[Hormonal and electrocardiographic studies in acrobatic and passenger hang-gliding flights].
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Biomedical subjects
Publications and source records attributed to D Blanc.
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Among the cutaneous manifestations of hyperparathyroidism, cases of panniculitis with calcification of the adipose tissue and necrosis of the skin have recently been reported, the mechanism incriminated being calciphylaxis, as defined by Selye on the basis of experiments. Experimental calciphylaxis consists of local or systemic calcium deposits followed by inflammatory necrosis or sclerosis. The deposits are induced by "provoking" or precipitating factors (metal salts, albumin, traumas) after a phase of sensitization (to parathyroid hormone, vitamins D2 or D3, dihydrotachysterol), provided a critical period is allowed between these two phases; the duration of that period depends on the experimental conditions. The case reported here concerns a 64-year old obese and diabetic woman who had presented with hard and tender nodosities and plaques in her abdominal and crural panniculi, ending in extensive and hyperalgesic necrosis (fig. 1 and 2). The panniculitis had occurred in a peculiar context: at the end of an episode of renal failure complicated with secondary hyperparathyroidism (serum PTH 12.9 mIU/ml; N = 1.5-4.4 mIU/ml) with moderate increase to 5,000 of the P x Ca product. Histological examination of a nodule of the thigh disclosed multiple foci of microcalcification (fig. 3, 4, 5) within the adipose lobules, in the interadipocyte spaces, in connective tissue septa and in the adventitia of small vessels (positive Von Kossa reaction). Electron microscopy showed dense calcium deposits between adipocytes, in subcutaneous septa (fig. 6, 8) and in more or less damaged vascular walls (fig. 9). Within the microfibrillar and granular fundamental substance, microcrystals looking like hydroxyapatite crystals (fig. 7) conglomerated into pincushion-like formations becoming increasingly denser and more compact.(ABSTRACT TRUNCATED AT 250 WORDS)
During the year 1985, 462 cases of septicemia were collected by SES group; 417 observations could be exploited. 73 patients died (17.3%). The statistical analysis of epidemiological and clinical data argued to factors correlated with high mortality rate: a shock, an acute respiratory distress syndrome, a pulmonary portal of entry lead to a high mortality rate. The fatal outcome increased with the age of the patients. A documented immunodeficiency (granulopenia, cytotoxic chemotherapy...), a previous broncho-pulmonary, neurologic or cardiovascular disease were factors of risk. The pulmonary or cutaneous localisations occurring within a septicemic phase were significantly related to death. Among fatal cases of bacteremia, 25% were Staphylococci, 25% Enterobacteria, 20% Pneumococci, 7% Pseudomonas. Pseudomonas, then Pneumococcus, then Staphylococcus bacteremias looks to have a worse prognosis. The more serious cases were prescribed several antibiotics, significantly much more than the mild cases. These results are compared with the results of former series; the main prognosis factors of actual septicemia are elicited in here.
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We have evaluated the serologic and T cell function inhibiting properties of 10 rat mAb reactive with the mouse LFA-1 molecule. Binding inhibition studies revealed that these mAb identified five topographic domains on LFA-1, including an immunodominant epitope region (A) defined by 6 mAb (H35-89, H68-96, H85-326, H129-37, H154-595, and H155-141) and four other spatially separate epitopes each defined by a single mAb (i.e., B, H154-266; C, H129-296; D, H154-163; and E, H155-78). Immunoprecipitation studies carried out with T cell hybridoma detergent lysate containing native or dissociated alpha and beta LFA-1 subunits permitted assignment of the epitopes A, C, and D to the alpha-chain, while expression of the epitopes B and E required homologous pairing of the alpha and beta LFA-1 subunits. These anti-LFA-1 mAb did not bind to the Mac-1 positive P388D1 cells. All the six mAb directed at epitope A inhibited, in the range of 50 to 95%, the proliferative responses of alloantigen- or soluble-antigen GAT-specific T cell clones and the cytolytic activity of I-Ak-specific CTL clones. MAb reactive with the epitopes C and D also blocked these T cell responses, although to a lesser extent. No inhibition was observed with mAb specific to epitope B, whereas the epitope E-specific mAb H155-78 potentiated control T cell responses by 20 to 40%. Suboptimal amounts of anti-L3T4 mAb H129-19 were found to synergistically enhance the T cell function inhibiting properties of mAb to LFA-1 epitopes A, C, and D. These studies reveal an unexpected diversification of LFA-1 between mouse and rat species and further the functional dissection of this molecule.
A series of BALB/c-derived T hybridoma cells, capable of producing interleukin 2 (IL 2) in response to poly(Glu60, Ala30, Tyr10) (GAT) presented by syngeneic B lymphoma cells in the context of Ad restriction determinants, was used as a model system to evaluate the roles of LFA-1 and L3T4 accessory molecules in antigen-specific T cell activation. Examination of the antigen requirement for optimal IL 2 responses revealed marked differences in the apparent avidity of these cells for GAT/Ad complexes. A relationship was observed between this parameter and the susceptibility of T hybridoma cells to inhibition by monoclonal antibodies directed at 5 distinct epitopes of LFA-1, and at A beta d allodeterminants. In contrast, L3T4a-specific monoclonal antibodies were found to block in a similar fashion the antigen-specific IL 2 responses of T hybridoma cells, regardless of the apparent avidity of their antigen receptors. It was also shown that both L3T4+ and L3T4- T hybridoma cells were capable of recognizing GAT plus Ad with high avidity. Thus, the quality of T cell antigen recognition appears to critically influence the involvement of LFA-1, and only to a marginal extent that of L3T4, in antigen-specific T cell activation. The implications of these findings are discussed in the context of recent data indicating that L3T4 may not only be an Ia-binding protein.
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Data of bony histomorphometry by transiliac biopsy were studied in 35 cases of multiple myeloma and 26 cases of benign monoclonal dysglobulinemia. In a first stage, the comparison between the two groups showed an osteoclastic resorption which was significantly higher in myeloma patients in osteolytic forms as well as asymptomatic forms, showing the diagnostic advantage of this measurement in these forms of the disease. Also, the association of a preservation of the bony trabecular volume with an osteoclastic hyper-resorption was only observed in myeloma patients. In a second stage, study of the evolution of myeloma patients permitted to demonstrate the pejorative prognostic value of an intense hyper-resorption (STRO greater than or equal to 6) from a vital point of view as well as the future of the bone; patients with an initial hyper-resorption develop an osteolysis during the first year and/or a hypercalcemia during the first 24 months; the search for a correlation between these parameters of bony resorption and known prognostic factors, has proven negative except for calcemia and the level of beta 2 serum microglobulins. This fact emphasizes the advantage of a treatment toward osteoclasts associated with the classic chemotherapy of multiple myeloma.
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Seventeen monoclonal anti-Thy-1 antibodies (mAb) derived from LOU/M rats immunized with mouse T cell clones were used to study the role of Thy-1 in antigen-independent T cell activation. These mAb identified Thy-1.2 or monomorphic determinants and immunoprecipitated a molecule of 25-28 kDa from detergent-solubilized, 125I-labeled T cell surface proteins. Competitive cross-inhibition binding assays demonstrated that these reagents defined 3 epitope groups including either Thy-1.2 (group A) or Thy-1 monomorphic (groups B and C) determinants. Experiments using high titered culture supernatants revealed that all 6 IgG mAb defining the epitope group C, and one IgG2c mAb directed at a determinant in group A were capable of stimulating the terpolymer-L-glutamic acid60-L-alanine33-Ltyrosine10 (GAT) plus I-Ad-reactive BALB/c T cell hybridoma T14-117.9 to produce interleukin 2 (IL2) in the absence of accessory cells. Cross-linking of cell-bound rat mAb by a BALB/c anti-rat kappa chain mAb, or the presence of B cell lymphomas in the culture resulted in an increase of the Thy-1-mediated IL2 responses of this hybridoma. Some mAb from group B required antibody doses exceeding 80 micrograms/ml in order to activate T cells, while others remained nonstimulatory at any dose tested. Striking synergy in mAb-mediated T cell activation was observed when nonmitogenic doses of mAb group groups A and C were mixed in the same culture. Analysis of a panel of GAT plus I-Ad-specific T cell hybridomas revealed that these cells markedly differed in the magnitude of their IL2 responses induced by a given amount of stimulating anti-Thy-1 mAb. Such reagents also stimulated normal thymocytes to express IL2 receptor on their surface. These studies show that the epitopic specificity and the amount of anti-Thy-1 mAb, and the susceptibility of the T cell examined represent important parameters for the triggering of the Thy-1 pathway of T cell activation.