Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Faecal iron excretion during continuous subcutaneous deferoxamine infusion was measured by flameless atom-absorption spectral photometry in 21 patients with homozygous ss-thalassaemia and one patient with Blackfan-Diamond anaemia. Taking into account faecal and urinary iron excretion, more iron was eliminated than was taken up during transfusion and by intestinal absorption. Urine contained 37.9%, faeces 62.1% of the amount of iron eliminated.
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PMID:[Deferoxamine in hemosiderosis. Fecal iron excretion during continuous subcutaneous infusion]. 648 81

Two strains of Friend virus differ in their in vivo actions in that one strain induces anemia (FVA), while the other induces polycythemia (FVP). This study characterizes differences in the in vitro effects of these viruses on hematopoietic cells of (BALB/c x DBA/2)F1 mice. Both variants induced erythroid bursts that proliferated and differentiated without added erythropoietin (EPO). However, while the bursts induced by FVP were well "hemoglobinized" (i.e., most cells contained hemoglobin), the cells of FVA-induced bursts contained little or no hemoglobin. The nonhemoglobinized bursts, induced by FVA, were established to be erythroid by cytochemistry, electron microscopy, and hormone sensitivity. FVA-induced cells appeared to be hypersensitive to EPO, since small concentrations of the hormone produced marked increases in hemoglobin production--even when the hormone was added to the culture 3 days post infection. Time-lapse photography documented that EPO stimulated hemoglobin synthesis in virally transformed cells rather than uninfected erythroid precursors. This observation of FVA-induced hypersensitivity prompted the reexamination of the hormone requirements of FVP-induced bursts--previously considered to be EPO-independent. Reduction of the serum in the cultures allowed the demonstration that FVP-induced erythroid cells also were hypersensitive to EPO. Thus FVA and FVP can be readily distinguished in vitro by the relative EPO sensitivity of virus-induced bursts. From these findings, a hypothesis is drawn: i.e., oncogenic transformation may result from increased sensitivity of progenitor cells for natural, physiologic regulators, and transformation is not necessarily accompanied by a block in differentiation. In addition, since hypersensitive virus-induced bursts could be recognized and picked from the cultures, these studies provide a method for obtaining highly purified erythroid precursors for the study of the regulation of terminal differentiation by EPO and other regulatory factors.
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PMID:Increased erythropoietin sensitivity after in vitro transformation of hematopoietic precursors by RNA tumor viruses. 657 60

Hematological assays of inbred specific pathogen-free (SPF) mice of ten different strains inoculated with Friend leukemia virus (FLV) were performed chronologically to assess whether the genetic control of the host may play an important role in viral oncogenicity. Mice strains C57BL/6J, B10 (H-2b) and B10D2 (H-2d) were FLV-resistant, BALB/c, DBA/2N (H-2d), RFM (H-2f), AKR and 80% of CBA/JN (H-2k) were FLV-sensitive (polycythemia) and C3H/He, B10Br and 20% of CBA/JN (H-2k) were FLV-sensitive (anemia). Only the AKR strain mice showed a spontaneous regression of splenomegaly. These results indicate that there is not a strong but a weak correlation between the H-2 haplotype and the reaction to FLV. The main phenomenon in the anemic mice was the monotonous proliferation of the naked blastic cell, whereas that in the polycythemic mice was the enormous increase of the mature erythroblast and the decrease of the naked blastic cell in the later phase. These facts suggest that the naked blastic cell in the mice with polycythemia are reactive and that in the mice anemia truly neoplastic.
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PMID:Relation between Friend leukemia virus-induced leukemia and genetic control of the host. 658 86

A 13 year old boy with Blackfan-Diamond anemia treated with frequent transfusions was investigated for endocrine abnormalities. Prepubertal plasms LH and FSH values, lack of sleep-related hormone rhythms of the gonadotropins, as well as prepubertal responses of LH and FSH to acute stimulation with LHRH strongly suggests that a hypothalamic-pituitary abnormality is the cause of the hypogonadotropic hypogonadism observed in this patient. As a result of impaired stimulation of the gonads plasm testosterone was prepubertal. A three-to fourfold increase of basal plasma PRL values was found without any signs of a typical sleep-dependent increase. Values obtained ranged between 21 ng/ml and 24 ng/ml (normal range 5-8 ng/ml). A normal response to TRH stimulation was found. These results suggest that hemosiderosis may be responsible for the hyperprolactinemia as a result of hypothalamic-pituitary dysfunction. Furthermore, dysfunction is demonstrated by prepubertal responses of LH and FSH to LHRH stimulation.
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PMID:Endocrine studies in Blackfan-Diamond anemia: evidence for hypothalamic-pituitary dysfunction under frequent transfusion therapy. 677 97

Appearance of tumorigenic cells was studied in DBA/2 and ICFW mice infected either with the polycythemia-inducing or the anemia-inducing strain of Friend leukemia virus. Tumorigenicity was defined by transplantability of virus-infected cells into the omentum of an isogeneic preirradiated host. Tumorigenic cells were detected in 50% of the leukemic donors 3 wk after infection by the polycythemia-inducing strain and 7-8 wk after infection by the anemia-inducing strain. These cells appeared first in the spleen and later in peripheral blood, bone marrow, and liver. They consisted of a heterogeneous population at different degrees of malignancy as determined by successive transfers in vivo and in vitro. The observations clearly show that leukemias induced by Friend viruses evolve by multistep processes, in which different stages of malignancy can be detected.
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PMID:Emergence of tumorigenic cells during the course of Friend virus leukemias. 694 62

In mice with "diffuse" hemoglobin (Hb), the decrease in the proportion of minor Hb during ontogeny qualitatively resembles the decline observed in human Hb F. Since Hb F reappears during some forms of erythroid stress, we investigated the effect of hematopoietic stress on minor Hb in DBA/2 mice. The stresses were acetlyphenylhydrazine-induced hemolysis, phlebotomy, or infection with Friend erythroleukemia virus. Recovery from anemia was associated with a transient increase in the synthesis of minor Hb similar to the reappearance of Hb F in man. Minor Hb synthesis also increased during the evolution of erythroleukemia induced by both the anemic and the polycythemic strains of virus. Thus, the mouse model can be used to study Hb regulation, since changes in the modulation of minor Hb synthesis occur under conditions which are associated with alterations in Hb F synthesis in humans.
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PMID:Increased mouse minor hemoglobin during erythroid stress: a model for hemoglobin regulation. 695 22

We studied the in vitro proliferative characteristics of marrow erythroid progenitors, colony forming unit-erythroid (CFU-E) and burst forming unit-erythroid (BFU-E), in two infants with Diamond-Blackfan syndrome before and during prednisone treatment. Patient 1, had a brisk erythropoietic response to prednisone and the anemia improved; Patient 2 was steroid-unresponsive. Marrow from Patient 1 yielded linear increases in numbers of colonies in erythropoietin dose-response studies, and the magnitude of response was much greater while on prednisone compared to pretreatment. Cultures of stem cell rich fractions of marrow from Patient 1 separated by unit gravity sedimentation (STA-PUT) revealed moderately reduced CFU-E and BFU-E numbers before prednisone, but normal colony numbers during treatment. Patient 2 differed because CFU-E and BFU-E were almost absent at all erythropoietin doses before and during therapy. Even stem cell rich marrow fraction initially yielded very low colony numbers which did not increase significantly while on prednisone. These findings suggest that in Patient 1 there were adequate numbers of progenitors that were able to differentiate normally only in the presence of prednisone. In Patient 2 the erythropoietic failure in vivo and in vitro was unaffected by prednisone.
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PMID:Diamond-Blackfan syndrome. I. Erythropoiesis in prednisone responsive and resistant disease. 709 63

Strain variation in the level of resistance to malaria was investigated in inbred strains of mice after infection with Plasmodium chabaudi. When infected intraperitoneally with 10(6) P. chabaudi-parasitized erythrocytes, mice of 11 inbred strains could be separated into two groups by using survival time as the criterion; C57BL/6J, C57L/J, DBA/2J, CBA/J, and B10.A/SgSn mice were found to be resistant to P. chabaudi, whereas A/J, DBA/1J, BALB/c, C3H/HeJ, AKR/J, and SJL/J mice were susceptible. An examination of F1 hybrids revealed that resistance was dominant over susceptibility. A segregation analysis of backcross and F2 progeny derived from susceptible A/J and resistant B10.A/SgSn parental mice suggested that host resistance in this strain combination was genetically controlled by a single, dominant, non-H-2-linked gene. Inheritance of resistance was autosomal, but expression of the trait was influenced by the sex of the host, female mice being more resistant than male mice. Phenotypic expression of the resistance gene was apparent within 6 days of infection as a significant difference between resistant and susceptible mice in the level of parasitemia. A preliminary analysis of the mechanism of resistance showed that compared with susceptible A/J mice, resistant B10.A/SgSn hosts had an augmented erythropoietic response during the course of malaria, as well as phenylhydrazine-induced anemia. These results suggest that the ability to replace destroyed erythrocytes quickly and efficiently may determine host survival after infection with P. chabaudi.
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PMID:Murine malaria: genetic control of resistance to Plasmodium chabaudi. 714 99

A patient with a pure red cell aplasia (Blackfan-Diamond Anemia), and with many congenital abnormalities and growth retardation, has been found to have a chromosome breakage syndrome. In this patient, the frequencies of spontaneous chromosome aberrations and micronuclei in PHA stimulated peripheral blood lymphocytes are elevated when compared to those in normal individuals. The frequency of sister chromatid exchanges is within normal range. The response to mitomycin C (MMC) in the micronucleus test, using lymphocytes, shows a similar increase in the patient's lymphocytes to that in normal individuals, indicating no increased sensitivity to MMC. The frequencies of X-ray induced dicentric chromosomes and micronuclei in the peripheral blood lymphocytes are elevated in the patient. But as the patient clinically does not have any signs of ataxia telangiectasia, this combination of clinical and laboratory findings of this case does not correspond with any of the other known 'chromosome breakage' syndromes.
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PMID:A case of pure red cell aplasia with a high incidence of spontaneous chromosome breakage: a possible X-ray sensitive syndrome. 720 68

Fetal-like erythropoiesis frequently accompanies marrow stress conditions such as Diamond-Blackfan syndrome and aplastic anemia. In contrast, patients with transient erythroblastopenia of childhood have erythrocytes which lack fetal characteristics at the time of diagnosis. This report describes nine children with transient erythroblastopenia of childhood in whom transient, fetal-like erythropoiesis was observed during the period of recovery. These patients initially presented with anemia, reticulocytopenia, erythrocytes of normal size for age, low levels of fetal hemoglobin, and i-antigen. During the recovery period, however, erythrocytes manifested one or more fetal characteristics. These included an increased fetal hemoglobin (in three of five patients), the presence of i-antigen (in four of six patients), and macrocytosis (in seven of nine patients). These fetal characteristics persisted more than 2 wk after the reticulocyte count returned to normal. Within one year from diagnosis, red blood cells contained no fetal characteristics.
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PMID:Fetal-like erythropoiesis during recovery from transient erythroblastopenia of childhood (TEC). 725 49


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