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Biomedical subjects

D H Chui

Publications and source records attributed to D H Chui.

120 records · Page 7Linked to original sources
PubMed1979

Hemoglobin ontogeny during normal mouse fetal development.

Pure populations of large, nucleated erythrocytes derived from yolk sac blood islands were obtained during normal fetal mouse development. Embryonic hemoglobins were present in these cells early in gestation. Later in gestation, an increasing amount of adults hemoglobin was also synthesized and accumulated in this population of primitive nucleated erythrocytes, as demonstrated by both biochemical and immunocytochemical techniques.

Animals↗
PubMed1979

Fetal erythropoiesis and hemoglobin ontogeny in tail-short (Ts/+) mutant mice.

Mutant Ts/+ fetuses are developmentally retarded as compared to normal +/+ littermates. Mutant fetuses have less total hemoglobin than do normal fetuses of the same gestational age. However, when compared to +/+ fetuses of similar body weight, Ts/+ fetuses have the appropriate amount of total hemoglobin, suggesting that the apparent anemia observed in mutant fetuses is most likely the result of delay in growth and development. Changes in proportions of embryonic hemoglobins during fetal development are similar in Ts/+ and +/+ fetuses at day 12 and later of gestation. Moreover, adult hemoglobin is detected in circulating primitive nucleated erythrocytes in the developmentally retarded Ts/+ mutant fetuses at about the same chronologic age as their +/+ normal littermates.

Aging↗
PubMed1978

Fetal erythropoiesis in steel mutant mice. III. Defect in differentiation from BFU-E to CFU-E during early development.

Erythroid progenitor cells in +/+ and Sl/Sld fetal livers manifested as burst-forming units-erythroid (BFU-E) and colony-forming units-erythroid (CFU-E) were assayed in vitro during early development. The proportion of BFU-E was higher as mutant than in normal fetal livers. On the other hand, the proportion of CFU-E was less in the mutant than in the normal. These results suggest that the defect in Sl/Sld fetal hepatic erythropoiesis is expressed at the steps of differentiation that effect the transition from BFU-E to CFU-E.

Animals↗
PubMed1975

Foetal erythropoiesis in steel mutant mice. II. Haemopoietic stem cells in foetal livers during development.

A rapid and reliable method of definitively identifying mutant (Sl/Sld) and wild type (+/+) mouse embryos in segregating litters is described, based on the mean cell volume determination of circulating foetal erythrocytes by an electronic particle counter. The mean cell volumes of yolk sac derived nucleated erythrocytes from +/+ and Sl/Sld embryos are similar, whereas the foetal liver derived non-nucleated red blood cells are much larger in Sl/Sld than +/+ embryos. There is no significant retardation in the growth of mutant embryos in spite of the severe anaemia which is macrocytic and normochromic. Evidence is also presented that the proportion of haemopoietic stem cells among hepatic erythroblasts, assayed by the macroscopic spleen colony technique, is higher in the mutant embryos, even though the total number of these progenitor cells present in each mutant foetal liver is less than the normal. Furthermore, these stem cells undergo active proliferation in Sl/Sld foetuses during development. The data indicate that the mutant Sl genes do not affect the primitive erythroid cell lineage derived from the yolk sac blood islands, but seriously interfere with the differentiation of the definitive erythroid cell lineage of foetal liver origin. It is further suggested that the mutant foetal liver fails to support or interferes with the normal rate of differentiation from immature precursor cells in to haemoglobinized erythroblasts. The reduction of total haemopoietic stem cells in mutant embryos may be secondary to this defect in cellular differentiation.

Animals↗
PubMed1975

Erythropoiesis in steel mutant mice: effects of erythropoietin in vitro.

Adult SI/SI-d mutant mice have severe macrocytic, normochromic anemia. Moreover these animals are unresponsive to the stimulation of erythropoietin in vivo. By means of a bone marrow cell suspension culture system, the present investigation shows that in adult SI/SI-d marrow, there are cells capable of responding in vitro to erythropoietin in a normal fashion. Moreover, the erythropoietin present in SI/SI-d serum is biologically active in vitro without any prior biochemical modification. These observations support the suggestion that there is a defect in differentiation in the erythroid cell lines of SI/SI-d mice in vivo due to an abnormal hemopoietic microenvironment.

Anemia, Macrocytic↗
PubMed1971

Erythropoietin effects on fetal mouse erythroid cells. I. Cell population and hemoglobin synthesis.

The effect of the hormone, erythropoietin, on cultures of erythroblasts derived from the livers of fetal C57BL/6J mice was examined. An increase both in the content and in the rate of synthesis of normal adult mouse globin chains was detected in hormone-treated cultures. The rate of protein synthesis by individual erythroblasts does not increase in response to the hormone, whereas the absolute number of hemoglobin-synthesizing cells does increase and accounts for the observed stimulation of hemoglobin synthesis. The principal effect of erythropoietin appears to be upon the population of immature erythroid precursor cells which persists in the presence of the hormone, the cells maintaining their ability to replicate, and their capacity to differentiate into hemoglobinizing erythroblasts. In the absence of hormone, already committed erythroblasts continue their development, but erythropoiesis is not sustained.

Animals↗
PubMedDate not supplied

Human ERMAP: an erythroid adhesion/receptor transmembrane protein.

A human cDNA and gene encoding for human ERMAP, a putative erythroid transmembrane adhesion/receptor protein, is reported. The predicted protein is made up of 475 amino acids and shares high homology with the murine ERMAP (73% identity and 14% conservative changes). Human Ermap is highly expressed in erythroid tissues and the protein localizes to the plasma membrane, particularly in sites of cell contact, and "cytoplasmic bodies." The extracellular segment contains one IgV fold that shares high homology with the butyrophilin family of milk proteins, autoantigens, and avian blood group antigens. In the intracellular region, there is a conserved B30.2 domain that is encoded by a single exon and is highly homologous with a similar domain in a diverse group of proteins, including butyrophilin, pyrin, and MID 1. The human Ermap gene is composed of 11 exons spanning 19 kb on chromosome 1p34.

Amino Acid Sequence↗