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Biomedical subjects

C Rosenfeld

Publications and source records attributed to C Rosenfeld.

At least 19 recordsLinked to original sources
PubMed1979

Computer-aided analysis of chromosomal aberrations occurring in an abnormal human karyotype.

A semi-automatic method for recognition of chromosomal changes is presented: from a coded description of an abnormal chromosome (formulated with the aid of an R-banding technique), a computer program makes simulations to reconstitute this chromosomal image from a group of normal chromosomes. Nine types of aberrations (see text) can thus be recognized and the aggregate structure of a group of abnormal chromosomes occurring in a human karyotype can also be rediscovered.

Chromosome Aberrations↗
PubMed1979

Tumour-promoting phorbol diester induces substrate-adhesion and growth inhibition in lymphoblastoid cells.

The treatment of human lymphoblastoid cell cultures with the phorbol diester, 12-O-tetradecanoyl-phorbol-13-acetate, a tumour promoter, caused at nM concentration surface structural changes associated with altered adhesion properties. The effect was observed in several cell lines from normal or leukaemic origin. In addition, the tumour promoter induced an early and transitory growth inhibition which was observed in all tested B-characteristic cells. The phorbol diester, 4-O-methyl-phorbol-12,13-didecanoate, which is devoid of tumour-promoting activity, was much less effective in altering cell adhesion properties and cell growth than the active derivative. These observations suggest that lymphoblastoid cells may be a useful model for studying the molecular alterations at the membrane level resulting from the action of tumour-promoting phorbol diesters.

Animals↗
PubMed1979

Thymosin modulation of suppressor function in mice and man.

The effect of thymosin on suppressor-cell function was evaluated in vivo in a murine tumor system and in vitro on human lymphocytes. In mice, the Lewis tumor system was used. We showed that splenocytes from tumor-bearing animals were able to enhance tumor growth in a syngeneic system. This enhancement was similar when thymocytes from tumor-bearing animals were used and disappeared after anti-Thy 1-2 antiserum treatment, suggesting a T-dependence. Treatment of the tumor-growth-enhancing lymphocytes with corticosteroids or irradiation caused this effect to disappear completely suggesting that the tumor-growth-enhancing T-lymphocytes were suppressor T-cells. Furthermore thymosin (fraction 5)-treated, tumor-growth-enhancing T-lymphocytes were not able to enhance tumor growth and even significantly decreased it. In the human system we showed that Con A-stimulated lymphocytes were able to suppress the response of normal lymphocytes to PHA, PWM, and Con A, and in MLC. This effect was significantly blocked in presence of thymosin fraction 5.

Animals↗
PubMed1978

Decreased microviscosity of membrane lipids in leukemic cells: two possible mechanisms.

Steady-state fluorescence polarization studies with the fluorescent lipid probe 1,6-diphenyl 1,3,5-hexatriene were done to determine the degree of microviscosity of cellular membrane lipids and serum lipoproteins in human normal donors and leukemic patients. The results show a marked decrease in microviscosity of cellular membrane lipids in both intact lymphocytes and isolated cellular plasma membranes obtained from leukemic patients in clinical relapse as compared to intact lymphocytes and isolated cellular plasma membranes obtained from normal donors and leukemic patients in complete clinical remission. Concomitant to these dynamic changes in cellular membrane lipids, the degree of microviscosity of lipids in the blood serum of leukemic patients in clinical relapse is markedly reduced as compared to serum obtained from normal donors and leukemic patients in complete clinical remission. Moreover, an in vitro incubation of leukemic lymphocytes with normal low density lipoproteins results in an increased microviscosity of cellular membrane lipids. In addition to the interrelation between cellular membrane lipids and serum lipoproteins, plasma membrane vesicles with a high degree of lipid microviscosity were isolated from the blood serum and pleural effusion of leukemic patients in clinical relapse. Such membrane vesicles could not be detected in normal serum. Therefore, we suggest that the two major mechanisms associated with the decreased microviscosity of membrane lipids in human leukemic cells are an abnormal exchange in lipids between the leukemic cell surface membrane and leukemic serum lipoproteins and an exfoliation of plasma membrane vesicles with a high degree of microviscosity from the cell surface of leukemic cells.

Cell Membrane↗
PubMed1978

A new lymphoid cell line, Reh 6, with characteristics of non-T and non-B cells, lacking the Epstein-Barr virus genome and derived from human acute lymphoblastic leukemia.

A new lymphoid cell line, Reh 6, has been established from the peripheral blood of a patient with acute lymphocytic leukemia. Reh 6 cells were assayed for the presence of Epstein-Barr virus (EBV) DNA by nucleic acid hybridization and for Epstein-Barr nuclear antigen (EBNA) by the immunofluorescence test. Reassociation kinetics between in vitro [3H]-labeled EBV DNA and Reh 6 cell DNA indicated the absence of detectable amounts of EBV DNA in Reh 6 cell DNA. In addition, attempts to detect EBNA by the immunofluorescence test in Reh 6 cells were unsuccessful. Thus, this new lymphoid cell line apparently lacks the EBV genome.

Antigens, Viral↗
PubMed1978

Comparative cytogenetic studies of normal and leukemic lymphoblastoid cell lines during the course of their establishment.

A comparative chromosomal analysis was made of 10 human lymphoblastoid cell lines, four of which originated from normal donor lymphocytes and six of which were from leukemic peripheral blood. For comparison of lymphoblastoid cells with respect to their normal or leukemic origin, cytogenetic studies have been carried out regularly since the beginning of the culture during more than 3 years. Samples were drawn during the three phases previously described for the establishment of these lines. The chromosome distribution remained diploid for at least 2 years in normal cell lines, and the cells were euploid. In contrast, an important variability of the chromosome set was demonstrated during the same period in leukemic cell lines. Moreover, in these lines, it was always possible to observe a nonsystemic pseudodiploidy. After 2 years, a clonal evolution was described in both types of cell lines that carried at least one marker. With a controlled-heating denaturation technique, it was possible to identify the markers as specific to each cell line. The cells with marker chromosomes appeared to have a selective advantage of growth.

Aneuploidy↗
PubMed1978

Modifications of lectin binding on human leukemic cells after neuraminidase treatment.

Cell surface modifications after vibrio cholerae neuraminidase treatment were investigated using three different tritiated lectins: Concanavalin A, Ricinus sanguineus agglutinin (R.S.A.) and Robinia pseudoacacia lectin. Lectin binding measurements were performed on untreated and enzyme treated cells. The cells used were from chronic and acute leukemic donors. After neuraminidase treatment, a significant increase in the number of receptor sites, from 1 to 3 times, was found in all cases tested and for all three lectins utilized with only one exception. The affinity constant was generally decreased after neuraminidase treatment. The increase in number lectin binding sites, indicating extensive modification of the cell surface, is completely consistant with the known importance of sialic acid in determining immunogenicity.

Binding Sites↗
PubMed1978

Metabolism of proline in a human leukemic lymphoblastoid cell line.

Amino acid analysis of the culture medium was carried out in a human leukemic lymphoblastoid cell line (REH) established from the lymphoblasts of a patient with acute lymphoid leukemia. The results are compared with those of a reference cell line (LHN13) established from normal human lymphocytes. The most striking difference between these two cell lines concerns proline. In LHN13 the concentration of this amino acid in the culture medium increases by 40 microgram/ml/10(6) cells during a 72-hr incubation. In REH there is a decrease under the same culture conditions. In both cell lines proline is derived from glutamic acid and from arginine, as found with the use of 14C-labeled precursors. Synthesis of proline in the REH line represents approximately 26% of the value measured in LHN13 when the precursor is glutamic acid and 15% when the precursor is arginine. The radioisotopic assay for delta1-pyrroline-5-carboxylate reductase showed that there is a deficiency of this enzyme in the REH cells. The defect in proline synthesis of REH was found at the establishment of this line and constitutes a metabolic marker that has persisted for more than 2 years.

Amino Acids↗
PubMed1977

[Serological identification of an antigen associated with acute lymphoid leukemia].

Using as references a lymphoblastoid cell line established from the pleural effusion of a lymphosarcoma patient and the corresponding autochtonous reactive serum, absorption typing assays resulted in the identification of a cell surface antigen associated with acute lymphoid leukaemia. This antigen, provisionally termed PON, may also be demonstrated on the cells of some acute myelomonocytic leukaemias and lymphosarcomas.

Antigens, Neoplasm↗
PubMed1977

[Nickel content of human lymphoblastoid cells cultured in a nickel sulfate-enriched medium].

Nickel is titrated by atomic absorption in nuclear and non-nuclear fractions of cells cultured in media supplemented by nickel sulphate. The living cell percentages are estimated in the same culture conditions. We try to connect the nickel presence in cellular fractions and the living cell percentages. These used cells seem to have mortality probability when nuclear fraction has 55 x 10(-6) of nickel and non-nuclear fraction has 33 x 10(-6) of nickel. We discuss the nickel stimulating effect for the start of DNA synthesis and the nickel penetration into cells.

Cell Nucleus↗