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1
Beckett, Cynthia Diane. "Navajo children and families living with fetal alcohol syndrome/fetal alcohol effects." Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/280150.
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The aim of the study was to develop a culturally sensitive Grounded Theory of Navajo parenting for families who are living with Fetal Alcohol Syndrome (FAS)/Fetal Alcohol Effects (FAE). The research question was: What are the social and cultural factors and processes that Navajo families use to mange care for a child with FAS/FAE? The philosophical perspectives that guided the study were: the Navajo philosophy, or view of life; resilience (middle range theory); the Family Stress Theory; and the Resiliency Mode of Family Stress, Adjustment, and Adaptation. Resilience was used as the over arching conceptual perspective for the study. A Grounded Theory of Navajo Parenting emerged from the data. Key categories to support the emerging theory were identified. The core category was Versatility through Transcendence. The supporting categories were: Strategies for Managing Challenges; Transcendence in Parenting; Intergenerational Alcohol Abuse, Violence and Suffering; and Knowledge/Acquisition of Needs. The families described their stories of transcendence through substance abuse, suffering, and violence to be able to parent their children who were living with the primary and secondary challenges of prenatal alcohol exposures. Further research is needed to test and expand this emerging theory of Navajo parenting of children with FAS/FAE. The challenges that were related to FAS/FAE were more easily managed with patterns of resilience within the families. Factors that influenced family's abilities to parent will be disseminated to assist other families who are managing the problems associated with FAS/FAE.
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Webber, Troy A. "Fetal Testosterone: Developmental Effects on Externalizing Behavior." Scholar Commons, 2015. https://scholarcommons.usf.edu/etd/7376.
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Fetal testosterone (FT) exposure influences sexual differentiation and may promote well-established sex differences in externalizing (EXT) behavior. Although puberty may be a critical period for these effects, it is unknown how FT exposure influences EXT as a function of pubertal development. We used a longitudinal, multi-sample design to test the relationships between two proxy indices of FT exposure and EXT as a function of age and pubertal development (approximately ages 6, 9, 11, 14, and 16). Twin data were used to approximate FT exposure (TT-FT) because testosterone is thought to cross the intrauterine membrane and cause variability in co-twin gonadal hormone exposure, with increasing exposure for males and participants with male co-twins. Increasing number of older siblings may also approximate increasing FT exposure (SI-FT), although existing research has yet to disentangle possible postnatal socialization effects from potential FT exposure using this variable. Given that biologically related siblings share a fetal and social environment while non-biologically related siblings simply share a social environment, we tested the independent effect of SI-FT on EXT using a sibling adoption design. Across four independent samples, SI-FT and TT-FT predicted externalizing for males alone. SI-FT predicted EXT over-and-above socialization influences and interacted with pubertal development in two independent samples, with elevated EXT for those in mid-late puberty that were exposed to increased FT. TT-FT predicted EXT differentially as a function of developmental period. Our data are consistent with the notion that exposure to FT promotes sexually differentiated, sexually selected behavior during reproductively relevant periods.
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Conliffe, Phyllis R. (Phyllis Rowena). "Effects of maternal diabetes on fetal development in rats." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39344.
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The mechanisms underlying the high incidence of fetal abnormalities including fetal lung immaturity during maternal diabetes are not fully understood. Utilizing streptozotocin-diabetic rats as the model, I have examined the role of fetal hyperglycemia and hyperinsulinemia and other factors on fetal adrenal and lung functions in culture. Insulin and glucose did not alter fetal adrenal and lung cell proliferation and adrenal corticosterone output. On the other hand, a novel protein-bound, low molecular weight non-proteinaceous cytotoxic factor was detected in the serum of diabetic animals. In addition, a novel protein with cytostatic activity was found in fetal lungs, the concentration of which increased during diabetes. Partial amino acid sequence and Western Blot analysis revealed this protein to be similar to histone H2B. An extra-nuclear role is suggested for this protein because it appears to be present in the microsomal fraction of fetal lungs. It is concluded that fetal lung immaturity during diabetes may be contributed by cytotoxic and cytostatic factors contained in the serum and fetal lungs, respectively.
4
Kelly, Mary Clare. "Maternal and fetal effects of intrathecal analgesia in obstetrics." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361287.
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Arkwright, P. D. "Effects of the human trophoblast on lymphocyte proliferation." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236250.
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Barrett, Robert Daniel. "Therapeutic hypothermia and its effects on the preterm fetal sheep." Thesis, University of Auckland, 2011. http://hdl.handle.net/2292/7200.
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There is compelling evidence that 72 h of moderate hypothermia initiated within 2 to 6 h after hypoxia-ischemia can protect against brain injury, disability and death in term newborn infants. Currently, there is no clinical treatment for hypoxic-ischemic encephalopathy for preterm infants. With the worldwide rates of preterm birth steadily increasing, there is much interest in using therapeutic hypothermia to treat preterm hypoxic-ischemic encephalopathy. The goal of this thesis was to investigate the effects and window of opportunity of therapeutic hypothermia on the brain and physiology after asphyxia in preterm fetal sheep. My first study showed that 68.5 h of selective head cooling, initiated 90 min after asphyxia, protected oligodendrocytes in the white matter (WM) and subventricular zone (SVZ) of the preterm fetal sheep brain at 3 days recovery from 25 min of umbilical cord occlusion. Overall proliferation of cells was not reduced by hypothermia in the WM or SVZ. The remainder of the studies focused on the use of 72 h of whole body hypothermia, and assessed effects at 7 days recovery from asphyxia. Two hypothermia protocols were examined, a 30 min onset after asphyxia protocol, and a clinically relevant, 5 h after asphyxia protocol. Whole body hypothermia was associated with mild bradycardia, mild changes in blood pressure and carotid blood flow and transitory suppression of EEG power. All physiological variables resolved to sham values by 96 h after asphyxia. Delayed hypothermia was associated with slower improvement of spectral edge frequency and EEG power than early onset hypothermia. The window of opportunity for SVZ protection was less than 5 h, with significant improvement in numbers of oligodendrocytes after only early onset but not delayed hypothermia. In contrast, there was no significant improvement in number of oligodendrocytes in the white matter tracts, with either early or late cooling. This was associated with reduced proliferation in the white matter, and no induction of microglia and caspase 3, which suggests that lack of replenishment of oligodendrocytes may have contributed to persistent reduction in numbers of oligodendrocytes after therapeutic hypothermia. Overall the studies in this thesis suggest that the window of opportunity for brain protection in the preterm infant is less than 5 hours and that synergistic treatment may be required to protect the WM after hypoxic-ischemic insults.
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Delorme, Danielle. "Effects of Interleukin-3 on murine fetal hemopoiesis in utero." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59630.
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The effect of interleukin-3 (IL-3), a candidate hemopoietic growth factor, on prenatal hemopoiesis is unclear. Microinjection of IL-3 directly into mouse fetuses (day 13) via the yolk sac, allowed us to evaluate the effects on morphogenetic events and more specifically on fetal liver populations using quantitative in vitro clonal assays for hemopoietic precursors. Control studies, required to distinguish stress effects of surgical laparotomy and microinjection, clearly revealed that the fetal liver is a sensitive organ responding with limited tissue disorganization, reduced cellularity and erythropoietic activity as identified 24 h after experimental intervention. Microinjection of 15 units of IL-3 promoted significant expansion of the depleted fetal liver hemopoietic cell populations and had stimulatory effects on connective tissue mast cells, absolute cell numbers including hemopoietic precursors (erythroid, granulocyte, macrophage, megakaryocyte) compared to controls. These studies suggest that fetal liver cells acquire a responsiveness to IL-3 early in development and that, IL-3 has a positive stimulatory effect on fetal liver cell populations, promoting the recovery of normal liver hemopoiesis.
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Samnakay, Naeem. "Antenatal bladder outflow obstruction : effects of morphology and apoptosis in the fetal kidney, and effects on fetal ACTH and cortisol levels in an ovine model." University of Western Australia. School of Women's and Infants' Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0151.
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Posterior urethral valves cause bladder outflow obstruction and damage to the developing fetal kidney. Posterior urethral valves affect 1 in 8000 new-born males. A third of these children develop end stage renal failure by adolescence, despite valve ablation in the early post-natal period, implying that majority of the damage to the kidneys occurs in utero. How does this damage occur, and should we intervene in utero? The answers to these questions require further research, and are the basis to this thesis. This thesis focused on the effect bladder outflow obstruction has on morphology and apoptosis in the fetal kidney in a fetal lamb model. It also looked at the effect of bladder outflow obstruction on fetal stress hormone levels. Bladder outflow obstruction was created surgically in fetal lambs at day 70 of gestation, and fetal kidneys were analysed at day 2, 5, 10, 20 and 30 after creation of obstruction. Controls undergoing sham surgery were used for comparison. Four aspects were investigated: - effects of bladder outflow obstruction on renal histology effects of bladder outflow obstruction on expression of pro-apoptosis gene Bax and anti-apoptosis gene Bcl-X - effects of bladder outflow obstruction on renal regional apoptosis effects of bladder outflow obstruction on serum fetal ACTH and cortisol levels. Bladder outflow obstruction resulted in sequential morphological change in the fetal kidney over time. By 2 days post-obstruction, cystic change was noted. In addition, patchy attenuation of the nephrogenic blastema was evident by 5 days post-obstruction, with more confluent blastemal attenuation as well as generalized renal architectural disorganization by 10 days post-obstruction. By 20 and 30 days post-obstruction, cystic renal dysplasia had developed. Bladder outflow obstruction resulted in an increase in the ratio of renal expression of pro-apoptosis gene Bax to anti-apoptosis gene Bcl-X. Regional apoptosis counts showed increased tubular apoptosis compared to controls at 2 days post-obstruction, and increased blastemal apoptosis compared to controls at 5 days post-obstruction. By 10 days post-obstruction, blastemal apoptosis counts were reduced compared to controls. There were no significant differences in fetal serum ACTH and cortisol levels between fetal lambs with bladder outflow obstruction and controls. In conclusion, the results of this thesis outline the spectrum of morphological change in the fetal kidney over 30 days of bladder outflow obstruction. They show that detectable changes in morphology occur within two days of bladder outflow obstruction. Likewise, detectable changes in gene expression occur within 2 days of bladder outflow obstruction. The increased ratio of expression of Bax to Bcl-X suggests a swing towards increased apoptosis in response to bladder outflow obstruction. Further research is required to ascertain if these changes are reversible. However, the early onset of these changes as shown in this thesis suggests that any fetal intervention to protect the fetal kidney from the effects of bladder outflow obstruction may need to be instituted very early in gestation
9
Almeida, Nisha. "Measures of maternal tobacco smoke exposure and foetal growth." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112375.
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Objective. Most biomarker studies of maternal smoking have been based on a single blood or urinary cotinine value, which is inadequate in capturing maternal tobacco exposure over the entire pregnancy. This thesis used maternal hair biomarkers to investigate the association between maternal active and passive smoking, and birthweight for gestational age (BW for GA).Methods. Subjects were 444 term controls drawn from 5,337 participants of a multi-centre nested case-control study of preterm birth in Montreal. Maternal hair, collected after delivery, was measured for average nicotine and cotinine concentration across the pregnancy, assuming hair growth of 1 cm/month. The BW for GA z-score used Canadian population-based standards. Multiple linear regression was used to assess effects on the z-score, after controlling for potential confounders.
Results. In regression models for maternal active smoking analysis, the addition of hair nicotine to models containing either self-report or hair cotinine or both self-report and cotinine explained significantly more variance in the BW for GA z-score (p=0.009, p=0.017, and p=0.033, respectively). In maternal passive smoking analysis, no significant effect of ETS on BW for GA was found using hair biomarkers.
Conclusion. These results indicate that hair biomarkers are sensitive tools capable of predicting reductions in birthweight for maternal active smoking. The stronger results obtained for nicotine are reflective of the fact that hair nicotine is a better measure of maternal smoking, but it could also suggest that nicotine plays an aetiologic role in affecting foetal growth.
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Heiberg, Ludvig. "An electrophoretic study of fetal mouse brain proteins after in vivo exposure to phenytoin and disulfiram." Master's thesis, University of Cape Town, 1990. http://hdl.handle.net/11427/27187.
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Although there have been two-dimensional electrophoretic studies on fetal brain tissue (for instance, Yoshida and Takahashi, 1980), the emphasis in most of this work has been on developmental changes in protein expression, and not on the effects that drugs have on fetal brain protein complement. Klose and co-workers (1977) did an early study using two-dimensional gel electrophoresis to determine the effects of various teratogens on whole embryos. No protein changes were found and that line of research was not continued. In this study two-dimensional gel electrophoresis is extensively used, in the belief that the usefulness of this technique to experimental teratology has not been fully evaluated. It is reasonable to suppose that a central nervous system teratogen administered during critical periods of susceptibility will led to perturbations of orderly brain development, and that these perturbations will be reflected as changes to the protein complement. The total brain protein complement of mice that have been exposed to drugs in utero will therefore be analysed, in the hope that any inductions or deletions of proteins as a result of drug exposure may provide a clue to the molecular events underlying drug injury to the fetus.
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Hashim, Ezat. "Reversible tracheal obstruction in the fetal sheep : effects on tracheal fluid pressure and lung growth with implications in fetal surgery." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55500.
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The purpose of this study was to determine the effect of reversible fetal tracheal occlusion on lung development. Nine fetal sheep were divided into two groups. Group 1 had intratracheal balloons placed and the balloons left inflated for 21-28 days. Group 2 consisted of littermates that served as controls. They had either uninflated balloons placed or were left unoperated. Tracheal pressure measurements were periodically recorded and the amniotic fluid pressure served as a reference. The animals were sacrificed near term and the lungs, heart and liver were weighed and corrected for body weight. Standard morphometry was used to compare the lungs further and the lung DNA and protein content were measured. Tracheal damage from the balloon catheter was also assessed.Tracheal pressure was 3.85 ($ pm$.49 S.E.) mm Hg in experimental animals while it was an average of $-$0.27 ($ pm$.27 S.E.) mm Hg in controls (p $<$.0001). Tracheal occlusion increased lung weight and volume by 2-3 times (p $<$.0001 and p =.0006, respectively) while heart and liver weights remained similar to controls. Airspace fraction and radial alveolar counts were raised (p =.044 and p =.0002, respectively) and alveolar number per body weight was doubled (p $<$.0001). The alveolar number per lung volume was preserved, however, as was the DNA and protein content per unit weight of lung tissue. The chronic indwelling balloon catheter caused some mucosal and submucosal damage at the balloon site and proximal to it.
These results show that tracheal occlusion leads to an elevation of intratracheal pressure that is associated with a tremendous increase in lung growth over a short period in the third trimester fetal sheep. The techniques used in this experiment may be easily modified for use with endoscopic surgical equipment.
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Potter, Susan M. "Effects of fetal cocaine and tobacco exposure on newborn information processing." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42119.
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Approximately 10% of women use cocaine and 20% smoke cigarettes during pregnancy. Animal studies indicate that both cocaine and nicotine are neuroteratogenic agents, although findings with humans are inconsistent. Studies with human infants have been plagued by unreliable subject identification procedures, poor control over confounding factors, and invalid measures of CNS integrity. The literature on prenatal cocaine and nicotine use is reviewed and two studies are presented along with an intriguing case report. The effects of maternal prenatal cocaine use (Study 1) and two levels of cigarette smoking (Study 2) on newborn information processing ability were examined using an auditory habituation-recovery paradigm. Case-control designs were employed in which subjects were individually matched on a number of maternal and infant factors. Cocaine exposure was determined by newborn meconium analysis, urine analysis, and maternal self-report. Maternal smoking was determined by self-report and a variation of the bogus pipeline method. Fetal cocaine- and nicotine-exposure were associated with differential impairments in neonatal information processing. Cocaine-exposed newborns exhibited deficits on measures of habituation and recovery to novelty. Dose-response effects of nicotine-exposure were evident on measures of orientation and habituation, but recovery to novelty was not consistently affected. The results imply that fetal cocaine-exposure severely impairs neonatal auditory information processing ability, whereas fetal tobacco-exposure is associated with deficits in information-processing which may be secondary to impairments in arousal regulation. These auditory processing deficits may be related to the later language impairments reported in follow-up studies with cocaine-and tobacco-exposed infants. Following the two studies, a case is presented of an infant born to a woman who reported using large amounts of cocaine throughout pregnancy, although the infant's meco
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Potter, Susan M. "Effects of fetal cocaine and tobacco exposure on newborn information processing." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ30361.pdf.
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Dunn, Stacey Leanne. "Fetal growth restriction : effects on the adrenal cortex in postnatal lambs /." Title page and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09SB/09sbd9231.pdf.
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Van, der Weyde Marlene P. "The effects of the beta-adrenergic agonist, ritodrine, in the fetal lamb." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30417.
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Ritodrine is a beta-adrenergic agonist commonly used to inhibit premature labor contractions in women. The primary goal of ritodrine tocolysis is to prolong gestation, however, other indications may include fetal distress. The purpose of the current study was to examine the metabolic and behavioral effects of ritodrine in the fetus, using the chronically instrumented pregnant sheep as an experimental model.
Ritodrine was infused continuously into 11 fetal lambs at a rate of 2.6 ug/minute for a period of 8, 12 or 24 hours. Samples were taken simultaneously at predetermined time periods from a fetal femoral artery, umbilical vein, maternal femoral artery and uterine vein for the analysis of fetal and maternal arterial and umbilical and uterine venous blood gases, acid-base status, hematocrit, ritodrine concentration, uterine and umbilical blood flow, and glucose, lactate and oxygen concentrations and fluxes. Cardiovascular and behavioral variables were monitored continuously.
The average concentration of ritodrine in fetal arterial plasma was 20.0 ± 2.7 ng/ml (range 9.5 to 3 4.7 ng/ml) at the end of the infusion. This concentration is within the range of cord levels obtained in ritodrine exposed human fetuses at birth (7 to 79 ng/mL) . Fetal arterial plasma ritodrine levels at 8 hours post-infusion were still sufficiently elevated to exert considerable fetal effects. The apparent tolerance of the fetus to given plasma levels of drug varied considerably among animals.
The infusion of ritodrine resulted in many typical beta-adrenergic receptor mediated responses in the fetus. Fetal arterial glucose levels rose to 79% above the control by the end of the infusion. This was associated with an increase in fetal glucose delivery (70% above the control), a decrease in the umbilical veno-arterial glucose concentration difference and a tendency for fetal glucose uptake to decline. Fetal arterial plasma lactate concentrations rose more than fivefold during the infusion of ritodrine. This was associated with a rise in fetal lactate delivery (540% above the control), a slight increase in the umbilical veno-arterial plasma lactate concentration difference and a tendency for fetal lactate uptake to rise.
Fetal oxygen consumption rose progressively and significantly throughout the infusion of ritodrine and during the first 8 hours of post-infusion, reaching a maximum of 22% above the control by 8 hours post-infusion. Umbilical blood flow remained unchanged, therefore umbilical oxygen delivery was not increased to meet the additional oxygen demands of the fetus. The rise in fetal oxygen consumption was hence accomplished through an increase in fetal fractional oxygen extraction (from a control value of 32.0±1.1% to a maximum of 51.6±1.8% by 1.5 hours of infusion). The rise in fetal oxygen extraction resulted in concurrent declines in fetal arterial Po₂ (78% of the control) and O₂ content (55% of the control) and a widening of the veno-arterial oxygen content difference. By the end of the infusion, umbilical venous Po₂ and O₂ content values had also fallen significantly to 78% and 75% of the control respectively. These latter changes resulted in a concurrent 25% decline in fetal oxygen delivery which in turn contributed to the rise in fetal oxygen extraction.
Fetal arterial and umbilical venous pH declined rapidly and significantly from control values of 7.370±0.004 and 7.401±0.005 to 7.274±0.025 and 7.306±0.023 respectively by the end of the infusion. The acidemia was reflected by significant declines in base excess values and appeared to be entirely metabolic in nature, resulting from elevated blood lactate levels. The acidemia likely contributed to the progressive fall in fetal blood O₂ content through a rightward shift of the oxyhemoglobin dissociation curve (Bohr effect).
The rise in fetal oxygen consumption was reflected by a similar (although nonsignificant) increase in uterine oxygen consumption. Uteroplacental oxygen consumption appeared to remain unaltered. The rise in uterine oxygen consumption was not accompanied by a corresponding increase in uterine oxygen delivery, hence uterine oxygen extraction rose to 23.8±1.9% (from a control value of 19.5±1.6%) by 1.5 hours post-infusion. The rise in uterine oxygen extraction resulted in significant declines in uterine venous Po₂ and CO₂ values which likely contributed to the fall in fetal oxygen delivery.
Fetal heart rate increased significantly to 21% (34 beats per minute, bpm) above the control (162±7 bpm) during the first 1.5 hours of ritodrine infusion. It remained elevated by an average of 16% (26 bpm) throughout the remainder of the infusion and the first 8 hours of post-infusion, returning to the control by the end of the post-infusion period. Fetal arterial pressure remained unchanged from the control (46.2±1.5 mm Hg).
The incidence of fetal breathing activity fell significantly from an overall average control value of 43.2±2.6% to an average of 28.1±6.8% during the ritodrine infusion period. In most animals, breathing was most depressed near the end of the infusion. The incidence of low voltage electrocortical (ECoG) activity also fell significantly by an average of 7.5% while that of high voltage ECoG rose by 7.3%. Alterations in intermediate voltage activity were not observed. The incidence of fetal rapid eye movement also tended to fall by an average of 8.2% during the infusion of ritodrine. These behavioral changes may have resulted from the development of fetal hypoxemia, rather than as a direct effect of ritodrine.
In conclusion, these data have demonstrated that ritodrine infusion to fetal lambs results in significant physiological and behavioral changes in the fetus. These effects may put the fetus at risk, particularly in situations where fetal oxygen delivery is already reduced, as in various states of compromised pregnancy.Medicine, Faculty of
Obstetrics and Gynaecology, Department of
Graduate
16
Zhang, Ruoyi, and 张若怡. "Protective effects of polysaccharides extracted from morinda officinalis on fetal rat hippocampal neurons." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44143199.
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Zou, Liangliang, and 邹亮亮. "Protective effects of icariin extracted from epimedii herba on fetal rat hippocampal neurons." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B44142900.
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Torres, Esperanza. "THE EFFECTS OF CAFFEINE INGESTION ON FETAL HEART RATE IN PREGNANT COLOMBIAN WOMEN." Thesis, The University of Arizona, 1985. http://hdl.handle.net/10150/275340.
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Morrison, Janna L. "The effects of sleep altering pharmacological agents on ovine fetal behavioural state." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq21051.pdf.
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Paquette, Hammond Andrea. "Short-term memory and learning in children with fetal alcohol syndrome/effects." Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/284282.
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Short-term memory function and learning in children with Fetal Alcohol Syndrome/Effects (FAS/E) was examined. Participants included twenty school-aged children diagnosed with either Fetal Alcohol Syndrome or Fetal Alcohol Effects (mean age = 11.13 years) and twenty normal controls (mean age = 11.11 years) matched on age and gender, all of which were Native American and lived on a rural reservation. All participants completed nine core subtests of the Wide Range Assessment of Memory and Learning. Results indicated that children with FAS/E performed significantly more poorly than controls on eight of the nine memory measures, including Number/Letter Memory, Sentence Memory, Story Memory, Finger Windows, Design Memory, Verbal Learning, Visual Learning, and Sound-Symbol. No statistically significant group differences were found on Picture Memory. Subsequent discriminant function analyses revealed that scores on the WRAML subtest provided useful discriminating information for children with FAS/E and controls. Scores on Story Memory, Design Memory, and Number/Letter Memory most strongly discriminated between groups. Implications of these results are discussed and recommendations for further research are provided.
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Simner, Claire Louise. "Vitamin D transport and the effects on placental function and fetal growth." Thesis, University of Southampton, 2015. https://eprints.soton.ac.uk/386933/.
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Boyd, Christopher M. "The behavioral effects of nonnutritive sucking on infants of differential fetal growth." Thesis, Virginia Tech, 1989. http://hdl.handle.net/10919/44702.
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Newborn infants with differential patterns of fetal growth, as determined by their weight-for-length, typically display behaviors which have been conceptualized as reflecting the integrity of the infant's behavioral organization. The newborn infant's sucking is one behavior that has been hypothesized to both reflect the effects of previous experiences on behavioral organization and affect the infant's future behavioral development. In particular, the infant's pattern of sucking activity may not only reflect the integrity of the infant's nervous system, it may also alter the temporal organization of the infant's behavioral state and motor activity by increasing behavioral quiescence. The purpose of this study was to compare the sucking activity of underweight-for-length (N = 30) and averageâ weightâ forâ length (N = 30) infants and its effects on behavioral state and motor activity. Fifteen low-PI and 15 averageâ PI infants were randomly assigned to each of two experimental conditions.
Master of Science
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Black, Rebecca Slain. "The maternal, fetal and neonatal effects of nitric oxide donors in pregnancy." Thesis, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271106.
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Gustafsson, Anna. "Anti-abortion legislation: What is the problem represented to be? : A critical policy analysis of the “heartbeat bills” in the United States." Thesis, Umeå universitet, Umeå centrum för genusstudier (UCGS), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-173003.
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Since the introduction of a new type of anti-abortion legislation in the United States which bans abortions after a fetal heartbeat can be detected, women’s options regarding abortion are being limited. How “problems” are represented or constituted in legislation shows that problems are time, place and context dependant. By using Carol Bacchi’s “What’s the problem represented to be?” approach to policy analysis, problem representations and subjectification effects in the heartbeat bills were identified. The problem representation of abortion as “lack of information” emerged as the central problem representation and the subject positions that were made available limits women’s choices regarding abortion. Fetal rights emerged as the core of the argumentation in the legislation, excluding women’s rights. How the problem of abortion is represented to be, the subjectification effects and the way rights are used and argued for in antiabortion legislation shows how they effectively limits women’s abortion choices.
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Algaba, Chueca Francisco. "Impact of gestational diabetes on fetal precursors and lipoprotein profile: effects on offspring." Doctoral thesis, Universitat Rovira i Virgili, 2020. http://hdl.handle.net/10803/669980.
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La diabetis mellitus gestacional (DMG) és una de les complicacions més comunes de l'embaràs i s'ha associat amb alteracions metabòliques i nutricionals maternes que pertorben les adaptacions metabòliques d'ell mateix. Aquests trastorns s'han associat amb patrons de creixement alterats i una major predisposició a desenvolupar malalties posteriors a la vida per la programació fetal. Les cèl·lules precursores fetals i el metabolisme dels lípids són components clau de la programació fetal que es poden veure directament afectats per la DMG. Aquest treball estudia l'impacte de la DMG en la funcionalitat de les cèl·lules precursores fetals trobades en la membrana amniòtica i en les característiques morfològiques i funcionals de les lipoproteïnes fetals, i també si aquestes alteracions potencials podrien programar el metabolisme fetal i contribuir directament a la major predisposició a malalties metabòliques i cardiovasculars durant el desenvolupament de la vida adulta. Portem a terme dos estudis observacionals cas-control amb DMG i embarassades amb tolerància normal a la glucosa. Vam demostrar que la DMG indueix canvis en les característiques biològiques de les cèl·lules mare mesenquimàtiques de la membrana amniòtica (AMSC), moltes de les quals estan relacionades amb paràmetres metabòlics fetals, el que suggereix que l'entorn de la DMG podria programar les cèl·lules mare i posteriorment afavorir la disfunció metabòlica més endavant en la vida. D'altra banda, trobem un contingut alterat de triglicèrids i lipoproteïnes de colesterol a la descendència de mares amb DMG dividida per categories de naixement. Concretament, els nounats amb pes adequat per a l'edat gestacional (AGA) mostren un perfil més similar als adults amb dislipidèmia i aterosclerosi que els nascuts de mares DMG. A més, trobem que les partícules de lipoproteïnes de baixa densitat (LDL) són biomarcadors potencials d'obesitat futura.La diabetes mellitus gestacional (DMG) es una de las complicaciones más comunes del embarazo y se ha asociado con alteraciones metabólicas y nutricionales maternas que perturban las adaptaciones metabólicas del mismo. Estos trastornos se han asociado con patrones de crecimiento alterados y una mayor predisposición a desarrollar enfermedades posteriores en la vida por la programación fetal. Las células precursoras fetales y el metabolismo de los lípidos son componentes clave de la programación fetal que pueden verse directamente afectados por la DMG. Este trabajo estudia el impacto de la DMG en la funcionalidad de las células precursoras fetales encontradas en la membrana amniótica y en las características morfológicas y funcionales de las lipoproteínas fetales, y también si estas alteraciones potenciales podrían programar el metabolismo fetal y contribuir directamente a la mayor predisposición a enfermedades metabólicas y cardiovasculares durante el desarrollo de la vida adulta. Llevamos a cabo dos estudios observacionales caso-control con DMG y embarazadas con tolerancia normal a la glucosa. Demostramos que la DMG induce cambios en las características biológicas de las células madre mesenquimatosas de la membrana amniótica (AMSC), muchas de las cuales están relacionadas con parámetros metabólicos fetales, lo que sugiere que el entorno de la DMG podría programar las células madre y posteriormente favorecer la disfunción metabólica más adelante en la vida. Por otro lado, encontramos un contenido alterado de triglicéridos y lipoproteínas de colesterol en la descendencia de madres con DMG dividida por categorías de nacimiento. Concretamente, los neonatos con peso adecuado para la edad gestacional (AGA) muestran un perfil más similar a los adultos con dislipidemia y aterosclerosis que los nacidos de madres DMG. Además, encontramos que las partículas de lipoproteína de baja densidad (LDL) son biomarcadores potenciales de obesidad futura.
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Nugent, Justine Lucy. "Effects of glucocorticoids on placental development and function : implications for fetal growth restriction." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/effects-of-glucocorticoids-on-placental-development-and-functionimplications-for-fetal-growth-restriction(b27d81f1-8d97-4be8-8fed-fa28743e42fa).html.
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Fetal growth restriction (FGR) signifies that the fetus has not achieved its growth potential and is associated with increased perinatal mortality and morbidity. The exact aetiology of FGR, in the absence of any identifiable fetal and maternal factors, remains unclear and is attributed to placental insufficiency. The FGR placenta has a characteristic phenotype including: increased resistance in the fetoplacental circulation, an alteration in trophoblast cell turnover and reduced activity of placental nutrient transport systems, the best characterised being the amino acid transporter, system A. The placenta strongly expresses the cortisol inactivating enzyme, 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). 11β-HSD2 activity was reduced in placentas from pregnancies complicated by FGR, suggesting increased exposure of the fetoplacental unit to maternal cortisol. In animal models, excessive exposure to glucocorticoids (GCs) is associated with a reduction in both fetal and placental weight. This reduction in placental weight was associated with abnormalities in placental function, consistent with those observed in the FGR placenta. This PhD investigated whether excess GC exposure during pregnancy is responsible placental insufficiency in human pregnancies and tested the hypotheses that excess GC exposure adversely affects placental vascular tone, trophoblast cell turnover and activity of the amino acid transporter, system A. Term placentas were collected from uncomplicated pregnancies and first trimester placental samples were obtained following elective surgical termination of pregnancy. Wire myography was used to explore the acute and chronic effects of GCs on term chorionic plate artery (CPA) function. The impact of GC treatment on trophoblast cell turnover in both first trimester and term placenta was investigated using the placental explant system. The effect of GCs on the activity of the system A transporter was also investigated in term explants and in isolated cytotrophoblasts where the expression of 11β-HSD2 was reduced using siRNA. Gene microarray studies on first trimester placental explants treated with GCs were utilised to identify genes regulated by GCs. Blunted constriction to thromboxane A2 was observed following acute GC treatment, whilst chronic exposure resulted in enhanced vasoconstriction, mimicking the altered reactivity of CPAs from pregnancies complicated by FGR. GC excess in first trimester placental explants increased apoptosis and decreased proliferation, thereby replicating the disordered turnover of the trophoblast observed in FGR placentas. No demonstrable effect was observed in cell turnover or system A activity in term placental explants treated with GCs, however, these experiments were hindered by the in-vitro regeneration of the syncytiotrophoblast in the model employed. The attenuation of 11β-HSD2 activity observed in FGR placentas was replicated in term primary cytotrophoblasts utilising siRNA to knock-down expression of 11β-HSD2. Preliminary results suggested an increase in system A activity in response to cortisol. Gene microarray studies identified a significant number of genes (~500) that were regulated by dexamethasone, confirming that GCs have an impact on many aspects of placental function. Potential mediators for the characteristic features of the FGR placenta replicated here in response to GC treatment were identified and validated at the mRNA level. The studies described in this thesis support the hypotheses that GC excess within the placenta contributes to the development of raised vascular resistance in the fetoplacental circulation and the disordered trophoblast turnover in placentas from pregnancies complicated by FGR. However, with the preliminary studies performed, the hypothesis that elevated levels of GCs contribute to the reduced placental amino acid transfer by the system A transporter in the FGR placenta can not be confidently disproven.
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Zhang, Ruoyi. "Protective effects of polysaccharides extracted from morinda officinalis on fetal rat hippocampal neurons." Click to view the E-thesis via HKUTO, 2010. http://sunzi.lib.hku.hk/hkuto/record/B44143199.
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Zou, Liangliang. "Protective effects of icariin extracted from epimedii herba on fetal rat hippocampal neurons." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B44142900.
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Illa, Armengol Míriam. "Brain effects of fetal growth restriction and their prevention in an animal model." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/565667.
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BACKGROUND: Chronic hypoxia due to placental insufficiency and prenatal undernutrition are probably the two major causes worldwide of an adverse intrauterine environment having an impact on neurodevelopment. Clinically, both situations manifest as an intrauterine growth restriction (IUGR), a situation defined as a significant reduction in fetal growth resulting in a birth weight below the 10th percentile. This situation is a well-recognized cause of neurobehavioral and cognitive impairments extending beyond childhood and early adulthood period. Although all these evidence, the structural ground of these functional impairments and the pathophysiological mechanisms are not fully characterized. An improvement in these two aspects would allow us to propose different therapeutic strategies aiming to ameliorate and even revert the long-lasting consequences of the IUGR.
HYPOTHESIS: We hypothesized that IUGR produces subtle structural brain changes that underlie the long-term neurobehavioral and cognitive impairments. The severity of the neurodevelopmental consequences might be related to the severity of the prenatal insult (reduction in nutrients with or without a reduction in oxygen). High-resolution brain imaging along with specific histological techniques focused on neuronal connectivity could evidence these structural brain changes. Additionally, we hypothesized that an early postnatal stimulation might ameliorate the structural and functional impairments that persist at the long-term period after IUGR.
METHODS: Two animal models of IUGR were used in this thesis: i. A cohort of pregnant rabbits was randomized to reproduce an undernutrition model based on maternal food reduction intake, ii. Another cohort of pregnant rabbits was randomized to the placental insufficiency model based on the surgical ligation of 40-50% of the uteroplacental vessels that irrigate each gestational sac. After the delivery in both models, IUGR and controls animals were followed up to the 70th postnatal days. At the 30th postnatal days, a subgroup of IUGR animals was randomized to an environmental enrichment strategy. In all the groups at the neonatal period, general motor skills, reflexes, and olfactory sensitivity were evaluated. Similarly, at the 70th postnatal days, anxiety, memory, and learning were evaluated. Afterward, animals were sacrificed and brains were fixed and diffusion MRI was then performed. In a subset of animals, changes at the microstructural level and differences in the number of fibers in two specific brain circuits (anxiety and memory circuits) were performed by using a Voxel-Based approach
(VBA) and Tractography analysis, respectively. Moreover, brain networks were obtained and evaluated by means of a Connectomics. Finally, a subgroup of animals was also histologically evaluated by means of dendritic spine and perineural nets evaluation in the Hippocampus.
RESULTS: IUGR animals showed poorer functional performance in both moments, especially in the model of placental insufficiency. At the long-term period, IUGR animals presented an altered brain network architecture, being again these differences more pronounced in the placental insufficiency model. Moreover, VBA analysis and Tractography analysis evidenced microstructural brain changes mostly affecting gray matter and a decreased in the number of fibers involved in the anxiety and memory circuits in the IUGR animals in comparison to controls. At the cellular level, IUGR animals presented abnormal neuronal connectivity with changes in the dendritic spine density and in the perineural nets. In contrast, stimulated IUGR animals presented a functional and structural improvement in comparison to non-stimulated IUGR animals over the long-term period.
CONCLUSIONS: This thesis adds to the previous evidence new insights regarding the pathophysiological mechanisms underlying IUGR and gives strong evidence linking IUGR with altered brain connectivity as the basis for the neurological sequelae associated with IUGR. Additionally, it gives preliminary evidence suggesting that a strategy based on physical, sensory, cognitive as well as social stimulation applied during early postnatal life, where brain plasticity is higher, might ameliorate the neurodevelopmental consequences of IUGR.
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Zehri, Aqib Hyder. "Differential Effects of Pulsatile vs. Chronic Hyperglycemia on Fetal Pancreatic Beta Cell Population." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/145129.
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Waylan, Ann Terese. "Effects of L-carnitine on fetal growth and the IGF system in pigs /." Search for this dissertation online, 2003. http://wwwlib.umi.com/cr/ksu/main.
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Audinis, Vilius. "Computer-based simulation of the effects of instrumental delivery on the fetal head." Thesis, University of East Anglia, 2017. https://ueaeprints.uea.ac.uk/63688/.
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Fetal head moulding is a phenomenon that happens during the process of human childbirth. Due to the highly deformable fetal scalp being in contact with the maternal anatomy, the shape of the fetal head changes. This can be beneficial when the fetal head dimensions are very similar to the dimensions of the female pelvis hence allowing the baby to progress safely through the birth canal. Conversely, excessive head moulding may have serious effects on the baby's wellbeing. The first part of this thesis presents a computer-based finite element model of fetal head moulding as an improvement on previously developed models. The second part of the research focuses on another cause of potentially excessive fetal head moulding, i.e. the incorrect use of obstetric instruments including the obstetric forceps and the ventouse (vacuum extractor). The degree of damage that may be caused by incorrectly placing a forceps (i.e. asymmetric placement of the blades) or a ventouse (i.e. placement on top of soft parts of the skull such as the fontanelles) was assessed by means of finite element analysis after developing a set of software tools to facilitate these experiments. The fi�nal results of this research included: an improved and more realistic model of fetal head moulding under conditions of normal delivery, and results that reveal the great potential of severe damage that obstetric forceps and/or the ventouse may cause to the baby's head when applied incorrectly.
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Barahona, Roberto G. Suazo. "Intrauterine position in pigs: effects on conceptus development and fetal fluids steroid content." Thesis, Virginia Tech, 1989. http://hdl.handle.net/10919/43288.
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The purpose of this study was to investigate the effect of intrauterine position and its possibly resultant steroid differential on conceptus growth and steroid content in allantoic and amniotic fluid of pigs. six conceptus variables (placental weight, placental length, fetal weight, fetal length, allantoic fluid volume and amniotic fluid volume) and seven steroids (progesterone, androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate, testosterone, estrone and estrone sulfate) were evaluated. Four fetal positions were studied: females between females (f2F), females between males (fOF) , males between females (m2F) and males between males (mOF).
Fetuses examined from ovariectomized (OVX) pregnenolone (PS)-treated gilts showed differences in placental
weight, allantoic fluid estrone and androstenedione content and amniotic fluid androstenedione content as a result of intrauterine position. Fetuses from OVX gilts treated with either medroxyprogesterone acetate (MPA) I or progesterone (P4) showed differences in placental length due to intrauterine position. Allantoic and amniotic fluid content of any of the steroids studied from OVX MPA- and P4-treated gilts was not altered as a result of intrauterine position. Intrauterine position appears to have a definite influence on conceptus development and possibly on steroid content. However, discrepancies' of results among trials possibly as a result of differences in type and amount of exogenous precursor enable us to draw stronger conclusions on the intrauterine position effect.Master of Science
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Li, Zheng. "The mechanisms of ethanol-induced damage to the developing cerebellum effects on the cerebellar granule cells /." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=3134.
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Thesis (Ph. D.)--West Virginia University, 2003.Title from document title page. Document formatted into pages; contains vii, 146 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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Copeland, Brenda Maureen. "Searching for, finding, and experiencing friendship, a qualitative study of friendship experiences of seven young adults with fetal alcohol syndrome or fetal alcohol effects." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ62546.pdf.
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Lanoue, Louise. "The effects of graded levels of dietary carbohydrate on fetal and neonatal glucose metabolism." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41670.
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The effects of maternal dietary glucose restriction on reproductive performance were investigated by feeding pregnant rats isocaloric diets containing graded levels of dietary glucose (0, 12, 24 and 60%) during pregnancy and during pregnancy and lactation, and by measuring the effects of glucose restriction on (1) maternal, fetal and neonatal metabolism, on (2) growth and composition of the mammary glands and placentas, and (3) on milk composition. Carbohydrate restriction induced maternal metabolic adaptations that were proportional to the severity of the glucose restriction. Placental growth and composition as well as mammary gland composition were not affected by dietary glucose restriction, whereas fetal growth and development and milk composition were significantly impaired when glucose was limited in the maternal diet. This suggests that the effects of dietary glucose on the fetus and on milk composition were not mediated by changes in placenta and mammary gland DNA, protein or glycogen concentrations. Complete dietary glucose restriction significantly depressed fetal liver, lung and heart glycogen concentrations; repletion of the maternal diets with 12 and 24% glucose restored cardiac glycogen to normal but not fetal lung glycogen and liver glycogen. Pups born to dams fed a glucose-free diet failed to survive longer than 24 h postpartum and that was associated with the low levels of tissue glycogen at birth in these pups. At birth, lung and liver glycogen concentration of pups of the 12 and 24% glucose diets was similar to pups of the control diet despite the fact that these reserves were depressed in utero; and these pups efficiently corrected the transient hypoglycemia observed following parturition. The effects of glucose restriction on fetal liver glycogen were not reflected by similar changes in fetal plasma insulin, glucagon and glucose levels or in glycogen synthase and phosphorylase activities. Maternal dietary glucose was an important determinant
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Jeffray, Treena. "The effects of cortisol on the development of the fetal hypothalamic-pituitary-adrenal axis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ41180.pdf.
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Alves, Teixeira Jeronima Maria. "The effects of maternal anxiety and disease on the fetal and neonatal cardiovascular system." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421465.
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Bales, Mary. "Knowledge of the Effects of Alcohol on Fetal Development Among Women of Childbearing Age." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/honors/22.
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While Fetal Alcohol Syndrome Disorder is a recognized problem with alcohol ingestion during the formation of facial features, Fetal Alcohol Spectrum Disorders are not as widely recognized. These disorders result from exposure to alcohol throughout pregnancy when the brain and nervous system are developing. The resulting disorders include attention deficit disorders, social disorders, inappropriate behaviors, learning disorders, and intellectual disability. The incidence of children with alcohol-related disorders is increasing as evidenced by children needing special services in the educational systems. It is unknown how much alcohol ingestion is safe during pregnancy or how genetic factors are involved in the development of these disorders. Women often get conflicting information from the media and other resources about safe levels of alcohol consumption during pregnancy. Abstinence of alcohol ingestion is the only known prevention of such intellectual disorders. It is hypothesized that women of childbearing age may not be knowledgeable of the relationship between drinking and the implications of alcohol exposure on fetal development.
The purpose of this research is to determine what women of childbearing age know about alcohol consumption during pregnancy and if there is a knowledge deficit that exists among women of a certain age or women that use specific resources for health information. The researcher surveyed 40 female students at East Tennessee State University by using true or false questions concerning alcohol consumption related to fetal development in order to determine if a knowledge deficit exists. Based on the findings, it may be determined if women of childbearing age need educational materials from a reliable source.
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Schlaeppi, Janine-Ai. "Effects of creatine treatment on neuronal phenotype and neurotoxicity in cultured fetal spinal cord /." Bern : [s.n.], 2006. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Adegoke, Korede K. "The Effects of Maternal Folate on Fetal Brain and Body Size among Smoking Mothers." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6793.
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The adverse effects of maternal smoking on infant mortality and morbidity has been well documented in the literature. Maternal tobacco use is causally associated with fetal growth restriction and correlates negatively with folate intake and metabolism. Studies have examined the association between smoking and folate levels during pregnancy, but very few have assessed this relationship using objective and accurate measures of both variables. Furthermore, despite evidence of a causal association between smoking in pregnancy and intrauterine growth restriction, and a plausible relationship between tobacco use and low maternal folate which is required for optimal fetal growth, no experimental study has investigated the potential benefit of folic acid in mitigating the adverse effects of maternal smoking on fetal outcomes.
The objectives of this study were to investigate the relationship between maternal smoking and folate levels and examine the efficacy of higher-strength folic acid supplementation, in combination with enrollment in a smoking cessation program, in promoting fetal body and brain growth. Our hypothesis was that women who smoke during pregnancy have lower peri-conceptional folic acid reserves than non-smoker pregnant women and that folic acid reserves will decrease with increasing cotinine level. Additionally, smoker pregnant women on higher-strength folic acid (4mg daily) in combination with smoking cessation programs will experience faster fetal brain growth and have infants with larger body size at birth compared to smokers on the standard dose of folic acid (0.8mg daily).
Participants were pregnant women (smokers and non-smokers) who received antenatal care between 2010-2014 at the Genesis Clinic of Tampa, a community health center affiliated with the Department of Obstetrics and Gynecology of the University of South Florida (USF). They were aged 18-44 years and had a gestational age of less than 21 weeks at study enrollment. To determine the peri-conceptional folic acid reserves in smoking versus nonsmoking women during pregnancy and associated sociodemographic factors, baseline (crosssectional) data from a double-blinded randomized controlled trial were analyzed using Tobit regression models (n=496). Smoking information was assessed using salivary cotinine, a sensitive and specific tobacco use biomarker. Folate reserve was measured using red blood cell folate. To investigate the efficacy of higher-strength folic acid on fetal body and brain size, baseline and follow-up data from pregnant smokers enrolled in the randomized controlled trial were utilized (n=345). All primary analyses of the clinical trial data were conducted on a modified intention-to-treat basis and included participants who completed the trial with an observed endpoint, irrespective of compliance to protocol. Multilevel modeling, linear regression, and log-binomial regression analyses were conducted.
A significant inverse association between salivary cotinine level and periconceptional red blood cell folate concentration was found among pregnant women in the early to midpregnancy period. Smokers on high-dose folate during pregnancy had infants with a 140.38g higher birth weight than infants of their counterparts on standard dose folate (P =0.047). Mothers who received higher strength folate had a 31.0% lower risk of having babies with SGA compared to their mothers on the standard-dose (adjusted relative risk-ARR=0.69, 95% CI: 0.46–1.03; (P =0.073)). High-dose folate had no significant effect on the intrauterine rate of growth in head circumference, and head circumference and brain weight at birth in our trial sample. However, the brain-body ratio of infants of mothers who received high-dose treatment was 0.33 percentage-point lower than that for infants of mothers who received the standard dose of folate (P =0.044).
Higher strength folic acid supplementation in pregnant women who smoke might be a cost-effective and safe option to improve birth outcomes and reduce low birth weight and SGA associated infant morbidity and mortality. Future studies with larger sample sizes and diverse populations are indicated to confirm or refute the results of this study. Randomized controlled trials starting during the preconception period and with follow-up until delivery are warranted, to identify the most folate-sensitive period of fetal growth and determine the optimal dose of folic acid supplement. Further research investigating several pathways through which the effects of prenatal smoking on adverse birth outcomes can be mitigated is needed.
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Gunn, J. K. L., C. B. Rosales, K. E. Center, A. V. Nunez, S. J. Gibson, and J. E. Ehiri. "The effects of prenatal cannabis exposure on fetal development and pregnancy outcomes: a protocol." BMJ, 2015. http://hdl.handle.net/10150/617200.
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UA Open Access Publishing FundIntroduction: The effects of exposure to marijuana in utero on fetal development are not clear. Given that the recent legislation on cannabis in the US is likely to result in increased use, there is a need to assess the effects of prenatal cannabis exposure on fetal development and pregnancy outcomes. The objective of this review is to assess the effects of prenatal exposure to cannabis on pregnancy outcomes (including maternal and child outcomes). Methods and analyses: Major databases will be searched from inception to the latest issue, with the aim of identifying studies that reported the effects of prenatal exposure to cannabis on fetal development and pregnancy outcomes. Two investigators will independently review all titles and abstracts to identify potential articles. Discrepancies will be resolved by repeated review, discussion and consensus. Study quality assessment will be undertaken, using standard protocols. To qualify for inclusion, studies must report at least one maternal or neonatal outcome post partum. Cross-sectional, case–control, cohort and randomised controlled trials published in English will be included. In order to rule out the effects of other drugs that may affect fetal development and pregnancy outcomes, studies will only be included if they report outcomes of prenatal exposure to cannabis while excluding other illicit substances. Data from eligible studies will be extracted, and data analysis will include a systematic review and critical appraisal of evidence, and meta-analysis if data permit. Meta-analysis will be conducted if three or more studies report comparable statistics on the same outcome. Ethics and dissemination: The review which will result from this protocol has not already been conducted. Preparation of the review will follow the procedures stated in this protocol, and will adhere to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Ethical approval of data will not be required since the review will use data that are already available in the public domain through published articles and other reports.
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Puzey, Martin Stanley. "The investigation of the calcium antagonist nifedipine on fetal umbilical artery Doppler waveforms." Master's thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/27134.
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The following thesis will describe the investigation of the effect of nifedipine (a calcium antagonist) on the Doppler flow velocity waveform of the umbilical artery. The thesis is divided into two parts. The first section is a literature review of the three main aspects of the thesis namely: 1. The uteroplacental circulation in humans and the pathophysiology related to this circulation in hypertension and intrauterine growth retardation (IUGR). 2. The biokinetics of nifedipine and a review of the experiments that have been performed using the drug in human and animal models. 3. The principles of Doppler ultrasound and the literature pertaining to its use in the study of the uteroplacental circulation. The second part of the thesis is devoted to the effect of nifedipine on fetal umbilical artery Doppler waveform analysis. In the first ·stage of the investigation the effect of the drug on hypertensive mothers has been examined, and in the second stage the effect on fetuses that have an increased resistance index of the umbilical artery Doppler waveform.
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Lowe, Victoria H., and Victoria H. Lowe. "Effects of Early Weaning Calves as a Management Tool." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625344.
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The goal of a cow-calf producer is to produce a calf each year per cow. Research suggests that first year heifers struggle breeding back with their second calf because of the adjustments to new range/main herd conditions and the partitioning of nutrients between gaining weight, milk production, and gestation. This study was conducted at the V-V ranch at the University of Arizona for five years and looked at the effects on young cows when calves were weaned from first year heifers at 80 days rather than 205 days. Early weaning allows for gestational benefits because they are given the opportunity to adapt to herd conditions by applying feed resources to the in utero fetus and their own body condition rather than lactation. All first year heifers were included over three years, and were randomly assigned to two groups, normal weaning (NW) or early weaning (EW). This resulted in 122 heifers in the group whose calves were EW and 119 heifers in the group whose calves were NW. Heifers that were in the EW group bred back at a 27% higher rate in their second year, and had 15% greater longevity in the herd. Calves that were in utero when the nursing calves were early weaned were 16.4 kg heavier at weaning. Part of this was due to the age of the calf and part to gestational health. Early weaning was an effective strategy for improving reproductive performance of first year heifers as well as their survival rate in the herd to 5 years of age. It also resulted in improved performance for their in utero calves.
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Catlin, Michelle Catherine. "Effects of ethanol on muscarinic receptor-induced responses in astroglia /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8444.
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Welham, Simon John Marshall. "The effects of maternal protein restriction in the rat, upon programming of blood pressure, renal structure and function." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300821.
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Nevalainen, Nina. "Effects of glial cell line-derived neurotrophic factor (GDNF) on mouse fetal ventral mesencephalic tissue." Thesis, Mälardalen University, Department of Biology and Chemical Engineering, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-615.
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The symptoms of Parkinson's disease occur due to degeneration of dopamine neurons in substantia nigra. It has been demonstrated that glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor when it comes to protect and enhance survival of dopamine neurons in animal models of Parkinson's disease. The aim of this study was to evaluate short- and long-term effects of GDNF on survival and nerve fiber outgrowth of dopamine cells and astrocytic migration in mouse fetal ventral mesencephalic (VM) tissue. Primary tissue cultures were made of mouse fetal VM tissue and evaluated at 7 and 21 days in vitro (DIV) in terms of dopaminergic nerve fiber outgrowth and astrocytic migration when developed with GDNF present, partially, or completely absent. The results revealed that VM tissue cultured in the absence of GDNF did not exhibit any significant differences in migration of astrocytes or dopaminergic nerve fiber outgrowth neither after 7 DIV nor after 21 DIV, when compared with tissue cultured with GDNF present. Migration of astrocytes and dopaminergic nerve fiber outgrowth reached longer distances when tissue was left to develop for 21 DIV in comparison with 7 DIV. In order to study the long-term effects of GDNF, mouse fetal dopaminergic tissue was transplanted into the ventricles of adult mice and evaluated after 6 months. No surviving dopamine neurons were present in the absence of GDNF. In contrast dopamine neurons developed with GDNF did survive, indicating that GDNF is an essential neurotrophic factor when it comes to long-term dopamine cell survival. More cases have to be assessed in the future in order to strengthen the findings. Thus, transplanted dopamine neurons will be assessed after 3 and 12 months in order to map out when dopamine neurons deprived of GDNF undergo degeneration.
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Coumans, Audrey Barbara Catharina. "Endotoxemia effects on the circulation and the brain : studies in fetal sheep and neonatal rats /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 2003. http://arno.unimaas.nl/show.cgi?fid=6028.
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Karalekas, Panagiotis. "Is S100A1 involved in the programming effects of fetal hypoxia on cardiac function in chickens?" Thesis, Linköpings universitet, Biologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-111556.
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Prolonged prenatal hypoxia has shown to cause fetal growth restriction inchickens due to restricted oxygen to the somatic tissue. The body goes through a critical periodof development. Insults during this critical period may have lifelong effects on the individual.Currently heart failure is treated either with symptomatic therapy using diuretics or by targetingthe renin-angiotensin-aldosterone system. Developing new successful treatments is importantwith the aging population and the increased rate of heart failure. Previous studies have shownsystolic contractile dysfunction in 5 week old broiler chicken hearts when the eggs have beenincubated in hypoxia until hatching. S100A1 in cardiomyocytes regulates the calcium-controllednetwork which plays a big role in cardiac contractility and in this study, using qPCR on S100A1(GOI), GADPH and β-actin to try and determine if the changes made to the heart while the fetusis developing is due to a lack of S100A1 expression resulting in a decreased handling of Ca2+uptake which causes contractile dysfunction A Roche Lightcycler 480 was used together with theRoche template running triplets of each sample at 15-15-15 seconds for 45 cycles No statisticalsignificance was observed between the control group and the experimental group. However inthis study only S100A1 gene is being considered but a better understanding of the whole S100family might give a better understanding of mechanisms causing the progressive deterioration ofcardiac function
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Phillips, Leilanie Cashandra. "The neuropsychological effects of prenatal exposure to alcohol." Thesis, Stellenbosch : Stellenbosch University, 2004. http://hdl.handle.net/10019.1/50170.
Full textAbstract:
Thesis (MA)--University of Stellenbosch, 2004.ENGLISH ABSTRACT: The objective of this thesis is to review and synthesize the scientific literature on cognitive and neuropsychological deficits associated with children who were exposed to alcohol prenatally and to highlight possible areas of future attention. High incidences of Fetal Alcohol Syndrome has been reported especially in patients from low socio-economic areas. The highest reported incidence is found in the Western Cape province in South Africa. The devastating part of FAS is that its affects are entirely preventable. Alcohol is a physical and a behavioural teratogen. Prenatal alcohol exposure causes structural damage to the central nervous system and the brain that is vulnerable throughout the pregnancy. A dose-response association exist as exposure to heavier amounts of alcohol can cause more harm. The timing and pattern of alcohol consumption also plays a role. To date though, no "safe" level of alcohol consumption during pregnancy can be advocated. Various neuropsychological decrements are found in individuals with fetal alcohol syndrome or alcohol related neuro-developmental deficits as evaluated on standardized tests. Mental retardation is commonly found and even individuals with normal IQ's still display other learning disabilities. IQ's remain stable over the life span. Along with impaired intellectual functioning they also struggle with mathematical tasks especially as their complexity increases. Speech and language development is also delayed in individuals with FAS. There is little variation in the pith and display poor language comprehension. Attentional deficits are also noted and especially impact on academic functioning. Clinically, children often present with ADHD but in-depth studies have revealed that neurobiologically there is some differences as children with FAS struggle more with encoding and shifting of attention as opposed to other patients with ADHD. Difficulties with visual-spatial functioning has also been found. Verbal learning and memory are also impaired in individuals with FAS. Their poor verbal learning are influenced by their shallow level of encoding. Problems with fine motor skills are also noted. It also appear that all executive functions are impaired. They demonstrate poor planning skills, initiation, cognitive shifting, slow information processing, their thinking is concrete and they have poor self-regulatory skills. Behavioural problems include impulsivity, hyperactivity, aggressiveness, poor social skills and impaired judgement. Early intervention is thus essential to lessen the impact of neuro-psychological deficits on functional adaptation. A sensitive battery of neuro-psychological tests are also required to identify all the impairments in affected individuals and to plan more focussed intervention strategies.
AFRIKAANSE OPSOMMING: In hierdie tesis word 'n oorsig aangebied van literatuur wat betrekking het op die disfunksie van kinders wie se moeders tydens swangerskap alkohol misbruik het. Leemtes asook moontlike areas van toekomstige navorsing, is bespreek. 'n Hoe voorkoms van fetale alkohol sindroom (FAS) word gerapporteer, pasiente uit die lae SES gebiede. Die hoogste voorkoms word gerapporteer in die Wes- Kaapse provinsie in Suid Afrika. Wat die probleem meer tragies maak, is die feit dat dit heeltemal voorkombaar is. Alkohol is 'n teratogeen wat fisieke, neurologiese en gedragsimplikasies het. Blootstelling aan alkohol voor geboorte veroorsaak strukturele veranderinge in die sentrale senuweestelsel en die brein. Blootstelling tot hoer volumes van alkohol veroorsaak noodwendig meer skade. Die spesifieke stadium van alkohol-inname tydens die swangerskap, en die moeder se drinkpatroon, speel 'n rol in die neurosielkundige uitkomste. Tot op hede kon geen veilige alkoholsvlak tydens swangerskap vasgestel word nie. Verskeie neurosielkundige uitvalle is gevind in kinders met FAS en ook kinders met alkohol-verwante neurologies ontwikkelings probleme, volgens neurosielkundige toetsing. Verstandelike gestremdheid kom algemeen voor in kinders met FAS. Kinders met FAS wat oor normale intellektuele vernoens beskik ervaar leerprobleme. Die intellektuele inkortings bly stabiel oor die lewenspan. Kinders met FAS ondervind erge probleme met wiskunde, veral wanneer die werk moeiliker raak. Die spraak-en taalontwikkeling wat kinders met FAS ervaar sluit in beperkte taalbegrip en intonasie. Hulle kort aandagspan affekteer veral hulle akademiese funksionering. Die aandagsteuring van kinders met FAS en kinders met aandagstekort-hiperaktiwiteit versteuring verskil neuro-biologies. Verdere verskille bestaan ook aangesien kinders met FAS spesifiek sukkel met swak enkoderingsvermoe en om kognitiewe aanpassings te maak. Visueel-ruimtelike verrnoe van kinders met FAS is ook benadeel. Hulle sukkel ook met verbale leer en hulle geheue is ook ingekort. Die inkortings dui op 'n oppervlakkige enkoderingsvermoe. Probleme met fyn-motoriese vaardighede is ook gevind, volgens toetseing. Toetse wat gemik is om uitvoerende funksies te evalueer, het verskeie uitvalle aan die lig gebring. Probleme in abstrakte redenering, beplanning, impulsiwiteit, self-regulering, en die lnlslerlnq en prosessering van informasie. Gedragsprobleme soos swak sosialiseringsvaardighede, aggresiwiteit, swak oordeel en hiperaktiwiteit. Die wye neurosielkundige uitvalle wat voorkom in kinders met FAS noodsaak vroee intervensie om die langtermyn-impak daarvan te verminder. Hiervoor word 'n sensitiewe battery neurosielkundige toetse benodig wat al die kognitiewe uitvalle kan identifiseer.