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fetal origins of adult disease

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https://www.readbyqxmd.com/read/28101838/renal-consequences-of-preterm-birth
#1
REVIEW
Amelie Stritzke, Sumesh Thomas, Harish Amin, Christoph Fusch, Abhay Lodha
BACKGROUND: The developmental origin of health and disease concept identifies the brain, cardiovascular, liver, and kidney systems as targets of fetal adverse programming with adult consequences. As the limits of viability in premature infants have been pushed to lower gestational ages, the long-term impact of prematurity on kidneys still remains a significant burden during hospital stay and beyond. OBJECTIVES: The purpose of this study is to summarize available evidence, mechanisms, and short- and long-term renal consequences of prematurity and identify nephroprotective strategies and areas of uncertainty...
December 2017: Molecular and Cellular Pediatrics
https://www.readbyqxmd.com/read/28099426/fetal-origins-of-adult-cardiac-disease-a-novel-approach-to-prevent-fetal-growth-restriction-induced-cardiac-dysfunction-using-insulin-like-growth-factor
#2
Tarek Alsaied, Khaled Omar, Jeanne F James, Robert B Hinton, Timothy M Crombleholme, Mounira Habli
BACKGROUND: Fetal growth restriction is a risk factor for adult cardiovascular disease. Intra-placental gene transfer of human insulin-like growth factor-1 corrects birth weight in our mouse model of fetal growth restriction. This study addresses long term effects of fetal growth restriction on cardiac function and the potential preventive effect of insulin-like growth factor-1. STUDY DESIGN: Laparotomy was performed on pregnant C57BL/6J mice at embryonic day 18 and pups were divided into 3 groups: Sham operated; fetal growth restriction (induced by mesenteric uterine artery ligation); treatment (intra-placental injection of insulin-like growth factor-1 after uterine artery ligation)...
January 18, 2017: Pediatric Research
https://www.readbyqxmd.com/read/27979377/review-sexual-dimorphism-in-the-formation-function-and-adaptation-of-the-placenta
#3
REVIEW
J I Kalisch-Smith, D G Simmons, H Dickinson, K M Moritz
Exposure of the embryo or fetus to perturbations in utero can result in intrauterine growth restriction, a primary risk factor for the development of adult disease. However, despite similar exposures, males and females often have altered disease susceptibility or progression from different stages of life. Fetal growth is largely mediated by the placenta, which, like the fetus is genetically XX or XY. The placenta and its associated trophoblast lineages originate from the trophectoderm (TE) of the early embryo...
December 8, 2016: Placenta
https://www.readbyqxmd.com/read/27959272/fetal-syndrome-of-endocannabinoid-deficiency-fsecd-in-maternal-obesity
#4
Natalia Schlabritz-Loutsevitch, Nadezhda German, Gary Ventolini, Eneko Larumbe, Jacques Samson
The theory of a fetal origin of adult diseases links many pathological conditions to very early life events and is known as a "developmental programming" phenomenon. The mechanisms of this phenomenon are not quite understood and have been explained by inflammation, stress, etc. In particular the epidemic of obesity, with more than 64% of women being overweight or obese, has been associated with conditions in later life such as mental disorders, diabetes, asthma, and irritable bowel syndrome. Interestingly, these diseases were classified a decade ago as Clinical Syndrome of Endocannabinoid Deficiency (CECD), which was first described by Russo in 2004...
November 2016: Medical Hypotheses
https://www.readbyqxmd.com/read/27903733/development-of-activity-in-the-mouse-visual-cortex
#5
Jing Shen, Matthew T Colonnese
: A comprehensive developmental timeline of activity in the mouse cortex in vivo is lacking. Understanding the activity changes that accompany synapse and circuit formation is important to understand the mechanisms by which activity molds circuits and would help to identify critical checkpoints for normal development. To identify key principles of cortical activity maturation, we systematically tracked spontaneous and sensory-evoked activity with extracellular recordings of primary visual cortex (V1) in nonanesthetized mice...
November 30, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27886132/the-future-is-the-past-methylation-qtls-in-schizophrenia
#6
REVIEW
Anke Hoffmann, Michael Ziller, Dietmar Spengler
Genome-wide association studies (GWAS) have remarkably advanced insight into the genetic basis of schizophrenia (SCZ). Still, most of the functional variance in disease risk remains unexplained. Hence, there is a growing need to map genetic variability-to-genes-to-functions for understanding the pathophysiology of SCZ and the development of better treatments. Genetic variation can regulate various cellular functions including DNA methylation, an epigenetic mark with important roles in transcription and the mediation of environmental influences...
November 24, 2016: Genes
https://www.readbyqxmd.com/read/27882215/epigenetic-changes-in-peripheral-leucocytes-as-biomarkers-in-intrauterine-growth-retardation-rat
#7
Xue-Feng Xu, Shan-Shan Xu, Lin-Cheng Fu, Qiong-Yao Hu, Ying Lv, Li-Zhong Du
Epigenetics plays an important role in the fetal origins of adult disease. Intrauterine growth retardation (IUGR) can cause increased histone acetylation of the endothelin-1 (ET-1) gene from pulmonary vascular endothelial cells or the whole lung tissue and persist into later life, likely resulting in increased risk of pulmonary hypertension or asthma later in life. However, little is known regarding the correlation of epigenetic changes between specific tissue and peripheral leucocytes. In the present study, an IUGR rat model was established by maternal nutrient restriction...
November 2016: Biomedical Reports
https://www.readbyqxmd.com/read/27817870/biological-features-of-placental-programming
#8
Kent L Thornburg, Kevin Kolahi, Melinda Pierce, Amy Valent, Rachel Drake, Samantha Louey
The placenta is a key organ in programming the fetus for later disease. This review outlines nine of many structural and physiological features of the placenta which are associated with adult onset chronic disease. 1) Placental efficiency relates the placental mass to the fetal mass. Ratios at the extremes are related to cardiovascular disease risk later in life. 2) Placental shape predicts a large number of disease outcomes in adults but the regulators of placental shape are not known. 3) Non-human primate studies suggest that at about mid-gestation, the placenta becomes less plastic and less able to compensate for pathological stresses...
December 2016: Placenta
https://www.readbyqxmd.com/read/27801895/prenatal-maternal-depression-is-associated-with-offspring-inflammation-at-25-years-a-prospective-longitudinal-cohort-study
#9
D T Plant, S Pawlby, D Sharp, P A Zunszain, C M Pariante
Animal studies and a handful of prospective human studies have demonstrated that young offspring exposed to maternal prenatal stress show abnormalities in immune parameters and hypothalamic-pituitary-adrenal (HPA) axis function. No study has examined the effect of maternal prenatal depression on offspring inflammation and HPA axis activity in adulthood, nor the putative role of child maltreatment in inducing these abnormalities. High-sensitivity C-reactive protein (hs-CRP) and awakening cortisol were measured at age 25 in 103 young-adult offspring of the South London Child Development Study (SLCDS), a prospective longitudinal birth cohort of mother-offspring dyads recruited in pregnancy in 1986...
November 1, 2016: Translational Psychiatry
https://www.readbyqxmd.com/read/27780972/developmental-origins-of-nafld-a-womb-with-a-clue
#10
REVIEW
Stephanie R Wesolowski, Karim C El Kasmi, Karen R Jonscher, Jacob E Friedman
Changes in the maternal environment leading to an altered intrauterine milieu can result in subtle insults to the fetus, promoting increased lifetime disease risk and/or disease acceleration in childhood and later in life. Particularly worrisome is that the prevalence of NAFLD is rapidly increasing among children and adults, and is being diagnosed at increasingly younger ages, pointing towards an early-life origin. A wealth of evidence, in humans and non-human primates, suggests that maternal nutrition affects the placenta and fetal tissues, leading to persistent changes in hepatic metabolism, mitochondrial function, the intestinal microbiota, liver macrophage activation and susceptibility to NASH postnatally...
October 26, 2016: Nature Reviews. Gastroenterology & Hepatology
https://www.readbyqxmd.com/read/27763252/myeloid-cell-origins-differentiation-and-clinical-implications
#11
Kipp Weiskopf, Peter J Schnorr, Wendy W Pang, Mark P Chao, Akanksha Chhabra, Jun Seita, Mingye Feng, Irving L Weissman
The hematopoietic stem cell (HSC) is a multipotent stem cell that resides in the bone marrow and has the ability to form all of the cells of the blood and immune system. Since its first purification in 1988, additional studies have refined the phenotype and functionality of HSCs and characterized all of their downstream progeny. The hematopoietic lineage is divided into two main branches: the myeloid and lymphoid arms. The myeloid arm is characterized by the common myeloid progenitor and all of its resulting cell types...
October 2016: Microbiology Spectrum
https://www.readbyqxmd.com/read/27752049/tissue-resident-macrophages-how-to-humanize-our-knowledge
#12
Andreas Schlitzer, Joachim L Schultze
Tissue macrophages of fetal and adult origin have pivotal roles in tissue homeostasis and organ inflammation. Recently several functional and transcriptomic studies have revealed their unique module-like transcriptomic organization leading to enormous tissue-dependent functional plasticity. In this review, we discuss the development, tissue adaption and function of resident murine and human macrophages. Finally, we discuss our limited knowledge on human tissue macrophages and provide our opinion on their relevance during disease and for clinical application...
October 18, 2016: Immunology and Cell Biology
https://www.readbyqxmd.com/read/27734997/gamete-and-embryo-fetal-origins-of-adult-diseases
#13
Manuela Monti
By putting together the most advanced evidences supporting the 'gamete and embryo-fetal origins of adult diseases' the two editors, Prof. He-Feng Huang and Prof. Jian-Zhong Sheng (Hangzhou, People's Republic of China) did a great workk.....
August 10, 2016: European Journal of Histochemistry: EJH
https://www.readbyqxmd.com/read/27680963/prenatal-food-restriction-induces-poor-quality-articular-cartilage-in-female-rat-offspring-fed-a-post-weaning-high-fat-diet-and-its-intra-uterine-programming-mechanisms
#14
Yang Tan, Yunpeng Wu, Qubo Ni, Yu Deng, Jing Li, Linlong Wang, Lang Shen, Yansong Liu, Jacques Magdalou, Hui Wang, Liaobin Chen
Epidemiological data show that osteoarthritis (OA) is significantly associated with lower birth weight, and that OA may be a type of fetal-originated adult disease. The present study aimed to investigate the prenatal food-restriction (PFR) effect on the quality of articular cartilage in female offspring to explore the underlying mechanisms of fetal-originated OA. Maternal rats were fed a restricted diet from gestational day (GD) 11 to 20 to induce intra-uterine growth retardation. Female fetuses and female adult offspring fed a post-weaning high-fat diet were killed at GD20 and postnatal week 24, respectively...
October 2016: British Journal of Nutrition
https://www.readbyqxmd.com/read/27666010/a-transient-developmental-hematopoietic-stem-cell-gives-rise-to-innate-like-b-and-t-cells
#15
Anna E Beaudin, Scott W Boyer, Jessica Perez-Cunningham, Gloria E Hernandez, S Christopher Derderian, Chethan Jujjavarapu, Eric Aaserude, Tippi MacKenzie, E Camilla Forsberg
The generation of distinct hematopoietic cell types, including tissue-resident immune cells, distinguishes fetal from adult hematopoiesis. However, the mechanisms underlying differential cell production to generate a layered immune system during hematopoietic development are unclear. Using an irreversible lineage-tracing model, we identify a definitive hematopoietic stem cell (HSC) that supports long-term multilineage reconstitution upon transplantation into adult recipients but does not persist into adulthood in situ...
December 1, 2016: Cell Stem Cell
https://www.readbyqxmd.com/read/27618559/preserving-of-postnatal-leptin-signaling-in-obesity-resistant-lou-c-rats-following-a-perinatal-high-fat-diet
#16
Anne-Laure Poher, Denis Arsenijevic, Mohamed Asrih, Abdul G Dulloo, François R Jornayvaz, Françoise Rohner-Jeanrenaud, Christelle Veyrat-Durebex
Physiological processes at adulthood, such as energy metabolism and insulin sensitivity may originate before or weeks after birth. These underlie the concept of fetal and/or neonatal programming of adult diseases, which is particularly relevant in the case of obesity and type 2 diabetes. The aim of this study was to determine the impact of a perinatal high fat diet on energy metabolism and on leptin as well as insulin sensitivity, early in life and at adulthood in two strains of rats presenting different susceptibilities to diet-induced obesity...
2016: PloS One
https://www.readbyqxmd.com/read/27604528/placental-origins-of-chronic-disease
#17
REVIEW
Graham J Burton, Abigail L Fowden, Kent L Thornburg
Epidemiological evidence links an individual's susceptibility to chronic disease in adult life to events during their intrauterine phase of development. Biologically this should not be unexpected, for organ systems are at their most plastic when progenitor cells are proliferating and differentiating. Influences operating at this time can permanently affect their structure and functional capacity, and the activity of enzyme systems and endocrine axes. It is now appreciated that such effects lay the foundations for a diverse array of diseases that become manifest many years later, often in response to secondary environmental stressors...
October 2016: Physiological Reviews
https://www.readbyqxmd.com/read/27577791/homage-to-the-h-in-developmental-origins-of-health-and-disease
#18
C S Rosenfeld
Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes...
February 2017: Journal of Developmental Origins of Health and Disease
https://www.readbyqxmd.com/read/27555292/transgenerational-cardiology-one-way-to-a-baby-s-heart-is-through-the-mother
#19
Patrick Y Jay, Ehiole Akhirome, Rachel A Magnan, M Rebecca Zhang, Lillian Kang, Yidan Qin, Nelson Ugwu, Suk Dev Regmi, Julie M Nogee, James M Cheverud
Despite decades of progress, congenital heart disease remains a major cause of mortality and suffering in children and young adults. Prevention would be ideal, but formidable biological and technical hurdles face any intervention that seeks to target the main causes, genetic mutations in the embryo. Other factors, however, significantly modify the total risk in individuals who carry mutations. Investigation of these factors could lead to an alternative approach to prevention. To define the risk modifiers, our group has taken an "experimental epidemiologic" approach via inbred mouse strain crosses...
November 5, 2016: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/27542533/increased-susceptibility-of-prenatal-food-restricted-offspring-to-high-fat-diet-induced-nonalcoholic-fatty-liver-disease-is-intrauterine-programmed
#20
Li Zhang, Lang Shen, Dan Xu, Linlong Wang, Yuming Guo, Zhongfen Liu, Yansong Liu, Lian Liu, Jacques Magdalou, Liaobin Chen, Hui Wang
The present study aims to explore the mechanisms of fetal origin of high susceptibility to adult high-fat diet induced-nonalcoholic fatty liver disease in rat offspring undergoing intrauterine growth retardation (IUGR) induced by prenatal food restriction (FR) from gestational day 11 until full-term delivery. We observed that adult IUGR offspring rats exhibited gender-dependent catch-up growth with lower serum corticosterone (CORT) but up-regulation of the insulin-like growth factor 1 (IGF1) pathway, higher hepatic Kleiner scores and lower lipid export and oxidation...
October 2016: Reproductive Toxicology
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