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M Faure

Publications and source records attributed to M Faure.

At least 109 records · Page 6Linked to original sources

In Xenopus laevis, the product of a developmentally regulated mRNA is structurally and functionally homologous to a Saccharomyces cerevisiae protein involved in translation fidelity.

We have performed a differential screen of a Xenopus egg cDNA library and selected two clones (Cl1 and Cl2) corresponding to mRNA which are specifically adenylated and recruited into polysomes after fertilization. Sequence analysis of Cl1 reveals that the corresponding protein is 67.5% identical (83% similar) to the product of the Saccharomyces cerevisiae SUP45 (also called SUP1 or SAL4) gene. This gene, when mutated, is an omnipotent suppressor of nonsense codons. When expressed in a sup45 mutant, the Xenopus Cl1 cDNA was able to suppress sup45-related phenotypes, showing that the structural homology reflects a functional homology. Our discovery of a structural and functional homolog in Xenopus cells implies that the function of SUP45 is not restricted to lower eukaryotes and that the SUP45 protein may perform a crucial cellular function in higher eukaryotes.

Amino Acid Sequence↗

Cutaneous mesenchymal tumour with haemangiopericytoma-like features.

A case of cutaneous mesenchymal haemangiopericytoma-like tumour affecting a 17-year-old male is presented. Clinical features were non-specific. The tumour was studied by light, electron microscopy and immunohistochemistry. The results of these studies suggested the diagnosis of a mesenchymal, poorly-differentiated tumour showing features of haemangiopericytoma. The clinical course after surgery was uneventful after a 9-month follow-up period.

Adolescent↗

Keratinocyte proliferation in epidermal keratinocyte disorders evaluated through PCNA/cyclin immunolabelling and AgNOR counting.

The assessment of cell proliferation is important to our understanding of hyperproliferative disorders. In this work we evaluated the proliferation characteristics of epidermal keratinocytes in diseases with abnormal keratinization by two different methods (immunostaining for the proliferating cell nuclear antigen--PCNA and histochemical staining for nucleolar organizer region--associated argyrophilic proteins--AgNORs). Twenty-seven specimens from diseases with an abnormal keratinization were studied and compared with specimens of normal human skin. As compared with the latter, the numbers of PCNA-positive epidermal keratinocytes were increased in psoriasis, congenital non-bullous ichthyosiform erythroderma, epidermolytic hyperkeratosis and chronic dermatitis and decreased in ichthyosis vulgaris, X-linked ichthyosis and pityriasis rubra pilaris. In most cases a parallel modification of AgNORs was found. We conclude that although PCNA immunolabelling and AgNOR staining do not provide strictly correlated values, both appear as useful markers for the assessment of keratinocyte proliferation in epidermal disorders.

Autoantigens↗

Identification of a human guanine nucleotide-releasing factor (H-GRF55) specific for Ras proteins.

A critical step in the activation of cellular Ras is the release of bound GDP. Oligonucleotide primers derived from a mouse cDNA sequence homologous to the Saccharomyces cerevisiae CDC25 gene product were used to screen a human brain cDNA library. The cloning led to the isolation of a 2.8-kb cDNA predicted to encode a protein of 488 amino acids. This protein was produced in Escherichia coli as a glutathione S-transferase fusion protein and functioned in vitro as a specific guanine nucleotide-releasing factor. Polyclonal antibodies raised against the last 281 amino acids of the protein allowed a protein in the molecular weight range of 55 kDa to be identified in human cortex homogenates. Analysis by Northern blotting led to the identification of a 5.5-kb mRNA in brain poly(A)+ RNA. The functionality of the encoded protein was evaluated after expression in different cells: (i) in Saccharomyces cerevisiae the effects of the cdc25.5 and RAS2 Ala-22 mutations were reversed; (ii) in chinese hamster ovary cells, a RAS-responsive element was transactivated as demonstrated by the expression of a CAT reporter gene under the control of the polyomavirus enhancer. Finally, in situ hybridization on of human chromosomes revealed a localization on band 15q2.4.

Amino Acid Sequence↗

[Hormonal assessment in a woman with acne and alopecia].

Acne, androgenogenetic alopecia, hyperseborrhea and hirsutism may result from hyperandrogenism in women. This may be peripheral "idiopathic" hyperandrogenism due to cutaneous metabolism of steroids, but in some cases hyperandrogenism is due to abnormal production or input of steroids with androgenic activity (hyperplasia, endocrine tumors, cysts, consumption of progestogens or other hormones with androgenic activity, menopause...). An assessment is useful only in cases of acne or alopecia if they are accompanied by other signs of peripheral hyperandrogenism and/or disturbed menstruation. The treatment is based on the administration of an anti-androgen (in France, usually cyproterone acetate), combined with other local or systemic treatments for the problem, depending on the age, dermatological signs and context.

Acne Vulgaris↗

Cyclic nucleotide phosphodiesterase of Dictyostelium discoideum and its glycoprotein inhibitor: structure and expression of their genes.

The genes coding for the cyclic nucleotide phosphodiesterase (PD) and the PD inhibitory glycoprotein (PDI) have been cloned and characterized. The PDI gene was isolated as a 1.6 kb genomic fragment, which included the coding sequence containing two small introns and 510 nucleotides of non-translated 5' sequence. From the deduced amino acid sequence we predict a protein with a molecular weight (MW) of 26,000 that, in agreement with previous data, contains 15% cysteine residues. Genomic Southern blot analysis indicates that only one gene encodes the inhibitor. Northern blot analysis shows a single transcript of 0.95 kb. The PDI gene is expressed early in development with little transcript remaining following aggregation. The appearance of PDI mRNA is prevented by the presence of cAMP, but when cAMP is removed the transcript appears within 30 minutes. When cAMP is applied to cells expressing PDI the transcript disappears with a half-life of less than 30 minutes. The PD gene of D. discoideum is transcribed into three mRNAs: a 1.9 kb mRNA specific for growth, a 2.4 kb mRNA specific for aggregation, and a 2.2 kb mRNA specific for late development. The 2.2 kb mRNA is also specific for prestalk cells, and is induced by differentiation-inducing factor. All three mRNAs contain the same coding sequence, and differ only in their 5' non-coding sequences. Each mRNA is transcribed from a different promoter, and by using the chloramphenicol acyltransferase gene as a reporter, we have shown that each promoter displays the same regulation as its cognate mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

3',5'-Cyclic-AMP Phosphodiesterases↗

Autism and family home movies: preliminary findings.

Preliminary analyses of 12 home movies taken by parents before the recognition of autistic disorders of their own child confirm the major value of this method for describing early signs: anomalies of eye contact, deficient variability of emotional expression, defect of attention and initiation of communication, motor abnormalities, etc. The possibilities of subsequently using these documents in a research context are described: behavior assignment with a rating scale, comparative analysis with movies of normal children, blind examination, and scoring by investigators not informed of the diagnosis.

Activities of Daily Living↗

Reactivity of indole derivatives towards oxygenated radicals.

The reactivity of a series of indole derivatives was assessed in the following systems: (i) oxidation of the indole derivatives induced by the thermolysis of 2,2'-azobis-(2-amidinopropane) (ABAP); (ii) oxidation of cumene induced by the thermolysis of 2,2'-azobis-(2-methyl propionitrile) (AIBN); (iii) lysozyme inactivation induced by the thermolysis of ABAP and (iv) brain homogenate autoxidation. In systems (ii) to (iv), addition of the indole derivatives decreases the rate of the process. The data obtained indicate that common factors (i.e., oxidation potential and presence of N-H bonds) control the reactivity of the indole derivatives in the four systems considered. However, in the brain homogenate autoxidation, hydrophobicity is an additional factor that affects the efficiency of antioxidants, as illustrated by Q1/2 values (the concentration of additive required to decrease the autoxidation rate to one half that observed in the absence of additive) of 0.1 mM and much greater than 8 mM for 3-methylindole and tryptophan, respectively.

Animals↗

Effect of additives on the inactivation of lysozyme mediated by free radicals produced in the thermolysis of 2,2'-azo-bis-(2-amidinopropane).

The inactivation of lysozyme caused by the radicals produced by thermolysis of 2,2'-azo-bis-2-amidinopropane can be prevented by the addition of different compounds that can react with the damaging free radicals. Compounds of high reactivity (propyl gallate, Trolox, cysteine, albumin, ascorbate, and NADH) afford almost total protection until their consumption, resulting in well-defined induction times. The number of radicals trapped by each additive molecule consumed ranges from 3 (propyl gallate) to 0.12 (cysteine). This last value is indicative of chain oxidation of the inhibitor. Uric acid is able to trap nearly 2.2 radicals per added molecule, but even at large (200 microM) concentrations, a residual inactivation of the enzyme is observed, which may be caused by urate-derived radicals. Compounds of lower reactivity (tryptophan, Tempol, hydroquinone, desferrioxamine, diethylhydroxylamine, methionine, histidine, NAD+ and tyrosine) only partially decrease the lysozyme inactivation rates. For these compounds, we calculated the concentration necessary to reduce the enzyme inactivation rate to one half of that observed in the absence of additives. These concentrations range from 9 microM (tryptophan and Tempol) to 5 mM (NAD+).

Amidines↗

[Acute lupus erythematosus disseminatus in adults: clinical aspects & course].

Acute systemic lupus erythematosus (SLE) is characterized by a variety of manifestations and by the almost constant presence of anti-nuclear antibodies. In order to distinguish it from other systemic diseases, eleven diagnostic criteria have been laid down, four of which at least must be present. In 50 p. 100 of the cases the disease is revealed by a non-destructive inflammatory polyarthritis which is highly suggestive when associated with a "butterfly" facial erythema. The main prognostic criteria are renal lesions and their histological type. Nervous system involvement seems to be less frequent and less severe nowadays, but it may leave sequelae. Pleuropericarditis and vascular thrombosis are commonly part of the clinical set up. Antinuclear antibodies are detected by immunofluorescence in more than 95 p. 100 of the patients, but they are not specific to SLE. Their absence in the initial phase of the disease may throw doubts on the diagnosis. Antibodies to DNA and Sm are more specific but inconstant. SLE is a chronic disease with intermittent flare-ups: 30 p. 100 of the patients may hope for a prolonged complete remission. At present, the survival rate at 10 and 20 years is higher than 80 p. 100 and 70 p. 100 respectively at the cost of a very close supervision but also of iatrogenic complications in increasing numbers.

Acute Disease↗

Action of staphylococcal exfoliative toxins on epidermal cell cultures and organotypic skin.

In the staphylococcal scalded skin syndrome, spontaneous intraepithelial cleavages are due to the exfoliative toxins A or B (ETA or ETB). Until now, these toxins have been studied either on epidermis or on organotypic skin cultures. In the present study, we compare the effects of these toxins on human keratinocyte cell cultures to those on human and mouse organotypic skin cultures. With concentrations of ETA or ETB of 1 mg/ml for 3 hours, spontaneous intraepithelial cleavages were noted in both cell and organotypic cultures. Keratinocyte cell cultures were as sensitive as organotypic skin cultures to these toxins. Since keratohyaline granules may represent a possible binding site for ETA or ETB, we tried to correlate the expression of keratohyaline granules with the appearance of intraepithelial clefts due to the toxins. However, when cultured in liquid medium, epithelia were not differentiated enough to allow the detection of the binding site of ETA-ETB.

Animals↗

Cultured epithelia from junctional epidermolysis bullosa letalis keratinocytes express the main phenotypic characteristics of the disease.

Keratinocytes from a 1-week-old male infant with junctional epidermolysis bullosa letalis (JEBL) were grown in vitro and then grafted as multi-layered epithelia onto nude mice, to investigate whether the defect in the dermo-epidermal cohesiveness in the disease is of epidermal and not mesodermal origin. In culture, there was a birefringent ring of cells at the edges of the keratinocyte colonies and in places some cells looked as though they had been ejected from the periphery of the colony. At confluence, the multi-layered epithelia were easily detached from the culture flasks using only mechanical agitation. On microscopy the fully-differentiated epithelium on days 21, 30 and 40 after grafting sometimes showed blistering at the dermal-epidermal junction. No labelling was noted using a GB3 monoclonal antibody, that reacts with normal human keratinocytes in culture and with the dermo-epidermal basement membrane zone in normal skin. This indicates that the defect of JEBL may be reproduced in culture and also after grafting the cultured epithelial onto a wound without an epidermis. This suggests a possible role for the junctional structure recognized by GB3 in dermo-epidermal cohesiveness.

Animals↗