Dissertationen zum Thema „Fetal“
Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an
Machen Sie sich mit Top-50 Dissertationen für die Forschung zum Thema "Fetal" bekannt.
Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.
Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.
Sehen Sie die Dissertationen für verschiedene Spezialgebieten durch und erstellen Sie Ihre Bibliographie auf korrekte Weise.
Cohen, Doron. „Human fetal phonocardiography and the detection of fetal activity“. Thesis, University of Cambridge, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235812.
Der volle Inhalt der Quelle冼世源 und Sai-yuen Sin. „Fetal cardiac function predicting fetal compromise: a prospective study“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31969823.
Der volle Inhalt der QuelleSin, Sai-yuen. „Fetal cardiac function predicting fetal compromise : a prospective study /“. Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21903566.
Der volle Inhalt der QuelleJaishankar, Gayatri. „Fetal Alcohol Syndrome“. Digital Commons @ East Tennessee State University, 1995. https://dc.etsu.edu/etsu-works/8867.
Der volle Inhalt der QuelleBarreira, Ana Raquel Matos Alves. „Hidrópsia fetal imune“. Master's thesis, Faculdade de Medicina da Universidade do Porto, 2010. http://hdl.handle.net/10216/61128.
Der volle Inhalt der QuelleProniaiev, D. V. „Fetal uterus anatomy“. Thesis, БДМУ, 2022. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/19329.
Der volle Inhalt der QuelleBarreira, Ana Raquel Matos Alves. „Hidrópsia fetal imune“. Dissertação, Faculdade de Medicina da Universidade do Porto, 2010. http://hdl.handle.net/10216/61128.
Der volle Inhalt der QuelleDamodaram, Mellisa. „Brain development in fetal growth restriction : a volumetric approach using fetal MRI“. Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9853.
Der volle Inhalt der QuellePrice, Robin Owen. „Maternal health and fetal brain development : altered fetal neurogenesis following maternal inflammation /“. May be available electronically:, 2009. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Der volle Inhalt der QuelleBeckett, 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.
Der volle Inhalt der QuelleEast, Christine Elizabeth. „Fetal intrapartum pulse oximetry /“. [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19387.pdf.
Der volle Inhalt der QuelleJoffe, Tracey Helene. „Fetal and infant encephalisation“. Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398119.
Der volle Inhalt der QuelleMcGinley, Susan. „Fetal Programming in Diabetes“. College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2010. http://hdl.handle.net/10150/622072.
Der volle Inhalt der QuelleCarneiro, Bruno Correia. „Sexagem Fetal por Ecografia“. Master's thesis, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/63715.
Der volle Inhalt der QuelleCarneiro, Bruno Correia. „Sexagem Fetal por Ecografia“. Dissertação, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/63715.
Der volle Inhalt der QuelleO'Connor, David. „The role of the fetal microenvironment in abnormal fetal haematopoiesis in Down syndrome“. Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/29169.
Der volle Inhalt der QuelleRuiz, Romero Aina. „Impacto de las cardiopatías congénitas en el sistema nervioso central“. Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/454999.
Der volle Inhalt der QuelleThis thesis is the summary of three studies carried out along the same line of work in relation to the role of angiogenic factors in the neurological development of foetuses with congenital heart diseases (CHD). Study 1: Placenta-related complications in women carrying a foetus with congenital heart disease Introduction: Recent studies pointed to an intrinsically angiogenic imbalance in CHD in the maternal and foetal circulation suggestive of impaired placentation. Objectives: To assess whether pregnant women with a CHD foetus are at greater risk of placenta-related complications. Methods: Perinatal results of women with a CDH foetus were compared with those of a nonselected population followed up at our centre. Results: 279 pregnancies with CHD foetuses were included. A significantly higher incidence of pre-eclampsia was observed in the CHD group compared with the normal population (5.7% vs 1.2% p< 0.0001). 9.7% of foetuses with CHD had < 3rd birth weight percentile compared with 3% for the normal population. A higher incidence of stillbirth was also observed in the CHD group compared with the normal population (2.5% vs 0.4%). Study 2: Longitudinal changes in fetal biometries and cerebroplacental haemodynamics in fetuses with congenital heart disease. Objectives: To determine the longitudinal behaviour of fetal biometries and cerebroplacental haemodynamics throughout gestation in fetuses with CHD. Methods: Fetal biometries and Doppler haemodynamic were serially measured in a cohort of consecutive fetuses diagnosed with CHD. Evaluations were made at various time points, from diagnosis (<25 weeks) to delivery. CHD fetuses were classified in 3 groups according to the expected pattern of brain blood supply. Results: 444 ultrasound examinations were performed on 119 CHD fetuses. CHD fetuses presented a small head at diagnosis (BPD -1.32 - 0.99 Zs, HC -0.79 - 1.02 Zs), which remained small throughout gestation. UtA and UA Doppler showed a significant increase towards the end of pregnancy, whereas no significant changes were observed in MCA or CPR with gestational age. Both MCA and CPR presented significant differences in longitudinal behaviour between CHD groups. Study 3: Brain angiogenic gene-expression in congenital heart disease Introduction: Increasing evidence support prenatal appearance of mechanisms that lead to poor neurodevelopmental outcome. Angiogenic unbalance has emerged as a possible contributor pathway in the pathogenesis of CHD. Objective: To analyze if differences exists in the expression of antiangiogenic and angiogenic factors as well as the genes of chronic hypoxia in cerebral tissue of euploid CHD compared to control fetuses. Methods: Gene expression profile was determined by real-time PCR quantification in brain tissue from 2 different areas: frontal cortex and basal ganglia and hypothalamus, obtained from 15 CHD and 12 control fetuses. Results: Both antiangiogenic/angiogenic factor mRNA expressions were significantly increased in the CHD group compared to controls in frontal cortex (sFlt-1, 48%, p=0.0431) and in basal ganglia and hypothalamus (sFlt-1, 72%, p=0.0369 and VEGF-A, 60%, p=0.0432). Conclusions: 1. Women carrying a foetus with CHD have a high risk of placenta-related complications (pre-eclampsia and IUGR). 2. CHD fetuses had smaller head biometries from the second trimester of pregnancy. Our results support the early onset appearance of mechanisms that could lead to a poorer neurodevelopment later in life in CHD cases. 3. CHD fetuses had and increasing resistance in UtA and UA Doppler suggestive of progressing degree of placental impairment. 4. An overall dysregulation of angiogenesis with a net balance towards an anti-angiogenic environment was observed in the cerebral tissue from fetuses with CHD, suggesting that CHD cases have an intrinsically-angiogenic impairment that could contribute to impaired brain perfusion and abnormal neurological development later in life.
GADELHA, Neylane Nyeria Coelho Batista. „Impactos do tratamento antimicrobiano no cérebro fetal devido a peritonite autógena fecal em ratas“. Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/21467.
Der volle Inhalt der QuelleMade available in DSpace on 2017-09-13T13:19:52Z (GMT). No. of bitstreams: 2 license_rdf: 811 bytes, checksum: e39d27027a6cc9cb039ad269a5db8e34 (MD5) NEYLANE - BIBLIOTECA.pdf: 8964969 bytes, checksum: 754bac3dafdb148836460ae5c4a86f75 (MD5) Previous issue date: 2016-02-24
Objetivo: Investigar a densidade neuronal do cérebro de ratos recém-nascidos cujas mães foram submetidas a peritonite autógena fecal e comparar com aqueles cuja mãe recebeu tratamento antimicrobiano agressivo. Métodos: Duas ratas prenhas se submeteram a peritonite com suspensão a 10% de fezes, na dose de 4 ml por quilograma, tendo uma recebido tratamento antimicrobiano venoso constituído por injeção de moxifloxacino na dose de 15 mg/kg e dexametasona na dose de 2,5 mg/kg (contidos em colírio de cloridrato de moxifloxacino a 0,5% e fosfato de dexametasona a 0,1%, além de dois mililitros de extrato alcoólico/aquoso da entrecasca de Schinus terebinthifolius raddi que foi injetada na cavidade abdominal. Ambos agentes antimicrobianos foram feitos 24 h após a indução da peritonite. Uma rata prenha não foi submetida a peritonite, nem intervenções, sendo caracterizada como grupo controle. Resultados: Os cérebros dos ratos recém-nascidos cujas mães receberam 4 ml/kg da suspensão de fezes a 10% evidenciaram menor tamanho e consistência mais amolecida do que aqueles das mães que tinham recebido tratamento antimicrobiano e os normais do grupo controle. A densidade neuronal do cérebro dos conceptos de mães não tratadas foi significantemente diminuída quando comparada com os grupos tratada e controle p < 0,01. Conclusão: Peritonite não tratada em ratas prenhas pode produzir dano cerebral nos conceptos. Tratamento efetivo precoce pode prevenir a diminuição da densidade neuronal do cérebro. A translação para humanos é que a infecção intra-abdominal em mulheres grávidas pode estar associada a dano cerebral nos conceptos. Isto pode ser prevenido usando abordagem terapêutica precoce e adequada.
Purpose: To investigate the neuronal density of newborn rat brain whose mothers were subjected to autogenously fecal peritonitis and compare with those whose mothers received aggressive antimicrobial treatment. Methods: Two pregnant rats underwent peritonitis with a 10% suspension of feces at a dose of 4 ml per kilogram. One of them received intravenous antimicrobial treatment consisting of a combination of moxifloxacin at a doses of 15 mg/kg and dexamethasone at a doses of 2.5 mg/kg as an eye drop solution (moxifloxacin cloridrat 0,5% and dexamethasone phosphate 0.1%), in addition of two milliliters of alcohol/aqueous extract of the inner bark of Schinus terebinthifolius raddi which was injected into the abdominal cavity. Both antimicrobial agents were injected 24 h after the induction of peritonitis. One pregnant rat didn’t receive peritonitis or treatment. It was reported as control group. Results: The brains of newborn rats whose mothers were given 4 ml / kg of 10% fecal suspension evidenced smaller and softer consistency than those from mothers that had received antimicrobial therapy and normal control group. The neuronal density in the brains of untreated fetuses mothers was significantly reduced when compared with the control and treated groups p <0.01. Conclusion: Peritonitis untreated in pregnant rats can produce brain damage. Early effective treatment can prevent the decrease of neuronal densities in the brain. The translation to human is the intra-abdominal infection in pregnant women may be associated with brain damage in her concepts. This can be prevented by using early and appropriate therapeutic approach.
Mäkikallio, K. (Kaarin). „Placental insufficiency and fetal heart: Doppler ultrasonographic and biochemical markers of fetal cardiac dysfunction“. Doctoral thesis, University of Oulu, 2002. http://urn.fi/urn:isbn:9514267370.
Der volle Inhalt der QuelleMassey, Valerie J. „Listening to the voiceless ones, women with fetal alcohol syndrome and fetal alcohol effect“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq21597.pdf.
Der volle Inhalt der QuelleVugt, Johannes Marinus Gerardus van. „Fetal artery Doppler velocimetry a study in the human fetus and the fetal lamb /“. Maastricht ; Rijksuniversiteit Limburg ; Maastricht : University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5436.
Der volle Inhalt der QuelleFinning, Kirstin M. „Prediction of fetal RhD blood group status using fetal genetic material in maternal blood“. Thesis, University of the West of England, Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275889.
Der volle Inhalt der QuelleDoro, Giovana Farina. „Avaliação da vascularização renal fetal em gestações de fetos com restrição de crescimento fetal“. Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-05012016-163757/.
Der volle Inhalt der QuelleINTRODUCTION: The association between intrauterine growth restriction (IUGR) and renal alterations refers to issues such as the relation between reduced renal vascularization in these fetuses and the fetal hemodynamics during pregnancy, which were not sufficiently investigated so far. Considering that the primary cause of nefrons reduction in these fetuses would be the renal hypoflow caused by the redistribution of the fetal hemodynamics resulting from hypoxic stimuli, it would be expected that the severety of the fetal impairment could result in worse renal vascularization in IUGR fetuses. OBJECTIVES: This study aimed at evaluating IUGR fetuses in order to (1) describe the pulsatility index of renal arteries, the renal volume and the renal vascularization indexes, as well as (2) verify correlations of the doppler findings in the umbilical arteries, middle cerebral artery, and venous duct with the pulsatility index of the renal arteries, the renal volume, and the renal vascularization indexes (VI, FI, VFI), and of the pulsatility index of the renal arteries, the renal volume, and the renal vascularization indexes with the amniotic liquid index. METHODS: 81 fetuses with IUGR were assessed with tridimentional power doppler in order to determine data regarding the pulsatility index of the renal arteries, the renal volume, the renal vascularization indexes, the pulsatility indexes of umbilical arteries, middle cerebral artery and venous duct, and the amniotic liquid index. Data were undertaken to statistical analysis for establishing eventual correlations among such assessed parameters. RESULTS: Pulsatility index of renal arteries ranged from 1.50 to 3.44 (median of 2.39 + 0.41); renal volume ranged from 1.90 to 18.90 (median of 8.54 + 3.43); renal VI ranged from 0.05 to 7.75 (median of 1.57 + 1.58); renal FI ranged from 19.04 to 40.0 (median of 28.29 + 5.06); and renal VFI ranged from 0.03 to 5.18 (median of 0.96 + 1.3. There was no correlation between the pulsatility index of renal arteries and the pulsatility indexes of the umbilical arteries, middle cerebral artery, and venous duct; correlations were not observed as well between the renal volume and the pulsatility indexes of the umbilical arteries, middle cerebral artery, and venous duct. Renal VI and VFI correlated negatively with the pulsatility index of the venous duct, and positively with the amniotic liquid index. There was no correlation betweem renal vascularization indexes and doppler findings in umbilical arteries and in middle cerebral artery, neither between pulsatility index of renal arteries, renal volume and renal FI and the amniotic liquid index. CONCLUSION: The pulsatility index of the venous duct was better predictive of alterations in renal vascularization index, suggesting that such alterations are more evident in IUGR fetuses with more severe hemodynamic impairments
Fritsch, Alessandra. „Hidropisia fetal não-imune : efeito da presença de cromossomopatia na mortalidade fetal e neonatal“. reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2004. http://hdl.handle.net/10183/5209.
Der volle Inhalt der QuelleFox, Alice J. Sophia Women's & Children's Health Faculty of Medicine UNSW. „Non-invasive procedure for fetal electrocardiography“. Awarded by:University of New South Wales. Women's & Children's Health, 2007. http://handle.unsw.edu.au/1959.4/41240.
Der volle Inhalt der QuelleCoşar, Fatma Sulak Osman. „Fetal dönem boyunca uterusun gelişimi /“. Isparta : SDÜ Sağlık Bilimleri Enstitüsü, 2004. http://tez.sdu.edu.tr/Tezler/TT00158.pdf.
Der volle Inhalt der QuelleEvcil, E. Hilal Malas Mehmet Ali. „Fetal dönem boyunca Diaphragma gelişimi /“. Isparta : SDÜ Sağlık Bilimleri Enstitüsü, 2005. http://tez.sdu.edu.tr/Tezler/TT00205.pdf.
Der volle Inhalt der QuelleDalton, Paola. „Maternal antibodies to fetal antigens“. Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270344.
Der volle Inhalt der Quelle黃康素 und Hong-soo Wong. „First trimester fetal echocardiographic normogram“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970813.
Der volle Inhalt der QuelleDonovan, Christine M. „Statistical aspects of fetal screening“. Thesis, University of Plymouth, 1995. http://hdl.handle.net/10026.1/2265.
Der volle Inhalt der QuelleHaigh, R. M. „Urogastrone and fetal lung maturation“. Thesis, University of Manchester, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377734.
Der volle Inhalt der QuelleDeng, Jing. „Dynamic three-dimensional fetal echocardiography“. Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412515.
Der volle Inhalt der QuelleKyriakopoulou, Vanesa. „Brain development in fetal ventriculomegaly“. Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11086.
Der volle Inhalt der QuelleSmith, Gordon C. S. „The expression of prostanoid receptor genes in uterine and fetal tissues : studies in the maternal and fetal baboon and the fetal and neonatal lamb“. Thesis, University of Glasgow, 2000. http://theses.gla.ac.uk/40962/.
Der volle Inhalt der QuelleGuszkowski, Andrea Jean. „Positive Patient Responses Regarding the Multidisciplinary Approach to Treatment of High Risk Pregnancies with Fetal Anomalies“. University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1179845686.
Der volle Inhalt der QuelleYoo, Sun Dong. „Maternal-fetal disposition, fetal pharmacodynamics and comparative pharmacokinetics of diphenhydramine in pregnant and nonpregnant sheep“. Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/29325.
Der volle Inhalt der QuellePharmaceutical Sciences, Faculty of
Graduate
Zavala, Coca Carlos Alberto. „Flujo venoso fetal e índice cerebro placentario como indicadores de hipoxia fetal en gestantes preeclámpticas severas“. Doctoral thesis, Universidad Nacional Mayor de San Marcos, 2010. https://hdl.handle.net/20.500.12672/1343.
Der volle Inhalt der QuelleObjective: To ascertain the value of cerebral-placental ratio and the abnormal fluxo of Aranzio´s Ductus Venous and for identifying newborns with neonatal morbidity in pregnancies complicated by severe preeclampsia. Study Design: A longitudinal and correlational study of 160 patients with severe preeclampsia (PA > 160/110, proteinuria 3+) was performed Doppler study done by one operador within 7 days before delivery. An abnormal cerebral-placental ratio and abnormal resistance and pulsabilility index of ductus venous were used to identificate fetal asphixia (cardiac insuficiency). The results belong 5 percentile were considered abnormal. These results were matched with perinatal results considered as abnormal. Results: Maternal characteristic were: age 33, parity 1, primigravid 45%, prenatal care 85%, gestational age at enrollment 35,1 weeks. The probability of detection IUGR is 65% and oligohydramnios 61,2%. Conclusion: The cerebral-placental ratio and abnormal fluxo of Aranzio´s Ductus venous identifies 65 % or more of the newborns with severe neonatal morbidity in pregnancies with severe preeclampsia.
Tesis
Zabihi, Sheller. „Fetal Outcome in Experimental Diabetic Pregnancy“. Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8739.
Der volle Inhalt der QuelleWomen with pregestational diabetes have a 2-5 fold increased risk of giving birth to malformed babies compared with non-diabetic women. Diabetes-induced oxidative stress in maternal and embryonic tissues has been implicated in the teratogenic process. The malformations are likely to be induced before the seventh week of pregnancy, when the yolk sac is partly responsible for the transfer of metabolites to the embryo, and the uterine blood flow to the implantation site determines the net amount of nutrients available to the conceptus. We aimed to evaluate the effect on embryogenesis caused by a diabetes-induced disturbance in yolk sac morphology, uterine blood flow or altered maternal antioxidative status in conjunction with a varied severity of the maternal diabetic state.
We investigated to which extent maternal diabetes with or without folic acid (FA) supplementation affects mRNA levels and protein distribution of ROS scavenging enzymes (SOD, CAT, GPX), vascular endothelial growth factor-A (Vegf-A), folate binding protein-1 (Folbp-1), and apoptosis associated proteins (Bax, Bcl-2, Caspase-3) in the yolk sacs of rat embryos on gestational days 10 and 11. We found that maternal diabetes impairs, and that FA supplementation restores, yolk sac vessel morphology, and that maternal diabetes is associated with increased apoptotic rate in embryos and yolk sacs, as well as impaired SOD gene expression. We assessed uterine blood flow with a laser-Doppler-flow-meter and found increased blood flow to implantation sites of diabetic rats compared with controls. Furthermore, resorbed and malformed offspring showed increased and decreased blood flow to their implantation sites, respectively. In mice with genetically altered CuZnSOD levels, maternal diabetes increased embryonic dysmorphogenesis irrespective of CuZnSOD expression. We thus found the maternal diabetic state to be a major determinant of diabetic embryopathy and that the CuZnSOD status exerts a partial protection for the embryo in diabetic pregnancy.
Drake, Amanda J. „The intergenerational consequences of fetal programming“. Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24536.
Der volle Inhalt der QuelleGazca, Lizzette. „Fetal Rights Regarding Prenatal Substance Abuse“. Scholarship @ Claremont, 2018. http://scholarship.claremont.edu/cmc_theses/1751.
Der volle Inhalt der QuelleDoğan, Şevkinaz Malas Mehmet Ali. „Fetal dönemde el ve ayak gelişimi /“. Isparta : SDÜ Sağlık Bilimleri Enstitüsü, 2004. http://tez.sdu.edu.tr/Tezler/TT00157.pdf.
Der volle Inhalt der QuelleCankara, Neslihan Sulak Osman. „İnsan fetuslarında fetal dönemde mesane gelişimi /“. Isparta : SDÜ Sağlık Bilimleri Enstitüsü, 2005. http://tez.sdu.edu.tr/Tezler/TT00204.pdf.
Der volle Inhalt der QuelleCrittenden, Mark E. „Real-time intrapartum fetal electrocardiogram analysis“. Thesis, University of Nottingham, 1997. http://eprints.nottingham.ac.uk/27969/.
Der volle Inhalt der QuelleAiken, Catherine Elizabeth Margaret. „A mitochondrial role in fetal programming?“ Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613207.
Der volle Inhalt der QuelleChan, Shiao-yng. „Thyroid status and fetal brain development“. Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418887.
Der volle Inhalt der QuellePeasgood, William. „Enhancement of the abdominal fetal electrocardiogram“. Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335851.
Der volle Inhalt der QuelleMurray, Henry G. „Evaluation of the fetal electrocardiogram (ECG)“. Thesis, University of Nottingham, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297895.
Der volle Inhalt der QuelleBartlett, M. L. „Automatic analysis of intrapartum fetal monitoring“. Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377449.
Der volle Inhalt der QuelleThomas, Margot Ross. „Fetal cells in the maternal circulation“. Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363337.
Der volle Inhalt der QuellePurnell, Sasha Justine. „Fetal dosimetry from natural alpha emitters“. Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311370.
Der volle Inhalt der Quelle