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)

The effect of varying the H-2 complex on the survival of parabiosed mice was investigated using a strain combination known to lead to about 50% long-term survival. While 45.6% of DBA/2J (H-2d) with (DBA/2J x C3H/HeJ)F1 (H-2d/H-2k) parabionts survive to 100 days or more, 69% of DBA/2J with (DBA/2J x C3H.NBSn)F1s (H-2d/H-2p) survive that long; only 16% of DBA/2J with (DBA/2Jx C3H.SWSn)F1s (H-2d/H-2b) survive to 100 days. The plot of hematocrits as a function of time after parabiosis differs significantly between the 45.6% surviving strain combination (which shows the classical pattern of parental polycythemia and F1 hybrid anemia) and the 69% surviving strain combination (which shows no divergence in parental and F1 hematocrit values). Furthermore, the 69% surviving strain combination often (5/14) persists in a chimeric state as judgec by starch gel electrophoresis of rec blood cell lysates; the other two strain combinations show no demonstrable red cell chimerism. The conclusion is suggested that the mechann these two generally successful strain combinations tested, and appears to be a function of the H-2types of the partners.
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PMID:The genetics of tolerance induction in histoincompatible parabiosed mice. 98 44

Intravenous injection of 5 x 10(7) C57BL/6 (B6) lymphocytes into adult (C57BL/6 x DBA/2)F1 recipient mice results in acute lethal graft-versus-host (ALGVH) disease. This disorder is characterized by anemia, a diminished number of splenocytes, impaired cytotoxicity (CTX) against third party alloantigen, and impaired natural killer cell (NK) activity. Parental anti-F1 CTX is critical to the induction of ALGVH disease, and CTX in general has been reported to be dependent upon the presence of the low molecular weight polyamines essential for cell growth and differentiation. We now report that DL-alpha-difluoromethylornithine, a specific inhibitor of polyamine biosynthesis, attenuates the clinical expression of disease in mice undergoing ALGVH disease.
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PMID:Attenuation of murine acute lethal graft-versus-host disease by the administration of DL-alpha-difluoromethylornithine. 145 28

1. The relationship between red cell aging and enzyme activities was studied in rabbit, guinea-pig, hamster, rats (F344/N and SD), and mice (BALB/c and DBA/2). 2. The activities of six enzymes: glucose-6-phosphate dehydrogenase (G-6-PD), 6-phosphogluconate dehydrogenase (6-PGD), hexokinase (Hx), glutamate oxaloacetate transminase (GOT), lactate dehydrogenase (LDH) and acetylcholinesterase (AChE), were measured in the red cells of different ages which were obtained either by centrifugation or experimental anaemia. 3. Hx, AChE and GOT activities were much higher in younger red cells than in older cells, hence the activities of these enzymes may be used as an indicator of age of the cells.
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PMID:The relationship between red cell aging and enzyme activities in experimental animals. 176 9

DBA/2FG-pcy mice developed the chronic renal failure by the progressive polycystic formation at five months old. Their bilaterally enlarged kidneys occupied about 15% of the body weight. It was about 9 times larger than the normal kidney of DBA/2N mice. A large number of various-sized cysts appeared in cortex and medulla of bilateral light-yellow kidneys of sponge-like shape. Blood urea nitrogen and creatinine increased. Red blood cells (746 +/- 39 x 10(4)/mm3), hemoglobin (8.8 +/- 0.4 g/dl) and hematocrits (31.1 +/- 1.5%) were lower than those of normal control mice. Serum erythropoietin level and reticulocytes did not increase. In addition, the treatment with exogenous erythropoietin improved the anemia in DBA/2FG-pcy mice. It was suggested that the anemia in DBA/2FG-pcy mice was due to the disorder of erythropoietin production caused by the progressive polycystic formation in kidneys.
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PMID:Renal anemia in polycystic kidney disease mouse. 183 4

Mechanisms for the development of anemia and the effects of recombinant human erythropoietin (r-HuEPO) on hematological parameters were studied in new congenital adult type polycystic kidney (DBA/2FG-pcy) mice. The majority of DBA/2FG-pcy mice showed progressive anemia and an elevation of blood urea nitrogen, while a minority showed progressive anemia following polycythemia. Kidneys with numerous cysts in the cortex and medulla occupied virtually the entire abdominal cavity, and the combined kidney weight taken as a percentage of body weight reached 13.5% in the DBA/2FG-pcy mouse. The osmotic fragility of DBA/2FG-pcy mice erythrocytes was significantly increased compared with that of normal control mice. In addition, two-fold increases in serum EPO levels, determined by radioimmunoassay, and a decreased number of colony forming unit-erythroid (CFU-E) were observed in the DBA/2FG-pcy mice. The administration of r-HuEPO during anemia significantly increased the red blood cell count, hemoglobin concentration, hematocrit and reticulocyte percentage in a dose-dependent manner. These findings indicate that anemia in the DBA/2FG-pcy mouse is due to increased fragility of erythrocytes, a deficiency in EPO for the degree of anemia and a decreased number or a decreased response of erythroid progenitor cells. We suggest that the DBA/2FG-pcy mouse is a useful spontaneous model of chronic progressive renal failure.
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PMID:Anemia in new congenital adult type polycystic kidney mice. 194 61

Rearrangements within the p53 gene are observed in a high proportion of independent erythroleukemic cell lines derived from the spleens of mice infected with Friend leukemia virus. The majority of cells with at least one rearranged p53 allele do not express detectable levels of p53 protein. Here, we show that in 4 out of 19 newly established erythroleukemic cell lines induced by infecting DBA mice with either the anemia (FV-A) or polycythemia (FV-P)-inducing strains of Friend virus, the p53 gene is rearranged as a result of integration of spleen focus-forming virus (SFFV). Integration of SFFV within the p53 gene resulted in inactivation of gene expression as determined by Western blot analysis. The sites of SFFV integration in the p53 gene were found, by Southern blot analysis and the polymerase chain reaction, to be localized in a 1-kbp region between introns 7 and 9. In addition, loss of the normal p53 allele was observed in three of the erythroleukemic cell lines that carried a rearranged p53 gene. Insertion of SFFV in these cell lines resulted in either the appearance of aberrant p53 transcripts or the complete lack of p53 expression. The results presented in this paper demonstrate that retroviral insertions can not only contribute to neoplastic transformation by activating dominant oncogenes but also by inactivating genes that normally function in a negative way to control cell growth. Thus, it may be possible to identify additional genes of this class by characterizing chromosomal sequences that are adjacent to common sites of retroviral integration in tumors.
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PMID:Insertional inactivation of the p53 gene during friend leukemia: a new strategy for identifying tumor suppressor genes. 210 28

Normal and autoimmune mice were studied with regard to signals eliciting differentiation and division of bone marrow stem cells. The erythropoiesis induced by anemia following serial bleedings was analyzed in young autoimmune New Zealand Black (NZB) mice and non-autoimmune strains. No difference in the response to the stimulus created by anemia was noted between the strains. After serial bleedings as a stimulus to stem cell proliferation, a five-fold increase in numbers of proliferating spleen cells occurred in both NZB and DBA/2 strains; the increased proliferating spleen cells in both strains were non-lymphoid. The bled animals had decreased percentages of B cells. The production of autoantibodies was not significantly altered by the experimentally induced anemia. In contrast, anti-immunoglobulin activation of resting B cells was increased in response to anemia. Young mice which had experimentally induced anemia had several characteristics in common with old autoimmune NZB mice. Both old NZB mice and young anemic animals had splenomegaly, increased numbers of proliferating spleen cells, decrease in splenic Ly 5+ cells and an increase in splenic colony forming units (CFUs). The anemic normal strains of animals lacked other characteristics of old NZB mice such as hyperimmunoglobulinemia or autoantibody production or elevated CD5+B cell numbers. This work supports the concept that the increase in spleen cell number, proliferating spleen cells, CFUs and the increased percentages of non-Ly-5 cells (which include erythroid precursors) found in the spleens of old NZB mice may in part result from their autoimmune hemolytic anemia.
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PMID:Effects of induced anemia in normal and autoimmune mice. 221 Aug 4

Long-term biological effects of cadmium-polluted rice and the effect of repeated reproductive cycles on them were examined. Female SLC-B6D2F mice (female C57BL/6, male DBA/2) were fed a rice diet containing 65% unpolished rice for about 2 years from 7 weeks of age. The unpolished rice preparations used were commercially available rice (non-Cd-polluted) and Cd-polluted rice (over 1.0 ppm). Average Cd contents in each diet class were 0.12, 0.48, 1.78, 1.75, and 47.1 ppm (50 ppm Cd as CdCl2 added). Some experimental mice were subjected to repeated reproductive cycles (parity group). Hematological, biochemical, and pathological examinations of urine, blood, and tissues, including Cd measurement, were carried out. Results after statistical analysis indicate Cd toxicities such as anemia and disturbances of Ca metabolism. These Cd effects were found to be enhanced by the reproductive cycles. Soft X-ray radiograms showed osteoporosis in the parity groups, especially in the groups with diets of higher Cd content. However, we could not find any sign of disturbance of renal function under our experimental conditions.
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PMID:An experimental study on the long-term effect of cadmium in mice fed cadmium-polluted rice with special reference to the effect of repeated reproductive cycles. 370 97

We report here results suggesting that cells of the megakaryocytic lineage or uncommitted precursor cells may be targets for Friend-virus-induced proliferation, and that genetic differences (other than Fv-2) between strains C57BL/6 and DBA/2 affect the susceptibility of these cells to Friend virus. The evidence suggesting this was derived from experiments with C57BL/6 in equilibrium DBA/2 allophenic mice. Within the first few weeks following infection of these mice with the polycythemic NB-tropic strain of Friend virus (FV-P), we observed a rapid shift in the genotypic composition of both red cells and platelets in favor of those of the DBA/2 genotype. Infection with the anemia-inducing strain of Friend virus (FV-A) also resulted in preferential production of DBA/2 strain erythrocytes, but its effect on platelet kinetics was nil. The FV-P- and FV-A-induced change in red cell composition is consistent with the view that erythroid precursors are target cells for Friend virus and that viral infection preferentially stimulates proliferation of susceptible strain (DBA/2) erythroid precursors. As for the platelet shifts induced by FV-P (and not FV-A), we believe the changes in platelet mosaicism also could be caused by viral-induced proliferation of DBA/2 platelet precursors, or more primitive progenitors, over the C57BL/6 ones. Thus, these results implicate the existence of nonerythroid target cells for FV-P-induced proliferation, as well as the existence of genetic differences between strains C57BL/6 and DBA/2 that modulate the responsiveness of such cells to infection.
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PMID:Genotype-limited changes in platelet and erythroid kinetics in Friend-virus-infected allophenic mice. 370 7

Female F1 mice (BDF1: C57BL/6 x DBA/2, BCF1: C57BL/6 x C3H/HeN, BBF1: C57BL/6 x BALB/c) were preimmunized with rat erythrocytes and then received splenic T cells from parental female C57BL/6 mice injected with hydrocortisone acetate before killing. In BDF1 and BCF1 mice, direct Coombs' test (DCT) positivity persisted for more than 4 months in almost all mice. They also showed haematological sign of anaemia, and the survival of infused 51Cr-labelled parental C57BL/6 erythrocytes was reduced. In BBF1 mice, DCT positivity returned to negative within 2 months. Autoantibodies were eluted from DCT-positive erythrocytes and their specificities were examined. They were capable of binding equally well to erythrocytes from all strains of mice tested, including the donor mice. They also cross-reacted with rat erythrocytes but not with sheep, rabbit or human erythrocytes. Isotypes of the autoantibodies eluted were also examined. Interestingly, isotypes of the autoantibodies obtained from individual mice were confined to one or other subclass of IgG isotype: IgG1, IgG2a or IgG2b.
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PMID:Induction of persistent autoimmune haemolytic anaemia in mice by combined use of rat erythrocyte preimmunization and chronic GVHR. 387 25


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