Christine May Briton-Jones. / "May 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 149-171). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Orientadores: Egle Cristina Couto de Carvalho, João Luiz Pinto e Silva, Ricardo Barini / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas / Made available in DSpace on 2018-11-27T11:27:06Z (GMT). No. of bitstreams: 1 Briganti_Luciana_M.pdf: 1660554 bytes, checksum: 4773ebf2931e4577e1b9c58a75770425 (MD5) Previous issue date: 2007 / Resumo: Introdução: As malformações de parede abdominal fetal ocorrem entre a quinta e a décima semanas de idade gestacional, devido a falhas na seqüência normal do desenvolvimento embrionário. Costumam ser diagnosticadas precocemente com o uso da ultra-sonografia, geralmente por volta de doze semanas de gestação. A gastrosquise e a onfalocele são os defeitos mais comuns da parede abdominal. A gastrosquise, em geral, ocorre isoladamente, enquanto a onfalocele apresenta maior incidência com o aumento da idade materna, e comumente associa-se a anomalias genéticas. A adequada assistência em casos de malformação de parede abdominal demanda experiência do serviço e conhecimento da história natural da lesão. Objetivo: Avaliar a freqüência dos defeitos da parede abdominal fetal em gestantes atendidas no Ambulatório de Medicina Fetal do CAISMUnicamp entre 1996 e 2006, além de dados epidemiológicos e resultados neonatais. Sujeitos e Métodos: Foi realizado um estudo descritivo retrospectivo, através da revisão de prontuários de gestantes com fetos acometidos por malformações da parede abdominal. Os dados foram analisados através de tabelas de freqüência. Resultados: A freqüência das malformações de parede abdominal fetal nas gestantes estudadas foi de 33,3 para cada 10.000 partos. A onfalocele foi diagnosticada em 43 casos e a gastrosquise em 31. Foram também encontrados doze casos de síndrome de Body-Stalk, cinco de extrofia de cloaca, seis de Pentalogia de Cantrell, dois de síndrome da banda amniótica e um de síndrome de Beckwith-Wiedemann. Foram excluídos 18 casos cujos partos ocorreram fora do serviço. Entre os 82 restantes, o tabagismo foi relatado por 14,7% das mulheres com fetos com onfalocele e por 22,2% nos casos de gastrosquise. As médias de idade materna e paridade foram 27,5 e 2,5 nos casos de onfalocele e 19,5 e 1,4 nos de gastrosquise, respectivamente. A cesariana foi realizada em 67,7% dos casos de onfalocele e em 81,5% dos casos de gastrosquise, e a maioria dos partos ocorreu com mais de 34 semanas de gestação (61,8% e 77,8%, respectivamente). A média de peso dos recém-nascidos com onfalocele foi 2151,2 e dos com gastrosquise foi 2243,3 gramas. O índice de Apgar de primeiro minuto foi maior ou igual a sete em 35,3% dos recém-nascidos com onfalocele e em 63% daqueles com gastrosquise. O de quinto minuto foi maior ou igual a sete em 58,8% e 96,3%, respectivamente. Os neonatos com gastrosquise foram submetidos à correção cirúrgica em 96,3% dos casos e receberam alta hospitalar vivos em sua maioria. Conclusão: A freqüência de malformações de parede abdominal encontrada no serviço estudado foi mais alta do que aquela relatada na literatura. A média de idade materna foi baixa nos casos de gastrosquise. Os maiores índices de Apgar foram obtidos pelos fetos com gastrosquise. Estes foram submetidos a correção cirúrgica e receberam alta vivos em sua grande maioria / Abstract: Introduction: Malformations of fetal abdominal wall occur between the fifth and the tenth weeks in pregnancy, and are due to disruptions during the normal sequence of embryo development. They have been diagnosed early in pregnancy using ultrasonography, mostly around twelve weeks. Gastroschisis and omphalocele are the most common defects of fetal abdominal wall. Gastroschisis usually occurs isolated, while omphalocele presents greater incidence as maternal age increases and is generally associated with genetic anomalies. The adecquate assistance for fetuses with abdominal wall defects demands experience of the staff and the knowing of its natural history. Objective: To evaluate the frequency of fetal abdominal wall defects in pregnant women receiving care at the Outpatient Department of Fetal Medicine at CAISM-Unicamp, whose deliveries occurred between 1996 and 2006, and to assess epidemiological data and neonatal outcome. Methods: A retrospective, descriptive study was carried out by reviewing records of patients whose fetuses had abdominal wall defects. Data was later analyzed by setting-up frequency tables. Results: The frequency of fetal abdominal wall defects in the sample of pregnant women studied was 33.3/10,000 deliveries. Omphalocele was diagnosed in 43 cases and gastroschisis in 31. In addition, 12 cases of Body Stalk anomaly, 5 of cloacal exstrophy, 6 cases of Pentalogy of Cantrell, 2 of amniotic band syndrome and 1 case of Beckwith- Wiedemann syndrome were found. Of these 100 cases, 18 were excluded from the study because delivery occurred in another institute. Of the remaining 82 cases, smoking was reported by 14.7% of women whose fetuses had omphalocele and by 22.2% whose fetuses had gastroschisis. Mean maternal age and parity were 27.5 and 2.5 in cases of omphalocele and 19.5 and 1.4 in cases of gastroschisis, respectively. Cesarean sections were performed in 67.7% of cases of omphalocele and in 81.5% of cases of gastroschisis, the majority of deliveries occurring after 34 weeks of gestation (61.8% and 77.8%, respectively). Mean weight of the newborn infants with omphalocele was 2,151.2 grams and of those with gastroschisis 2,243.3 grams. Apgar score at the 1st minute was =7 in 35.3% of the newborn infants with omphalocele and in 63% of those with gastroschisis. Apgar score at the 5th minute was =7 in 58.8% and 96.3%, respectively. Infants with gastroschisis were submitted to corrective surgery in 96.3% of cases and most were alive at the time of discharge from hospital. Conclusion: The frequency of abdominal wall defects found in this service was higher than those reported in the literature. In cases of gastroschisis, mean maternal age was lower, the fetuses had higher Apgar scores, were submitted to corrective surgery and most were alive at the time of hospital discharge / Mestrado / Tocoginecologia / Mestre em Tocoginecologia

Lam Audrey Carmen. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 166-195). / Abstracts in English and Chinese. / Acknowledgements --- p.vi / Publications --- p.vii / Abbreviations --- p.x / Abstract --- p.xiii / Chapter Chapter One - --- Introduction --- p.1 / Chapter Section 1.1 --- Hematopoietic Stem Cells --- p.1 / Chapter 1.1.1 --- Hematopoiesis --- p.1 / Chapter 1.1.2 --- Hematopoietic Stem and Progenitor Cells --- p.1 / Chapter Section 1.2 --- Stem Cell Transplantation --- p.4 / Chapter 1.2.1 --- Stem Cell Transplantation --- p.4 / Chapter 1.2.2 --- Sources of Hematopoietic Stem Cells for Transplantation --- p.4 / Chapter 1.2.3 --- Cord Blood as a Source of Hematopoietic Stem Cells --- p.6 / Chapter 1.2.3.1 --- Advantages of Cord Blood Transplant --- p.6 / Chapter 1.2.3.2 --- Disadvantages of Cord Blood Transplant --- p.7 / Chapter Section 1.3 --- Ex Vivo Expansion --- p.8 / Chapter 1.3.1 --- Optimization of Expansion Conditions --- p.10 / Chapter 1.3.1.1 --- CD34+ Cell Selection --- p.10 / Chapter 1.3.1.2 --- Cytokines --- p.11 / Chapter 1.3.1.2.1 --- Thrombopoietin --- p.12 / Chapter 1.3.1.2.2 --- Stem Cell Factor --- p.14 / Chapter 1.3.1.2.3 --- Flt-3 Ligand --- p.15 / Chapter 1.3.1.2.4 --- Granulocyte-Colony Stimulating Factor --- p.16 / Chapter 1.3.1.2.5 --- Interleukin-3 --- p.17 / Chapter 1.3.1.2.6 --- Interleukin-6 --- p.18 / Chapter 1.3.1.2.7 --- Comparison of Flt-3 Ligand and Stem Cell Factor --- p.20 / Chapter 1.3.1.3 --- Culture Medium --- p.20 / Chapter 1.3.2 --- Mannose-Binding Lectin --- p.22 / Chapter 1.3.3 --- Ex Vivo Expansion for Clinical Transplantation --- p.23 / Chapter Section 1.4 --- Non-Obese Diabetic/Severe Combined Immunodeficient Mouse Transplantation Model --- p.29 / Chapter Chapter Two - --- Objectives --- p.32 / Chapter Chapter Three - --- Materials and Methodology --- p.34 / Chapter Section 3.1 --- Collection of Cord Blood Samples / Chapter Section 3.2 --- Cryopreservation and Thawing of Cord Blood --- p.34 / Chapter Section 3.3 --- Enrichment of CD34+ Cells --- p.35 / Chapter Section 3.4 --- Ex Vivo Expansion --- p.38 / Chapter 3.4.1 --- Effects of Flt-3 Ligand and stem Cell Factor on the Expansion of Megakaryocytic Progenitor Cells --- p.39 / Chapter 3.4.1.1 --- Ex Vivo Expansion of Cord Blood CD34+ Cells with Flt-3 Ligand or Stem Cell Factor --- p.39 / Chapter 3.4.1.2 --- Flt-3 Receptor Assay --- p.40 / Chapter 3.4.2 --- Effects of Mannose-Binding Lectin on the Ex Vivo Expansion of Hematopoietic Stem and Progenitor Cells --- p.41 / Chapter 3.4.2.1 --- Ex Vivo Expansion of Cord Blood CD34+ Cells with Mannose-Binding Lectin --- p.41 / Chapter 3.4.2.2 --- Effects of Mannose-Binding Lectin on the Preservation of Early Stem and Progenitor Cells --- p.41 / Chapter 3.4.2.3 --- Transplantation of Expanded Cells into NOD/SCID Mice --- p.42 / Chapter 3.4.3 --- "Optimization of Culture Duration, Culture Media, Autologous Plasma and Cytokine Combinations for the Preclinical Ex Vivo Expansion of Hematopoietic Stem and Progenitor Cells" --- p.42 / Chapter 3.4.3.1 --- "Comparison of Culture Duration, Culture Media and Cytokine Combinations" --- p.42 / Chapter 3.4.3.2 --- Effects of Autologous Cord Blood Plasma --- p.43 / Chapter 3.4.3.3 --- Effects of Flt-3 Ligand and Dosage of Thrombopoietin and Stem Cell Factor --- p.43 / Chapter 3.4.3.4 --- Transplantation of Expanded Cells into NOD/SCID Mice --- p.44 / Chapter Section 3.5 --- Progenitor Colony-Forming Assays --- p.44 / Chapter 3.5.1 --- Colony-Forming Unit Assay --- p.44 / Chapter 3.5.2 --- Colony Forming Unit Megakaryocyte --- p.46 / Chapter 3.5.3 --- Calculations of CFU --- p.46 / Chapter Section 3.6 --- Flow Cytometry Analysis --- p.47 / Chapter Section 3.7 --- Transplantation of Non-Obese Diabetic/Severe Combined Immunodeficient Mice --- p.48 / Chapter Section 3.8 --- Assessment of Human Cell Engraftment in Transplanted NOD/SCID Mice --- p.49 / Chapter 3.8.1 --- Flow Cytometry Analysis --- p.49 / Chapter 3.8.2 --- PCR Analysis --- p.50 / Chapter Section 3.9 --- Statistical Analysis --- p.52 / Chapter Chapter Four - --- Effects of Flt-3 Ligand and Stem Cell Factor on the Expansion of Megakaryocytic Progenitor Cells --- p.53 / Chapter Section 4.1 --- Results --- p.53 / Chapter 4.1.1 --- Ex Vivo Expansion of CD34+ Cells --- p.53 / Chapter 4.1.2 --- Identification of Flt-3 Receptors --- p.55 / Chapter Section 4.2 --- Discussion --- p.55 / Chapter Chapter Five- --- Effects of Mannose-Binding Lectin on the Ex Vivo Expansion of Hematopoietic Stem and Progenitor Cells --- p.68 / Chapter Section 5.1 --- Results --- p.68 / Chapter 5.1.1 --- Ex Vivo Expansion of CD34+ Cells with Mannose-Binding Lectin --- p.68 / Chapter 5.1.2 --- Effects of Mannose-Binding Lectin on the Preservation of Early Stem and Progenitor Cells --- p.72 / Chapter 5.1.3 --- Transplantation of Expanded Cells into NOD/SCID Mice --- p.75 / Chapter Section 5.2 --- Discussion --- p.76 / Chapter Chapter Six - --- "Optimization of Culture Duration, Culture Media, Autologous Plasma and Cytokine Combinations for the Preclinical Ex Vivo Expansion of Hematopoietic Stem and Progenitor Cells" --- p.111 / Chapter Section 6.1 --- Results --- p.111 / Chapter 6.1.1 --- Kinetics of Expansion --- p.111 / Chapter 6.1.2 --- Assessment of Culture Media --- p.113 / Chapter 6.1.3 --- Effects of Autologous Cord Blood Plasma --- p.115 / Chapter 6.1.4 --- Effects of Granulocyte-Colony Stimulating Factor --- p.117 / Chapter 6.1.5 --- Effects of Interleukin-6 --- p.118 / Chapter 6.1.6 --- Effects of Increased Dosage of Thrombopoietin and Stem Cell Factor --- p.119 / Chapter 6.1.7 --- Effects of Flt-3 Ligand --- p.120 / Chapter 6.1.8 --- Transplantation of Expanded Cells into NOD/SCID Mice --- p.121 / Chapter Section 6.2 --- Discussion --- p.123 / Chapter Chapter Seven- --- General Discussion and Conclusion --- p.163 / Bibliography --- p.166

Le concept de DOHaD (Developmental Origins of Health and Disease) qui découle de la théorie de Barker, replace l’origine des maladies métaboliques de l’adulte au moment du développement fœtal et/ou périnatal. De nombreuses données épidémiologiques indiquent qu’une dysnutrition maternelle (dénutrition, surnutrition) a des répercussions sur la croissance fœtale qui se traduisent par une anomalie du poids à la naissance (retard de croissance intra utérin : RCIU / gros poids de naissance : Macrosomie) et prédisposent l’individu au développement des maladies métaboliques. Afin de mieux comprendre les mécanismes susceptibles de transmettre de génération en génération cette vulnérabilité métabolique, nous avons développé un modèle transgénérationnel chez le rat associant la programmation fœtale chez la F0 par dénutrition maternelle (modèle FR30) et une dysnutrition chez la F1 avec un régime alimentaire hyperlipidique.Nos résultats montrent qu’une restriction alimentaire de 70% durant toute la grossesse (modèle FR30) contribue à une sensibilité accrue chez la descendance F1 femelle au développement de traits de syndrome métabolique. Les femelles F1 issues de mères dénutries présentent à l’âge adulte une intolérance au glucose et une hyperleptinémie. Les femelles de la F1 soumises à un régime hyperlipidique « high fat » (HF) ne présentent pas d’obésité que ce soit celles issues de mères contrôle que de mères dénutries. La faible appétence du régime, et la carence en hydrates de carbone qui l’accompagnent ne permettent pas le développement de l’obésité. En revanche, ce régime accentue les perturbations métaboliques chez des animaux sensibilisés par la programmation.Lorsque les femelles F1 sont mises en reproduction, on observe qu’en réponse à la programmation fœtale (FR) et/ou au régime alimentaire (Standard ou HF) la trajectoire de croissance dans la descendance F2 conduit à des phénotypes différents à la naissance. Les nouveau-nés de mères F1 issues de mères C ou FR et ayant suivi un régime HF en prégestation et en gestation (C HF-HF et FR HF-HF) ont un RCIU. A l’inverse, les nouveau-nés issus de mères F1 issues de mères dénutries et ayant eu un régime HF en prégestation puis un régime standard durant la gestation (FR HF-S) ont une macrosomie. Les perturbations métaboliques et hormonales des mères F1 ne pouvant expliquer à elles seules la survenue de ces phénotypes, nous nous sommes intéressés à l’organe situé à l’interface entre les compartiments maternels et fœtaux permettant le dialogue entre la mère et le fœtus : le placenta.L’analyse morphologique et moléculaire du placenta nous indique que cet organe est non seulement sensible aux modifications métaboliques de la mère, mais s’adapte à la demande du fœtus. On observe de fortes variations géniques qui se traduisent par une surexpression ou sous expressions géniques selon le phénotype observé RCIU ou macrosomie. Il est important de noter que les variations présentent un dimorphisme sexuel. Nos travaux suggèrent donc que les phénotypes de RCIU ou macrosomie sont le résultat d’anomalies métaboliques et hormonales maternelles mais également de l’adaptation génique placentaire sexe-spécifique. / The concept of DOHaD (Developmental Origins of Health and Disease) which derives from the theory of Barker, replace the origin of metabolic diseases in adults during fetal development and / or perinatal period. Many epidemiological data indicate that maternal dysnutrition (undernutrition, overnutrition) affects fetal growth showing abnormal birth weight (intrauterine growth retardation : IUGR / large birth weight macrosomia) and predispose individuals to development of metabolic diseases. To better understand the mechanisms invovle in transmission of the metabolic vulnerability from one generation to another, we have developed a model combining transgenerational rat fetal programming in the F0 by maternal undernutrition (model FR30) and dysnutrition in F1 with an hyperlipidic diet.Our results show that dietary restriction of 70% throughout pregnancy (FR30 model) contributes to emphasize development of metabolic syndrome traits into female F1 progeny. F1 females from undernourished mothers have an adult glucose intolerance and hyperleptinemia. These metabolic disturbances will be increase by a high fat diet (HF) but will not lead to obesity in female F1 regardless of the mother (F0) diet/statut. This can be explain by the low palatability of the diet, and the lack of carbohydrates largely involve in the development of obesity. These F1 phenoypes conduce to different F2 phenotypes at birth depending of fetal growth trajectory.Newborns from F1 mothers C or FR with HF diet during pregestation and gestation (C HF-HF and FR HF-HF) present IUGR. In contrast, infants born from F1 undernourished mothers with HF diet during pregestation following by standard diet during pregnancy (FR HF-S) show macrosomia. Like metabolic and hormonal disturbances into F1 mothers can not explain themselves the occurrence of these phenotypes, we studied the organ at the interface between maternal and fetal compartments in charge of the crosstalk between mother and fetus : the placenta. Morphological and molecular analysis indicate that placenta is not only sensitive to metabolic changes in the mother, but also able to adapt to the fetus needs. We observe strong correlation between gene expression (decrease or increase) and phenotype (IUGR/macrosomia) with gender specificity.Our work therefore suggests that IUGR or macrosomia phenotypes are not only depending on maternal hormonal and metabolic abnormalities but also in the sex-specific placental gene response to these exposure.

Introdução: o timo é importante órgão linfoide do sistema imunológico. Estudos mostraram que, durante o período fetal, a atrofia desse órgão faz parte da resposta adaptativa do feto ao ambiente intrauterino adverso, como a desnutrição crônica causada pela insuficiência placentária. Essa situação pode explicar a associação entre restrição de crescimento intrauterino e as alterações no sistema imunológico após o nascimento, na infância e na adolescência. Objetivos: analisar as dimensões do timo fetal pela ultrassonografia em gestações com insuficiência placentária, comparando com gestações de alto risco sem insuficiência placentária e gestações de baixo risco. Métodos: estudo prospectivo com 30 gestações com insuficiência placentária (Doppler de artéria umbilical com índice de pulsatilidade > p95) comparadas com 30 de alto risco e 30 de baixo risco (grupo controle). Os critérios de inclusão foram: idade gestacional entre 26 e 37 semanas, feto único e vivo, ausência de malformações fetais, membranas íntegras, ausência de sinais de trabalho de parto, ausência de infecção materna ou fetal e não realização de corticoterapia antes da avaliação ultrassonográfica fetal. O timo fetal foi identificado na interface com os pulmões, na altura dos três vasos da base do coração, no corte do tórax fetal. Foram realizadas três medidas do diâmetro transverso (DT) e do perímetro (P) do timo, e as médias foram utilizadas para análise, transformadas em escores zeta, de acordo com a idade gestacional em que se efetuou a medida. Foram realizadas as medidas ultrassonográficas da circunferência cefálica (CC) e do comprimento do fêmur (CF) fetal, com as quais se calculou as relações DT/CF, DT/CC, P/CF e P/CC. Resultados: o grupo com insuficiência placentária apresentou mediana significativamente maior do escore zeta do IP da artéria umbilical quando comparado ao grupo de alto risco e controle (4,6 vs. -0,5 vs. -0,2, p < 0,001). As medidas do timo fetal no grupo com insuficiência placentária [escore zeta do DT (média=-0,69; DP=0,83) e escore zeta do P (média=-0,73; DP=0,68)] foram significativamente (p < 0,001) menores quando comparadas aos grupos de alto risco [escore zeta do DT (média=0,49; DP=1,13) e escore zeta do P (média=0,45; DP=0,96)] e controle [escore zeta do DT (média=0,83; DP=0,85) e escore zeta do P (média=0,26; DP=0,89)]. Nas relações estudadas, houve diferença significativa (p < 0,05) na média dos grupos: insuficiência placentária (DT/CC=0,10, P/CF=1,32 e P/CC=0,26); alto risco (DT/CC=0,11, P/CF=1,40 e P/CC=0,30) e controle (DT/CC=0,11, P/CF=1,45 e P/CC=0,31). Conclusão: em gestações complicadas pela insuficiência placentária, ocorre redução das dimensões do timo fetal sugerindo que pode ser decorrente da adaptação fetal ao ambiente intrauterino adverso / Introduction: thymus gland is an important lymphoid organ involved in immune response. Studies have shown that during fetal life, thymus atrophy is part of an adaptive response to a compromised intrauterine environment, like chronic malnutrition due to placental insufficiency. This may explain the association between intrauterine growth restriction and later altered immune function. Objective: to evaluate fetal thymus by ultrasonography in pregnancies with placental insufficiency and compare to high risk pregnancies without placental insufficiency and low risk pregnancies. Methods: a prospective study with 30 pregnancies with placental insufficiency (umbilical artery Doppler with pulsatility index > p95), compared to 30 high risk pregnancies and 30 low risk pregnancies (control group). The inclusion criteria were: gestational age ranging from 26 to 37 weeks, singleton pregnancies, absence of fetal malformations, intact membranes, not in labor, no signs of maternal or fetal infection, and no corticotherapy before the ultrasound evaluation. Fetal thymus was identified in its interface with the lungs, at the level of the tree-vessel view of the fetal thorax. Three measures of thymus transverse diameter (TD) and perimeter (P) were made, and the media were converted into zeta score according to the gestational age. Head circumference (HC) and femur length (F) were also measured and used in the calculation of the relations TD/F, TD/HC, P/F, P/HC. Results: the group with placental insufficiency presented median of umbilical artery PI elevated, when compared to high risk pregnancies and low risk pregnancies (4.6 vs. -0.5 vs. -0.2, p < 0.001). Fetal thymus measurements were significantly (p < 0.001) lower in pregnancies with placental insufficiency [TD zeta score (media=-0.69; SD=0.83) and P zeta score (media=-0.73; SD=0.68)] when compared to high risk pregnancies [TD zeta score (media=0.49; SD=1.13) and P zeta score (media=0.45; DP=0.96)] and control group [TD zeta score (media=0.83; SD=0.85) and P zeta score (media=0.26; SD=0.89)]. There was significant difference (p < 0,05) in the relations studied among the groups: pregnancies with placental insufficiency (TD/HC=0.10, P/F=1.32 e P/HC=0.26), high risk pregnancies (TD/HC=0.11, P/F=1.40, P/HC=0.30) and control group (DT/HC=0.11, P/F=1.45, P/HC=0.31). Conclusion: fetal thymus measurements are reduced in pregnancies with placental insufficiency, suggesting that it is a fetal adaptive response for adverse environment

Publicación a texto completo no autorizada por el autor / Determina la utilidad del método clínico mediante 2 técnicas como la fórmula de Johnson-Toshach (FJT) y palpación para estimar el peso fetal en gestaciones a término. El estudio es de tipo analítico, observacional de tipo transversal. Se realizó en el Hospital Nacional Docente Madre Niño San Bartolomé, Lima, Perú. Participaron en el estudio las gestantes (e hijos) cuyo parto se atendió en dicho hospital. Se estudió 124 historias clínicas, registrándose la estimación clínica del peso fetal (calculada 24 horas antes del parto mediante FJT y palpación) y los pesos de nacimiento. Las principales medidas de resultados son peso al nacer (PAN), peso fetal estimado (PFE) según FJT o palpación y error absoluto (%E: diferencia entre el PFE clínico y el PAN respecto del PAN, en porcentaje). El PAN resultó 3470±394g, el PFE según palpación fue 3393g (p=0.016) y por FJT fue 3410g (p=0.375). El error absoluto de FJT (5.7%) y el de palpación (6.2%) no fueron estadísticamente diferentes (p=0.223). Al comparar las estimaciones útiles (%E≤10%) realizadas por FJT (74.2%) y por palpación (71.8%), no se halló diferencias (p=0.774). Existió correlación lineal positiva moderada entre ambos métodos y el PAN. Se concluye que los métodos FJT y palpación son útiles clínicamente (y económicos) para estimar el PAN, no se halló diferencias en la precisión de sus estimaciones y tuvieron moderada correlación con el PAN. Palabras clave: Peso fetal, fórmula de Johnson, palpación, peso al nacer. / Tesis

Objetivos: El objetivo principal de la investigación fue determinar si una cabeza fetal no encajada es un factor de riesgo para parto por operación cesárea en nulíparas con 41 semanas o más de gestación atendidas en el Hospital Docente Madre Niño San Bartolomé durante el año 2014. Materiales y métodos: Estudio analítico de cohortes retrospectivo. No se realizó muestreo, se trabajó con la totalidad de historias clínicas de las nulíparas con 41 semanas o más de gestación atendidas durante el año 2014 que cumplían los criterios de inclusión. El grupo expuesto hizo referencia a las pacientes que presentaron una cabeza fetal no encajada a una estación de -5 (fuera de pelvis) y -4. El grupo no expuesto a las que presentaron una cabeza fetal a estación -2 y -1. Los datos fueron procesados con el programa STATA 12. Se analizó la presencia de una cabeza fetal no encajada asociada a parto por operación cesárea calculando el Odds Ratio (OR) y luego ajustando su valor con un análisis de regresión logística a las variables de confusión. Resultados: El 73% de las pacientes con una cabeza fetal no encajada a una estación de -5 y -4 culminaron el parto por operación cesárea, mientras que solo lo hizo el 10% de las pacientes con una cabeza fetal a estación de -2 y -1. La indicación predominante para parto por operación cesárea fue trastornos por detención del trabajo de parto (33 de 79 pacientes con una cabeza fetal a estación de -5 y -4). En el análisis de regresión ajustado a las variables IMC pre-gestacional, dilatación inicial e inducción del trabajo de parto, una cabeza fetal no encajada a estación -5 y -4 tiene 17 veces el riesgo de tener un parto por operación cesárea (IC 95% 5.7 – 50.5) en comparación con una cabeza fetal a estación de -2 y -1. Conclusiones: Las pacientes nulíparas con 41 semanas o más de gestación con una cabeza fetal no encajada a estación -5 y -4 tienen 17 veces más riesgo de tener un parto con operación cesárea en comparación con las pacientes que presenten una cabeza fetal a estación de -2 y -1. / Tesis

Based on a large series of epidemiological studies, it has been proposed that exposure to an increased nutrient supply before birth increases the risk of developing obesity in postnatal life. The physiological mechanisms underlying the association between increased nutrition before birth and later obesity are, however, poorly understood. This thesis has investigated the impact of an increased fetal nutrient supply on the programming of key systems within the appetite - regulating network and / or the adipocytes before and after birth. The studies in this thesis have demonstrated that plasma concentrations of the adipostatic hormone leptin are directly related to adiposity and the size of adipose cells in fetuses of ewes fed at or above maintenance energy requirements, which suggests that leptin may act as a peripheral signal of fat mass before birth. It has also been demonstrated that the components of the central network for appetite regulation are expressed in the hypothalamus of the fetal sheep from at least 110 d gestation ( term = 150 ± 3 d gestation ), and that the expression of the appetite - regulating neuropeptides is responsive to signals of increased nutrient supply before birth. This thesis has also demonstrated that an increase in maternal nutrition in late pregnancy results in increases in both food intake and glucose concentrations in the lamb in early postnatal life and in a significant increase in subcutaneous adiposity on postnatal day 30. Importantly, increased maternal nutrition resulted in an altered relationship between signals of increased fat mass and nutrition and expression of a central appetiteinhibitory neuropeptide, CART, in the lamb hypothalamus. It was also demonstrated that there was an interaction between the prenatal and postnatal nutritional environments in the determination of lipogenesis in the early postnatal period. The findings presented in this thesis provide evidence that programmed changes to the sensitivity of the appetite - regulating neuropeptides to signals of increased adiposity and nutritional status in early postnatal life are an important part of the physiological pathway through which exposure to an increased nutrient supply before birth may lead to an increased risk of obesity in later life. / Thesis (Ph.D.)--School of Molecular and Biomedical Science, 2006.

Thesis (B.A.)--Haverford College, Dept. of Economics, 2007. / Includes bibliographical references.

The thesis contends that holistic, community-based treatment is preferable to carceral options for offenders with fetal alcohol conditions, presents emerging support for this contention, identifies barriers to the implementation of community-based treatment, and culminates with analyses of ways of influencing policy reform or of legally mandating non-carceral treatment options. Potential avenues that will be examined include:<P> &bull;&#x00A0;&#x00A0; Charter of Rights and Freedoms, s. 15, including an analysis from Eldridge, Law, and Auton, based on the duty to accommodate disabilities;<BR> &bull;&#x00A0;&#x00A0; Constitution Act, 1982, s. 35 and its recognition and affirmation of such relevant treaty right as the alcohol ban, particularly as the ban operates as a contextual factor in a s. 15 Charter analysis as applied to affected treaty beneficiaries; and<BR> &bull;&#x00A0;&#x00A0; Articles 23, 24 and 40 of the Convention on the Rights of the Child, and Article 12(1) of the International Covenant on Economic, Social and Cultural Rights, particularly as they influence the s. 1 analysis under the Charter. <P> A remedy mandating a positive state obligation to provide community-based treatment likely would require favourable cost-benefit analyses, as well as evidence of effectiveness of the treatment (the latter to be studied in a subsequent interdisciplinary Ph.D. program using qualitative research techniques). The implications of a finding of disability and mental disorder related to fetal alcohol conditions will be examined. The present research topic is at the interface of health and justice, and indeed is multidisciplinary in nature as fetal alcohol influences every aspect of affected individuals' lives. Moreover, the problem is situated in its historical, ideological, global, and trans-disciplinary context.