Thematische Bibliographien / Maternal physiology

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Auswahl der wissenschaftlichen Literatur zum Thema „Maternal physiology“

Autor: Grafiati

Veröffentlicht am 24. Juni 2021

Zuletzt aktualisiert am 12. Februar 2022

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Zeitschriftenartikel zum Thema "Maternal physiology"

Jansson, Lauren M., Martha L. Velez, Krystle McConnell, Lorraine Milio, Nancy Spencer, Hendree Jones und Janet A. DiPietro. „Maternal buprenorphine treatment during pregnancy and maternal physiology“. Drug and Alcohol Dependence 201 (August 2019): 38–44. http://dx.doi.org/10.1016/j.drugalcdep.2019.03.018.

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BLECHNER, JACK N. „Maternal-Fetal Acid- Base Physiology“. Clinical Obstetrics and Gynecology 36, Nr. 1 (März 1993): 3–12. http://dx.doi.org/10.1097/00003081-199303000-00004.

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STERRETT, MARY. „Maternal and Fetal Thyroid Physiology“. Clinical Obstetrics and Gynecology 62, Nr. 2 (Juni 2019): 302–7. http://dx.doi.org/10.1097/grf.0000000000000439.

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Goulopoulou, Styliani. „Maternal Vascular Physiology in Preeclampsia“. Hypertension 70, Nr. 6 (Dezember 2017): 1066–73. http://dx.doi.org/10.1161/hypertensionaha.117.08821.

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Heidemann, Bernhard H., und John H. McClure. „Changes in maternal physiology during pregnancy“. BJA CEPD Reviews 3, Nr. 3 (Juni 2003): 65–68. http://dx.doi.org/10.1093/bjacepd/mkg065.

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Taylor, Lucy, Brenda Kelly und Paul Leeson. „Maternal Smoking and Infant Cardiovascular Physiology“. Hypertension 55, Nr. 3 (März 2010): 614–16. http://dx.doi.org/10.1161/hypertensionaha.109.146944.

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Kadic, Aida Salihagic, und Maja Predojevic. „Fetal and Maternal Physiology and Ultrasound Diagnosis“. Donald School Journal of Ultrasound in Obstetrics and Gynecology 7, Nr. 1 (2013): 9–35. http://dx.doi.org/10.5005/jp-journals-10009-1267.

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ABSTRACT Fetal developmental potential is determined at the moment of conception by genetic inheritance. However, this development is modulated by environmental factors. It is important to recognize that both, the mother and the fetus, actively participate in the maintenance of the physiological intrauterine environment. Unfortunately, the fetus is not entirely protected from harmful influences of the external factors. By altering the intrauterine environment, these factors can have a long-term effect on fetal health. How to cite this article Kadic AS, Predojevic M, Kurjak A. Fetal and Maternal Physiology and Ultrasound Diagnosis. Donald School J Ultrasound Obstet Gynecol 2013;7(1):9-35.

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Hauth, John C. „Oral Concurrent Session A Maternal Fetal Physiology“. American Journal of Obstetrics and Gynecology 170, Nr. 1 (Januar 1994): 268–70. http://dx.doi.org/10.1016/s0002-9378(94)01022-7.

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Norwitz, Errol R., Valentine Edusa und Joong Shin Park. „Maternal Physiology and Complications of Multiple Pregnancy“. Seminars in Perinatology 29, Nr. 5 (Oktober 2005): 338–48. http://dx.doi.org/10.1053/j.semperi.2005.08.002.

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Miller, Margaret, und Amanpreet Kaur. „General Management Principles of the Pregnant Woman“. Seminars in Respiratory and Critical Care Medicine 38, Nr. 02 (April 2017): 123–34. http://dx.doi.org/10.1055/s-0037-1602167.

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AbstractPregnancy is a dynamic process that consists of profound physiological changes mediated by hormonal, mechanical, and circulatory pathways. Understanding of changes in physiology is essential for distinguishing abnormal and normal signs and symptoms in a pregnant patient. These physiological changes also have important pharmacotherapeutic considerations for a pregnant patient. Although there are limited data to guide decisions regarding medications and diagnostic procedures in pregnancy, a careful review of risks should be balanced with review of risk of withholding a medication or procedure. Interventional pulmonary procedures can be safely performed in pregnant women while keeping in mind the maternal anatomic and physiologic changes. Furthermore, management of a maternal cardiopulmonary arrest requires important modifications in patient positioning and intravenous access to ensure adequate efficacy of chest compressions, circulation, and airway management. This review will provide an overview of maternal physiologic changes with a focus on cardiopulmonary physiology, pharmacotherapeutic considerations, diagnostic and interventional pulmonary procedures during pregnancy, and cardiopulmonary resuscitation in pregnancy.

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Dissertationen zum Thema "Maternal physiology"

McAllister, Kelli. „Effect of maternal care on maternal responsiveness and astrocyte plasticity in the medial amygdala and medial preoptic nucleus in the rat“. Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112541.

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Estrogen acts on maternal circuitry to establish maternal behaviour in otherwise non-maternal rats. The precise mechanisms by which estrogen primes maternal circuitry are unknown; however, the medial preoptic area (MPOA) stimulates maternal behaviour whilst the medial amygdala (MeA) inhibits it. This thesis aimed to address the link between estrogen sensitivity, astroglia and maternal behaviour. Maternal care influences maternal behaviour of female offspring. One mechanism underlying this influence is differential estrogen sensitivity within the MPOA. Estrogen receptor alpha (ERalpha) expression was examined in offspring of High and Low licking/grooming (LG) dams within the MPOA. Enhanced expression ERalpha was limited to the medial preoptic nucleus in offspring of High LG dams and the anteroventral periventricular nucleus in Low LG dams. Adult nulliparous offspring of High and Low LG dams were assessed for maternal responsiveness using the pup sensitization paradigm. Offspring of Highs showed maternal behaviour significantly earlier than offspring of Lows. Brains of pup-exposed and pup-naive High and Low offspring were analyzed for astroglial markers glial fibrillary acidic protein (GFAP) and glutamine synthetase. Pup-naive animals showed more GFAP positive cells within the posteroventral MeA, with no differences within the MPOA and no effect of maternal care. Glutamine synthetase, a glial-derived enzyme necessary for glutamate production, showed greater expression within the MeA of High LG pup-naive animals; with no maternal care differences observed in pup-experienced animals. Thus, long-lasting changes within maternal circuitry established in early life are reflected in regionally specific enhanced estrogen sensitivity and latency to display maternal behaviour, but the effects are less clear with respect to astroglia.

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Doherty, N. Nicola. „Neurobehavioural effects of maternal diabetes on the fetus“. Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388050.

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Robertson, Anthony J. „Hormonally mediated maternal effects in birds“. Thesis, University of Glasgow, 2009. http://theses.gla.ac.uk/803/.

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The main aim of this thesis was to investigate the effects of environmental conditions, particularly unpredictable or potentially negative ones, on the maternal transmission of the primary avian stress hormone, corticosterone, to developing embryos. We currently lack information on the extent to which conditions in the maternal environment are transmitted to the offspring in birds via egg compositional changes. It is possible that maternally derived hormonal signals communicate information about the external environment to developing embryos and directly influence the fitness of their offspring in a negative or positive way. I found, using captive zebra finches, that the experimental stressor of unpredictable food availability (as these birds are used to ad libitum food) experienced by mothers can elevate yolk CORT concentrations, but only when combined with the additional demand of laying a replacement clutch (potentially a buffering system to prevent mild stressors impacting on CORT transmission to the embryo). I then looked at yolk CORT concentrations in two populations of gulls (herring and lesser black-backed gulls) in which the population trajectories differed depending on environmental conditions (potentially a reflection of different exposures to stressful stimuli). The results however did not support this hypothesis, as there were no differences according to habitat type or between species (where they coexist). This would suggest that the different environmental circumstances (harsher for the herring gull) experienced by these two species are not reflected in differences in their eggs (at least in terms of CORT). This could be the result of the eggs being buffered from the maternal CORT environment or it may be that the difficult environmental conditions are not occurring during the breeding season. We also identified that experimental human disturbance during the laying period does not appear to elevate yolk CORT concentrations, although there was a trend for concentrations to be higher following the loss of the first clutch in the herring gull (as seen in the zebra finches). I also measured yolk CORT concentrations in Common Eider eggs and looked for differences according to the degree of nest shelter. I found no relationship between shelter and yolk CORT, but birds that laid in more sheltered sites had, on average, smaller eggs. This may indicate lesser quality birds are nesting in the sheltered sites and that yolk CORT is not affected by maternal condition. Finally, I looked at another mechanism through which information relating to the maternal environment could be transferred to the embryo. I investigated whether there were any links between maternally derived immunity and CORT by comparing the anti-microbial lysozyme and CORT concentrations in the albumen. I found no correlation between CORT and lysozyme, suggesting that CORT may not affect lysozyme production. It may be that other factors such as colony density and ‘cleanliness’ are more important in determining the concentrations of lysozyme deposited in the egg or that lysozyme production is not sufficiently costly to be influenced by the maternal stress state. The overall theme of my findings is that CORT concentrations in eggs do not appear to vary much with maternal environments. I will discuss these findings in their broader ecological and evolutionary context and discuss if stress hormones are indeed being used as adaptive signals for preparing the embryo for its postnatal environment.

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Woo, Chit-shing Jackson, und 胡哲誠. „Ochratoxin A: endocrine disruption potential,transplacental kinetics and maternal exposure assessment“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B4979954X.

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Mycotoxin contamination in food commodities is an age-old problem. Due to the detrimental impact of mycotoxins on human health, exposure to mycotoxins and their health implications have been increasingly recognized. Ochratoxin A (OTA), one of the mycotoxins, has been found to cause diverse toxicities in animals, with potential impact on human health. OTA has been reported to be teratogenic and interfere with steroidogenesis in vivo. Chronic exposure of pregnant women to OTA may be hazardous for the human foetus, especially when endocrine and developmental toxicities are taken into consideration. Accordingly, in the first part of this project, I hypothesized that OTA may interfere with enzymes involved in human placental steroidogenesis. By evaluation of human placental 3β–hydroxysteroid dehydrogenase/isomerase (3β-HSD) at both mRNA and protein (hormonal) levels, my results showed that OTA could up-regulate 3β-HSD1 expression in human placental cells with concentration relevant to human exposure. This study is the first to report the endocrine disruption potential of OTA in human placental cells. As several mycotoxins have been demonstrated previously to cross human placental barrier and OTA has been associated with developmental toxicity in vivo, I further hypothesized that OTA may be transferred through human placenta and accumulate in foetal compartment. In the second part of this project, human perfused placenta was used to investigate the placental toxicokinetics of OTA using concentrations found in serum of pregnant women. Findings from this study clearly showed that the transfer of OTA through term human placenta was minimal, contradicting the existing epidemiological studies reporting higher foetal OTA levels than maternal. This is the first study where transplacental kinetics of OTA has been studied in human perfused placenta. To assess the relevance of the study findings, it is very important to provide information on maternal OTA exposure during pregnancy. Currently there is limited information regarding OTA exposure of pregnant women. The third part of this project aimed at evaluating the frequency and level of exposure to OTA in pregnant women from Egypt, where exposure to dietary mycotoxins is common due to the environmental conditions. Biomonitoring of both serum and urinary OTA levels showed that more than 70% of pregnant women were exposed to OTA with a geometric mean of 0.27 ng/ml in serum and 37.21 pg/mg creatinine in urine indicating frequent exposure of this subpopulation. As an ultimate aim, maternal-foetal risk assessment served as a conclusive part of this project to predict and evaluate both maternal and foetal risk of exposure to OTA during pregnancy. Data from the exposure of pregnant women in Egypt to OTA were further ultilized to conduct maternal-foetal risk assessment in relation to OTA exposure. Based on the refined Klaassen equation for exposure estimation during pregnancy and the benchmark dose approach for risk assessment, this subpopulation of pregnant women generally was not exposed to OTA in a high-risk manner. However, considering the suspected chronic exposure beginning from early pregnancy with high foetal susceptibility and diverse toxic effects, and in particular the potential endocrine disruption of OTA, keeping OTA exposure to a minimum is recommended.
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Biological Sciences
Doctoral
Doctor of Philosophy

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Bagot, Catherine Nancy. „An investigation of the role of maternal hoxiao in embryonic implantation“. Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250192.

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Burton, Nicholas O. (Nicholas Oscar). „Maternal environment and offspring physiology : the inheritance of information across a generation“. Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/111294.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2017.
Cataloged from PDF version of thesis.
Includes bibliographical references.
From the 4th century BC until the late 19th century AD philosophers and biologists ranging from Hippocrates to Charles Darwin hypothesized that information about the environment could be passed from parents to progeny. However, in 1893, German biologist August Weismann tested these hypotheses and based on his observations concluded that information about the environment could not be transmitted from parents to progeny. Weismann's hypothesis became known as the Weismann barrier and served as one of the founding pillars of modern evolutionary synthesis, which postulates that genetic and phenotypic variability in plant and animal populations are brought about by genetic recombination resulting from sexual reproduction and random mutations. Nonetheless, throughout the 20th century there have been several observations of plants and animals where parental exposure to environmental stress modified offspring physiology. These changes in progeny physiology sometimes enhanced progeny survival in response to repeated environmental stress, suggesting that information about the environment might be passed from parent to progeny. The mechanisms by which parental environment can alter progeny physiology to enhance survival remain unknown. To explore such mechanisms I investigated how parental exposure of the nematode C. elegans to osmotic stress affects its progeny's response to continued osmotic stress. First, I found that C. elegans arrests its development during periods of osmotic stress to enhance survival and that this developmental arrest is caused by a loss of insulin-like signaling to the intestine. I then discovered that exposure of parents to mild osmotic stress enhances progeny resistance to osmotic stress and determined that this adaptation is the result of a loss of insulin-like signaling to the maternal germline, which results in increased expression of the glycerol biosynthetic enzyme GPDH-2 in embryos; the increased GPDH-2 expression results in increased glycerol production, which in turn protects progeny from osmotic stress. These results indicate that insulin can cross the Weismann barrier and suggest that changes in maternal insulin signaling might be responsible for effects of the maternal environment on human diseases that involve insulin signalling, such as obesity and type-2 diabetes. From a screen for mutants that fail to arrest development in response to osmotic stress I identified the cytosolic sulfotransferase SSU-1 and found that SSU-1 functions in the ASJ sensory neurons to control development and insulin-sensitivity in response to osmotic stress.
by Nicholas O. Burton.
Ph. D.

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Dakin, Rachel Sarah. „Effects of postnatal and maternal diet-induced obesity on physiology and vascular function“. Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/8256.

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In recent years there has been an explosion in the rates of obesity, defined as a body mass index greater than 30kg/ m2, and associated cardiovascular disease. Alterations in peripheral glucocorticoid metabolism have been suggested to play a role in the development of obesity. Obesity occurs in both sexes, but the risk of associated metabolic disturbance and vascular dysfunction is greater in men. Although there is no accepted definition of obesity in rodents, the term is used to describe animals with a significant increase in fat pad mass often achieved by feeding a high fat diet. Although animal models of obesity have been useful in delineating potential mechanisms linking obesity with its metabolic and vascular sequelae, most studies have been in male animals and, thus, have not addressed sex differences. Additionally, emerging evidence shows that obesity during pregnancy is associated with increased cardio-metabolic and vascular disease in offspring, although the processes underlying such ‘programming’ effects are unclear. This thesis addresses the hypothesis that exposure to postnatal, or maternal obesity will alter both metabolism and vascular function in mice. Male and female mice maintained on a high fat and sugar diet from 5 weeks of age had increased adipose tissue deposition in adulthood. However there were striking sex differences in glucose homeostasis, mRNA levels and glucocorticoid metabolism, with males being more severely affected. Treatment of male mice with 17β-estradiol ameliorated a number of the effects of the high fat diet, including weight gain and altered glucose homeostasis; additionally estradiol altered glucocorticoid metabolism in the adipose so that it resembled that of females. Suprisingly, given the changes in metabolism, obesity in adult mice produced only small changes in vascular function and did not alter vascular remodelling following injury. The effects of maternal obesity were studied using male offspring aged 3 and 6 months. The offspring of obese mothers had similar body weight, adiposity, plasma lipid and plasma hormone concentrations to controls. In contrast, exposure to obesity in utero was associated with receptor specific changes in agonist-mediated contraction and decreased endothelium-dependent relaxation in male offspring. Despite these changes in vascular function, no alterations in blood pressure or vascular remodelling following injury were present. These results demonstrate that the more profound changes in glucose-insulin homeostasis associated with obesity in male humans can be recapitulated in rodent models and imply that estradiol plays a role in protecting the metabolism of female mice, potentially by alteration of glucocorticoid metabolism. Despite altered metabolism in postnatal obesity vascular function remained normal suggesting metabolic and vascular dysfunction are not intrinsically linked. Conversely, maternal obesity did not cause any overt changes in offspring metabolism but caused vascular dysfunction implying these parameters can be programmed independently.

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Calley, John Nels 1961. „The Drosophila maternal-effect mutantcappuccino and its interactors“. Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/288825.

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cappuccino (capu) is a Drosophila melanogaster gene required for establishing the dorsal-ventral and anterior-posterior axes of the developing egg and embryo. Egg chambers mutant for capu exhibit cytoplasmic streaming during mid-oogenesis that does not normally occur until late oogenesis. All known capu alleles stream at the same speed. Since capu alleles do differ in their effects on the dorsal-ventral axis, it is unlikely that premature streaming is a cause of the dorsal-ventral defects. Premature streaming may, however, cause the posterior defects. Streaming occurs at the same speed if isolated egg chambers are treated with the actin depolymerizing drug cytochalasin D, which suggests that CAPU may act in the actin cytoskeleton. A screen for proteins which physically interact with CAPU identified profilin, a regulator of the actin cytoskeleton as a probable partner of CAPU. This again suggests that CAPU acts in the actin cytoskeleton. CAPU is a member of the formin homology (FH) family of proteins. Sequence analysis of this family makes it possible to multiply align all family members throughout their carboxy-terminal halves. This makes possible better predictions of secondary structure, phylogenetic analysis, and identification of novel regions of conserved sequence. Analysis of the amino-terminal halves suggests that significant alignment is also possible in these more highly divergent regions. Members of the rho family of small GTPases have been implicated in the regulation of the actin cytoskeleton. They physically associate with members of the FH family, including CAPU. All four rho-like proteins tested associate with CAPU in the Interaction Trap system. There are also indications of genetic interactions between capu and the rho-like genes dcdc42 and drac1.

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Astbury, Stuart M. „The influence of maternal diet on intestinal adaptation in the mother and offspring“. Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/31390/.

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The effect of maternal nutrition on fetal and offspring growth and risk of disease in later life is well established. Animal models have shown that the small intestine can be preferentially affected by growth restriction compared with other organs, yet the effect of maternal diet on gastrointestinal (GI) development has not been well studied. Furthermore, both the maternal GI tract and microbiome undergo significant adaptations during pregnancy in response to the increased nutritional demands of the growing fetus, which may be further modulated by the maternal diet. Inadequate development of the GI tract may result in an increase in intestinal permeability, as demonstrated in inflammatory bowel diseases. Compromised gut barrier function has been linked to the development of obesity through the passage of endotoxin on Gram-negative bacteria leading to low-level inflammation of the liver and adipose tissue. The aim of this thesis was to use two animal models of maternal dietary manipulation that are representative of suboptimal nutrition characterised by the nutritional excess of macronutrients found in many Western diets. The effect of either fat in the form of palm oil and carbohydrate in the form of fructose were therefore examined with particular focus on the gut. This was undertaken in a pig model to examine the effects around the time of birth and in the juvenile offspring, whilst in a rat model both the mothers and offspring were studied. Addition of 10% fructose to drinking water in two generations of pregnant Wistar rats induced impaired glucose tolerance and raised serum triglycerides, but only in the second generation. Sequencing of the maternal microbiome in first generation dams through pregnancy revealed significant changes in microbial diversity from pre-mating to late pregnancy, both between and within dams. Consumption of the fructose diet led to further changes in microbial diversity. Offspring of fructose-fed mothers were growth restricted and had significantly shorter small intestines compared to controls. Changes in gene expression in the ileum and jejunum were indicative of raised intestinal permeability in second-generation dams, and included the epithelial tight junction genes occludin (OCLN), claudin (CLDN) and junctional adhesion molecule (JAM). In both generations the fructose diet significantly upregulated glucose transporters 2 and 5, and sodium-glucose linked transporter 1 in the ileum and jejunum suggesting that a relatively low level supplementation of fructose gradually increases the absorptive capacity of the small intestine for both glucose and fructose. This may explain the significantly impaired glucose tolerance and insulin resistance observed in second-generation offspring. To study maternal fat supplementation, sows were fed a standard commercial diet supplemented with palm oil (6.6% added to commercial feed) throughout gestation. Median birth weight offspring born to fat supplemented mothers sampled at 7 days demonstrated no growth restriction, but significant downregulation in OCLN, CLDN and JAMA expression, suggesting increased intestinal permeability. No changes in offspring body composition were observed at either time point, and effects on gene expression did not persist up to 6 months of age. In conclusion, a suboptimal diet through pregnancy in which macronutrient composition is raised has the potential to compromise gut function in the mother and offspring. The magnitude of effect can however be temporary and dependent on the animal model used as well as the macronutrient targeted.

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Girsén, A. (Anna). „Preeclampsia and maternal type-1 diabetes: new insights into maternal and fetal pathophysiology“. Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514291104.

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Abstract Abnormal placentation is associated with preeclampsia and placental insufficiency, both of which increase the risk for fetal growth restriction. So far the early recognition of the risk population for preeclampsia has been problematic. The first hypothesis of this study was that in preeclampsia, the maternal serum proteomic profile is different from that in uncomplicated pregnancies, and this difference is detectable already in early pregnancy. The findings of this study demonstrate that in clinical preeclampsia the maternal serum proteomic profile is different from that in uncomplicated pregnancies with increased levels of placental proteins and antiangiogenic factors in pregnancies with clinical preeclampsia. Furthermore, the early pregnancy maternal serum proteomic profile in women who later develop preeclampsia revealed a distinct and different pattern compared with the profile in clinical preeclampsia. In early pregnancy, the differentially expressed proteins belong to placental proteins, vascular and/or transport proteins and matrix and/or acute phase proteins, while angiogenic and antiangiogenic proteins were not significantly expressed in early pregnancy. Preeclampsia, placental insufficiency, fetal growth restriction and type-1 diabetes may have an impact on fetal cardiovascular hemodynamics. The second hypothesis in this thesis was that in placental insufficiency, abnormalities in fetal cardiovascular status correlate with biochemical markers of cardiac dysfunction and chronic hypoxia. In placental insufficiency, increases in fetal N-terminal pro-atrial (NT-proANP) and pro-B-type natriuretic peptide (NT-proBNP) and in fetal erythropoietin concentrations were related to increased pulsatility in the fetal umbilical artery and descending aorta. In addition, these fetuses demonstrated increased pulsatility in their systemic venous blood velocity waveforms. Thus, in placental insufficiency, biochemical markers of cardiac dysfunction and chronic hypoxia are associated with signs of increased fetal cardiac afterload and systemic venous pressure. Increased NT-proANP and NT-proBNP levels were also detected in fetuses of type-1 diabetic mothers with normal umbilical artery velocimetry. In these pregnancies, NT-proANP and NT-proBNP levels were related to poor maternal glycemic control during early pregnancy.

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Bücher zum Thema "Maternal physiology"

Maternal physiology. Washington, D.C: Council on Resident Education in Obstetrics and Gynecology, 1985.

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P, Belfort, Pinotti José Aristodemo 1934- und Eskes, T. K. A. B., Hrsg. Maternal physiology and pathology. Carnforth, Lancs, UK: Parthenon Pub. Group, 1989.

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Maternal, fetal & neonatal physiology: A clinical perspective. 2. Aufl. St. Louis, MO: Saunders, 2003.

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Maternal, fetal, & neonatal physiology: A clinical perspective. 4. Aufl. Amsterdam: Elsevier Saunders, 2013.

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Lee, Loper Donna, Hrsg. Maternal, fetal, and neonatal physiology: A clinical perspective. Philadelphia: Saunders, 1992.

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Fetal and neonatal physiology. 4. Aufl. Philadelphia: WB Saunders Co., 2011.

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H, Nicolaides K., Hrsg. Maternal and fetal thyroid function in pregnancy. New York: Parthenon Pub. Group, 1996.

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Windows to the womb: Revealing the whole baby from conception to birth. Berkeley, Calif: North Atlantic Books, 2012.

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1938-, Teoh Eng-Soon, Ratnam S. S und Macnaughton Malcolm C, Hrsg. Maternal physiology and pathology: The proceedings of the XIIIth World Congress of Gynaecology and Obstetrics, Singapore, September 1991. Carnforth, Lancs, UK: Parthenon Pub. Group, 1993.

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Barker, David. The best start in life: How a woman's diet can protect her child from disease in later life. London: Century, 2003.

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Buchteile zum Thema "Maternal physiology"

Pipkin, Fiona Broughton. „Maternal Physiology“. In Dewhurst's Textbook of Obstetrics & Gynaecology, 1–17. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119211457.ch1.

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Broughton Pipkin, Fiona. „Maternal Physiology“. In Dewhurst's Textbook of Obstetrics & Gynaecology, 1–15. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781119979449.ch1.

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Longo, Lawrence D. „Maternal Physiology of Pregnancy“. In The Rise of Fetal and Neonatal Physiology, 217–80. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7483-2_10.

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Caughey, Aaron B. „Maternal Blood Gas Physiology“. In Critical Care Obstetrics, 69–86. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119129400.ch5.

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Bobrowski, Renee A. „Maternal-Fetal Blood Gas Physiology“. In Critical Care Obstetrics, 53–68. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444316780.ch5.

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Itskovitz-Eldor, Joseph. „Fetal and Maternal Cardiovascular Physiology“. In Doppler Ultrasound in Obstetrics & Gynecology, 107–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-86441-4_7.

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Bridges, Robert S., und Elizabeth M. Byrnes. „Neuroendocrine Regulation of Maternal Behavior“. In Neuroendocrinology in Physiology and Medicine, 301–15. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-707-9_17.

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Lemley, Caleb O., Leticia E. Camacho und Kimberly A. Vonnahme. „Maternal Recognition and Physiology of Pregnancy“. In Bovine Reproduction, 245–56. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118833971.ch25.

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Smiley, Kristina O., Sharon R. Ladyman, Papillon Gustafson, David R. Grattan und Rosemary S. E. Brown. „Neuroendocrinology and Adaptive Physiology of Maternal Care“. In Neuroendocrine Regulation of Behavior, 161–210. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/7854_2019_122.

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Savine, Rachel, und Lui G. Forni. „Renal Physiology during Normal Pregnancy“. In Principles and Practice of Maternal Critical Care, 413–18. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43477-9_30.

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Konferenzberichte zum Thema "Maternal physiology"

Wulan Akbar, Putri, Florentina Sustini, Hermanto Tri Juwono und Handayani. „Maternal Anthropometrics as a Predictor of Preeclampsia Risk Factor“. In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007336702410243.

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Lebold, Katie, Matthew Drake, Allison Fryer, Nancy Lee, James Lee und David Jacoby. „Maternal interleukin-5 and/or eosinophils affect airway physiology of offspring“. In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2089.

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Block, Janice. „19th Century Homeopathic Materia Medica Texts Predict Source Materials Whose Physiology Influences Thyroid Activity“. In HRI London 2019—Cutting Edge Research in Homeopathy: Presentation Abstracts. The Faculty of Homeopathy, 2020. http://dx.doi.org/10.1055/s-0040-1702099.

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Leman, A. M., Mohd Mahathir Suhaimi Shamsuri, Azian Hariri, Aeslina Abdul Kadir, Ahmad Fu’ad Idris und Azizi Afandi. „Correlation between plant physiology and CO2 removable“. In 3RD ELECTRONIC AND GREEN MATERIALS INTERNATIONAL CONFERENCE 2017 (EGM 2017). Author(s), 2017. http://dx.doi.org/10.1063/1.5002203.

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Lubis, Desy, Marnala Tobing, Dian Mayasari, Lina Pangaribuan und Siti Wahidah. „Development of e-Book As A Teaching Material In Anatomy Physiology Course“. In Proceedings of the 2nd Annual Conference of Engineering and Implementation on Vocational Education (ACEIVE 2018), 3rd November 2018, North Sumatra, Indonesia. EAI, 2019. http://dx.doi.org/10.4108/eai.3-11-2018.2285603.

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Tsoukantas, George, Konstantinos Salonitis, Panagiotis Stavropoulos und George Chryssolouris. „Overview of 3D laser materials processing concepts“. In Medical Imaging 2003 Physiology and Function: Methods, Systems, and Applications, herausgegeben von Alexis Carabelas, Giuseppe Baldacchini, Paolo Di Lazzaro und Dimitrios Zevgolis. SPIE, 2003. http://dx.doi.org/10.1117/12.513639.

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Bendero, J. M. S., M. E. R. Doon, K. C. A. Quiogue, L. C. Soneja, N. R. Ong, Z. Sauli und R. Vairavan. „Ergonomics study on mobile phones for thumb physiology discomfort“. In 3RD ELECTRONIC AND GREEN MATERIALS INTERNATIONAL CONFERENCE 2017 (EGM 2017). Author(s), 2017. http://dx.doi.org/10.1063/1.5002469.

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Auzel, Francois E. „Single-mode laser diode at absolute predetermined wavelength via intracavity Er3+-doped material absorption“. In Medical Imaging 2003 Physiology and Function: Methods, Systems, and Applications, herausgegeben von Alexis Carabelas, Giuseppe Baldacchini, Paolo Di Lazzaro und Dimitrios Zevgolis. SPIE, 2003. http://dx.doi.org/10.1117/12.513640.

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Polyzos, I., G. Tsigaridas, M. Fakis, V. Giannetas, Peter Persephonis und J. Mikroyannidis. „Three-dimensional data storage in photochromic materials based on pyrylium salt by two-photon-induced photobleaching“. In Medical Imaging 2003 Physiology and Function: Methods, Systems, and Applications, herausgegeben von Alexis Carabelas, Giuseppe Baldacchini, Paolo Di Lazzaro und Dimitrios Zevgolis. SPIE, 2003. http://dx.doi.org/10.1117/12.513598.

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Sukirman, Melani, Pringgo Widyo Laksono, Ilham Priadythama, Susy Susmartini und Bambang Suhardi. „Conceptual design of wearpack with physiology detector feature based on wearable instrumentation“. In 3RD INTERNATIONAL MATERIALS, INDUSTRIAL AND MANUFACTURING ENGINEERING CONFERENCE (MIMEC2017). Author(s), 2017. http://dx.doi.org/10.1063/1.5010665.

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Berichte der Organisationen zum Thema "Maternal physiology"

Comstock, Sarah. Examining the Effect of Maternal High-Fat Diet Consumption on the Physiology and Pancreas Development of Fetal and Juvenile Nonhuman Primate Offspring. Portland State University Library, Januar 2000. http://dx.doi.org/10.15760/etd.551.

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