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Добірка наукової літератури з теми "Fetus Growth"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 29 січня 2023

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Статті в журналах з теми "Fetus Growth"

Kim, O. H., and K. S. Shinn. "Postnatal growth of fetus-in-fetu." Pediatric Radiology 23, no. 5 (September 1993): 411–12. http://dx.doi.org/10.1007/bf02011978.

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Pilliod, Rachel A., Jessica M. Page, Teresa N. Sparks, and Aaron B. Caughey. "The Growth-Restricted Fetus." Obstetrical & Gynecological Survey 74, no. 7 (July 2019): 383–85. http://dx.doi.org/10.1097/01.ogx.0000569524.58213.11.

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Denis, Danièle, Maud Righini, Claudie Scheiner, Françoise Voloty, L. Boubli, X. Dezard, J. Vola, and J. B. Saracco. "Ocular Growth in the Fetus." Ophthalmologica 207, no. 3 (1993): 117–24. http://dx.doi.org/10.1159/000310417.

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Denis, Danièle, Françoise Faure, Françoise Volot, Claudie Scheiner, L. Boubli, Xavier Dezard, and J. B. Saracco. "Ocular Growth in the Fetus." Ophthalmologica 207, no. 3 (1993): 125–32. http://dx.doi.org/10.1159/000310418.

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Shamsuddin, L., and A. K. M. Shamsuddin. "Growth pattern of Bangladeshi fetus." International Journal of Gynecology & Obstetrics 70 (2000): B30. http://dx.doi.org/10.1016/s0020-7292(00)86183-4.

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Harding, JE, and BM Johnston. "Nutrition and fetal growth." Reproduction, Fertility and Development 7, no. 3 (1995): 539. http://dx.doi.org/10.1071/rd9950539.

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Nutrient supply to the fetus is a key factor in the regulation of fetal growth. However, the direct supply of nutrients to provide building blocks for tissue growth is likely to be only a minor component of this regulation. The indirect effects of nutrition on fetal endocrine and metabolic status, and on the interaction between the fetus, placenta and mother all of which must be coordinated to allow fetal growth are also important. Maternal undernutrition may alter the growth of the fetus and its different component tissues in a way which cannot be explained solely on the basis of reduced substrate supply during the rapid growth phase of the tissues involved. Adaptation to altered substrate supply, during both undernutrition and refeeding, involves sequential changes in the metabolic and endocrine interactions between the fetus and the placenta. In addition, undernutrition has long-term consequences for the fetus. There is evidence for nutritional programming of fetal endocrine and cardiovascular systems before birth. Nutritional effects may also persist over more than one generation. The effects of nutrition on fetal growth are far more complex than simply those of substrate deprivation.

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Hart-Elcock, Laura, R. D. Baker, and H. W. Leipold. "Growth of the Early Bovine Fetus." Journal of Veterinary Medicine Series A 37, no. 1-10 (February 12, 1990): 294–99. http://dx.doi.org/10.1111/j.1439-0442.1990.tb00908.x.

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Mathai, M., S. Thomas, A. Peedicayil, A. Regi, P. Jasper, and R. Joseph. "Growth pattern of the Indian fetus." International Journal of Gynecology & Obstetrics 48, no. 1 (January 1995): 21–24. http://dx.doi.org/10.1016/0020-7292(94)02237-2.

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Hema, Karumpuzha R., and Richard Johanson. "Management of the growth-restricted fetus." Obstetrician & Gynaecologist 2, no. 2 (April 2000): 13–20. http://dx.doi.org/10.1576/toag.2000.2.2.13.

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Robinson, J., S. Chidzanja, K. Kind, F. Lok, P. Owens, and J. Owens. "Placental control of fetal growth." Reproduction, Fertility and Development 7, no. 3 (1995): 333. http://dx.doi.org/10.1071/rd9950333.

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Анотація:

The placenta exerts its effects on the growth of the fetus from the beginning of pregnancy via metabolic and endocrine mechanisms. To achieve this, the placenta exchanges a wide array of nutrients, endocrine signals, cytokines and growth factors with the mother and the fetus. These exchanges modulate or programme fetal growth and development. This review concentrates on the function and structure of the placenta in humans and in animals, and the effects of experimental perturbation of placental size and function on fetal growth. The consequences for fetal growth of varying the abundance of peptides or, by deleting genes, insulin-like growth factors or cytokines, are also described. Maternal nutritional and hormonal state from as early as the first few days after fertilization, can influence the growth rate of the placenta and the fetus and also the length of gestation. Influences on placental development and their consequences will clearly have an impact on the placental control of fetal growth. Variations in the maternal environment and consequent perturbation of the metabolic and endocrine environment of the placenta and fetus are implicated as being responsible for the associations between prenatal growth of the placenta and its fetus and the subsequent risk of adult disease. The next challenge will be to determine the dominant influences at each stage of fetal and placental growth.

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Дисертації з теми "Fetus Growth"

Koch, Jill Marie. "Periconceptional treatment with growth hormone alters fetal growth and development in sheep." Morgantown, W. Va. : [West Virginia University Libraries], 2008. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5713.

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Thesis (Ph. D.)--West Virginia University, 2008.
Title from document title page. Document formatted into pages; contains ix, 128 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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Carr, Jillian M. "Insulin-like growth factor binding proteins (IGFBPs) in growth and development of the ovine fetus." Adelaide Thesis (Ph.D.) -- University of Adelaide, Department of Biochemistry, 1994. http://hdl.handle.net/2440/21607.

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Lunshof, Maria Simone. "Circadian rhythms in the normal and growth-retarded fetus and infant." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/81110.

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Hoelle, Katharina. "The role of System A amino acid transport in fetal growth and development." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609768.

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Zablith, Nadine. "The association between amniotic fluid albumin, prealbumin or transferrin and the fetal growth /." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98526.

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The study objectives were to measure the concentrations of albumin, prealbumin and transferrin in amniotic fluid (AF), and to establish if these concentrations were associated with infant birth weight (BW). At St Mary's Hospital (Montreal, Quebec), 294 AF samples were collected from mothers undergoing routine amniocentesis (12-19 weeks gestation). Exclusion criteria included subjects having gestational diabetes, multiple births or fetal genetic abnormalities. AF samples were analyzed by capillary electrophoresis (CE) at 190 nm. Analysis of variance and multiple linear regressions were performed. AF prealbumin could not be detected by CE. However, ANCOVA showed that transferrin was different among BW categories. Multiple regressions showed the parameter estimates for transferrin and albumin were negative, but neither was associated with BW in our study population. In contrast, transferrin was negatively associated with BW in our LBW infants. Our study shows that 2nd trimester AF transferrin may emerge as a biomarker for poor in-utero growth.

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De, Blasio Miles Jonathon. "Placental restriction and endocrine control of postnatal growth." Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phd2869.pdf.

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Sibley, Colin. "The nutrient exchange phenotype of the placenta in fetal growth restriction : characterization, adaptation and regulation." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/the-nutrient-exchange-phenotype-of-the-placenta-in-fetalgrowth-restriction-characterization-adaptation-and-regulation(35a27da9-ad7c-4e7e-8e91-8742304a5c9c).html.

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An essential function of the placenta is the exchange of nutrients, and wasteproducts of fetal metabolism, between mother and fetus. The placenta thereforeplays a key role in determining fetal growth and size at birth. Fetal growthrestriction (FGR) is a complication affecting around 5% of pregnancies. Thereare several possible causes of FGR but the most common in the Western world isplacental dysfunction. The FGR baby is at much greater risk of stillbirth andneurodevelopmental morbidities than the normally grown baby. Furthermore, thesmaller baby per se has an increased risk of a range of morbidities as an adult.The thrust of the work covered in this thesis was to improve understanding of theabnormalities in placental exchange physiology associated with FGR. The goalwas (and is) to develop new placental diagnostic biomarkers for the disease andnew treatments based on improving placental function.The first tranche of work described showed that there are specific changes intransporter activities in the placenta in FGR. My colleagues and I showed thatSystem A amino acid transporter activity in the microvillous plasma membrane(MVM) of the syncytiotrophoblast (transporting epithelium of the placenta) isreduced, per mg membrane protein, and that this reduction is related to theseverity of the disease. This contrasted with our observation in normal pregnancythat MVM System A activity, per mg protein, is inversely related to size of the babyat birth, and first suggested the concept of placental adaptation to fetal growthdemand. We, and others, went on to show that a number of other transporters inthe syncytiotrophoblast are altered in FGR. However, not all transporters areaffected and at least one is upregulated. This led me to hypothesise that some ofthese changes are causal to FGR and some are responses, or adaptations, toabnormal fetal growth. The direct causes of transporter activity changes are notknown but our work, and that of others, suggests that glucocorticoids play a role.We also showed that transporter activities in the placenta are affected in othercomplications where fetal growth is aberrant. Furthermore, we provided evidencethat denuded areas of the syncytiotrophoblast might be the morphologicalcorrelate of a route of passive transfer of hydrophilic solutes across the placenta.Our studies in a mouse model of FGR suggest that abnormalities in such aparacellular route may be part of the placental dysfunction in the disease.In the final group of publications of this thesis I describe work showing gestationalchanges in placental transporter activities. I suggest that these are primarilyregulated to maintain fetal growth trajectory, but may also provide for specificnutrient demands at particular times in gestation. This explanation was supportedby work with genetically modified mice showing experimentally that placentaltransporter activity is regulated, or adapted, in relation to fetal growth demand. Itappears from several studies described here that there is a matching of fetalgrowth demand and placental nutrient supply. However, other work shows that thematernal nutritional environment does modify this matching.The studies described here have led to three ongoing lines of investigation: (1)applying knowledge of placental phenotypes of FGR to assist in early diagnosis ofwomen at risk; (2) using mouse models of FGR to test drugs for treating thedisease in humans; (3) investigations into the nature of the fetal nutrient demandsignal(s) to the placenta, and whether these signals are altered in FGR.

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Lassala, Arantzatzu Leticia. "Arginine and fetal growth in ovine models of intrauterine growth restriction." [College Station, Tex. : Texas A&M University, 2008. http://hdl.handle.net/1969.1/ETD-TAMU-3238.

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Burrage, Deborah. "The impact of reduced nutrition on growth and cardiovascular control in the fetus." Thesis, University of Southampton, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430705.

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Carr, D. "Evaluation of prenatal adenoviral vascular endothelial growth factor gene therapy in the growth-restricted sheep fetus and neonate." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1401185/.

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Background - Fetal growth restriction (FGR) is associated with reduced uterine blood flow (UBF). In normal sheep pregnancies, adenovirus (Ad) mediated over-expression of vascular endothelial growth factor (VEGF) in the uterine arteries (UtA) increases UBF. It was hypothesised that enhancing UBF would improve fetal substrate delivery in an ovine paradigm of FGR characterised by reduced UBF from mid-gestation. Methods - Singleton pregnancies were established using embryo transfer in adolescent ewes subsequently overnourished to generate FGR (n=81). Ewes were randomised mid-gestation to receive bilateral UtA injections of 5x1011 particles Ad.VEGF-A165 or inactive treatment (saline or 5x1011 particles Ad.LacZ, a control vector). Fetal growth/wellbeing were evaluated using serial ultrasound. Late-gestation study: UBF was monitored using indwelling flowprobes until necropsy at 0.9 gestation. Vasorelaxation, neovascularisation in perivascular adventitia and placental mRNA expression of angiogenic factors/receptors were examined. A group of control-fed ewes with normally-developing fetuses was included (n=12). Postnatal study: Pregnancies continued until spontaneous delivery near to term. Lambs were weighed and measured weekly and underwent metabolic challenge at 7 weeks, dual-energy X-ray absorptiometry at 11 weeks, and necropsy at 12 weeks postnatal age. DNA methylation of somatotropic genes was examined in hepatic tissues. Results - Ultrasonographic fetal growth velocity was greater in Ad.VEGF-A165-treated versus control-treated FGR fetuses at 3-4 weeks post-injection. In late gestation fewer fetuses were markedly growth-restricted following Ad.VEGF-A165 therapy. There was evidence of mitigated brain sparing. No effect was seen on UBF/neovascularisation although Ad.VEGF-A165-transduced vessels showed enhanced vasorelaxation. Flt1/KDR expression was increased in the maternal placental compartment. At birth Ad.VEGF-A165-treated lambs tended to be heavier with increased placental efficiency. Postnatal growth, lean tissue accretion and insulin secretion were also increased, however no epigenetic changes were observed. Conclusions - Ad.VEGF-A165 safely increases fetal growth in this ovine model of FGR. This work has supported a successful application to translate this therapy into the clinic.

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Книги з теми "Fetus Growth"

Le, Dai-Trang ELizabeth. The role of insulin, insulin-like growth factors I and II, insulin- like growth factor binding protein 3, and their receptors in the regulation of human fetal growth. [New Haven, Conn: s.n.], 1993.

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Pasqualini, Jorge R. Hormones and the fetus. Oxford [Oxfordshire]: Pergamon Press, 1985.

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1937-, Carrera José María, ed. Ultrasound and fetal growth. New York: Parthenon Pub. Group, 2001.

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P, Smotherman William, and Robinson Scott R. 1952-, eds. Behavior of the fetus. Caldwell, N.J: Telford Press, 1988.

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Life before birth and a time to be born. Ithaca, N.Y: Promethean Press, 1992.

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Detmer, Ann. Intrauterine growth retardation: An experimental study of fetal growth, regional blood flow and hepatic lipid metabolism in the anaesthetized guinea pig. Uppsala: Sveriges Lantbruksuniversitet, 1992.

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England, Marjorie A. Life before birth. 2nd ed. London: Mosby-Wolfe, 1996.

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F, Hawkins D., ed. Your pregnancy: Questions and answers. Shaftesbury, Dorset: Element, 1997.

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Judith, Schuler, ed. Yun ma mi quan shu: Huai yun qian dao sheng chan hou jian kang zhi nan. Taibei Xian Xindian Shi: Shi mao chu ban she, 2003.

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Spanish Biochemical Society. Perinatal Biochemical Group. Meeting. Endocrine and biochemical development of the fetus and neonate. New York: Plenum Press, 1990.

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Частини книг з теми "Fetus Growth"

Lin, Chin-Chu. "Fetal Growth Retardation." In The High-Risk Fetus, 360–95. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9240-8_20.

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Moss, Timothy J. M., Cheryl A. Albuquerque, and Richard Harding. "Intrauterine Growth and Development." In Anesthesia and the Fetus, 1–18. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118477076.ch1.

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Ganguly, Chameli, Gitanjaly Guha Thakurata, Sukla Ghosh, K. L. Mukherjee, and Niranjan Bhattacharya. "Human Fetus: Carbohydrate Metabolism." In Human Fetal Growth and Development, 85–98. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-14874-8_7.

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Thorburn, G. D., C. A. Browne, A. W. Hey, S. Mesiano, and I. R. Young. "Growth Hormone and Fetal Growth: Historical Perspective." In The Endocrine Control of the Fetus, 1–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-72975-1_1.

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Ober, Carole. "Immunogenetics of Fetal Growth and Development." In The High-Risk Fetus, 85–97. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9240-8_4.

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Tamura, Ralph K., and Rudy E. Sabbagha. "Ultrasound Evaluation of Fetal Age and Growth." In The High-Risk Fetus, 221–43. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9240-8_12.

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Nissley, S. Peter, Lynne A. Gaynes, and Robert M. White. "Somatomedin/Insulinlike Growth Factor in the Human Fetus." In Human Growth Hormone, 621–34. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_50.

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Styne, D. M., G. Van Vliet, A. M. Rudolph, J. Kitterman, H. Iwamoto, S. L. Kaplan, and M. M. Grumbach. "Somatomedin C in the Ovine Fetus and Neonate." In Human Growth Hormone, 635–42. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_51.

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Ganguly, Chameli, Bimal Samanta, Gitanjaly Guha Thakurata, Nemaichand Chandra, Sukla Ghosh, K. L. Mukherjee, and Niranjan Bhattacharya. "Anthropometric Measurement of the Human Fetus." In Human Fetal Growth and Development, 67–83. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-14874-8_6.

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Guardamagna, Ornella, and Paola Cagliero. "Lipid Metabolism in the Human Fetus Development." In Human Fetal Growth and Development, 183–95. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-14874-8_12.

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Тези доповідей конференцій з теми "Fetus Growth"

Liu, Muye. "Approximate Growth Curve of Fetus Pancreas by Monotone Splines Regression." In international Conference on Intelligent Computing and Information Engineering (ICIE). VOLKSON PRESS, 2017. http://dx.doi.org/10.26480/icie.01.2017.41.44.

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Kumaresh, S., M. Sabareesh, and R. Srihari. "Non-invasive fetus heart rate and growth measurement with abnormality detection using IoT." In 2016 International Conference on Electrical, Electronics and Optimization Techniques (ICEEOT). IEEE, 2016. http://dx.doi.org/10.1109/iceeot.2016.7755390.

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Bhalla, Prerna, Ramesh K. Sunkaria, and Anterpreet Bedi. "Evolutionary Techniques on Fetal Head Segmentation." In International Conference on Women Researchers in Electronics and Computing. AIJR Publisher, 2021. http://dx.doi.org/10.21467/proceedings.114.18.

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In Obstetrics, Ultrasound is used to access fetus growth which can be measured by Head Circumference. Accurate segmentation of fetal head is important for calculating Head Circumference. As Deep Learning is gaining popularity because of its state of the art performance, the various Deep Learning techniques for the segmentation of fetal skull are discussed in this article.

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Nagaoka, Tomoaki, Tetsu Niwa, and Soichi Watanabe. "Specific absorption rate in human fetus with fetal growth for RF far-field exposure." In 2013 Asia Pacific Microwave Conference - (APMC 2013). IEEE, 2013. http://dx.doi.org/10.1109/apmc.2013.6694857.

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Nowlan, Niamh C., Paula Murphy, and Patrick J. Prendergast. "Mechanical Stimuli Resulting From Embryonic Muscle Contractions Promote Avian Periosteal Bone Collar Formation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-172077.

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Mechanical forces due to muscle contractions play an essential role in embryonic skeletal development. In neuromuscular conditions such as congenital myotonic dystrophy, where movement of the fetus in utero is reduced or absent, the bones and joints of the newborn often show malformations [1]. In this paper, we examine the effect of muscle contractions on embryonic bone development. We propose the hypothesis that mechanical loading due to muscle contractions promotes periosteal ossification and we test this hypothesis using computational and experimental methods. A set of FE analyses were performed using anatomically realistic morphologies and loading conditions, at several timepoints during development, in order to identify biophysical stimuli active during bone formation. Avian immobilization experiments were performed to examine bone growth in the absence of skeletal muscle contractions.

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Farah, Huda Mohamed, Muram Elmubarak Elamin, Rahaf Nader Nader Nader, Rana Said Alabsi, Salma Bouazza Bouabidi, Sara Elgaili Khogali Suleiman, Shahd Mohammad Nasr, Shouq Fahad Al-Rumaihi, Zain Zaki Zakaria, and Maha alasmakh Alasmakh. "Metagenomic Analysis of Oral Microbiome during pregnancy." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0135.

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Pregnancy is a dynamic physiological process associated with significant hormonal, immune and metabolic changes to support the growth and development of the fetus. Several studies have highlighted the role of gut microbiota during pregnancy1. The composition of gut microbiota changes dramatically during the course of pregnancy with an increase in Proteobacteria and Actinobacteria, a decline in butyrate-producing bacteria and a reduction in bacterial richness at the end of pregnancy2. These modifications were anticipated to favour the increased metabolic demand during pregnancy, which will, in turn, support healthy fetal growth3. Gut microbiota has also been suggested to contribute to weight gain during pregnancy via increased absorption of glucose and fatty acids, induction of catabolic pathways, increased fasting-induced adipocyte factor secretion, and stimulation of the immune system2, 4. The oral cavity houses the second most diverse microbiota after the gut harbouring over 700 species of bacteria. Oral microbiota plays a crucial role in maintaining oral homeostasis, protecting the oral cavity and preventing disease development5. Little is known about the role of the oral microbiome during pregnancy. One study examined changes in oral microbiota during pregnancy on Japanese women and found that the total viable microbial counts were higher during pregnancy, as were levels of the pathogenic bacteria Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, and Candida6. Several studies have also found correlations between oral infections and pregnancy complications, further suggesting mechanisms connecting the oral microbiome with the state of pregnancy7. The Qatari Birth Cohort (QbiC) was successfully developed in July 2018 by Qatar Biobank. It is an epidemiological study that aims to assess the synergetic role of environmental exposure and genetic factors in the development of chronic disease. It monitors the health of women throughout their pregnancy and after birth. The present study is designed to explore changes in the salivary microbiome, using high throughput sequencing during pregnancy and to explore key microbial clades involved in pregnancy.

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Fu, Luoyu, Peiqi Yi, Zikun Gao, and Yan Gan. "Design and Research of Flexible Wearable Medical Testing Equipment for Pregnant Women." In 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1001478.

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Pregnant women, as a special group, bear the mission of nurturing and continuing human life. Pregnant women need to experience psychological and physiological changes in the tenth month of pregnancy. In the special "post-epidemic era", it is hard and unsafe for pregnant women to go to the hospital regularly for birth check-up. In order to make pregnant women have a better prenatal experience, our team wants to design a wearable device, which can monitor the fetal heart rate and the frequency of fetal movement, so that pregnant women can also realize routine detection of the fetal condition at home, and protect the growth health and safety of the fetus. In this design, questionnaire interview, literature search and collaborative story telling are used to deeply understand the pain points of pregnant women's antenatal examination, the development status of wearable devices for pregnant women at home and abroad, pregnant women's preferences and so on. Then, determine the product use process, product functional structure and product packaging. This design adopts cutting-edge technologies such as flexible sensors, and combines ergonomics and kansei engineering. The product obtains the data and information of pregnant women and fetuses, and then through sorting and analysis, the results are intuitively transmitted to pregnant women, pregnant women's relatives or doctors in the matching APP, so that users can clearly obtain the health data of pregnant women in real time. Realize early warning of physical abnormalities of infants and mothers, early warning and early treatment, so as to better protect the safety and health of pregnant women and fetuses during pregnancy. After the usability test, the interviewed pregnant women thought that the design had a certain effect.

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Bukowski, Michael, Brij Singh, James Roemmich, and Kate Larson. "Lipidomic analysis of TRPC1 Ca2+-permeable channel-knock out mouse demonstrates a vital role in placental tissue sphingolipid and triacylglycerol homeostasis under high-fat diet." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/tjdt4839.

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Placental function including oxygen delivery and nutrient transport are critical determinants of fetal growth, moderating the risks of obesity and metabolic diseases later in life. Previously, we demonstrated in a mouse model that parental diet and exercise play important roles in placental lipid content and inflammation. Transient receptor potential canonical channel 1 (TRPC1) is a Ca2+-permeable integral membrane protein. We have demonstrated that TRPC1 increases total body adiposity in mice by decreasing the efficacy of exercise to limit adipose accumulation under a high fat (HF) diet. Importantly, intracellular calcium may regulate total body adiposity and increased total body adiposity could promote placental lipid accumulation. Similarly, intracellular calcium regulates membrane lipid content via the activation of the protein kinase C. Membrane lipids such as sphingomyelin are key regulators of cell signaling. Maternal HF diets increase placental tissue lipid concentrations resulting in compromised nutrient transport to fetus. However, the specific lipid species that accumulate due to the absence of the placental TRPC1 gene under maternal HF diet feeding is not yet known. We hypothesized that placental tissue response to a maternal HF diet is disrupted in TRPC1 mice fed a maternal HF diet resulting in greater cellular sphingomyelin concentrations. Results showed placentae from TRPC1 KO mice fed high fat diet (45% en, HF) had increased sphingomyelin concentrations compared to control diet (16% en, NF). Placentae from WT mice fed HF diet exhibited diet-dependent increases in ceramide concentration with no concomitant increase in sphingomyelins compared to NF fed WT mice. Additionally, 11 placental triacylglycerol (TAG) species were different based on diet, 16 based on genotype, and 5 were affected by both diet and genotype. These results suggest that during a HF diet, loss of TRPC1 function reduces placental sphingomyelin hydrolysis into ceramide and that placental TAG concentrations respond in diet- and genotype-dependent manner.

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Ohnaka, H., Y. Kojima, S. Kishimoto, Y. Ohno, and T. Mizutani. "Fabrication of CNT-FETs using PECVD-grown nanotubes." In Digest of Papers Microprocesses and Nanotechnology 2005. 2005 International Microprocesses and Nanotechnology Conference. IEEE, 2005. http://dx.doi.org/10.1109/imnc.2005.203851.

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Bjork, M. T., K. E. Moselund, H. Schmid, H. Ghoneim, S. Karg, E. Lortscher, J. Knoch, W. Riess, and H. Riel. "VLS-grown silicon nanowires — Dopant deactivation and tunnel FETs." In 2010 Silicon Nanoelectronics Workshop (SNW). IEEE, 2010. http://dx.doi.org/10.1109/snw.2010.5562587.

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Звіти організацій з теми "Fetus Growth"

Spencer, Thomas E., Elisha Gootwine, Arieh Gertler, and Fuller W. Bazer. Placental lactogen enhances production efficiency in sheep. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7586543.bard.

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The key objectives of this BARD project were to: (1) study long-term effects of immunization of prepubertal ewes against recombinant ovine placental lactogen (roPL) on subsequent birth weights of their lambs and their milk production; (2) optimize the anti-roPL immunization protocol using adjuvant preparations acceptable to producers and regulatory agencies; and (3) determine the physiological mechanism(s) whereby immunization against oPL increases fetal growth and development and mammogenesis. These objectives were based on key findings from a previous BARD project that: (a) immunization of ewes against roPL increased lamb birth weight and ewe milk production during lactation; (b) roPL and recombinant ovine growth hormone (roGH) increased the proliferation and differentiated function of endometrial glands that, in turn, would enhance uterine secretions necessary for fetal and placental growth; and (c) exogenous roPL and roGH stimulated mammogenesis and milk production during lactation. The BARD projects address central problems in sheep production, including reproductive failure due to embryonic/fetal mortality, low birth weight of lambs especially in prolific breeds, and reduced milk yields which affect neonatal survival. The sheep placenta secretes both lactogenic (oPL) and somatogenic (oGH) hormones. The receptors for those hormones are present in the fetus and placenta as well as maternal uterus, and mammary gland. Our research has focused on determining the biological role of these placental hormones in development and differentiation of the uterus during gestation and the mammary gland during pregnancy and lactation. Studies conducted in the current BARD project indicated that the effects of anti-roPL immunization were variable in ewes and that commercially available and widely acceptable adjuvant preparations were not effective to produce high anti-roPL titers in pre-pubertal ewes. In the non-prolific Rambouillet ewe in Texas and in the Awassi and the Assaf in Israel, anti-roPL immunization increased lamb birth weight; however, the magnitude of this effect and the inherent variability precluded our ability to determine the physiological mechanism of how the immunization increases fetal growth. Collectively, our findings suggest that anti-roPL immunization is not currently feasible as an easy and efficacious tool for the producer to increase flock reproductive and production efficiency. The variability in response of individual ewes to anti-roPL immunization likely includes modifying the recombinant hormone and the type of adjuvant used for the immunization. In particular, the oPL may need to be modified to ensure maximum antigenicity in a broad range of breed types. Nonetheless, the investigators continue to collaborate on identifying fundamental mechanisms that can be improved by genetics or management to enhance the efficiency of uteroplacental function and, in turn, fetal growth and development. High prolificacy is a desirable trait in intensive sheep production systems. One of the main limitations of using prolific breeds of sheep is that increased litter size is associated with low birth weights and increased mortality of lambs. Further, low birth weight is associated with an increased propensity for adult diseases and decreased production efficiency. Indeed, our recent studies find that the birth weights of lambs born in large litters can be improved by both genetics and management. Future cooperative research will continue to focus on reproductive efficiency of sheep that have broader implications for improving production efficiency in all types of ruminant livestock.

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