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Biomedical subjects

C Béraud

Publications and source records attributed to C Béraud.

At least 19 recordsLinked to original sources

Binding of the HTLV-I Tax1 transactivator to the inducible 21 bp enhancer is mediated by the cellular factor HEB1.

Transcription driven by the HTLV-I promoter is strongly activated by the viral transactivator protein Tax1. This effect is mediated via a 21 bp sequence which is imperfectly repeated three times in the viral promoter. We showed previously that a single 21 bp copy exhibits a strong Tax1-inducible enhancer activity and is able to bind different cellular proteins, namely ATF, HEB1 and HEB2. We have further investigated the molecular mechanism involved in the Tax1 induction of the 21 bp motif's enhancer activity by analysing Tax1 interaction with this DNA sequence. For this purpose a HeLa cell line constitutively expressing a functional Tax1 protein was established and nuclear extracts of these cells were used to perform a DNA affinity precipitation assay. This experimental approach allowed us to show that Tax1 specifically binds to the 21 bp motif. The same sequence elements of the 21 bp motif are required both for Tax1 binding and for Tax1-induced enhancer activity. Chromatographic fractionation of the HeLa tax nuclear extract showed that the binding is indirect and is mediated by the cellular factor HEB 1.

Base Sequence

Tax1 induction of the HTLV-I 21 bp enhancer requires cooperation between two cellular DNA-binding proteins.

Activation of the HTLV-I promoter by the viral Tax1 transactivator is mediated by a 21 bp sequence motif imperfectly repeated three times and composed of three exactly conserved domains (A, B and C from 5' to 3'). We show here that the Tax1 response requires the integrity of the B domain and of at least one of the flanking A or C domains. We have identified three cellular proteins which bind specifically to the 21 bp motif. One of these is the already well-characterized transcription factor ATF. The other two, namely HEB1 and HEB2, are specific for the 21 bp motif. HEB1 can bind to either domain A or C, but binding of ATF and HEB2 is determined by domain B. However, neither domain B alone, nor ATF/CREB binding sites respond significantly to Tax1. We therefore propose that Tax1 induction of the 21 bp enhancer element requires interaction with the two different cellular proteins identified in this study: HEB1 and HEB2, rather than binding of the ATF factor.

Base Sequence

[Evaluation of decontamination procedures used at digestive endoscopy units in Gironde].

Decontamination procedures used for endoscopes were noted in 23 digestive endoscopy units, public and private, in the department of Gironde and compared to recommended procedures. Serial, bacteriological samples were obtained from one esogastroscope and one colonoscope in each unit, after upper endoscopy and colonoscopy diagnostic procedures at the end of the endoscopy session. Six units of 23 used complete decontamination procedures. In the 17 other units, principal errors of decontamination procedures were: inadequate cleaning of internal channel of scopes (12 units) and lack of utilization of glutaraldehyde between each endoscopy (8 units). Bacteriological samples were negative in 11/12 endoscopes after a complete decontamination procedure and in 8/39 after an inadequate procedure (p less than 0.01). Complete procedures are efficacious but not used often enough. Information and changes in endoscopic practices are necessary in digestive endoscopy units.

Bacterial Infections

[Congenital hepatic fibrosis disclosed late by hepatic encephalopathy].

A case of hepatic encephalopathy revealing congenital hepatic fibrosis in a 47-year-old woman is reported. The characteristic features of this observation were: a) the long clinical latency of a congenital disease usually discovered in childhood or in adolescence; b) the existence of hepatocellular insufficiency which appeared without any other reason than an ordinary infection; c) the absence of digestive bleeding or portacaval shunt, factors always found in the rare, previously described cases of encephalopathy in congenital hepatic fibrosis.

Ammonia

[Evolution of serum gammaglutamyl transpeptidase activity in treated hyperthyroid and hypothyroid patients].

The pattern of gammaglutamyl transpeptidase levels was studied in the sera of 25 subjects with hyperthyroidism and 11 subjects with hypothyroidism, before and after treatment, and in 14 age- and sex-matched control subjects. Gammaglutamyl transpeptidase levels were significantly increased in hyperthyroidism (65 +/- 59 U/l) (p less than 0.01) and significantly decreased under treatment (40 +/- 27 U/l) (p less than 0.001). Before treatment, gammaglutamyl transpeptidase levels correlated with alkaline phosphatase levels and 5'-nucleotidase levels, the correlation persisting after treatment with 5'-nucleotidase. Alkaline phosphatase levels significantly increased under treatment (p less than 0.01). The percentages of gammaglutamyl transpeptidase variation correlated with thyroxine (r = 0.44, p less than 0.03), triiodothyronine (r = 0.47, p less than 0.02) and latent fixation capacity (r = 0.44, p less than 0.03) variations. Subjects with hypothyroidism had significantly decreased gammaglutamyl transpeptidase levels before treatment (18 +/- 9 U/l, p less than 0.01). Alkaline phosphatase levels were significantly decreased before treatment, and significantly increased after treatment. For all subjects with hyperthyroidism of hypothyroidism, the percentages of gammaglutamyl transpeptidase variations correlated with thyroxine (r = 0.48, p less than 0.003) and triiodothyronine (r = 0.39, p less than 0.016) variations. These results suggest that variations in gammaglutamyl transpeptidase levels in hyperthyroidism and hypothyroidism are, at least in part, in relation with variations in thyroid hormone levels.

Adult

[Changes in circulating lymphocyte subsets in alcoholic hepatopathies. Respective role of alcohol, hepatocellular insufficiency and malnutrition].

Peripheral lymphocyte subpopulations have been quantified by a direct and indirect, immunofluorescence technique, using monoclonal antibodies, in 22 patients with continued heavy drinking, hepatocellular dysfunction (spider angiomata, ascites, and factor V decrease) (group I), in 16 patients with a history of heavy drinking and abstinence maintained for at least 6 months and hepatocellular dysfunction (group II) and in 28 patients admitted for continued heavy drinking, without hepatocellular dysfunction (group III). Sixteen normal subjects were studied as controls. The total number of lymphocytes and T lymphocytes (OKT3+) were significantly reduced (p less than 0.001) in groups I and II. A significant decrease of B lymphocytes was observed in group II (p less than 0.02). The OKT8+ lymphocytes were significantly reduced in group I (p less than 0.01) and in group II (p less than 0.001); the decrease of the OKT4+ lymphocytes was significant in group II (p less than 0.01) only. The OKT4/OKT8 ratio was higher in group I (p less than 0.05) and group II (p less than 0.01) than in the control group. Normal values of total lymphocytes, B lymphocytes, T lymphocytes subsets and OKT4/OKT8 ratio were observed in group III. In group III, the lymphocyte subpopulations and OKT4/OKT8 ratio were similar in patients with or without abnormalities of liver function tests. In group I and II, no correlation was found between the lymphocyte subpopulations or the OKT4/OKT8 ratio and factor V or nutritional status assessed by anthropometrical and biological tests. T-cell imbalance in alcoholic liver disease does not seem to be related to alcohol consumption, factor V decrease or malnutrition.

Adult

Circadian rhythm of bile secretion in the rat.

In rats the bile flow and the estimated bile acid independant flow (BAIF) were significantly lower at 17.00 h than at 08.00 and 24.00 h. The decrease in BAIF paralleled the decrease in liver weight. Bile acid excretion was not different.

Animals