Relevant bibliographies by topics / Fetal origins of adult disease

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Fetal origins of adult disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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Journal articles on the topic "Fetal origins of adult disease"

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Morley, Ruth, and Terence Dwyer. "Fetal Origins of Adult Disease Fetal Origins Of Adult Disease?" Clinical and Experimental Pharmacology and Physiology 28, no. 11 (November 2001): 962–66. http://dx.doi.org/10.1046/j.1440-1681.2001.03557.x.

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Bora, Rishabh, and Neharika Malhotra Bora. "Fetal Origin of Adult Disease." Donald School Journal of Ultrasound in Obstetrics and Gynecology 8, no. 2 (2014): 164–77. http://dx.doi.org/10.5005/jp-journals-10009-1352.

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ABSTRACT Fetal origins of adult disease, a concept first popularized by Dr David Barker, has subsequently led to many studies which have provided the evidence that certain diseases do have links pointing to fetal origins—adverse influences early in development, and particularly during intrauterine life, can result in permanent changes in physiology and metabolism, which result in increased disease risk in adulthood. Links that are well-established are—reduced birth weight and increased risk of coronary heart disease, hypertension and stroke in adulthood. The concept of a fetal origin of adult disease have been extended well-beyond coronary heart disease and being a risk factor for coronary heart disease, and now includes investigations of the development of the central nervous system, early origins of adult mental health and cognitive function. By understanding fetal origin of adult disease, health care professionals and policy makers will make this issue a high health care priority and implement preventive measures and treatment for those at higher risk for chronic diseases. How to cite this article Malhotra N, Malhotra J, Bora NM, Bora R, Malhotra K. Fetal Origin of Adult Disease. Donald School J Ultrasound Obstet Gynecol 2014;8(2):164-177.
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Simmons, Rebecca. "Fetal Origins of Adult Disease." NeoReviews 5, no. 12 (December 2004): e511-e515. http://dx.doi.org/10.1542/neo.5-12-e511.

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Choi, Gyu Yeon. "Fetal origins of adult disease." Korean Journal of Obstetrics and Gynecology 53, no. 6 (2010): 475. http://dx.doi.org/10.5468/kjog.2010.53.6.475.

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Morley, Ruth. "Fetal origins of adult disease." Seminars in Fetal and Neonatal Medicine 11, no. 2 (April 2006): 73–78. http://dx.doi.org/10.1016/j.siny.2005.11.001.

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Langley-Evans, Simon C. "Fetal origins of adult disease." British Journal of Nutrition 81, no. 1 (January 1999): 5–6. http://dx.doi.org/10.1017/s0007114599000070.

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Calkins, Kara, and Sherin U. Devaskar. "Fetal Origins of Adult Disease." Current Problems in Pediatric and Adolescent Health Care 41, no. 6 (July 2011): 158–76. http://dx.doi.org/10.1016/j.cppeds.2011.01.001.

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Barker, DJP. "The fetal origins of adult disease." Fetal and Maternal Medicine Review 6, no. 2 (May 1994): 71–80. http://dx.doi.org/10.1017/s0965539500001005.

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Recent studies have shown that babies who are small for dates at birth, or who fail to grow in infancy, have, in adult life, raised blood pressure, impaired glucose tolerance, abnormal serum lipids, raised fibrinogen and high death rates from coronary disease, stroke and obstructive lung disease. This has led to the hypothesis that these diseases are ‘programmed’ in utero in response to an adverse environment.
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Hanson, M. "Fetal origins of adult disease: introduction." Heart 91, no. 7 (July 1, 2005): 863. http://dx.doi.org/10.1136/hrt.2004.047357.

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Robinson, R. "The fetal origins of adult disease." BMJ 322, no. 7283 (February 17, 2001): 375–76. http://dx.doi.org/10.1136/bmj.322.7283.375.

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Dissertations / Theses on the topic "Fetal origins of adult disease"

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Huxley, Rachel R. "A critical appraisal of the fetal-origins hypothesis of adult disease : a meta-analysis and a retrospective cohort study." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393401.

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Liang, Chengya. "High Saturated Fat Diet Induces Gestational Diabetes, Perinatal Skeletal Malformation and Adult-Onset Chronic Diseases." Diss., Virginia Tech, 2009. http://hdl.handle.net/10919/26700.

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Adult exposure to high fat diet (HFD) has been linked to increased risk of musculoskeletal, cardiovascular, and metabolic diseases; however, the contribution of gestational HFD to elevated oxidative stress (OS), perinatal cardiovascular, skeletal, and metabolic dysfunction as well as long-term effects on adult offspring are incompletely understood. Pathophysiologic mechanisms linking gestational HFD, OS, and insulin resistance to perinatal development and adult-onset chronic diseases are explored in the present study, and maternal antioxidant (quercetin) is offered as a potential preventive dietary supplement to reduce fetal and maternal sequelae of HFD. Female C57BL/6 mice were fed â cafeteria-styleâ HFD (including 32.1% saturated fat to mimic a typical fast food menu) with or without quercetin for one month prior to conception, and throughout gestation. HFD dams developed gestational diabetes with significantly increased placental OS and vasculopathy. Neonates were smaller at birth than age-matched controls, and surviving offspring developed type 2 diabetes, hypertension and osteoporosis during adulthood, despite having been fed healthy diet throughout their postnatal life. Additional measures of bone using three-dimensionally reconstructed computed tomographic image analysis (microCT) revealed microarchitectural changes of bone at birth, and at 6 and 12 months postnatally. Fetuses from HFD dams displayed diminished bone mineral density (BMD) and disrupted endochondral and intramembranous ossification with significantly shortened distal limb lengths, as compared to offspring of standard rodent chow dams. Skeletal malformation persisted into adulthood despite the fact that both control and HFD offspring were fed conventional rodent chow throughout postnatal life. The offspring gestationally exposed to HFD showed significant decreased femoral BMD at 6 months of age and dysregulation of distal femoral trabecular architecture at 12 months of age, indicating development of osteoporosis. We were able to reduce incidence of placental vasculopathy, fetal maldevelopment and adult-onset type 2 diabetes, hypertension and osteoporosis with concurrent maternal quercetin supplementation during pregnancy. Collectively, these data suggested that maternal HFD increases placental OS and vascular damage during pregnancy, which are associated with fetal malformation and elevated adult-onset multisystemic chronic diseases. Maternal quercetin supplementation must be further explored as a potential dietary intervention for improved placental integrity, fetal development and lifelong health.
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Maisonet, Mildred, Simo Näyhä, Debbie A. Lawlor, and Michele Marcus. "Prenatal Exposures to Perfluoroalkyl Acids and Serum Lipids at Ages 7 and 15 in Females." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/etsu-works/29.

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Background In some cross-sectional epidemiologic studies the shape of the association between serum concentrations of perfluoroalkyl acids (PFAAs) and lipids suggests departures from linearity. Objectives We used statistical approaches allowing for non-linearity to determine associations of prenatal exposures of perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) with lipid concentrations. Methods PFAAs were measured in serum from pregnant women collected in 1991–1992 at enrollment in the Avon Longitudinal Study of Parents and Children and lipids in serum from their daughters at ages 7 (n = 111) and 15 (n = 88). The associations of PFAAs with lipids were first explored by cubic splines, followed by piecewise linear regressions by tertiles to obtain regression coefficients (β) and their 95% confidence limits (95% CL) (in mg/dL per 1 ng/mL). Results At age 7, total cholesterol was positively associated with prenatal PFOA concentrations in the lower tertile (β = 15.01; 95% CL = 2.34, 27.69) but not with PFOA concentrations in the middle (β = − 3.63; 95% CL = − 17.43, 10.16) and upper (β = − 1.58; 95% CL = − 4.58, 1.42) tertiles. At age 15, a similar pattern was noted as well. Positive associations between LDL-C and prenatal PFOA concentration in the lower tertile were observed in daughters at ages 7 (β = 14.91; 95% CL = 3.53, 28.12) and 15 (β = 13.93; 95% CL = 0.60, 27.26). LDL-C was not associated with PFOA concentrations in the middle or upper tertile at any age. Neither HDL-C nor triglycerides was associated with prenatal PFOA exposure. Non-linear patterns of association of total cholesterol and LDL-C with prenatal PFOS were less consistently noted. Conclusion Exposure to low levels of PFOA during prenatal development may alter lipid metabolism later in life. Given the small sample size further replication of the association in large independent cohorts is important.
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Godfrey, Keith Malcolm. "Maternal nutrition, fetal development and adult disease." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285785.

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Sherman, Rachel Caroline. "The role of the renin-angiotensin system in the fetal origins of hypertension." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300922.

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Tegethoff, Marion. "Fetal origins of pediatric disease fetoplacental plasticity and intrauterine programming by stress and glucocorticoids." Göttingen Cuvillier, 2009. http://d-nb.info/999629417/04.

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Kajantie, Eero. "Mechanisms of growth in small preterm infants and early life origins of adult cardiovascular disease." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/kajantie/.

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Forsén, Tom. "Early growth and adult disease : programming of coronary heart disease, type 2 diabetes and hypertension by fetal and childhood growth." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kansa/vk/forsen/.

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Siemienowicz, Katarzyna Joanna. "Fetal programming of adult disease : causes and consequences of metabolic dysregulation in an ovine model of PCOS." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28977.

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Polycystic ovary syndrome (PCOS) is a common and complex endocrine condition with reproductive and metabolic complications, affecting up to 10% of reproductive-age women. Hyperandrogenemia, ovulatory dysfunction, and luteinising hormone hypersecretion are characteristic traits of PCOS however, it seems that the most concerning long-term key issues are metabolic problems associated with the syndrome, such as hyperinsulinemia, insulin resistance, obesity, dyslipidaemia and non-alcoholic liver disease. Despite the numerous studies on PCOS, its origin and pathophysiology are still not fully understood. However, there is increasing evidence that the adult PCOS phenotype is programmed in fetal life by androgen excess. Exposure to increased levels of testosterone in utero in rodents, sheep and monkeys result in adult reproductive and metabolic pathologies that parallel those seen in PCOS women. Since hyperandrogenemia is a hallmark of PCOS and daughters of PCOS mothers have elevated levels of androgens at birth, it is likely that prenatal androgenisation during early life predispose to the future development of PCOS. Animal models of PCOS provide an opportunity to examine the developmental aetiology and molecular mechanisms underlying the pathogenesis of this condition. Over last 10 years our lab has successfully utilised a well-established ovine model of PCOS, where pregnant ewes were treated with testosterone propionate (TP) through mid-gestation. From this model, we had a large sample bank of fixed and frozen tissues from the fetal, lamb and adolescent prenatally androgenised animals that allowed to carry a broad range of experiments. In addition, a new cohort of prenatally androgenised adult sheep enabled additional in vivo analysis. Past research documented that prenatal androgenisation result in hyperinsulinemia with altered pancreas structure and function, and early fatty liver without difference in body weight in adolescent sheep. This thesis examines the effects and consequences of increased in utero androgen exposure on metabolic dysregulation in adolescent and adult female sheep. During puberty, but not fetal or early life, there was decreased adipogenesis in subcutaneous adipose tissue (SAT), but not visceral adipose tissue (VAT), accompanied by decreased circulating concentrations of fibroblast growth factor 21 (FGF21), leptin and adiponectin, and increased concentrations of fasting free fatty acids (FFA) in prenatally androgenised sheep. This was countered by upregulated expression of FFA transporters in liver. As adults, TP-exposed animals had increased body weight, elevated fasting insulin and FFA concentrations but normal FGF21, leptin and adiponectin levels. Histological analysis revealed that adult TP-exposed animals had SAT hypertrophy, which was associated with increased expression of inflammatory markers and correlated with increased fasting FFA. Therefore, it is likely that impaired preadipocyte differentiation in SAT during adolescence resulted in hypertrophy and inflammation of adult SAT. This consequently lowered capacity of SAT to safely store fat and potentially explains metabolic perturbations observed in PCOS-like female sheep. To further investigate potential causes of obesity in adult PCOS-like sheep postprandial thermogenesis (PPT), an important constituent of energy expenditure, was measured through implantation of datalogger thermometers into interscapular adipose tissue. Adult prenatally androgenised sheep had decreased amplitude of PPT, without difference in basal body temperature, despite receiving the same caloric intake, and independent of obesity. These findings indicate that adult PCOS-like sheep have reduced capacity for energy expenditure, which is mirrored in women with PCOS. This reduced capacity for postprandial thermogenesis was correlated with hyperinsulinemia decreased noradrenaline levels and reduced thermogenic potential of brown and/or beige adipose tissue. This suggests that women with PCOS might be prenatally programmed to become obese. In summary, findings documented in this thesis provide better understanding into the pathophysiology of PCOS from puberty to adulthood and give opportunities for early clinical intervention to ameliorate the metabolic phenotype of PCOS.
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Brenseke, Bonnie Margaret. "The Role of Maternal High Fat Diet in the Pathogenesis of Metabolic and Bone Disease in the Adult Offspring." Diss., Virginia Tech, 2013. http://hdl.handle.net/10919/49590.

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Chronic diseases such as osteoporosis, type 2 diabetes, and cardiovascular disease are diseases of long duration, slow progression, and are by far the leading cause of death worldwide. A growing body of evidence links adverse exposures in early development with an increased risk of chronic diseases in adult life. The studies presented in this dissertation sought to exploit this phenomenon to determine the extent to which gestational and lactational exposure to a high fat diet predisposes the offspring to certain diseases in later life and if the eating habits of adult offspring would be able to mitigate or exacerbate these conditions.  In the study presented in Chapter III, dams fed an atherogenic high fat diet prior to conception and throughout gestation and lactation experienced excess hepatic lipid accumulation and poor birth outcome as characterized by smaller litter sizes and higher post-delivery mortality. In the offspring, gestational and lactational exposure to such a diet resulted in growth restriction and skeletal aberrations indicative of osteoporosis, despite being fed a standard rodent diet post-weaning. We propose that dietary-induced hyperlipidemia, along with pregnancy-associated factors, resulted in fatty liver and subsequently reduced litter sizes and increased early mortality, and that the skeletal aberrations seen in the mature offspring represent dietary-induced inhibition of osteogenesis in favor of adipogenesis. In the study presented in Chapter IV, early exposure to a high fat diet resulted in central obesity, elevated lipid levels, hyperglycemia, and additional markers used in the diagnosis of the metabolic syndrome. Altering the diets of the mature offspring demonstrated that the eating habits of adulthood have the potential to mitigate or exacerbate certain metabolic parameters established earlier in life. Mechanisms contributing to the observed metabolic aberrations could include developmental plasticity and mismatch, catch-up growth, and altered programming of the appetite regulatory network. Collectively, this research suggests that early exposure to a fat-rich diet can lead to metabolic and skeletal aberrations in the adult offspring and adds support to the developmental origins of health and disease hypothesis by finding that adverse nutritional exposures in early life can play a role in the chronic diseases of adulthood.

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Books on the topic "Fetal origins of adult disease"

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Huang, He-Feng, and Jian-Zhong Sheng, eds. Gamete and Embryo-fetal Origins of Adult Diseases. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-007-7772-9.

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Langley-Evans, S. C., ed. Fetal nutrition and adult disease: programming of chronic disease through fetal exposure to undernutrition. Wallingford: CABI, 2004. http://dx.doi.org/10.1079/9780851998213.0000.

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Marelyn, Wintour E., and Owens Julie A, eds. Early life origins of health and disease. New York, N.Y: Springer Science+Business Media, 2006.

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Gregory, Bock, Whelan Julie, and Symposium on the Childhood Environment and Adult Disease (1990 : Ciba Foundation), eds. The Childhood environment and adult disease. Chichester: Wiley, 1991.

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C, Azmitia Efrain, Björklund Anders 1945-, and New York Academy of Sciences., eds. Cell and tissue transplantation into the adult brain. New York, N.Y: New York Academy of Sciences, 1987.

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A perinatal strategy for preventing adult disease: The role of long-chain polyunsaturated fatty acids. Boston, Mass: Kluwer Academic Publishers, 2002.

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Fetal & Infant Origins of Adult Disease. Bmj Publishing Group, 1992.

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Fetal and Infant Origins of Adult Disease. Amer College of Physicians, 1992.

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Huang, He-Feng, and Jian-Zhong Sheng. Gamete and Embryo-fetal Origins of Adult Diseases. Springer, 2016.

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Huang, He-Feng, and Jian-Zhong Sheng. Gamete and Embryo-fetal Origins of Adult Diseases. Springer, 2013.

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Book chapters on the topic "Fetal origins of adult disease"

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Huang, He-Feng, Guo-Dian Ding, Shen Tian, and Qiong Luo. "Gamete/Embryo-Fetal Origins of Diabetes." In Gamete and Embryo-fetal Origins of Adult Diseases, 79–93. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7772-9_4.

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Zhang, Dan, He-Feng Huang, Feng Zhang, Run-Ju Zhang, Yang Song, and Jing-Yi Li. "Gamete/Embryo-Fetal Origins of Tumours." In Gamete and Embryo-fetal Origins of Adult Diseases, 109–36. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7772-9_6.

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Huang, He-Feng, Min Jin, and Xian-Hua Lin. "Gamete/Embryo-Fetal Origins of Obesity." In Gamete and Embryo-fetal Origins of Adult Diseases, 137–56. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7772-9_7.

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Zhu, Xiao-Ming, Yu Zhang, Xi-Jing Chen, and He-Feng Huang. "Gamete/Embryo-Fetal Origins of Infertility." In Gamete and Embryo-fetal Origins of Adult Diseases, 173–96. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7772-9_9.

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Longo, Lawrence D. "Epigenetics and the Fetal Origins of Adult Health and Disease." In The Rise of Fetal and Neonatal Physiology, 207–34. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7921-5_11.

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Longo, Lawrence D. "Epigenetics and the Fetal Origins of Adult Health and Disease." In The Rise of Fetal and Neonatal Physiology, 501–34. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7483-2_16.

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Sheng, Jian-Zhong, Li Zhang, Gu-Feng Xu, and Ying Jiang. "Gamete/Embryo-Fetal Origins of Cardiovascular Diseases." In Gamete and Embryo-fetal Origins of Adult Diseases, 95–108. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7772-9_5.

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Qu, Fan, Lu-Ting Chen, Hong-Jie Pan, and He-Feng Huang. "Gamete/Embryo-Fetal Origins of Mental Disorders." In Gamete and Embryo-fetal Origins of Adult Diseases, 157–71. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7772-9_8.

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Ye, Ying-Hui, Le-Jun Li, Yue-Zhou Chen, He-Feng Huang, and Zhong-Yan Liang. "Physiology of Gametogenesis." In Gamete and Embryo-fetal Origins of Adult Diseases, 1–38. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7772-9_1.

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Zhu, Yi-Min, Xiao-Ling Hu, Yan-Ting Wu, Chun Feng, and He-Feng Huang. "Assisted Reproductive Technology and Gamete/Embryo-Fetal Origins of Diseases." In Gamete and Embryo-fetal Origins of Adult Diseases, 197–219. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7772-9_10.

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Conference papers on the topic "Fetal origins of adult disease"

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Dodson, Reuben B., Kendall S. Hunter, and Virginia L. Ferguson. "Elastic Properties of the Human Umbilical Cord in Preeclampsia." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53673.

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Maternal diseases of pregnancy have been found to detrimentally affect the fetal circulatory system, with consequences lasting well into adulthood. In 1995, Barker introduced the idea that major disorders of adult life (including coronary heart disease, hypertension, stroke and diabetes) arise not only through an interaction between factors in our lifestyle, such as a high-fat diet, obesity and smoking, and a genetically determined susceptibility but also through development in utero [1]. Epidemiological evidence continues to support the notion that adult cardiovascular disease (CVD) has fetal origins [2–5].
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Tai, Andrew S. N., Haily Tran, Mary Roberts, Nadeene Clarke, John W. Wilson, and Colin F. Robertson. "Pediatric Origins Of Adult Chronic Obstructive Pulmonary Disease(COPD): Childhood Asthma." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2275.

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Abshire, T., L. Fink, J. Christian, J. O'Connell, and W. Hathaway. "THE DYSFIBRINOGEN OF CHILDHOOD NEPHROSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643334.

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An abnormal fibrinogen (Fib) related to increased sialic acid (SA) has been described in adults with liver disease. This dysfibrinogen (Dysfib) seems most like fetal Fib. A review of 11 patients with nephrosis revealed an unexplained prolonged thrombin time (TT) and otherwise normal coagulation studies. Based on these observations, we sought to answer whether the prolonged TT defined a Dysfib and if this abnormal Fib was similar to fetal Fib. Pooled adult, fetal plasma, and the plasma of 3 patients with nephrosis were studied with TT and reptilase times (RT). Fib was measured by functional (Fib-act) and immunologic (Fib-ag) assays. An enzyme linked immunosorbent assay (ELISA) was established using antifibrinogen as the first antibody and either peroxidase conjugated Fib or a lectin (Limulus Polyphemus) specific for SA as the second antibody. The optical density was recorded per μgm Fib for both conjugated antifibrinogen or lectin and the ratio compared in order to estimate SA reactivity. Patient 3 was also studied by: 1) crossed immunoelectrophoresis (CIE) employing lectin in the first dimension and 2) polyacrylamide gel electrophoresis (PAGE) with transfer to nitrocellulose paper using Western Blot technique.Results of the CIE showed patient 3 and fetal plasma were similar in electrophoretic pattern and different from adult plasma. The PAGE with Western Blot revealed a similar pattern of Fib for patient 3, fetal and adult plasma. We conclude that the prolonged TT and RT, the greater amount of Fib-ag when compared to Fib-act in patients 1-3 and fetal plasma and the absence of evidence for Fib degradation products, support the diagnosis of Dysfib. The similarity of the CIE for patient 3 and fetal plasma and the difference between ELISA lectin/Fib ratio of patients 1-3 and fetal compared with adult plasma suggest that the Dysfib of nephrosis may be similar to fetal Fib.
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Soker, Shay, Dawn Delo, Samira Neshat, and Anthony Atala. "Amniotic Fluid Derived Stem Cells for Cardiac Muscle Therapies." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192492.

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Many forms of pediatric and adult heart disease are accompanied by high morbidity and mortality, as the heart muscle has limited regenerative potential. Cell therapy has been proposed as a means to promote the regeneration of injured heart muscle. We have established lines of broad spectrum multipotent stem cells derived from primitive fetal cells present in human amniotic fluid (hAFS) cells (1). AFS cells offer several advantages: They are easy to isolate and grow (no feeder layers needed), are highly expansive including clonal growth and they can differentiate into all germ layers. In the current study, we demonstrate that AFS cells can differentiate into cardiac muscle cells and be used for cardiac tissue regeneration.
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Oliveira, Sayd Douglas Rolim Carneiro, Carlos Jorge Maciel Uchoa Gadelha, Dara da Silva Mesquita, and Tereza Cristina Ribeiro Brito. "SARS-CoV-2 infection during pregnancy and risk of neurodevelopmental disorders in neonatals: a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.031.

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Introduction: With the emergence of SARS-CoV-2 and its rapid spread, a concern with the pregnant women have increased, since viruses have a wide range of obstetric and neonatal issues. Recent findings indicate that the gestational period and the postpartum period make mothers and their offspring more susceptible to COVID-19 and the rapid progression to the critical stage of the disease. Objectives: To carry out a bibliographic study on SARS-CoV- 2 during pregnancy and the potential risk of neurodevelopmental disorders in neonates. Methods: A review, developed from articles selected on the following bases: PubMed, Web of Science and Scopus. In the search, articles indexed until March 2021 and published in English, using the descriptors: “COVID-19”; “Pregnancy”; “Offspring”; “Neonatal”; “Neurodevelopment”; “Anomalies” and “Complications”. Exclusion criteria: duplicates and articles outside the scope of the study. Results: The initial search resulted in 533 articles, 498 from PubMed, 2 from Web of Science and 33 from Scopus. After reading the title and abstract, the application of the inclusion and exclusion criteria, the sample of 48 documents were included. In the studies, 89.0% of all patients had cesarean delivery (n = 201), 33.3% had gestational complications, 35.3% had premature delivery and about 2.5% were stillborn or had neonatal death. Among those tested, 6.45% of neonates diagnosed positive for COVID-19. In another study, the newborn showed neurological issues similar to the adult patients and transient neurological complications due to cerebral vasculitis. Conclusions: The results demonstrate that further investigations are needed to determine the potential for vertical intrauterine transmission in pregnant women with COVID-19 and possibles fetal and neonatal consequences.
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