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Biomedical subjects

M Santos

Publications and source records attributed to M Santos.

At least 217 records · Page 12Linked to original sources
PubMed1985

Surface T-antigen expression in simian virus 40-transformed mouse cells: correlation with cell growth rate.

Cell growth control appears to be drastically altered as a consequence of transformation. Because the cell surface appears to have a role in modulating cell growth and simian virus 40 (SV40)-transformed cells express large T antigen (T-Ag) in the plasma membrane, we investigated whether surface T-Ag expression varies according to cell growth rate. Different growth states were obtained by various combinations of seeding density, serum concentration, and temperature, and cell cycle distributions were determined by flow microcytofluorometry. Actively dividing SV40-transformed mouse cell cultures were consistently found to express higher levels of surface T-Ag and T-Ag/p53 complex than cultures in which cells were mostly resting. In addition, the T-Ag/p53 complex disappeared from the surface of tsA7-transformed cells cultured under restrictive conditions known to induce complete growth arrest (39.5 degrees C), although the surface complex did not disappear from other tsA transformants able to keep cycling at 39.5 degrees C. These results suggest that surface SV40 T-Ag or surface T-Ag/p53 complex, or both, are involved in determining the growth characteristics of SV40-transformed cells.

Animals↗
PubMed1984

Dengue haemorrhagic fever in Cuba. II. Clinical investigations.

Clinical and serological studies were carried out on 114 patients admitted to hospital in Havana, Cuba with Dengue Haemorrhagic Fever and Dengue Shock Syndrome (DHF/DSS). Serological confirmation of dengue was obtained in 90% of cases, with 5% of cases primary and 95% secondary. Fever, haemorrhagic manifestations, vomiting and headache were the most frequent signs and symptoms. Among haemorrhagic manifestations, petechiae and vaginal bleeding were reported in a larger number of patients. 21 patients presented shock and, of these, 20 were secondary infections. The disease appeared more frequently in white persons and in women. The aetiopathogenicity of the syndromes is discussed. 95% of the cases could be explained on the basis of the secondary infection hypothesis.

Adolescent↗
PubMed1984

Dynamic nature of the association of large tumor antigen and p53 cellular protein with the surfaces of simian virus 40-transformed cells.

A molecular complex of simian virus 40 large tumor antigen (T-Ag) and p53 cellular protein is present on the surface of simian virus 40-transformed mouse cells. The stability of the association of the two proteins with the cell surface was characterized. Cells were either surface iodinated by the lactoperoxidase technique or metabolically labeled with [35S]methionine, and surface antigens were detected by differential immunoprecipitation with specific antibodies immediately after labeling or after incubation at 37 degrees C. A rapid, concomitant disappearance of T-Ag and p53 from the cell surface was observed. The half-life of iodinated surface T-Ag was less than 30 min, whereas that of [35S]methionine-labeled surface T-Ag was 1 to 2 h. Although T-Ag and p53 were rapidly lost, both were also rapidly replaced on the cell surface, since newly exposed molecules could be detected when cells were reiodinated after a 2-h chase period. Control experiments established that the loss of the surface molecules was not induced by the iodination reaction. The appearance of surface T-Ag was prevented when cellular protein synthesis was inhibited with cycloheximide. The disappearance and replacement of T-Ag and p53 appeared to be energy-independent processes, as neither was inhibited by sodium azide or 2,4-dinitrophenol. Incubation of iodinated cells at 4 degrees C did block the loss of T-Ag and p53. These observations suggest that T-Ag and p53 are coordinately turned over in the plasma membrane. The nature of the association of the T-Ag-p53 complex with the cell surface can best be described as highly dynamic.

Animals↗
PubMed1984

Antigenic structure of simian virus 40 large tumor antigen and association with cellular protein p53 on the surfaces of simian virus 40-infected and -transformed cells.

The antigenic structure of simian virus 40 (SV40) large tumor antigen (T-ag) in the plasma membranes of SV40-transformed mouse cells and SV40-infected monkey cells was characterized as a step toward defining possible biological function(s). Wild-type SV40, as well as a deletion mutant of SV40 (dl1263) which codes for a truncated T-ag with an altered carboxy terminus, was used to infect permissive cells. Members of a series of monoclonal antibodies directed against antigenic determinants on either the amino or the carboxy terminus of the T-ag polypeptide were able to precipitate surface T-ag (as well as nuclear T-ag) from both SV40-transformed and SV40-infected cells. Cellular protein p53 was coprecipitated with T-ag by all T-ag-reactive reagents from the surface and nucleus of SV40-transformed cells. In contrast, T-ag, but not T-ag-p53 complex, was recovered from the surface of SV40-infected cells. These results confirm that nuclear T-ag and surface T-ag are highly related molecules and that a complex of SV40 T-ag and p53 is present at the surface of SV40-transformed cells. Detectable levels of such a complex do not appear to be present on SV40-infected cells. Both the carboxy and amino termini of T-ag are exposed on the surfaces of SV40-transformed and -infected cells. The possible relevance of the presence of a T-ag-p53 complex on the surface of SV40-transformed cells and its absence from SV40-infected cells is considered.

Animals↗
PubMed1982

Detection of a complex of SV40 large tumor antigen and 53K cellular protein on the surface of SV40-transformed mouse cells.

The possible interaction between simian virus 40 (SV40) large tumor antigen (T-ag) and cellular proteins in the plasma membrane of SV40-transformed mouse cells was investigated. The presence of SV40 T-ag, 53,000 (53K) cellular protein, and histocompatibility (H-2) antigens on the surface of SV40-transformed cells was demonstrated by immunofluorescence. The use of lactoperoxidase-catalyzed cell surface iodination and a differential immunoprecipitation technique established that large T-ag is associated with the 53K host-coded protein on the surface of the transformed cells. In contrast, no detergent-stable complex between large t-ag and H-2 antigens was detected. Both labeled T-ag and 53K protein were coprecipitated from surface-iodinated SV40-transformed cells by monoclonal antibodies directed against either the viral or the cellular protein. Based on the unique antigenic sites recognized by the anti-T monoclonal antibodies, it appears that both the carboxy and amino termini of the T-ag polypeptide are exposed on the surface of SV40-transformed mouse cells. The nature of the association between surface T-ag and 53K protein, as well as that between the molecular complex and the plasma membrane, remains to be determined. The possible effect of the surface-associated T-ag/53K complex on cellular proliferation is considered.

Animals↗
PubMed1980

Chemoimmunotherapy with Corynebacterium parvum in acute myelocytic leukemia.

The purpose of this study is to see if immunotherapy with C. parvum and prevention of central nervous system relapse with intrathecal methotrexate can prolong duration of complete remission and survival as well as avoid central nervous system relapse. For induction, three weekly I.V. injections of vincristine and Daunorubicin were given with daily prednisone orally, followed by 5-day courses of Cytosine Arabinoside and 6-mercaptopurine. The patients were randomized to chemotherapy or chemoimmunotherapy. Maintenance consisted of vincristine, Daunorubicin, and prednisone one week every odd month, and a 5-day course of Cytosine Arabinoside and 6-mercaptopurine every even month. Every week, the chemoimmunotherapy group also received, without chemotherapy, one injection of C. parvum 4 mg, subcutaneously. All patients received five weekly injections of intrathecal methotrexate 13 mg/m2 right after complete remission was achieved. Out of 181 evaluable cases, 80 (44%) achieved complete remission, 45 were randomized to chemotherapy, and 35 to chemoimmunotherapy. In the chemoimmunotherapy group 32/35 relapsed, and in the chemotherapy group 36/45. Median duration of complete remission and survival were: for group chemotherapy, 8 and 15 months; for group chemoimmunotherapy, 5 and 10 months. This difference is not significant. Intrathecal methotrexate was given to all patients. Six patients (7%) had central nervous system leukemia at the time of the first injection. None had central nervous system relapse after prevention with intrathecal methotrexate. This method seems useful in preventing central nervous system relapse in patients with acute myeloblastic leukemia, but does not seem to prolong complete remission.

Adolescent↗