996 resultados para NCX 1000
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Baluzianus
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Colbertinus
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Colbertinus
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Puteanus
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Puteanus
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Colbertinus
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Acquis le 1er avril 1837 de MM. de Bure, "manuscrits provenant de la bibliothèque de Rosny, ou plutôt de M. Lepelletier de Rosambo", pour le prix de 100 francs 50 centimes; cf. B.n.F., département des Manuscrits, registre des acquisitions 1833-1848, n° 2029; Rosny 2371, cf. Delisle, Cab. des mss., II, 294 n. 4; — bibliothèque de Rosny, cf. ex-libris gravé aux armes de Marie-Caroline de Bourbon-Sicile, duchesse de Berry et cote "45" (contreplat sup.); Catalogue Rosny, n° 2371; — Louis Le Peletier de Rosambo (?); — Pierre Pithou, cf. ex-libris "P. Pithoei" (1); B.n.F., département des Manuscrits, nouv. acq. fr. 5527, f. 13; — , cote "26" (dos)
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Iowa has approximately 1000 bridges that have been overlaid with a nominal 2" of portland cement concrete. A Delamtect survey of a sampling of the older overlaid bridges indicated delaminations in several of them. Eventually these bridges as well as those that have not received an overlay must be programmed for rehabilitation. Prior to rehabilitation the areas which are delaminated must be identified. There are currently two standard methods of determining delaminated areas in bridge decks; sounding with a metal object or a chain drag and sounding with an electro-mechanical sounding system (Delamtect). Sounding with a metal object or chain drag is time consuming and the accuracy is dependent on the ear of the operator and may be affected by traffic noise. The Delamtect requires less field time but the graphical traces require that data reduction be done in the office. A recently developed method of detecting delamination is infrared thermography. This method is based on the temperature difference between sound and delaminated concrete. A contract was negotiated with Donohue and Associates, Inc. of Sheboygan, Wisconsin, to survey 18 p.c. concrete overlaid bridge decks in Iowa using the infrared thermography method of detecting delaminations.
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Glioblastoma multiforme (GBM) is the most common malignant primary brain tumor in adults. Standard therapeutic approaches provide modest improvement in the progression-free and overall survival, necessitating the investigation of novel therapies. We review the standard treatment options for GBM and evaluate the results obtained in clinical trials for promising novel approaches, including the inhibition of angiogenesis, targeted approaches against molecular pathways, immunotherapies, and local treatment with low voltage electric fields.
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Anti-idiotype antibody therapy of B-cell lymphomas, despite numerous promising experimental and clinical studies, has so far met with limited success. Tailor-made monoclonal anti-idiotype antibodies have been injected into a large series of lymphoma patients, with a few impressive complete tumour remissions but a large majority of negative responses. The results presented here suggest that, by coupling to antilymphoma idiotype antibodies a few molecules of the tetanus toxin universal epitope peptide P2 (830-843), one could markedly increase the efficiency of this therapy. We show that after 2-hr incubation with conjugates consisting of the tetanus toxin peptide P2 coupled by an S-S bridge to monoclonal antibodies directed to the lambda light chain of human immunoglobulin, human B-lymphoma cells can be specifically lysed by a CD4 T-lymphocyte clone specific for the P2 peptide. Antibody without peptide did not induce B-cell killing by the CD4 T-lymphocyte clone. The free cysteine-peptide was also able to induce lysis of the B-lymphoma target by the T-lymphocyte clone, but at a molar concentration 500 to 1000 times higher than that of the coupled peptide. Proliferation assays confirmed that the antibody-peptide conjugate was antigenically active at a much lower concentration than the free peptide. They also showed that antibody-peptide conjugates required an intact processing function of the B cell for peptide presentation, which could be selectively inhibited by leupeptin and chloroquine.(ABSTRACT TRUNCATED AT 250 WORDS)
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Until now it was thought that the retrovirus mouse mammary tumor virus preferentially infects B cells, which thereafter proliferate and differentiate due to superantigen-mediated T cell help. We describe in this study that dendritic cells are infectable at levels comparable to B cells in the first days after virus injection. Moreover, IgM knockout mice have chronically deleted superantigen-reactive T cells after MMTV injection, indicating that superantigen presentation by dendritic cells is sufficient for T cell deletion. In both subsets initially only few cells were infected, but there was an exponential increase in numbers of infected B cells due to superantigen-mediated T cell help, explaining that at the peak of the response infection is almost exclusively found in B cells. The level of infection in vivo was below 1 in 1000 dendritic cells or B cells. Infection levels in freshly isolated dendritic cells from spleen, Langerhans cells from skin, or bone marrow-derived dendritic cells were compared in an in vitro infection assay. Immature dendritic cells such as Langerhans cells or bone marrow-derived dendritic cells were infected 10- to 30-fold more efficiently than mature splenic dendritic cells. Bone marrow-derived dendritic cells carrying an endogenous mouse mammary tumor virus superantigen were highly efficient at inducing a superantigen response in vivo. These results highlight the importance of professional APC and efficient T cell priming for the establishment of a persistent infection by mouse mammary tumor virus.
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OBJECTIVE: To compare interval breast cancer rates (ICR) between a biennial organized screening programme in Norway and annual opportunistic screening in North Carolina (NC) for different conceptualizations of interval cancer. SETTING: Two regions with different screening practices and performance. METHODS: 620,145 subsequent screens (1996-2002) performed in women aged 50-69 and 1280 interval cancers were analysed. Various definitions and quantification methods for interval cancers were compared. RESULTS: ICR for one year follow-up were lower in Norway compared with NC both when the rate was based on all screens (0.54 versus 1.29 per 1000 screens), negative final assessments (0.54 versus 1.29 per 1000 screens), and negative screening assessments (0.53 versus 1.28 per 1000 screens). The rate of ductal carcinoma in situ was significantly lower in Norway than in NC for cases diagnosed in both the first and second year after screening. The distributions of histopathological tumour size and lymph node involvement in invasive cases did not differ between the two regions for interval cancers diagnosed during the first year after screening. In contrast, in the second year after screening, tumour characteristics remained stable in Norway but became prognostically more favorable in NC. CONCLUSION: Even when applying a common set of definitions of interval cancer, the ICR was lower in Norway than in NC. Different definitions of interval cancer did not influence the ICR within Norway or NC. Organization of screening and screening performance might be major contributors to the differences in ICR between Norway and NC.