Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leukocyte kinetic studies using chromium-51 were performed in four patients with acute myelocytic leukemia (AML). Intravascular leukocyte survival was prolonged in comparision with granulocyte survival in normal subjects. Significant splenic pooling occurred in three patients, none of whom had splenomegaly. In one patient studied, circulating leukemic cells were shown to return to the bone marrow. The prolongation of intravascular leukocyte survival in AML in relapse, as in chronic myelocytic leukemia, probably depends on several factors including the presence of immature leukemic cells and the recycling of these cells from the spleen and bone marrow.
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PMID:Study of leukocyte kinetics in acute myelocytic leukemia utilizing chromium-51. 106 22

Three Beagles with chronic anemia and reticulocytosis were studied. The dogs originated from a large breeding colony and appeared clinically normal with the exception of splenomegaly. The PCV ranged from 30 to 39% (normal, 46 to 56%), with reticulocyte indices of 2.3 to 9.9. Red blood cells were morphologically normal, and examination of marrow aspirates revealed erythroid hyperplasia. Shortened chromium-51 RBC life-spans (7.2 to 15.4 days in anemic dogs; 22.2 to 25.2 days in control dogs) documented a hemolytic anemia. Acquired causes of hemolytic anemia were ruled out. Red blood cells had normal glycolytic enzyme activities, no evidence of unstable or abnormal hemoglobin, and had altered osmotic fragility curves. The breeding of 2 anemic dogs resulted in offspring with anemia and reticulocytosis. Polyacrylamide gel electrophoresis revealed no abnormalities in RBC membrane cytoskeletal proteins in all anemic adult dogs and in 3 offspring.
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PMID:Hereditary nonspherocytic hemolytic anemia in beagles. 245 89

A patient had extensive foreign-body granulomatous inflammation of multiple skin sites and of the inguinal lymph nodes with splenomegaly, cutaneous anergy to common skin antigens, and peripheral blood eosinophilia. The patient had an elevated serum angiotensin-converting enzyme level. Histologically, the granulomas were of the foreign-body type with lymphocytes, histiocytes, eosinophils, and giant cells, some that contained doubly refractile crystalline material. Electron-probe x-ray microanalysis identified silicon, magnesium, iron, calcium, phosphorus, zinc, titanium, and chromium in the crystalline material. These findings suggest talc, cement, and inorganic pigment as possible sources of the crystals. This case is reported for its unusual clinical, laboratory, and morphologic features.
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PMID:Widespread foreign-body granulomas and elevated serum angiotensin-converting enzyme. 629 13

Natural killer (NK) cytotoxic activity was measured against the standard target cell line YAC-1 in a four-hour chromium release assay. Effector cells were taken from spleen and bone marrow of BDF1 mice inoculated 3, 7, 14 or 21 days earlier with 2 X 10(6) Lewis lung carcinoma (LL) cells. The peak of cytotoxic activity both in spleen and bone marrow appeared in mice 3 days after tumor inoculation. There were no differences in cytotoxic effect between tumor bearing and normal mice on day 7. The significant decrease was observed in tumor bearing mice on day 14 and 21. However, at that time the spleen cellularity increased 2.7 and 3.8 times, respectively suggesting a possible dilution effect of NK cells in mice with splenomegaly. Bone marrow cellularity remained unchanged as compared to control. The possible mechanisms of decrease in NK cytotoxic activity and its implications for progression of tumor growth are considered.
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PMID:Changes in natural killer cells activity in mice bearing subcutaneously implanted Lewis lung carcinoma. 648 51

Two sets (four lines) of chickens, lines 7 and 6 and lines P and N, the former of each set susceptible and the latter resistant to Marek's disease, were examined for their relative histocompatibility and immunocompetence. Results from the in vivo graft-versus-host response splenomegaly assay, and graft-versus-host chorioallantoic membrane pock formation assay confirmed the within-line, B-locus homozygosity of chickens of lines 7, 6, and N and the heterozygosity of line-P chickens. These assays further confirmed that line-7 and line-6 chickens share identical alleles at the major histocompatibility locus. The capacity of the lines of chickens to elicit specific cell-mediated immune lysis as measured by the release of chromium 51 generally agreed with the in vivo graft-versus-host responses. These data demonstrate that the 51Cr-release assay is a reliable measure of histocompatibility within the avian system.
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PMID:Studies of histocompatibility and immune response of chickens selected for resistance and susceptibility to Marek's disease. 684 51

With the very long life expectancy of Polycythaemia Vera late complications are often observed: progressive resistance to treatment, bad tolerance to maintenance by phlebotomy, progression towards myelofibrosis. Resistance to phosphorus 32 is reflected by a progressive reduction in the duration of remission and by a gradually decreasing remission rate. A complete resistance appears after a mean duration of disease of 7 years. In the maintenance treatment by hydroxyurea, there is a secondary resistance in one third of cases with a poor control of the excess platelets. Resistance to Pipobroman is less frequent (10%). The phosphorus resistance could be delayed by addition of maintenance treatment by Hydroxyurea. In the presence of resistance to 32 P, Hydroxyurea and Pipobroman often remain effective. In the case of resistance to Hydroxyurea or Pipobroman, we have several possibilities: inversion of chemotherapy, other chemotherapy as Busulfan, 32 phosphorus. Intolerance of phlebotomy as baseline treatment is almost constant. Three complications lead to discontinuation of phlebotomy: development of cardiovascular complications, raised platelet count to above 800,000 and often more than 1 million, progressive increase in the size of the spleen with appearance of signs of myeloid splenomegaly. Exclusive phlebotomies are not indicated as baseline treatment of Polycythaemia Vera. The progression towards myelofibrosis (spent phase, post polycythaemia myeloid splenomegaly) increases with the duration of the disease and the frequency of transformation differs according to the type of treatment. The time to transformation is much shorter in the patients treated by phlebotomy. The transformation towards myelofibrosis is demonstrated by bone marrow biopsy and isotope investigations (bone marrow scintigraphy and kinetic by iron 59 and chromium 51).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and laboratory assessment and therapeutic problems in longstanding polycythaemia vera. 803 42

Vaccination of mice with a live attenuated vaccine virus induces potent protection against subsequent challenge with pathogenic Friend retroviral complex. The kinetic studies presented here demonstrate protection from acute splenomegaly as early as 1 week postvaccination. At this time point virus-specific cytotoxic T lymphocytes (CTL) were demonstrable in direct chromium release assays. However, during the first 2 weeks after vaccination protection was incomplete since the mice were not protected against establishment of low-level persistent infections in the spleen. By 3 weeks postvaccination the animals were protected against the establishment of persistent virus as well as acute splenomegaly. The timing of this complete protection correlated with the presence of both virus-neutralizing antibodies and primed CTL in the immunized mice. Within 3 days of virus challenge, vaccinated mice showed high levels of activated B cells and CD4(+) and CD8(+) T cells, indicating an efficient priming of all lymphocyte subsets. Despite very limited replication of the vaccine virus, the protective effect was long lived and was still present 6 months after immunization.
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PMID:Kinetics of the development of protective immunity in mice vaccinated with a live attenuated retrovirus. 1048 95