J. E. Infeld

Bio: J. E. Infeld is an academic researcher. The author has contributed to research in topics: Placenta & Fetus. The author has an hindex of 2, co-authored 2 publications receiving 105 citations.

Growth and in-vitro metabolism of placental tissues of cows from day 100 to day 250 of gestation.

Abstract: Weight of placental tissues of cows increased exponentially from Day 100 to Day 250 of gestation, but at much slower relative and absolute rates than fetal weight. In addition, growth rate of fetal placental tissues was less than that of maternal placental tissues. Concentrations of DNA, RNA and protein, however, increased in fetal placental but not in maternal placental tissues. Fetal placental tissues therefore exhibited hyperplasia, which probably contributes to increased functional capacity of the placenta during late gestation. The rate of O2 uptake in vitro was greatest for maternal placental tissues, suggesting that the maternal portion of the placenta accounts for most of the large rate of placental O2 utilization in vivo. Compared with other placental tissues, rate of secretion of macromolecules by intercaruncular endometrium was high, but decreased from Day 100 to 250, suggesting that uterine glandular secretory activity may decrease as gestation advances. Rate of secretion of macromolecules also was high for intercotyledonary tissues and increased with day of gestation, suggesting a role for secretory products of chorioallantois in gravid uterine function.

Angiogenic activity of placental tissues of cows.

Abstract: In Exp. 1, maternal (caruncle) and fetal (cotyledon) portions of the placenta as well as uterine endometrium were obtained from cows at mid-gestation and evaluated for angiogenic activity by placing tissue samples on chick chorioallantoic membranes (CAM). Only caruncular tissues exhibited angiogenic activity in the CAM assay. In Exp. 2, lyophilized homogenates of caruncular tissues obtained from cows at mid-gestation were evaluated for angiogenic activity on CAM and for their ability to stimulate mitosis of bovine aortic endothelial cells in vitro. Homogenates of caruncular tissues again were angiogenic on the CAM and also were mitogenic for endothelial cells. In Exp. 3, maternal (caruncle and endometrium) and fetal (cotyledon and fetal membrane) portions of the placenta were obtained from cows at mid-gestation and fine minces (explants) of each were cultured for 24 h. Explant-conditioned media were then tested for angiogenic activity by their abilities to stimulate mitosis and migration of bovine aortic endothelial cells in vitro. Conditioned media from caruncular explants, but not from explants of other tissues, exhibited both mitogenic and migration-stimulating activities. When pools of caruncular explant-conditioned media were fractionated by ultrafiltration, mitogenic activity was not present in fractions of Mr less than 10,000, less than 30,000 and less than 100,000, but was retained in fractions of Mr greater than 10,000, greater than 30,000 and greater than 100,000. Mitogenic activity was not observed in any fractions subjected to heat treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiogenesis in the Placenta

Abstract: The mammalian placenta is the organ through which respiratory gases, nutrients, and wastes are exchanged between the maternal and fetal systems. Thus, transplacental exchange provides for all the metabolic demands of fetal growth and development. The rate of transplacental exchange depends primarily on the rates of uterine (maternal placental) and umbilical (fetal placental) blood flows. In fact, increased uterine vascular resistance and reduced uterine blood flow can be used as predictors of high risk pregnancies and are associated with fetal growth retardation. The rates of placental blood flow, in turn, are dependent on placental vascularization, and placental angiogenesis is therefore critical for the successful development of viable, healthy offspring. Recent studies, including gene knockouts in mice, indicate that the vascular endothelial growth factors represent a major class of placental angiogenic factors. Other angiogenic factors, such as the fibroblast growth factors or perhaps the angiopoietins, also may play important roles in placental vascularization. In addition, recent observations suggest that these angiogenic factors interact with the local vasodilator nitric oxide to coordinate placental angiogenesis and blood flow. In the future, regulators of angiogenesis that are currently being developed may provide novel and powerful methods to ensure positive outcomes for most pregnancies.

Angiogenesis in the female reproductive system.

Abstract: In adult tissues, capillary growth (angiogenesis) occurs normally during tissue repair, such as in healing of wounds and fractures. Rampant capillary growth is associated with various pathological conditions, including tumor growth, retinopathies, hemangiomas, fibroses and rheumatoid arthritis. The female reproductive organs (i.e., ovary, uterus, and placenta) exhibit dynamic, periodic growth and regression accompanied by equally dramatic changes in rates of blood flow. It is not surprising, therefore, that they are some of the few adult tissues in which angiogenesis occurs as a normal process. Thus, the female reproductive system provides a unique model for studying regulation of angiogenesis during growth and differentiation of normal adult tissues. Ovarian, uterine, and placental tissues recently have been shown to contain and produce angiogenic and anti-angiogenic factors. This review discusses the current state of knowledge regarding angiogenic processes and their regulation in female reproductive tissues. In addition, implications of this research for regulation of fertility as well as for control of angiogenesis in other normal and pathological processes are discussed.

Utero-placental vascular development and placental function.

Abstract: The rate of fetal growth and subse- quent birth weight are major determinants of postna- tal survival and growth. Because the placenta is the organ through which respiratory gases, nutrients, and wastes are transported between the maternal and fetal systems, its primary function is to supply the metabolic substrates necessary to support fetal growth. Placental growth and development, therefore, are critical for normal fetal growth and development. During the last half of gestation in mammals, growth of the fetus is exponential, whereas utero-placental growth slows or ceases. Nevertheless, unless placental transport capacity keeps pace with the continually increasing demands of the fetus, fetal growth will be compromised. Studies over the last two decades have shown that placental transport capacity does indeed keep pace with fetal growth. This increase in placental function can be accounted for primarily by continual increases in placental (uterine and umbilical) blood flows, associated with increased placental vascularity. Placental vascular growth and development, in turn, are probably regulated by angiogenic factors produced by the placental tissues themselves. These placental angiogenic factors are produced primarily by the maternal placental tissues, are heparin-binding, and seem to be related to the fibroblast growth factor family. Further elucidation of the factors responsible for placental growth and vascular development is critical for an improved understanding of utero- placental-fetal interactions, which result in delivery of a healthy offspring.

Effects of dietary fiber on intestinal growth, cell proliferation, and morphology in growing pigs.

Abstract: Growing pigs (initial BW 14.3 +/- 1.2 kg) were fed isocaloric (3.26 Mcal of ME/kg) and isonitrogenous (16% CP) diets containing either 0 (low fiber, LF; n = 4) or 10% (high fiber, HF; n = 4) wheat straw for ad libitum intake for 14 d. On d 14, each pig was injected i.v. with bromodeoxyuridine (BrdU, a thymidine analog; 5 mg/kg) and was slaughtered 1 h later. Visceral organs (liver, pancreas, and intestines) were weighed, and tissue samples were obtained. Feed consumption, daily gain, gain: feed, and final BW did not differ between treatments. Neither visceral weights nor visceral weights per unit of eviscerated BW were affected by diets. Tissue concentrations of DNA (milligrams/gram of tissue) were lower (P < .03) in HF than in LF only for jejunum, ileum, and liver. Contents of DNA and protein (milligrams) did not differ between LF and HF for intestinal segments or liver. Content of RNA (milligrams) was greater (P < .04) in HF than in LF only for colon. The number of crypt cell nuclei that were labeled with BrdU (indicating DNA synthesis and thus cell proliferation) was increased (P < .03) in HF relative to LF for jejunum and colon. The number of epithelial cells exhibiting DNA fragmentation (indicating programmed cell death) was greater (P < .07) in the HF than in the LF group for jejunum and ileum. Width of intestinal villi was increased (P < .10) in HF vs LF for jejunum and ileum. Depth of intestinal crypts was increased (P < .08) in HF vs LF for jejunum, ileum, and colon.(ABSTRACT TRUNCATED AT 250 WORDS)

Large Offspring or Large Placenta Syndrome? Morphometric Analysis of Late Gestation Bovine Placentomes from Somatic Nuclear Transfer Pregnancies Complicated by Hydrallantois

Abstract: Somatic nuclear transfer (NT) in cattle is often complicated by fetal oversize (i.e., large offspring syndrome), hydrallantois, and placentomegaly in late gestation. The aims of this work were to obtain data on the placentome structure in NT-recipient cows with hydrallantois (NTH) and to relate these with fetal and placental weights to better understand the abnormalities observed in NTH pregnancies during the third trimester. Pregnant cows were slaughtered between Gestation Days 180 and 280. The fetuses were weighed, and the placentomes were numbered and weighed. Placentomes were examined by histologic and stereological techniques. Macroscopic data showed that placental overgrowth preceded fetal overgrowth, and the ratio of the fetal to the total placentome weight in the NTH group was lower than that in controls after Gestation Day 220. This suggests that placental overgrowth is due to placental default rather than due to fetal overgrowth, as shown also by stereological analysis showing primary deregulation of the growth of cotyledonary tissues. Observed alterations, such as thinning of the maternal epithelium within placentomes and increased trophoblastic surface, could be secondary adaptations. Thus, placental growth deregulations would be due to modifications of the expression of placental factors. Various examples of placental deficiency were observed, suggesting that some fetal abnormalities observed in NTH calves, such as enlarged heart, enlarged umbilical cord, and abdominal ascites, are consequences of placental dysfunction. Therefore, the condition described by the term "large offspring syndrome" might better be described by "large placenta syndrome," because this syndrome affects an average of 50% of late-gestation NT pregnancies. No conclusion can be drawn from this work on apparently normal pregnancies.