El objetivo del estudio fue determinar las principales diferencias en los resultados perinatales entre gestantes con embarazo prolongado y evidencia ultrasonográfica de calcificaciones placentarias y oligohidramnios en comparación con gestantes con embarazo prolongado sin evidencia ultrasonográfica de calcificaciones placentarias y oligohidramnios. En el Instituto Nacional Materno Perinatal de Lima – Perú se realizó un estudio observacional, retrospectivo y transversal comparando 50 gestantes con embarazo prolongado con evidencia ultrasonográfica de calcificaciones placentarias y oligohidramnios con 70 gestantes con embarazo prolongado sin evidencia ultrasonográfica de calcificaciones placentarias y oligohidramnios. El análisis estadístico se realizó con el programa SPSS 14.0. La incidencia de embarazo prolonagado fue 0,73%. El 41,7% de gestantes con embarazo prolongado tuvo evidencia ultrasonográfica de calcificaciones placentarias y oligohidramnios. El 38,3% (n igual 46) de gestantes con embarazo prolongado presentó resultado perinatales adversos. Existió mayor riesgo de resultados perinatales adversos en embarazos prolongados con evidencia ultrasonográfica de calcificaciones placentarias y oligohidramnios (OR 4,58; 95% IC 2,74 – 7,65).

Thesis (M. Phil.)--University of Hong Kong, 1978. / Typewritten.

Background: Prenatal ethanol exposure (PNEE) causes irreversible intellectual and behavioral disabilities, clinically known as fetal alcohol spectrum disorder. Few neuropathologic studies of human brain exist. Hypotheses: First, markers of oxidative stress persist following PNEE. Second, PNEE is associated with inhibitory and excitatory neuron changes. Methods: Human brain autopsies (153) with known PNEE were reviewed; 18 cases (fetus to adult) and controls were selected. Oxidative stress and neuronal differentiation markers were used for immunohistochemistry. Results: There were no obvious differences between control and PNEE brains using oxidative stress markers. In human PNEE brains, glutamatergic neurons were reduced 15.96 % and 18.03% in dentate gyrus and temporal cortex, respectively. GABAergic neurons reactive for parvalbumin were reduced in all hippocampal regions (CA1= 57.86%, CA3= 65.15%, and DG= 53.39%) and temporal cortex (44.13%) in all age groups. Conclusion: GABAergic neuron reduction in human following PNEE could explain motor and behavior distractibility in FASD individuals.

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

Not available / text

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

published_or_final_version / Zoology / Master / Master of Philosophy

Arsenic is a metalloid present throughout the world, and the primary sources of exposure are through air, soil, and water. Arsenic is currently ranked as the most hazardous substance among environmental toxicants, and is well recognized as a human carcinogen, as well as a contributor to metabolic and cardiovascular diseases. However, cardiovascular effects have been mostly evaluated in epidemiological studies, and the direct mechanisms of pathogenesis remain largely unknown. The scope of studies described in this dissertation characterizes the cardiovascular pathophysiology associated with exposure to environmentally-relevant arsenic concentrations (100 µg/L), and attempts to elucidate the molecular mechanisms behind impaired vascular function. The effects of chronic arsenic exposure on blood pressure regulation were examined using a mouse model exposed to 100 µg/L for 22 weeks. Chronic exposure to arsenic results in the development of hypertension and concentric left ventricular hypertrophy. Furthermore, data presented here demonstrates that in utero exposure contributes to the development of metabolic syndrome throughout adulthood. Results indicate the development of hyperglycemia, hypercholesterolemia and nonalcoholic fatty liver disease. Mechanistic studies demonstrate the effects of arsenicals on endothelial nitric oxide synthase (eNOS) and its role in arsenic-induced vascular relaxation impairment. Biochemical assessment of eNOS conclude that decreased nitric oxide availability does not occur through alterations in protein levels or phosphorylation changes; however, decreased activity is likely a result of protein dimer stability through alterations in zinc tetrathiolate binding.

ABSTRACT Introduction: Human newborn and animal studies provide support for the intersensory redundancy hypothesis, which posits that learning is more effective when information is presented simultaneously in two modalities than one alone. Whether the same is true in the human fetus is unknown and was examined in this study. Methods: 63 low-risk fetuses (≥36 weeks gestation) were randomly assigned to one of 6 experimental groups: each group included one of 3 stimulus conditions [unimodal (music), unimodal (maternal sway) or bimodal (music and maternal sway)], and one of 2 pieces of music (music A, 4/4 time; music B, 3/4 time) composed for the study. Laboratory pre-testing included a 2 min no-music, 2 min music (A or B), 2 min no-music observation while fetal heart rate (FHR) and body movements were recorded. Subsequently, mothers carried out the assigned intervention at home, twice a day for 5 days. On day 6, laboratory testing was repeated first with the familiar (A or B) and then the novel music. Results: The initial testing showed a difference between Music A and Music B, F (1, 61) = 8.203, p <.01, where FHR decreased to Music A and increased to Music B. The same FHR response was found when fetuses were exposed to the opposite music for the first time in the novelty testing, F (1, 44) = 4.543, p <.05, following intervention. Music A elicited a response in both the unimodal music only and sway only groups, F (29, 203) = 1.871, p < .01, and F (29, 174) = 1.818, p < .01, respectively. In music B only the multimodal group showed an effect of intervention, F = (29, 203) = 1.914, p < .005. Conclusions: Fetal response to music A and B was qualitatively different. During pretesting, FHR decreased to music A and increased to music B. When the stimulus elicited an attention response (FHR decrease) learning was observed in both the unimodal or multimodal conditions. This is seen with music A (4/4 time) music where the fetus learns the stimulus. When the stimulus did not elicit a FHR decrease (Music B, 3/4 time), there was evidence that a multimodal stimulus was more effective providing some support for the intersensory redundancy hypothesis. / Thesis (Master, Nursing) -- Queen's University, 2007-10-18 16:52:55.68

In recent years, increased focus has been placed on the role of intrauterine infection and inflammation in the pathogenesis of fetal brain injury leading to neurodevelopmental disorders such as cerebral palsy. At present, the mechanisms by which inflammatory processes during pregnancy cause this effect on the fetus are poorly understood. Our previous work has indicated an association between experimentally-induced intrauterine infection, increased proinflammatory cytokines, and increased white matter injury in the guinea pig fetus. In order to further elucidate the pathways by which inflammation in the maternal system or the fetal membranes leads to fetal impairment, a number of studies investigating aspects of the disease process have been performed. These studies represent a body of work encompassing novel research and results in a number of human and animal studies. Using a guinea pig model of inflammation, increased amniotic fluid proinflammatory cytokines and fetal brain injury were found after a maternal inflammatory response was initiated using endotoxin. In order to more closely monitor the fetal response to chorioamnionitis, a model using the chronically catheterized fetal ovine was carried out. This study demonstrated the adverse effects on fetal white matter after intrauterine exposure to bacterial inoculation, though the physiological parameters of the fetus were relatively stable throughout the experimental protocol, even when challenged with intermittent hypoxic episodes. The placenta is an important mediator between mother and fetus during gestation, though its role in the inflammatory process is largely undefined. Studies on the placental role in the inflammatory process were undertaken, and the limited ability of proinflammatory cytokines and endotoxin to cross the placenta are detailed herein. Neurodevelopmental disorders can be monitored in animal models in order to determine effective disease models for characterization of injury and use in therapeutic strategies. Our characterizations of postnatal behaviour in the guinea pig model using motility monitoring and spatial memory testing have shown small but significant differences in pups exposed to inflammatory processes in utero. The data presented herein contributes a breadth of knowledge to the ongoing elucidation of the pathways by which fetal brain injury occurs. Determining the pathway of damage will lead to discovery of diagnostic criteria, while determining the vulnerabilities of the developing fetus is essential in formulating therapeutic options. / Thesis (Ph.D, Anatomy & Cell Biology) -- Queen's University, 2008-03-06 20:24:03.417