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Biomedical subjects

L Sachs

Publications and source records attributed to L Sachs.

At least 361 records · Page 20Linked to original sources
PubMed1970

In vitro induction of granulocyte differentiation in hematopoietic cells from leukemic and non-leukemic patients.

Human spleen-conditioned medium can induce the formation in vitro of large granulocyte colonies from normal human bone marrow cells. The granulocyte colonies contained cells in various stages of differentiation, from myeloblasts to mature neutrophile granulocytes. Human spleen-conditioned medium also induced colony formation with rodent bone-marrow cells, whereas rodent spleen-conditioned medium induced colony formation with rodent bone marrow but not with human cells. This in vitro system has been used to determine the potentialities for cell differentiation in bone-marrow and peripheral blood cells from patients with a block in granulocyte differentiation in vivo. The cloning efficiency, colony size, and number of mature granulocytes in bone-marrow colonies from patients with congential neutropenia, whose bone marrow contained only 1% mature granulocytes, were not less than in people whose bone marrow had the normal level of about 40% mature granulocytes. The cloning efficiency of peripheral blood cells from patients with acute myeloid leukemia was 350 times higher, with 10 times larger colonies, than the cloning efficiency of peripheral blood cells from normal people. The cytochemical properties and number of mature granulocytes in colonies from the leukemic patients were the same as in colonies from non-leukemic people. The results indicate that a block in cell differentiation in vivo, in these cases with neutropenia and acute myeloid leukemia, was overcome in vitro, in the presence of an inducer in the conditioned medium. In patients with chronic myeloid leukemia, colony formation was induced only in some of the cases. This indicates that there are blast cells with different potentialities for the development of colonies in different patients.

Bone Marrow Cells↗
PubMed1970

Ion metabolism in a Halobacterium. I. Influence of age of culture on intracellular concentrations.

Work is described on the changes in cell ions during growth of cultures of a species of Halobacterium isolated from the Dead Sea. Cell K concentration fell from 5.5 to 3.8 moles per kg cell water during the logarithmic phase of growth and maintained the latter value during the stationary phase (initial medium concentration, 7 mM). Cell Na and Cl followed a complex series of roughly parallel changes. The logarithmic phase ion concentrations were: Na, 1.0-2.3 moles/kg cell water; Cl, 2.3-3.7 moles/kg cell water. The final stationary phase values were: Na, 0.5 moles/kg cell water; Cl, 2.3-2.9 moles/kg cell water (medium NaCl concentration, 3.9 Molal). It is suggested that most of the K(+) is bound within the cytoplasm.

Centrifugation↗
PubMed1969

Feedback inhibition of the development of macrophage and granulocyte colonies. II. Inhibition by granulocytes.

It has been shown that mature normal rat granulocytes produce a substance that inhibits the activity of the inducer required for the development of macrophages (M) and granulocyte (G) colonies from normal hematopoietic cells seeded in soft agar. The granulocyte inhibitor inhibited the activity of the inducer when tested with normal hematopoietic cells from embryonic or adult organs. The inhibitor was not dialyzable, and was obtained in an active form in granulocyte-conditioned medium. The results indicate that the control mechanism that regulates the growth and development of normal macrophages and granulocytes includes a feedback inhibition of the activity of the inducer by inhibitors produced by mature granulocytes and macrophages, presumably at the end of their differentiation process. The inhibition of both M and G colonies by the feedback inhibitors produced by macrophages and granulocytes suggests that both types of colonies may be derived from a common stem cell. A line of primitive myeloid leukemia did not inhibit the activity of the inducer, and the cells of this line were not inhibited by the feedback inhibitors produced by normal granulocytes and macrophages.

Animals↗
PubMed1969

Interaction of the carbohydrate-binding protein concanavalin A with normal and transformed cells.

It has been shown that the carbohydrate-binding protein concanavalin A (ConA) can agglutinate leukemic cells and cells transformed by polyoma virus, simian virus 40, chemical carcinogens, and X-irradiation. This protein did not agglutinate normal cells under the same conditions. The agglutination was reversed by competition with alpha-methyl-D-glucopyranoside (alpha-MG), a carbohydrate that strongly binds to ConA, but not by the carbohydrates alpha-methyl-L-fucopyranoside or N-acetylglucosamine, with no binding or weak binding to ConA. Destruction of the alpha-MG binding sites of the native protein by removal of bivalent metal ions abolished the agglutination produced by the native protein. The treatment of cells with trypsin resulted in the agglutination of normal cells by ConA and a decrease of agglutinability of transformed cells. When nonagglutinating untransformed 3T3 cells were infected with simian virus 40 and normal rat cells were infected with polyoma virus, the infected cells became agglutinable several days after virus infection. The percentage of cells agglutinated, about 50 per cent, was much higher than the percentage of cells hereditarily transformed. The results indicate that the surface membrane of transformed cells contains sites that interact with the alpha-MG binding sites of ConA, that such sites can be found on the surface membrane of normal cells after treatment with trypsin, and that the change in the surface structure from normal to transformed occurs in cells that are abortively transformed.

Agglutination↗
PubMed1969

Enzymatic hydroxylation of benzopyrene and its relationship to cytotoxicity.

Aryl hydrocarbon hydroxylase, an inducible microsomal enzyme system, has been measured in cultures of normal and transformed hamster, mouse, and human cells. In order to determine the highest level of enzyme, the cells were induced by pretreatment with benz(a)anthracene. A correlation was found between the level of enzyme activity and the susceptibility of the cells to the cytotoxicity produced after treatment with benzopyrene. The results indicate that aryl hydrocarbon hydroxylase is the enzyme system responsible for cell susceptibility to the cytotoxic effect of benzopyrene and the toxic effect of benzopyrene is due to its enzymatic conversion to a cytotoxic metabolite. 3-Hydroxybenzopyrene, one of the products of the enzymatic hydroxylation of benzopyrene, was found to be cytotoxic to cells that were either susceptible or resistant to the cytotoxic effect of benzopyrene.

Animals↗