147 research outputs found
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An electrophoretic analysis of the coelomic and blood sera of the developing and metamorphosing bullfrog tadpole (Rana catesbeiana)
Albumin, as a percent of total proteins in both the coelomic
serum and the blood serum, was determined for four groups of
developing Rana catesbeiana tadpoles by cellulose acetate electrophoresis.
Also, using Folin phenol reagent, the total protein of
each the blood serum of metamorphosing tadpoles and the coelomic
serum was determined, along with the coelomic fluid weights relative
to the total body weights of these tadpoles. Coelomic fluid cells were
identified and percentages for them calculated.
Blood protein levels (1.68Ā±SE 0.01 g/100 ml) are significantly
higher than the coelomic fluid proteins (1.04Ā±SE 0.01 g/100 ml) in
metamorphosing animals. The percentage of albumin of total protein
in the coelomic fluid (Group I, 18.3Ā±2.3; II, 21.5Ā±1.07; III, 22.7Ā±0.68; IV, 31.3Ā±1.25) is significantly higher than that in the blood (Group I, 18.3Ā±2.30; II, 18.2Ā±0.82; III, 20.1Ā±0.82; IV, 27.7Ā±1.16)
for the last three Developmental Groups (Gosner stages 32-46). Percentages
of albumin in the blood and in the coelomic fluid did not
appear to increase at p<0.05, except in the last Group (IV).
The coelomic fluid weight decreased during the last five metamorphic
stages both absolutely, and also relative to tadpole weight.
The majority of the coelomic cells identified were lymphocytes
(51-85%). Monocytes accounted for 3-14%, and eosinophiles, erythrocytes,
histiocytes, neutrophiles and thrombocytes combined,
accounted for 4-23%
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Placental Origins of Chronic Disease.
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. Fetal development is underpinned by the placenta, the organ that forms the interface between the fetus and its mother. All nutrients and oxygen reaching the fetus must pass through this organ. The placenta also has major endocrine functions, orchestrating maternal adaptations to pregnancy and mobilizing resources for fetal use. In addition, it acts as a selective barrier, creating a protective milieu by minimizing exposure of the fetus to maternal hormones, such as glucocorticoids, xenobiotics, pathogens, and parasites. The placenta shows a remarkable capacity to adapt to adverse environmental cues and lessen their impact on the fetus. However, if placental function is impaired, or its capacity to adapt is exceeded, then fetal development may be compromised. Here, we explore the complex relationships between the placental phenotype and developmental programming of chronic disease in the offspring. Ensuring optimal placentation offers a new approach to the prevention of disorders such as cardiovascular disease, diabetes, and obesity, which are reaching epidemic proportions.The authors thank the various funding agencies that have generously supported their research over the years; GJB, the Medical Research Council, the Wellcome Trust and Action Medical Research; ALF, the Biotechnology and Biological Sciences Council, the Medical Research Council and the Wellcome Trust; KLT, the National Institutes of Child Health and Human Development, the Nation Heart Lung and Blood Institute, the National Institute of Diabetes and Digestive and Kidney Diseases, the National Institute of Aging, the American Heart Association and the M. Lowell Edwards Endowment.This is the author accepted manuscript. The final version is available from the American Physiological Society via https://doi.org/10.1152/physrev.00029.201
4-D Computational Modeling of Cardiac Outflow Tract Hemodynamics over Looping Developmental Stages in Chicken Embryos
Cardiogenesis is interdependent with blood flow within the embryonic system. Recently, a number of studies have begun to elucidate the effects of hemodynamic forces acting upon and within cells as the cardiovascular system begins to develop. Changes in flow are picked up by mechanosensors in endocardial cells exposed to wall shear stress (the tangential force exerted by blood flow) and by myocardial and mesenchymal cells exposed to cyclic strain (deformation). Mechanosensors stimulate a variety of mechanotransduction pathways which elicit functional cellular responses in order to coordinate the structural development of the heart and cardiovascular system. The looping stages of heart development are critical to normal cardiac morphogenesis and have previously been shown to be extremely sensitive to experimental perturbations in flow, with transient exposure to altered flow dynamics causing severe late stage cardiac defects in animal models. This paper seeks to expand on past research and to begin establishing a detailed baseline for normal hemodynamic conditions in the chick outflow tract during these critical looping stages. Specifically, we will use 4-D (3-D over time) optical coherence tomography to create in vivo geometries for computational fluid dynamics simulations of the cardiac cycle, enabling us to study in great detail 4-D velocity patterns and heterogeneous wall shear stress distributions on the outflow tract endocardium. This information will be useful in determining the normal variation of hemodynamic patterns as well as in mapping hemodynamics to developmental processes such as morphological changes and signaling events during and after the looping stages examined here
From Fatalism to Mitigation: a Conceptual Framework for Mitigating Fetal Programming of Chronic Disease by Maternal Obesity
Prenatal development is recognized as a critical period in the etiology of obesity and cardiometabolic disease. Potential strategies to reduce maternal obesity-induced risk later in life have been largely overlooked. In this paper, we first propose a conceptual framework for the role of public health and preventive medicine in mitigating the effects of fetal programming. Second, we review a small but growing body of research (through August 2015) that examines interactive effects of maternal obesity and two public health foci ā diet and physical activity ā in the offspring. Results of the review support the hypothesis that diet and physical activity after early life can attenuate disease susceptibility induced by maternal obesity, but human evidence is scant. Based on the review, we identify major gaps relevant for prevention research, such as characterizing the type and dose response of dietary and physical activity exposures that modify the adverse effects of maternal obesity in the offspring. Third, we discuss potential implications of interactions between maternal obesity and postnatal dietary and physical activity exposures for interventions to mitigate maternal obesity-induced risk among children. Our conceptual framework, evidence review, and future research directions offer a platform to develop, test, and implement fetal programming mitigation strategies for the current and future generations of children
Fetal Myocardial Expression of GLUT1: Roles of BPA Exposure and Cord Blood Exosomes in a Rat Model
Dietary exposure to Bisphenol A (BPA), an industrial chemical present in food containers, affects nutrient metabolism in the myocardium of offspring during intrauterine life. Using a murine model, we observed that fetal hearts from mothers exposed to BPA (2.5 mu g/kg/day) for 20 days before mating and for all of the gestation had decreased expression of glucose transporter-1 (GLUT1), the principal sugar transporter in the fetal heart, and increased expression of fatty acid cluster of differentiation 36 transporter (CD36), compared to control fetuses from vehicle-treated mothers. We confirmed the suppression of GLUT1 by exposing fetal heart organotypic cultures to BPA (1 nM) for 48 h but did not detect changes in CD36 compared to controls. During pregnancy, the placenta continuously releases extracellular vesicles such as exosomes into fetal circulation. These vesicles influence the growth and development of fetal organs. When fetal heart cultures were treated with cord blood-derived exosomes isolated from BPA-fed animals, GLUT1 expression was increased by approximately 40%. Based on our results, we speculate that exosomes from cord blood, in particular placenta-derived nanovesicles, could contribute to the stabilization of the fetal heart metabolism by ameliorating the harmful effects of BPA on GLUT1 expression
Long-Term Effects of Placental Growth on Overweight and Body Composition
Obesity is programmed in utero and small babies generally have small placentas. In some circumstances, an undernourished fetus can expand its placental surface to extract more nutrients. We hypothesize that this results in an imbalanced nutrient supply to the fetus leading to obesity. To determine whether placental size determines overweight and body composition, we studied 2003 subjects in adult life. Associations between placental surface area and indices of overweight were restricted to people who carried the Pro12Pro genotype of the PPARĪ³2 gene. For every 1 SD increase in placental surface area, the odds ratio for overweight was 1.37 (95% CI 1.10 to 1.71; P = 0.005). Expansion of the placental surface in compensation for fetal undernutrition increases the risk of overweight and a higher body fat percentage in people carrying the Pro12Pro genotype. We suggest that similar underlying multifactorial mechanisms affect the development of obesity in general
TranspoGene and microTranspoGene: transposed elements influence on the transcriptome of seven vertebrates and invertebrates
Transposed elements (TEs) are mobile genetic sequences. During the evolution
of eukaryotes TEs were inserted into active protein-coding genes, affecting
gene structure, expression and splicing patterns, and protein sequences.
Genomic insertions of TEs also led to creation and expression of new functional
non-coding RNAs such as micro- RNAs. We have constructed the TranspoGene
database, which covers TEs located inside proteincoding genes of seven species:
human, mouse, chicken, zebrafish, fruit fly, nematode and sea squirt. TEs were
classified according to location within the gene: proximal promoter TEs,
exonized TEs (insertion within an intron that led to exon creation), exonic TEs
(insertion into an existing exon) or intronic TEs. TranspoGene contains
information regarding specific type and family of the TEs, genomic and mRNA
location, sequence, supporting transcript accession and alignment to the TE
consensus sequence. The database also contains host gene specific data: gene
name, genomic location, Swiss-Prot and RefSeq accessions, diseases associated
with the gene and splicing pattern. In addition, we created microTranspoGene: a
database of human, mouse, zebrafish and nematode TEderived microRNAs. The
TranspoGene and micro- TranspoGene databases can be used by researchers
interested in the effect of TE insertion on the eukaryotic transcriptome
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Perinatal growth restriction decreases diuretic action of furosemide in adult rats
Perinatal growth restriction programs higher risk for chronic disease during adulthood
via morphological and physiological changes in organ systems. Perinatal growth
restriction is highly correlated with a decreased nephron number, altered renal function
and subsequent hypertension. We hypothesize that such renal maladaptations result in
altered pharmacologic patterns for life. Maternal protein restriction during gestation and
lactation was used to induce perinatal growth restriction in the current study. The
diuretic response of furosemide (2mg/kg single i.p dose) in perinatally growth restricted
rats during adulthood was investigated. Diuresis, natriuresis and renal excretion of
furosemide were significantly reduced relative to controls, indicative of decreased
efficacy. While a modest 12% decrease in diuresis was observed in males, females
experienced 26% reduction. It is important to note that the baseline urine output and
natriuresis was similar between treatment groups. The in vitro renal and hepatic
metabolism of furosemide, the in vivo urinary excretion of the metabolite, and the
expression of renal drug transporters was unaltered. Creatinine clearance was
significantly reduced by 15% and 19% in perinatally growth restricted male and female
rats, respectively. Further evidence of renal insufficiency was suggested by decreased
uric acid clearance. Renal protein expression of sodium-potassium-chloride
cotransporter, a pharmacodynamic target, was unaltered. In summary, perinatal growth
restriction could permanently imprint pharmacokinetic processes affecting drug
response.Keywords: perinatal growth restriction, furosemide, pharmacokinetics, fetal programming, renal insufficiency, in utero growth restrictio
The relationship between umbilical cord length and chronic rheumatic heart disease: a prospective cohort study.
BACKGROUND: One previous, preliminary study reported that the length of the umbilical cord at birth is related to the risk of developing chronic rheumatic heart disease in later life. We sought to replicate this finding. DESIGN: Prospective, population-based birth cohort. METHODS: We traced 11,580 individuals born between 1915 and 1929 in Uppsala, Sweden. We identified cases with a main or secondary diagnosis of chronic rheumatic heart disease in the Swedish national inpatient, outpatient or death registers. Archived obstetric records provided data on umbilical cord length, gestational age, birthweight and placental weight. RESULTS: There were 136 patients with chronic rheumatic heart disease (72 men and 64 women) with a mean age at first hospital admission of 68Ā years (range 36-92). There was evidence of a positive association between umbilical cord length and risk of subsequent chronic rheumatic heart disease. The overall hazard ratio in the Swedish study (1.13, 95% confidence interval 1.01 to 1.27) was similar to that of the previous study, with some suggestion of larger effect in men than in women. No other birth characteristics were predictive except for weak evidence of a protective effect of higher birthweight in men. CONCLUSIONS: People with longer umbilical cords at birth are more likely to develop chronic rheumatic heart disease in later life. As longer umbilical cords have more spiral arteries and a higher vascular resistance, we hypothesize that the increased pressure load on the heart leads to changes in endothelial biology and increased vulnerability to the autoimmune process initiated by infection with Ī²-haemolytic streptococci
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