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Biomedical subjects

C André

Publications and source records attributed to C André.

At least 19 recordsLinked to original sources
PubMed1992

Characterization of two human monoclonal IgM antibodies that recognize nuclear lamins.

Using immunofluorescence and immunoblotting techniques, we have identified monoclonal IgM lambda from two patients that are specific for lamins A and C and lamin B, respectively. Lamins A, B, and C are peripheral membrane proteins of the nuclear envelope with structural similarities to cytoplasmic intermediate filament proteins. When studied by indirect immunofluorescence on rat tissues, the serum containing anti-lamin B IgM stained smooth and striated muscles in addition to nuclear envelopes. Lamin B antibodies affinity purified from this serum were able to label muscle cells, suggesting that lamin B shares an epitope(s) with an unidentified muscular component(s). Since in an enzyme-linked immunosorbent assay there was no reactivity with a panel of proteins which are frequent targets of "natural" antibodies, these monoclonal IgM appear to belong to the rare category of IgM that possess a restricted specificity.

Animals↗
PubMed1992

Small repeated sequences and the structure of plant mitochondrial genomes.

The structure of plant mitochondrial genomes has proven to be complex and difficult to study. Recombination across large and small repeated sequences can result in genome diversity within individual plants, as well as rapid evolutionary change in genome structure. The role of these repeats is becoming more obvious as mitochondrial genomes are examined in detail.

DNA, Mitochondrial↗
PubMed1992

Sclerodermatous chronic graft-versus-host disease. Analysis of seven cases.

BACKGROUND: Sclerodermatous chronic graft-versus-host disease is a disabling complication after allogeneic bone marrow transplantation from HLA-identical sibling donors. Only a few series of patients have been reported and the dermatologic features have never been extensively described. OBJECTIVE: The purpose of the study was to describe clinical and biologic features of chronic sclerodermatous graft-versus-host disease and to compare them with scleroderma. METHODS: We reviewed 196 patients grafted between April 1973 and July 1987 with survival times sufficient to be at risk of chronic graft-versus-host disease. Seven had the sclerodermatous form. RESULTS: Most patients had disseminated sclerosis of the trunk and the proximal portions of the limbs. In two cases, atrophy of the skin was predominant, corresponding with a severe clinical evolution. Periorbital pigmentation was observed as an initial manifestation in three cases. Visceral manifestations resembled those observed in scleroderma but histologic and immunologic studies demonstrated clear differences. Response to therapy was variable. CONCLUSION: Chronic sclerodermatous graft-versus-host disease may realize two different patterns. Major atrophy is associated with a more severe progression.

Adolescent↗
PubMed1992

Identification and characterization of a new set of nucleolar ribonucleoproteins which line the chromosomes during mitosis.

We investigated the perichromosomal architecture established during mitosis. Entry into mitosis brings about a dramatic reorganization of both nuclear and cytoplasmic structures in preparation for cell division. While the nuclear envelope breaks down, nuclear proteins are redistributed during chromosome condensation. Some of these proteins are found around the chromosomes, but little is known concerning their nature and function. Ten autoimmune sera were used to study the microenvironment of chromosomes and, in particular, the chromosome periphery. They were selected for their anti-nucleolar specificity and were found to recognize three nucleolar proteins that coat the chromosomes during mitosis. The distribution of these antigens was followed through the cell cycle by confocal laser scanning microscopy. The antigens dispersed very early during prophase and simultaneously with the chromosome condensation suggesting a correlation between these two processes. The antigens have apparent molecular weights of 53, 66, and 103 kDa on SDS-PAGE migration. Elution of the antibodies and immunopurification showed that they are RNA-associated proteins. The coimmunoprecipitating RNA moiety involved in these RNPs appeared to be U3, but the antigens are not related to the fibrillarin family. Therefore, small nucleolar RNPs follow the same distribution during mitosis as that described for small nuclear RNPs. Possible functions for these antigens are discussed.

Antibodies, Antinuclear↗
PubMed1992

[Adverse prognostic influence of diabetes mellitus and hyperglycemia on the clinical course of cerebral infarction].

We accessed the potential impact of diabetes mellitus and hyperglycemia on early prognosis in a study of 109 cases of CT proved brain infarction. Main end-points of this study were 30-days case-fatality rates and the probability of early discharge or prolonged hospitalization. Proportions of patients exhibiting diverse evolutions were compared by Fisher's test and, when the number of observations permitted, by chi-square test. Diabetes mellitus was diagnosed by history in 15.6% (17 patients). In 86 cases analysed within 72 hours of admission, hyperglycemia (glucose level higher than 110 mg/dL) was detected in 67.4% (including all 14 diabetic patients (35.3% vs 21.7%; p = 0.18), but these patients probably were discharged early less frequently (23.5% vs 51.1%; p = 0.06). Compared to the normoglycemic patients, hyperglycemic patients also fared worse, when considering altogether the early discharge and case fatality rates and the need for prolonged hospitalization (p = 0.06). They also exhibited a nonsignificant increase in early case fatality rate (31% vs 15.4%; p = 0.21) and a markedly reduced chance of obtaining early hospital discharge (37.9% vs 65.4%; p = 0.03). Case fatality rates were maximal in diabetic hyperglycemic patients (42.9%) and seemed intermediate in non-diabetic hyperglycemic patients (27.3%). Considering the three end-points evaluated, the apparent differences between non-diabetic hyper and normoglycemic patients did not reach statistical significance (p = 0.19). These results suggest that both diabetes mellitus and hyperglycemia "per se" have deleterious effects on the clinical evolution of patients with cerebral infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Adverse prognostic influence of diabetes mellitus and hyperglycemia on the clinical course of cerebral infarction].

In non-diabetic patients, the appearance of hyperglycemia in the acute phase of stroke is related to the extension of cellular injury, and hence to the physiologic stress response. In animal models of ischemic insult, the deleterious effects of hyperglycemia depend heavily on the production of lactic acid "via" activation of the glycolytic anaerobic pathway. The abnormal production of lactic acid and consequent tissular acidosis appear mainly in the early post-reperfusion period, or in states of marked but partial reduction of blood flow. A direct reduction of cerebral blood flow and, perhaps, the production of a hyperosmolar state may contribute to worsening of the ischemic injury. In diabetic patients, previous hemorrheologic and microcirculatory changes, and a greater susceptibility to infections may additionally reduce the chances of complete recovery after stroke.

Brain Ischemia↗
PubMed1992

Genomic organization of the human c-kit gene: evolution of the receptor tyrosine kinase subclass III.

The c-kit proto-oncogene encodes a transmembrane tyrosine kinase receptor. It belongs to receptor tyrosine kinase subclass III, which also includes the colony-stimulating factor I receptor (c-fms), platelet-derived growth factor receptors A and B (PDGFRA and PDGFRB), as well as FLT1 and FLT3/FLK2. c-kit and PDGFRA, c-fms and PDGFRB, FLT1 and FLT3/FLK2 are grouped by pair in three clusters in man on chromosome 4 band q11-q13, chromosome 5 band q31-q33 and chromosome 13 band q12 respectively. Here, we report the genomic organization of the human c-kit gene, which is composed of 21 small coding exons, distributed over 80 kb. Comparison of the c-kit and c-fms oncogenes shows that they share identified exon/intron boundaries in their two kinase domains, as well as a similar exon/intron organization in the extracytoplasmic domain. Comparison with the kinase domains of tyrosine kinase genes not belonging to subclass III suggests that the exon/intron organization of c-kit and c-fms is a characteristic feature of subclass III. The genomic similarities between c-kit and c-fms, in conjunction with the location in pairs on different chromosomes of the subclass III genes, has led us to hypothesize that cis and trans duplications gave rise to this group of genes.

Amino Acid Sequence↗
PubMed1991

Substitution of leucine for isoleucine in a sequence highly conserved among retroviral envelope surface glycoproteins attenuates the lytic effect of the Friend murine leukemia virus.

Friend murine leukemia virus is a replication-competent retrovirus that contains no oncogene and that exerts lytic and leukemogenic properties. Thus, newborn mice inoculated with Friend murine leukemia virus develop severe early hemolytic anemia before appearance of erythroleukemia. To identify the retroviral determinants regulating these effects, we used chimeric infectious constructions and site-directed point mutations between a virulent Friend murine leukemia virus strain and a naturally occurring variant attenuated in lytic and leukemogenic effects. We found that severe hemolytic anemia was always associated with higher numbers of blood reticulocytes with budding retroviral particles. Furthermore, a remarkably conservative leucine to isoleucine change in the extracellular SU component of the retroviral envelope was sufficient to attenuate this lytic effect. Also, this leucine at position 348 of the envelope precursor protein was located within the only stretch of five amino acids that is conserved in the extracellular SU component of all murine, feline, and primate type C and type D retroviral envelopes. This observation suggested an important structural function for this yet undescribed conserved sequence of the envelope. Lastly, we observed that lytic and leukemogenic effects were attenuated by a deletion of a second repeat in the transcriptional enhancer region of the viral long terminal repeats of the variant strain.

Amino Acid Sequence↗
PubMed1991

Transient intraepidermal bullous reaction after skin graft for toxic epidermal necrolysis. Ultrastructural and immunohistochemical features similar to those of inherited epidermolysis bullosa simplex.

Blister formation in skin graft donor or recipient sites is uncommon. We describe a 49-year-old female patient with bullae in sites of grafts used in the treatment of toxic epidermal necrolysis. Generalized loss of skin developed 3 weeks after she had ingested phenobarbital. Sixty days after the beginning of the toxic epidermal necrolysis, the reepidermization was only 80% and skin grafts were placed on lower-extremity and abdominal wounds using the first healed sites as donor sites. Several bullae and erosions were noted on grafted areas 3 weeks later. Skin biopsy specimens revealed separation at the dermoepidermal junction, and no autoantibodies were detected by direct and indirect immunofluorescence. Electron microscopy demonstrated that the blister was formed through the basal keratinocytes and that the dermoepidermal junction, including hemidesmosomes and anchoring fibrils, was normal. Immunofluorescence mapping was performed using polyclonal antibodies from the serum of patients with bullous pemphigold and epidermolysis bullosa acquisita and monoclonal antibodies against GB3 antigen and collagen type VII. All but the bullous pemphigold serum gave positive results; only faint and focal staining of the dermoepidermal junction was observed with bullous pemphigold serum. These findings are the same as those encountered in hereditary epidermolysis bullosa simplex. A biopsy performed 1 year later in the same site as the first one revealed that bullous pemphigold antigen was normally expressed. Keratinocytes autografted in the treatment of toxic epidermal necrolysis may become transiently, functionally abnormal because of the alteration of recipient sites.

Blister↗
PubMed1990

[Idiopathic nephrotic syndrome. Effect of oral cromoglycate].

The occurrence of idiopathic nephrotic syndrome may be due to environmental antigens, and in particular to the ingestion of certain foods, as indicated by the result of food eviction tests. This led us to prescribe oral cromoglycate (800 mg/day for 2 weeks) combined with the avoidance of specific foods. Twelve patients with corticosteroid-dependent (n = 6) or corticosteroid-resistant (n = 6) idiopathic nephrotic syndrome with proteinuria greater than 1.50 g/24 h were thus treated without modification of steroid dosage. In 3 of these patients hypersensitivity to certain foods had previously been demonstrated. In 5 of the 12 patients, proteinuria was reduced by more than 50 percent; these 5 patients had received cromoglycate for 2 weeks with a free diet. After evictions were stopped, 3 patients relapsed; in 2 cases proteinuria remained absent. In 3 of the 12 cases, we subsequently used cromoglycate and evictions in corticosteroid-dependent patients in complete remission by gradual reduction of steroid dosage in the hope of lowering the dependence threshold. In one patient, the corticosteroid therapy could be discontinued during 3 months without relapse; in the other 2 patients no effect was observed. Thus, oral cromoglycate could be used together with food eviction in certain cases of idiopathic nephrotic syndrome, this being a therapeutic approach as well as a diagnostic test.

Administration, Oral↗
PubMed1989

Desensitization of alpha 2-adrenergic receptors in NG 108 15 cells by (-)-adrenaline and phorbol 12-myristate 13-acetate.

alpha 2-Adrenergic receptors on NG 108 15 cell membranes were identified by [3H]rauwolscine binding: Bmax. = 661 +/- 81 fmol/mg of protein, Kd = 6.9 +/- 2.5 nM (mean +/- S.E.M., n = 6). On intact cells, stimulation of these receptors by (-)-adrenaline inhibited the prostaglandin-E1-stimulated adenylate cyclase activity by about 60%. The effect of (-)-adrenaline was pertussis-toxin-sensitive, indicating the involvement of an inhibitory G protein. (-)-Adrenaline/[3H]rauwolscine competition-binding experiments revealed that only 50% of the alpha 2 receptors were coupled to G proteins (i.e. displayed high agonist affinity). Pre-treatment of the cells with 20 microM-(-)-adrenaline provoked homologous desensitization of the alpha 2 receptors. The alpha 2-adrenergic response decreased after a time lag of about 2 h, to reach a minimum after 12 h. The bradykinin and muscarinic responses were not affected. The alpha 2-receptor concentration decreased without time lag. The high-agonist-affinity sites disappeared more rapidly (t1/2 = 42 min) than did the low-affinity uncoupled sites (t1/2 approx. 20 h). In contrast, pertussis-toxin-mediated [32P]ADP-ribosylation of inhibitory G proteins was unaffected by the pre-treatment. Pretreatment of intact NG 108 15 cells with 1 microM-phorbol 12-myristate 13-acetate (PMA) provoked a rapid decrease of the alpha 2-adrenergic response. The effect was nearly complete after 40 min. PMA also decreased the bradykinin response, suggesting a heterologous desensitization process. The alpha 2-receptor concentration, the (-)-adrenaline competition-binding curves and the pertussis- and cholera-toxin-mediated [32P]ADP-ribosylation of their respective G proteins were not affected.

Adenylyl Cyclases↗