna contribuiu para o retardo de crescimento da criança no primeiro ano de vida. Verificou-se ainda um retardo no crescimento das crianças cujas mães apresentaram patologias próprias ou associadas à gravidez, mesmo quando classificadas como nutridas ou obesas, mas os filhos de desnutridas patológicas apresentaram ainda um maior déficit no seu crescimento. Concluiu-se que, além da desnutrição materna, também a presença de patologias durante a gestação associou-se com um retardo do crescimento fetal e pós-natal. Além disso, foi possível verificar que a desnutrição e a presença de patologias exerceram um efeito cumulativo sobre o retardo do crescimento fetal e pós-natal. / The weight curves proposed by SIQUEIRA for the diagnosis of maternal malnutrition in normal pregnant women were applied to two pregnant population samples which attended the Obstetric Clinic (Prenatal and Clinical Obstetrics) of the \"Hospital das Clinicas\" of the Federal University of Goiás (U.F.Go) One group (the Normal Group) consisted of expectant women who had no pathological history, either prior to or related to pregnancy, and the other group (the Pathological Group) consisted of expectant mothers who had a history of pathological condition. Several variables related to pregnancy were studied prepregnancy weight, weight-gain during pregnancy weight at and of nregnancy, mother\'s height, maternal cephalic circumference, mother\'s age, weight of placenta and gestational age by Capurro\'s and Last Menstrual Period (LMP) methods as were also some related to thc new-born child (weight, lenght, cephalic and thoracic circumferences) for both of the above groups in accordance with the nutritional status of the mother (undernourished, well-nourished and obese). The results led to the conclusion that the weight curves proposed by SIQUEIRA are applicable to other kinds of populations, whether of nor mal pregnant women or pathological pregnant women. The anthropometric measurements (weight, lenght, cephalic and thoracic circumferences) of the 42 children born to the Normal Group and of the 23 children born to the Pathological Groun were taken at birth and at the end of the 1st·, 6st., gst. and 12th. months, according to the nutritional status of the mother (undernourished, well-nourished and obese). The gestational age of 65 children was also studied, using the Capurro and LMP methods. The results led to the conclusion that maternal malnutrition contributed to the retardation of the child\'s growth in the first year of life. Further, it was discovered that there was a retardation in the growth of children whose mothers presented a pathological history either prior to or associated with pregnancy, even when these were classified as well-nourished or obese. However the children of undernourished mothers wi th a pathological history showed an even greater growth deficiency. The conclusion drawm was that the presence of a pathological condition during pregnancy was associated with retardation of fetal and postnatal growth beyond that caused by maternal malnutrition. It was also possible to establish that malnutrition and the presence of a pathological condition exercised a cumulative effect on the retardation of fetal and postnatal growth.

Alcohol consumption during pregnancy can result in fetal alcohol spectrum disorders (FASD), which encompass a range of physical, behavioral, learning, emotional and social disturbances. Many mechanisms for this array of alcohol-derived fetal injuries have been proposed, but none fully accounts for the deficiencies observed. Alcohol is a ubiquitous drug that may affect the brain at any or all stages of development and at multiple sites; regional differences in vulnerability of different brain structures during different periods of exposure have been demonstrated. This study investigates possible mechanisms for the alcohol induced neurodevelopment damage seen as a result of prenatal alcohol exposure, and also includes evaluation of a potential intervention strategy (glutamine). These experiments all utilized the sheep model, which has distinct advantages over the rodent model for third trimester-equivalent studies (a time of increased vulnerability to the effects of alcohol). The fetal hippocampal formation (pyramidal cells in the CA1 and CA2/3 fields and granule cells of the dentate gyrus) and olfactory bulb (mitral cells) have been altered in response to alcohol exposure in rodent model studies. This study examined the effects on the fetal hippocampal formation and olfactory bulb in response to all three trimester-equivalent alcohol exposure in the sheep model, a species in which the third trimester-equivalent occurs in utero (as opposed to post-natal as occurs in the rodent). It is known that both maternal and fetal cortisol levels increase in response to alcohol. The role of cortisol in mediating fetal cerebellar Purkinje cell loss (known to occur with alcohol exposure) was analyzed. Lastly, the availability of circulating amino acids, both maternal and fetal, in response to alcohol are reported. The results of administration of a single acute dose of glutamine to the ewe, concurrent with alcohol, was evaluated for its ability to prevent the amino acid and pH perturbations known to occur in response to alcohol.

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (p. 255-271).

Research Doctorate - Doctor of Philosophy (PhD) / Maternal asthma is associated with low birth weight, a risk factor for disease in adult life. To determine the mechanisms involved, the relationships between mother, placenta and fetus were examined in asthmatic and non-asthmatic pregnancies. Maternal asthma and its treatment (no glucocorticoid or glucocorticoid) was monitored throughout pregnancy. Fetal growth was examined during gestation, and at birth, neonatal size and sex were determined. Placental 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) enzyme activity and umbilical vein plasma cortisol and estriol concentrations were measured. Placental cytokine, growth factor and glucocorticoid receptor (GR) mRNA were determined using quantitative RT-PCR. Birth weight of female neonates in the no glucocorticoid asthmatic group only, was significantly reduced compared to females of the non-asthmatic group. Male neonates were unaffected by asthma or its treatment. Asthmatic women pregnant with a female fetus showed a significant increase in circulating monocytes and glucocorticoid treatment as pregnancy progressed, while those pregnant with a male fetus did not, suggesting that maternal asthma worsens in the presence of a female fetus. 11beta-HSD2 activity was significantly reduced in placentae from female neonates of the no glucocorticoid group compared to other female neonates and was associated with a trend towards higher plasma cortisol, reduced fetal adrenal activity demonstrated by lower cord blood estriol, reduced placental GR expression, no alteration in placental or fetal insulin-like growth factors or their binding proteins and a significantly increased Th2:Th1 cytokine mRNA ratio, which was inversely correlated with 11beta-HSD2 activity in all females. Reduced placental 11beta-HSD2 activity may be an important component leading to decreased female fetal growth in pregnancies complicated by asthma. This study provides strong evidence for a fetal sex-specific effect on the maternal immune system which can have adverse effects on the female fetus. The female fetus alters maternal inflammatory pathways, which when not controlled by the use of inhaled glucocorticoids results in reduced placental 11beta-HSD2 activity, contributing to suppressed fetal adrenal function and a late gestation decrease in female fetal growth.

Thesis (M.D.)--Dept. of Obstetrics and Gynaecology, University of Adelaide, 1970. / Includes bibliographical references (leaves 284-298).

Thesis (M.A.)--York University, 2006. Graduate Programme in Psychology. / Typescript. Includes bibliographical references (leaves41-48). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR29619

Thesis (M.S.P.H.)--University of Michigan, 1939.

Thesis (M.S.P.H.)--University of Michigan, 1939.

Thesis (M.Med.Sc.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 25-30). Also available in print.

Thesis (Ph.D) - University of Queensland, 2006. / Includes bibliography.