Hypertension in pregnancy is associated with autonomic dysregulation whereas the effects of obesity in pregnancy on maternal cardiac autonomic function are poorly understood. Furthermore, hypertension in pregnancy is associated with placental insufficiency and fetal growth restriction, whereas obesity in pregnancy is associated with placental inflammation and macrosomia. Fetal growth restriction is associated with an increased risk for language deficits at 2-5 years of age. However, maternal cardiac autonomic function and fetal auditory processing in pregnancies complicated by hypertension compared to obesity have not been examined and are the focus of this study. Maternal short-term cardiac autonomic modulation in the supine and standing postures as well as spontaneous and auditory elicited fetal behaviours were compared in 61 mother-fetal pairs (n=20 hypertensive; n=20 overweight; n=21 normal weight comparison pregnancies) from 34 to 40 weeks gestation. Maternal cardiovascular measures included systolic arterial finger-cuff blood pressure and electrocardiographic recordings of heart rate. Spontaneous observations of fetal heart rate, body and breathing movements, muscle tone and an estimate of amniotic fluid were made. Finally, each fetus received a 2 min recording of their mother and the mother’s voice in reverse (counterbalanced over subjects). When standing (othostatic stress), all three groups of women exhibited a decrease in the average baroreflex slope, parasympathetic nervous system indicator and high frequency power compared to the supine position. In a 20 min observation of spontaneous behaviour in the maternal supine compared to the standing position, fetuses of hypertensive mothers had, on average, fewer heart rate accelerations ≥ 15 bpm while the mother was supine; fetuses in the normal weight comparison group experienced more accelerations while the mother was supine. The average number of heart rate accelerations did not change in the two maternal positions for fetuses in the obese group. Fetuses in the three groups showed differential responses to the mother’s voice played forward and backward. It was concluded that there were no differences in maternal heart rate variability measures in the group of mildly hypertensive women compared to those with obesity and the normal weight comparison group. Differential spontaneous fetal heart rate accelerations and responses to the mother’s voice among the three groups needs further study with sufficient sample size to examine behaviour as a function of gestational age. / Thesis (Master, Nursing) -- Queen's University, 2009-03-13 17:45:41.837

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No description available.

No description available.

Fetal and neonatal immune thrombocytopenia (FNIT) is a severe bleeding disorder which results from fetal platelet destruction by maternal antibodies against platelet antigens, including GPIIbIIIa (αIIbβ3 integrin) and GPIbα. β3 integrin is also expressed by angiogenic endothelial cells (ECs) and is required for angiogenesis. Therefore, we investigated whether anti-β3 antibodies in FNIT cross-react with blood vessels of the fetus/neonate and contribute to pathogenesis. Antibodies to GPIbα were used as controls. To mimic human FNIT, β3 integrin- or GPIbα-deficient female mice were immunized with wild-type platelets and bred with wild-type male mice. Pups in both groups had thrombocytopenia but intracranial hemorrhage was only observed in anti-β3-mediated FNIT. Anti-β3-mediated FNIT pups had increased apoptosis in the brain and impaired vascularization of the brain and retina. In addition, anti-β3 sera inhibited proliferation and vascular-like tube formation by ECs in vitro. Therefore, anti-β3 antibodies in FNIT likely impair angiogenesis in the developing fetus/neonate.

Fetal and neonatal immune thrombocytopenia (FNIT) is a severe bleeding disorder which results from fetal platelet destruction by maternal antibodies against platelet antigens, including GPIIbIIIa (αIIbβ3 integrin) and GPIbα. β3 integrin is also expressed by angiogenic endothelial cells (ECs) and is required for angiogenesis. Therefore, we investigated whether anti-β3 antibodies in FNIT cross-react with blood vessels of the fetus/neonate and contribute to pathogenesis. Antibodies to GPIbα were used as controls. To mimic human FNIT, β3 integrin- or GPIbα-deficient female mice were immunized with wild-type platelets and bred with wild-type male mice. Pups in both groups had thrombocytopenia but intracranial hemorrhage was only observed in anti-β3-mediated FNIT. Anti-β3-mediated FNIT pups had increased apoptosis in the brain and impaired vascularization of the brain and retina. In addition, anti-β3 sera inhibited proliferation and vascular-like tube formation by ECs in vitro. Therefore, anti-β3 antibodies in FNIT likely impair angiogenesis in the developing fetus/neonate.

Bakgrunn: Intrauterin fosterdød er en hendelse som har ringvirkninger langt utover den rammede kvinnen og hennes familie. Det handler i sin ytterste mening om kvinner og barns helse og likhet i helse for alle. Utviklingen mot et flerkulturelt samfunn innebærer andre utfordringer enn tidligere i forhold til kultur, kommunikasjon, kvinne-og familieperspektiv, livsstil og medisinske problemstillinger. Formål: Denne studiens formål har vært å kartlegge forekomsten av intrauterin fosterdød (IUFD) hos innvandrerkvinner sammenlignet med svenske kvinner, og å undersøke faktorer som kan være assosiert med IUFD. Materiale og metode: Registerdata på 904 646 fødte og deres mødre i perioden 1992-2001 ble undersøkt med bivariate analyser. Det ble også gjort en systematisk litteraturgjennomgang av relevant nasjonal og internasjonal forskning på feltet. Resultat: Analysen viser en økt risiko for IUFD hos innvandrerkvinnene sammenlignet med svenske kvinner. IUFD forekommer oftere hos de ikke-europeiske innvandrerkvinnene;OR:1,45(95% CI 1,28-1,63). Litteraturgjennomgangen viser at ikke-europeiske innvandrerkvinner har 2-3 ganger så høy risiko for IUFD sammenlignet med totalpopulasjonen, men også at lav sosio-økonomisk status (SøS), alder, inngifte, røyking, reduksjon av medisinske risikofaktorer og kvaliteten på den antenatale omsorgen påvirker den perinatale dødeligheten. Konklusjon: En forbedret folkehelse i Norden de siste tiårene har bidratt til en reduksjon av den perinatale dødeligheten. Men ikke alle befolkningsgrupper har fått tatt del av denne utviklingen. De ikke-europeiske innvandrerkvinnene har signifikant høyere odds for IUFD. De har ofte lav SøS, hvilket i seg selv er assosiert med IUFD. Kunnskap om ulikheter i helse og sykdom blant ulike kategorier mennesker i samfunnet vårt er viktig og kan bidra til en mer tilpasset omsorg og en bedre medisinsk behandling. Det er behov for videre forskning fra flere fagområder for å kunne kartlegge livsstil, levekår og effekten av språkbarrierene og for å få en oppfatning om hvordan ulikheter i helse kan utjevnes. / Background: Stillbirths or intrauterine fetal death have wide effects on families. This is  about women’s and children’s health as well as equity in health for all. As Sweden becomes more multicultural, new challenges in equity on women’s and children’s health develope related to culture, communication, women –and family matters, lifestyle and medical issues. Aim: The aim of this study was to assess the occurence of stillbirths in immigrant women compared to Swedish women and investigate factors related to stillbirths. Method: Data from 904 646 newborns and their mothers during the period 1992-2001 was analysed using bivariat analyses. A literature study was undertaken with a systematic appraisal of relevant national and international research in the field. Results: The analyses showed that stillbirth was more common in non-European immigrant women. OR: 1,45 (95% CI 1,28-1,63). Non-European immigrant women in Sweden had higher odds of stillbirths compared to the background population. The litterature showed that non-European immigrant women have 2-3 times the risk of stillbirths, and the risk of stillbirths is also increased in women of lower socioeconomic status (SES). Other risk factors indicated to be important are age, consanguinity, smoking and the quality of perinatal care. Conclusions: Non-European immigrant women in Sweden have higher odds of stillbirths compared to the background population. These women also have an increased risk of low SES, which is itself a riskfactor of stillbirth. Appropriate knowledge of difference in health needs in different groups in the community is important for filling the health care needs and improving the medical treatments. Further research is needed from different sectors to assess the importance of lifestyle, language limitations and how these women are treated by the health care system. / <p>ISBN 978-91-85721-30-6</p>

Background: Prenatal alcohol exposure causes behavioural, growth and central nervous system deficits in the offspring, termed Fetal Alcohol Spectrum Disorder (FASD). Our lab has previously shown that structured saccadic eye movement tasks probe executive functioning and can be used to measure cognitive dysfunction in children with an FASD, because performance of these tasks reflects the structural integrity of brain areas shown to be vulnerable to prenatal alcohol exposure. Recently developed portable electroencephalographic (EEG) devices record brain activity using a single dry-sensor electrode. Our objectives were: 1) to assess attention and working memory via a delayed memory-guided saccadic eye movement task of varying mnemonic load and 2) to explore the use of a portable single-channel EEG recording device in measuring differences in frontal lobe activity in children with FASD during the performance of this eye movement task. Methods: A total of 18 children with an FASD diagnosis and 19 typically developing control children performed a memory-guided saccadic eye movement task with one, two or three target stimuli. During the task, frontal lobe EEG was recorded using the Neurosky Mindwave Mobile® portable recording device. Results: In the delayed, memory-guided task when two or three target stimuli were required to be held in working memory, children with an FASD performed the task correctly less often than children in the control group. During task performance, children with FASD exhibited a reduction in theta frequency band power, and in alpha frequency band power only at higher mnemonic loads, suggesting that children with FASD recruited more cognitive resources to complete the task. Conclusion: The results of this study suggest that a portable EEG recording device can be used to assist in the recognition of underlying neural mechanisms of executive functioning deficits in children with FASD. Portable devices offer greater user comfort than typical EEG recording equipment as well as flexibility for use outside the laboratory. This could greatly facilitate the study of children with FASD, and other groups who may be less tolerant of typical laboratory environments. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2013-08-14 20:22:10.995

Developmental ethanol exposure causes both structural and functional changes in the brain that can result in cognitive and behavioral abnormalities. The hippocampal formation, an area of the brain strongly linked with learning and memory, is particularly vulnerable to the teratogenic effects of ethanol. Research in this thesis focused on uncovering the effects of developmental ethanol exposure on hippocampal function in adulthood, particularly synaptic plasticity (a putative neurobiological mechanism of learning and memory). The first experiment sought to determine the temporal vulnerability of hippocampal synaptic plasticity as a function of exposure to ethanol during a single trimester. Ethanol exposure during the 1st or 3rd trimester equivalent resulted in minor changes in synaptic plasticity in adult offspring. In contrast, ethanol exposure during the 2nd trimester equivalent resulted in a pronounced decrease in long-term potentiation (LTP), indicating that the timing of exposure determines the severity of the deficit. The second experiment was aimed at determining the effects of prenatal ethanol exposure (1st and 2nd trimester equivalent combined) on bidirectional synaptic plasticity. Prenatal ethanol exposure resulted in a profound reduction in LTP but did not affect long-term depression. These findings show that prenatal ethanol exposure creates an imbalance in bidirectional synaptic plasticity. The third experiment sought to determine if prenatal ethanol exposure alters the affect of acute ethanol exposure in adulthood on synaptic plasticity. Acute exposure to ethanol in adulthood attenuated LTP in control offspring. Conversely, the magnitude of LTP was not affected by acute ethanol application in prenatal ethanol offspring. These results suggest that prenatal ethanol exposure alters the physiological response to ethanol in adulthood. Together, the results from the experiments undertaken in this thesis demonstrate long-lasting alterations in synaptic plasticity as the result of developmental ethanol exposure. Furthermore, these results allude to a malfunction of neural circuits within the hippocampal formation, perhaps relating to the learning and memory deficits observed in individuals with fetal alcohol spectrum disorders. / Graduate

Human Cytomegalovirus (HCMV) is the most common cause of congenital infection in newborns. One mechanism for this virus to reach the fetus is to cross the placenta through the syncytiotrophoblast layer. Accumulation and protection of pathogens in the syncytiotrophoblast could affect the systemic distribution of pathogens and prolong maternal infections leading to increased incidence of fetal infections. Primary infections, reactivation or reinfection with another strain during pregnancy are risk factors for intrauterine HCMV transmission to the fetus. All lead to an active infection; however, viral load in blood or urine does not correlate with intrauterine transmission. I have shown that HCMV reversibly binds to the syncytiotrophoblast in vitro, protecting it from degradation. Furthermore, I demonstrated in vivo that HCMV is present in the placenta, even when cleared from maternal blood and urine. This evidence suggests increased potential for fetal transmission by virtue of continued virus localized at the maternal-fetal interface.