SEARCH · PubMed Health

Results for “ERYTHROBLASTOSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

PubMed1985

High-frequency transduction of c-erbB in avian leukosis virus-induced erythroblastosis.

Twenty-one cases of Rous-associated virus type 1-induced erythroblastosis have been analyzed for novel restriction endonuclease fragments of c-erbB. Twenty of the erythroleukemias contained novel c-erbB fragments; 10 of these were found to contain a proviral insertion in c-erbB, and 10 were found to have a new transduction of c-erbB. Each of the proviral insertions was in the same transcriptional orientation as c-erbB, and most appeared to have retained both long terminal repeats as well as 5' viral sequences that signal packaging of RNA into virions. Each of the new c-erbB transducing viruses had a characteristic EcoRI fragment that contained a spliced form of c-erbB sequences. When inoculated into 1-week-old chickens, the new transducing viruses caused rapid-onset erythroblastosis.

Animals↗

PubMed1986

Structural domains of the avian erythroblastosis virus erbB protein required for fibroblast transformation: dissection by in-frame insertional mutagenesis.

Avian erythroblastosis virus (AEV) induces erythroblastosis and fibrosarcomas. The viral erbB protein is required for AEV-mediated oncogenesis. To explore the structural aspects of the v-erbB polypeptide necessary for its oncogenic function, we created a series of small in-frame insertions in different domains of the v-erbB oncogene. AEV genomes bearing lesions within the v-erbB kinase domain demonstrated a drastically decreased ability to transform avian fibroblasts, establishing a functional role for this structurally conserved oncogene domain. In contrast, mutations in the extracellular domain, between the transmembrane region and the kinase domain, or at the extreme C terminus of the v-erbB protein had no effect on AEV-mediated fibroblast transformation. One lesion within the v-erbB kinase domain, a 10-amino acid insertion, produced a temperature-sensitive mutant capable of fibroblast transformation at 36 degrees C but not at 41 degrees C, suggesting that small in-frame insertions have general utility for the in vitro creation of conditional mutants.

Alpharetrovirus↗

PubMed1986

Mammalian cell transformation by a murine retrovirus vector containing the avian erythroblastosis virus erbB gene.

A recombinant murine retrovirus vector containing the v-erbB gene of avian erythroblastosis virus was constructed to investigate v-erbB as a transforming gene for mammalian cells. A restriction fragment containing the v-erbB sequences from a molecular clone of avian erythroblastosis virus was inserted into a Moloney murine leukemia virus vector. The construct, designated MuLV/erbB, transformed NIH 3T3 cells at a high efficiency in the DNA transfection assay. Individual MuLV/erbB transfectants grew in soft agar and were tumorigenic. The transfectants contained v-erbB DNA sequences, expressed v-erbB-specific transcripts, and synthesized v-erbB-related glycoproteins. The majority of transfectants produced two major v-erbB gene products of 58 and 66 kilodaltons. However, some transfectants produced much smaller v-erbB-specific proteins. Tunicamycin experiments revealed that the size heterogeneity observed between different transfectants was not due to variations in glycoprotein processing, implying that, in some cases, alterations in the MuLV/erbB genome occurred during the transfection process. These findings indicate that expression of the complete v-erbB gene product is not required for transformation of NIH 3T3 cells. A transmissible murine v-erbB (M-erbB) virus was generated by infection of nonproducer transfectants with amphotrophic murine leukemia virus. Transmission of the rescued M-erbB virus was confirmed by DNA, RNA, and protein analyses. The introduction of a transforming v-erbB gene into mammalian cells by virus infection provides a means of analyzing the mechanism by which this epidermal growth factor receptor-related gene alters the growth and differentiation of cells from various lineages.

Alpharetrovirus↗

PubMed1989

Avian erythroblastosis virus transforms a novel mast cell-basophil precursor target in the Japanese quail.

Hematopoietic cells of the Japanese quail were transformed by avian erythroblastosis virus in vivo and in vitro. In both circumstances, the infected hematopoietic tissues exhibited a dual oncogenic response of erythroid and mast cell-basophil elements. The erythroid transformants escaped the avian erythroblastosis virus block in differentiation and progressed to hemoglobinization. Resulting basophilic cells were morphologically, biochemically, and ultrastructurally identical to mast cell-basophils observed in other species. None of the virally transformed cells actively produced reverse transcriptase activity. Nonproducer cell lines synthesized viral RNA and both v-erbA and v-erbB proteins. These results indicate that the Japanese quail has a viral target cell different from that of the chicken. The implications of a single bipotential transformation target yielding both erythroid and mast cell-basophil colonies is discussed.

Alpharetrovirus↗

PubMed1986

A single amino acid substitution in v-erbB confers a thermolabile phenotype to ts167 avian erythroblastosis virus-transformed erythroid cells.

A library of recombinant bacteriophage was prepared from ts167 avian erythroblastosis virus-transformed erythroid precursor cells (HD6), and integrated proviruses from three distinct genomic loci were isolated. A subclone of one of these proviruses (pAEV1) was shown to confer temperature-sensitive release from transformation of erythroid precursor cells in vitro. The predicted amino acid sequence of the v-erbB polypeptide from the mutant had a single amino acid change when compared with the wild-type parental virus. When the wild-type amino acid was introduced into the temperature-sensitive avian erythroblastosis virus provirus in pAEV1, all erythroid clones produced in vitro were phenotypically wild type. The mutation is a change from a histidine to an aspartic acid in the temperature-sensitive v-erbB polypeptide. It is located in the center of the tyrosine-specific protein kinase domain and corresponds to amino acid position 826 of the human epidermal growth factor receptor sequence.

Alpharetrovirus↗

PubMed1977

Leuco-erythroblastosis following withdrawal from glucocorticoid therapy.

Leuco-erythroblastosis has many known associations (Burkett, Cox and Fields, 1965; Weick, Hagedorn and Linman, 1974; Retief, 1964), but the only ones related to drug therapy are the well established response to haematinics (Burkett et al., 1965) and one possible case following anti-epileptic therapy (Retief, 1964). The case described below is of leuco-erythroblastosis following steroid withdrawal in a young man with primary polymyositis.

Adult↗

PubMed1984

Oncogenecity of an avian erythroblastosis virus in mutant strains of Japanese quails.

The susceptibility of 12 mutant strains of Japanese quails to the R strain of avian erythroblastosis virus (AEV) was examined. Three strains, SBPP, PNN and CWE, showed high susceptibility and developed various types of tumors including erythroblastosis, hemangioma and myeloblastic leukemia. In relatively resistant WE strain, increased incidence and various types of tumors were observed by modification of host conditions. These results indicate pluripotential oncogenicity of AEV in quails as well as partial control of AEV-oncogenesis by genetical background of the host.

Alpharetrovirus↗

PubMedDate not supplied

Anorexia as the probable cause of plasma alpha-lipoprotein changes seen in avian erythroblastosis.

The plasma alpha-lipoprotein bands seen on starch-gel electrophoresis are progressively split and retarded as avian erythroblastosis progresses. Similar changes may be produced in normal birds by starvation, and by pair-feeding methods. Anorexia appears to be a major cause, if not the total cause, of the plasma alpha-lipoprotein changes seen in erythroblastosis.

Alpharetrovirus↗

PubMed1990

Immune abnormalities in avian erythroblastosis virus-infected chickens.

Infection of animals with retroviruses frequently leads to immunosuppressed states. The immune status of chickens injected with the replication-defective avian erythroblastosis virus (AEV), with its naturally occurring subgroup B helper virus (avian erythroblastosis-associated virus; AEAV), was evaluated daily and compared to the immune status of age-matched uninfected control chickens. Spleen cells from AEV-infected chickens gave depressed responses to concanavalin A, phytohemagglutinin, and pokeweed mitogen beginning 3 days after injection of the virus and continuing until death. Spleen cells from AEV-infected chickens suppressed the T-cell mitogen-induced blastogenic responses of spleen cells from uninfected chickens. The ability of spleen cells from infected chickens to suppress mitogen-induced blastogenic responses of spleen cells from normal chickens in coculture was transient beginning 4 days following viral inoculation, reaching peak levels of suppression on day 7 and disappearing by day 12. Cytolysis of splenic cells from AEV-infected chickens with polyclonal anti-T-cell-serum removed the suppressor activity. Addition of conditioned medium rich in T-cell growth factor resulted in a partial restoration of the blastogenic responsiveness of splenic cells from 6-day post-AEV-infected chickens. Addition of exogenous T-cell growth factor had no effect on the suppressed blastogenic responsiveness of spleen cells from 12-day post-AEV-infected chickens, and it had no effect on coculture suppression. In addition to suppressed T-cell responses to polyclonal mitogen-induced proliferation in vitro and transiently expressed T-suppressor cells, thymic atrophy and structural disruption was observed in AEV-infected chickens.

Alpharetrovirus↗

PubMed1982

Japanese quail embryo cell line persistently infected with erythroblastosis virus.

A Japanese quail embryo cell line transformed by avian retrovirus, designated QERC-31F, was further characterized in virological and cytological aspects. Infectious virus produced by this cell line was found to belong to subgroup A. The virus failed to transform quail embryo cells, whereas it induced erythroblastosis by injection into neonatal quails. Injection of QERC-31F cells into neonatal quails resulted in the induction of solid tumors which morphologically diagnosed as undifferentiated sarcoma. Mitosis of pro-erythrocytic cells with also detected in the peripheral blood of the tumor bearing animals. Antiserum to chicken erythrocyte histone V fraction which was also shown to react specifically with the nucleus of quail erythrocytes stained the nucleus of QERC-31F cells. These results suggested that this cell line maintains characteristics of the erythroblast and possibly produces avian erythroblastosis virus as well as helper virus of subgroup A.

Alpharetrovirus↗

PubMed1953

Experimental erythroblastosis fetalis in rabbits. II. The passage of blood group antigens and their specific isoantibodies across the placenta.

Female rabbits became immunized during pregnancy to the rabbit blood group factors G or g in five out of ten instances in which the red cells of the fetuses carried one of the factors absent in the mother. Antibodies so produced were of low titer and disappeared in all cases within 6 weeks after the birth of the litter. Repeated pregnancies did not result in additive increases in titer. Antibodies to the G-g factors, whether produced by the injection of red cells or by pregnancy, crossed the placenta readily from mother to fetus and were found at birth (and prior to nursing) associated with the red cells and in the serum of the fetuses. The rabbit placenta appeared to be equally permeable to the agglutinating and coating antibodies. The implications of these findings and their relation to the pathogenesis of erythroblastosis fetalis are briefly touched upon.

Animals↗

PubMed1956

Management of erythroblastosis fetalis.

The practical management of the problem of erythroblastosis depends primarily on the prenatal determination of which pregnancies might result in an erythroblastotic infant. The physician primarily concerned with the care of the child must attend the delivery of every Rh-negative woman whose serum contains anti-Rh antibodies. At present, prompt confirmation of the suspected diagnosis immediately following birth and immediate exchange transfusion in infants with laboratory or clinical evidence of the disease are necessary to reduce morbidity and prevent kernicterus.

Child↗

PubMed1988

Erythroblastosis and reticulocytosis in anemic fetuses.

The fetal blood erythroblast and reticulocyte counts were determined in umbilical cord samples obtained at 17 to 36 weeks' gestation from 127 pregnancies complicated by red blood cell isoimmunization. The reticulocyte count increased linearly with fetal anemia, and the erythroblast count increased exponentially. Significant erythroblastosis was observed only when the hemoglobin concentration deficit was greater than 7 gm/dl. Of the 52 fetuses with a hemoglobin concentration deficit greater than 7 gm/dl, 35 had ultrasonographic evidence of hydrops. These data suggest that medullary hematopoiesis is stimulated by mild anemia and that recruitment of extramedullary sites occurs when anemia is severe. Extensive hepatic erythropoiesis may be the cause of fetal hydrops in red blood cell isoimmunization.

Anemia↗

PubMed1987

Measurement of human fetoplacental blood volume in erythroblastosis fetalis.

The fetoplacental blood volume of the human fetus was measured with the change in hematocrit at the time of intravascular transfusion for severe erythroblastosis. A total of 121 measurements were made between 18 and 31 weeks' gestation. The volume ranged from 117 ml/kg at 18 weeks to 93.1 ml/kg at 31 weeks. These values compare closely with those reported for the sheep fetus and, when they are extrapolated to term, are similar to the blood volume of human newborns plus the residual placental blood volume.

Blood Transfusion, Intrauterine↗

PubMedDate not supplied

[Erythroblastosis in a live newborn infant with triploidy--a sequela of fetomaternal macrotransfusion?].

Hematologic changes in an infant, live-born and surviving 46 hours are reported. The main characteristics were a decrease of red blood cells and an increase of mean corpuscular volume and mean corpuscular hemoglobin concentration. Some morphological abnormalities were found. The smears showed prematurity of the red cells, many of them with degenerative nucleal changes. The described alterations looks like a chronic erythroblastosis. The explanation might be an antepartum feto-maternal transfusion because a great amount of fetal erythrocytes could be found in the maternal blood.

Abnormalities, Multiple↗

PubMed1987

[Fetal erythroblastosis in Kell incompatibility].

The case study reported here concerned an intrauterine death as a result of a Kell erythroblastosis. Allergization had been caused by the administration of Kell-positive banked blood. Irregular antibodies are on the increase as a result of the increasing number of blood transfusions. It is recommended that the Kell system be considered in the selection of banked blood for girls and women of childbearing age--a practice that has been followed at the Innsbruck University Clinics for almost four years now. The indirect Coombs' test should be performed in order to establish Kell antibodies and other clinically significant antibodies. The enzyme test is recommended as a supplementary examination, but should never be used as the sole antibody test. As with rhesus incompatibility, and insofar as the determination of the father's Kell characteristics show him to be an antigen carrier, monitoring of allergized pregnant women must be carried out with the help of antibody titer follow-ups, amniocenteses, and ultrasonographic examinations at short notice.

Adult↗

PubMed1994

Erythroblastosis fetalis--the discovery and partial elimination of rhesus incompatibility--the origins of exchange transfusion in Australia.

The first 2 exchange transfusions in Australia for Rhesus-induced erythroblastosis (hemolytic disease of the newborn) were conducted in the 9 mth period from December 1945 to August 1946. These pioneering endeavours in medical research were undertaken by 3 transfusionists who were, or had been, directors of the Red Cross Blood Transfusion Service in Australia. Called "substitution transfusion" or "exsanguination transfusion" they were conducted prior to the international publication of the first case series of exchange transfusions for "Rhesus Disease". The first successful exchange transfusion in Australia, and one of the first in the world, was performed by Dr George Kelsall at the King Edward Memorial Hospital for Women, in Perth. Dr Kelsall had monitored pregnancies with serum raised himself from blood from a Rhesus monkey in the Perth Zoo. The second exchange transfusion, and the first with volume-monitoring, was successfully undertaken in Brisbane by Dr Eric Shaw, pathologist and Director of the Queensland Red Cross Blood Transfusion Service, and Dr Noel Gutteridge, a former Director and senior pathologist of Brisbane. Dr Kelsall's pioneering transfusion in Perth was a direct non-anticoagulated transfusion which was undertaken within minutes of birth and was completed within 5 min. The first volume-controlled exchange transfusion, in which the input-discard volumes were matched, used a plastic tube obtained from the Telephone Branch of the Postmaster General's Department, and employed citrated blood. These heroic exchanges (heroic for the infants and families concerned as well as for the operators) form a significant milestone in the history of blood transfusion, serology and preventive medicine in Australia.

Australia↗

PubMed1986

Fetomaternal AB0 incompatibility and erythroblastosis fetalis.

Ninety-one of 330 fetuses undergoing intrauterine fetal transfusion (IUT) had sufficient residual fetal red cells in their cord blood samples that their AB0 blood groups could be determined. Ten of the 91 (11%) were AB0 incompatible with their mothers. The degree of Rh disease was severe in all 10. Three were hydropic in utero; 5 had the syndrome of hepatocellular damage; in 6, IUT were required between 22 and 26 weeks gestation. The expected incidence of AB0 incompatible pregnancies in which the fetuses required IUT if AB0 incompatibility had no effect on severity of Rh disease, is 9.7% versus the 11% observed. AB0 incompatibility has no effect on ameliorating severity of erythroblastosis after Rh immunization has developed. AB0 incompatibility between mother and father should not be taken into account when making decisions regarding the management of an Rh immunized pregnancy.

ABO Blood-Group System↗