Biomedical subjects
Publications and source records attributed to P Vigier.
We analyzed the DNA sequences taking as an elementary pattern segments of increasing length from the codon to the gene. We have thus been able to identify part of the constraints from which originates the use of the code degeneracy in each gene. Our results show that the strategy of codon use is not solely related to the translation apparatus characteristics.
The statistical study of polynucleotide sequences constituting the genes of E. coli, bacteriophages lambda and T7 reveals that constraints act upon nucleic acids (DNA or RNA) and contribute to determine the choice between the synonymous codons. The existence of synonymous codons seems to be the way of satisfying these constraints, keeping the possibility of specifying a large variety of polypeptides. At least in the case of amino acids with a small number of codons, these constraints are strong enough to influence the primary structure of proteins.
The authors present diagnosis particularities in 32 cases of hypertrophic pyloric stenosis, from 1980 to 1984, whom 21 cases since 1982 (25 boys, 7 girls). The diagnosis of HPS was confirmed by sonographic and roentgen explorations, isolated or associated: ultrasound alone 3 cases, ultrasound and roentgen combined 29 cases either roentgen first (22) or ultrasound first (7). Fiability was made for 22 cases; two times, error came from false interpretation; eight times were "false negative" results, corrected by roentgenogram, and corresponding with a voluminous pylorus (3) or little, sclerosis pyloric lesions (5). Amelioration of results give, from the last year, right diagnosis in 85 per cent, about 13 cases.
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In order to investigate a possible correlation between in vitro transformation and tumorigenicity in ovo, a new temperature-sensitive class T mutant of Rous Sarcoma Virus was isolated with a lower (39 degrees 5C) restrictive temperature for morphological transformation. This lower restrictive temperature was compatible with the survival of chicken and duck eggs for the tumorigenicity studies. In chicken embryo fibroblasts (CEF) infected by this new mutant, PA 17, and cultured at 39 degrees 5C, increase of hexose uptake, plasminogen activator production and anchorage-independent growth were only partially restricted, requiring incubation at 41 degrees 5C for a complete shut-off. Tumorigenicity in chicken and duck eggs inoculated with CEF infected and transformed by PA 17 was restricted at 39 degrees 5C, correlating well with the restriction of morphological transformation at this temperature. The kinase activity of the transforming protein pp60src in lysates of PA 17 infected cells cultured at permissive or restrictive temperatures was labile in RIPA buffer, as in the case of some previously examined ts T mutants. In the non-ionic detergent NP40 buffer, the kinase activity of PA17 infected cell lysates was better conserved and showed a moderate temperature dependence. These results suggest that, in spite of the correlations between the transformed cell phenotype in vitro and cell tumorigenicity in ovo, it is difficult to establish a quantitative relationship.
Chicken embryo fibroblasts and hamster BHK cells transformed by Rous sarcoma virus (RSV) release in their culture media growth factors which enhance markedly anchorage-independent colony formation in gelified medium, at the restrictive temperature (41 degrees 5 C), of chicken embryo fibroblasts (CEF) infected by RSV mutants with a ts mutation of the src gene. This action is not observed with uninfected CEF, and, therefore, appears to require some expression of the viral src gene in the target cells. The enhancing factors are proteins related to the family of the transforming growth factors (TGFs) by their molecular weight (about 20 kd), their heat and acid resistance, and their sensitivity to dithiothreitol. They do not compete with 125I EGF for binding on the EGF receptors of the membrane of A431 cells. As chicken embryo fibroblasts are devoid of EGF receptors, their activity is not potentiated by EGF.
Avian sarcoma viruses (ASV) produced by Japanese quail embryo fibroblasts (QEF) were inactivated to the same degree as ASV produced by chick embryo fibroblasts (CEF), with or without complement, by rabbit antisera to CEF and to membrane antigens of chick embryo and adult chicken erythrocytes, in particular their unique age-specific antigens. ASV produced by duck embryo fibroblasts (DEF) were only inactivated by the antisera to the chicken erythrocyte antigens. Hence, viruses produced by QEF and DEF bear on their envelope antigens related to the chicken antigens picked up by ASV in CEF. These antigens are presumably coded by the quail and duck cells, since antigens related to the chicken antigens were found on QEF and on quail and duck erythrocytes. Antigens related to the chicken antigens have also been found on ASV shed in low amounts by semi-permissive rat sarcoma cells (line 17RBI77) and on the surface of these cells, as well as on that of another semi-permissive cell line (RBH) originating from a hamster sarcoma produced by inoculation of the rat cells. The origin of these antigens, which may play a role in semi-permissiveness, remains to be explained since they do not appear to be normally expressed by rat or hamster cells. It was also found that, contrary to an earlier conclusion and in agreement with a recent report, uninfected CEF bear on their membrane an antigen that is related or identical to the specific antigen of chick embryo erythrocytes. Therefore, only the antigen related to the adult-specific chicken erythrocyte antigen does not pre-exist on CEF.
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Treatment of Chick embryo fibroblasts (CEF) with 5-bromodeoxyuridine considerably increases the expression on the cell membrane of a cellular antigen related to an antigen specific to Chick embryo erythrocytes, present on the envelope of avian sarcoma oncoviruses produced by CEF.
Avian sarcoma viruses (ASV) of subgroups A to D, produced by chick embryo fibroblasts (CEF), are inactivated to a high degree by rabbit antisera to the membrane antigens of adult chicken and chick embryo erythrocytes, notably by antisera to an antigen of embryo erythrocytes, which is lost by adult erythrocytes and to another antigen specific to the latter erythrocytes. Contrary to virus inactivation by anti-CEF serum reported earlier, virus inactivation by the antisera to these two age-specific antigens does not require complement and is not paralleled by virolysis but by aggregation of virions. The two antigens related, or identical, to the age-specific erythrocyte membrane antigens thus shown to be present on the virus envelope do not pre-exist, or pre-exist only in a low amount, on the CEF membrane, since the virus-inactivating capacity of their antisera is not removed by absorption with CEF. Their appearance on the virus does not depend on cell transformation but only on infection, since both antigens are found on a ts ASV mutant produced at restrictive temperature by untransformed CEF and the virus-inactivating capacity of their antisera is removed by absorption with CEF infected with Rous-associated virus (RAV-1). These findings suggest that infection of CEF by avian oncoviruses may elicit the appearance, or enhance the expression at the cell surface of antigens characteristic of another cell type which may contribute to the formation of specific virus budding sites.
Neoplastic transformation by avian oncogenic retroviruses, notably by sarcoma viruses, the best known of all, results from the expression of a specific viral gene (oncogene), presumably of cellular origin. The protein coded for by this gene appears to act on different targets controlling the various modified cellular characters. A proteic factor coded for by the cell, and derepressed or activated by the expression of the oncogene, is involved in the maintenance of morphological transformation. This factor is also produced by cells transformed by other viruses or oncogenic agents. Other cellular factors, derepressed or activated, may also act as effectors for other parameters of transformation.
The number of Rous viral genomes in the cellular DNA from two subclones (RS2/3, RS2/6) derived from the same clone of hamster BHK-21 cells transformed by Rous sarcoma virus was determined by hybridization with viral complementary DNA made in vitro, and the capacity of the cellular DNA to infect (transfect) chicken embryo fibroblasts was compared before and after shearing this DNA to about the size of the provirus (6 x 10(6) to 7 x 10(6) daltons). The two subclones differed widely both in their capacity to give rise to virus (inducibility) after fusion with chicken embryo fibroblasts and in level of expression of viral proteins. It was shown that cells of both subclones contain a single copy of Rous DNA and yield infectious DNA. However, whereas transfection of chicken embryo fibroblasts was successful with both unsheared (>/=18 x 10(6) daltons) and sheared DNA from the most inducible subclone (RS2/3 subclone), which also expresses viral proteins to an appreciable amount, transfection with DNA from the least inducible subclone (RS2/6 subclone), in which viral proteins are not expressed, succeeded only with sheared DNA. It was then about as successful as with sheared or unsheared RS2/3 DNA. The lack of infectivity of unsheared RS2/6 DNA may be explained by the hypothesis proposed by Cooper and Temin (G. M. Cooper and H. T. Temin, J. Virol. 17:422-430, 1976) to explain the lack of infectivity of DNA from certain chicken cells producing spontaneously low amounts of RAV-0 and resistant to exogenous RAV-0 infection, that is, that the viral genome (proviral DNA) is linked to a cis-acting control element which blocks its expression. This linkage might originate, in RS2/6 cells, from translocation of cellular DNA containing the single proviral copy.
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The present report describes a typical case of tumoral calcinosis. Differential diagnosis was initially directed towards sarcoma suggested by fibrous connective tissue surrounding cystlike cavities. The course of this disease led to chronic multiple fistulae with secondary infection in spite of two attempts of surgical excision. This case adds further support to the results of earlier reports showing no specific biological abnormalities. The present sutyd indicates otherwise that tumoral calcinosis and lipo-calcino-granulomatosis of Teutschlaender are the same condition. The pathogenesis of this affection remains enigmatic; there is no evidence that the lipidic excess should be the beginning of the process, but this disease must be considered as a distinctive form of calcinosis. The surgical exeresis is the only possible treatment, even if it doesn't prevent recurrence.