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Biomedical subjects

S B Krantz

Publications and source records attributed to S B Krantz.

At least 145 records · Page 8Linked to original sources
PubMed1976

Quantitation of Friend spleen focus-forming virus by a nine-day 59Fe assay.

A previously described 3-day 59Fe assay for quantitation of Friend spleen focus-forming virus has been modified to produce a 200-fold more sensitive 9-day 59Fe assay. A characterization of this assay is reported here. Male BALB/c mice received intravenous injections of appropriately diluted Friend polycythemia virus (FVP); control mice received virus diluent. All mice were allowed food and water ad libitum for 6 days, and on day 6 after virus injection were fasted by removal of food but not water. On day 3 of the fast (the 9th day after virus injection) each mouse received an intraperitoneal injection of 1 muCi of 59Fe. Six hours later the mice were sacrificed and the splenic radioactivity was determined. The percent splenic incorporation of 59Fe was directly related to the logarithm of spleen focus-forming units (SFFU) of FVP injected in a range of approximately 25 to 1,000 SFFU. Using a standard FVP preparation in a dose range of 25 to 1,000 SFFU, it was possible to determine the SFFU titers of unknown samples by extrapolation of the percent splenic 59Fe incorporation to the logarithm of SFFU. SFFU titers obtained by the 9-day 59Fe assay were similar to those obtained by the enumerative-response assay. Advantages of the 9-day 59Fe assay over the enumerative-response assay include a 50-fold greater virus dose range, an easier and a more objective counting procedure, and a reduced coefficient of variation.

Animals↗
PubMed1976

Bone-marrow imaging in pure red blood cell aplasia.

Bone-marrow scintigraphy with indium chloride in 111 was performed on a patient with pure red blood cell aplasia before and after successful treatment with immunosuppressive drugs. The return of erythroid precursors to the bone marrow was accompanied by a substantial increase in the marrow uptake of 111In. The distribution of 111In in the posttreatment scan was indistinguishable from that of 52Fe. These results indicate that indium chloride in 111 is a useful agent for the delineation of erythroid cellularity within bone marrow.

Adult↗
PubMed1975

Chromosome band analysis in 19 cases of chronic myeloid leukemia: 9 chronic, 10 blastic, two with Ph1 (22q-) translocation on 17 short arm.

The results of Giemsa band analyses of the marrow cells of 19 cases of CML in the chronic or blast phase are reported. All but one of the 14 Ph1 positive cases showed the 9q+pattern, the exceptional one being 16p+. All 10 blast cases showed additional rearrangements, which are described. In two of the cases, one blastic, one chronic, which were -22, Ph1 negative, the 22q- member was identified as a translocation on the short arm of one 17 which was dicentric.

Chromosome Aberrations↗
PubMed1975

Studies on pure red cell aplasia. VII. Presence of proerythroblasts and response to splenectomy: a case report.

An 18-yr-old female with chronic active hepatitis developed a severe anemia due to a lack of red cell production. Her bone marrow showed many large proerythroblasts but an almost complete lack of more mature erythroblasts. Incubation of the marrow cells in a normal medium with erythropoietin concentrate led to increased erythropoiesis as indicated by the development of mature erythroblasts as well as a ninefold increase in hemoglobin synthesis. The patient's plasma was cytotoxic for erythroblasts. Following splenectomy, a remission of the disease occurred. This study indicates that in some cases the anemia associated with abundant marrow proerythroblasts and the absence of mature erythroblasts has the same pathogenesis as pure red cell aplasia and that splenectomy may be beneficial when there is a lack of response to immunosuppressive drugs.

Adolescent↗
PubMed1973

Studies on red cell aplasia. V. Presence of erythroblast cytotoxicity in G-globulin fraction of plasma.

The marrow cells of a patient with pure red cell aplasia markedly increased their rate of heme synthesis when they were freed from the host environment and were incubated in vitro. When the red cell aplasia was treated with cyclophosphamide and prednisone, marrow cell incorporation of (59)Fe into heme in vitro increased several weeks before a reticulocytosis was apparent, and was the earliest effect noted. The plasma gammaG-globulins of this patient inhibited heme synthesis by normal marrow cells or the patient's own marrow cells obtained after remission of the disease. Since the inhibition of heme synthesis could be the result of damage to erythroblasts, the patient's posttreatment marrow cells or normal marrow cells were labeled with (59)Fe and were then incubated with the patient's pretreatment, treatment, and posttreatment gammaG-globulins as well as normal gammaG-globulins. At the end of this incubation the supernatant and cells were separated and counted. Heme was extracted and also was counted. Treatment of the cells with the patient's pretreatment gammaG-globulins resulted in a release of 40% of the radioactive heme from the cells. This represented the loss of radioactive hemoglobin and was an index of erythroblast cytotoxicity. A progressive disappearance of the cytotoxic factor in the gammaG-globulins occurred in the 3 wk period preceding the onset of reticulocytes in the patient's blood. Posttreatment and normal gammaG-globulins did not produce this effect and increased injury of red cells and lymphocytes was not produced by the patient's pretreatment gammaG-globulins. These studies demonstrate a method for measuring erythroblast cytoxicity and show that red cell aplasia is associated with gammaG-globulins that specifically damage erythroblasts. Whether interference with new erythroblast development also occurs and contributes to the inhibition of heme synthesis has not yet been ascertained.

Anemia, Aplastic↗