1,105 results on '"Ferrarini, M"'
Search Results
252. Comparison of various tests for Fc receptors on different human lymphocyte sub populations.
- Author
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Winchester, R. J., Hoffman, T., Ferrarini, M., Ross, G. D., and Kunkel, H. U.
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CELL receptors ,LYMPHOCYTES ,T cells ,B cells ,IMMUNOGLOBULIN G ,LYMPHOID tissue ,MACROPHAGES - Abstract
Six different immune complex test systems for the detection of IgG Fc receptors were applied to the study of various human lymphocyte populations. The extent of binding varied widely according to the system and the cell type employed. Two systems bound preferentially to a high proportion of B lymphocytes from peripheral blood or tonsils, one of which bound with only a very few T cells. In contrast, four other test systems which bound well with the Fc receptors on T lymphocytes gave weaker reactions with Fc receptors on B cells. The reactivity of Fc receptors on null or third population lymphocytes was similar to that of the Fc-positive T cells. Pronase digestion experiments showed a graded selective loss of reactivity with the different Fc reagents. No one system was optimal for all of the lymphocyte populations, although aggregated IgG exhibited the broadest spectrum of reactivity. A pronounced effect of temperature was evident on the binding reactions, and native IgG showed strong binding at 4°C, particularly to the Fc receptors on T cells. [ABSTRACT FROM AUTHOR]
- Published
- 1979
253. Lymphocyte membrane immunoglobulins: similarities between human IgD and mouse IgD-like molecules.
- Author
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Sitia, R., Corte, G., Ferrarini, M., and Bargellesi, A.
- Published
- 1977
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254. A study of the immunoglobulin classes present on the membrane and in the cytoplasm of human tonsil plasma cells.
- Author
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Ferrarini, M., Viale, Giovanna, Risso, Angela, and Pernis, B.
- Published
- 1976
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255. Membrane Ig on human lymphocytes: rate of turnover of IgD and IgM on the surface of human tonsil cells.
- Author
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Ferrarini, M., Carte, G., Viale, Giovanna, Durante, Maria L., and Bargellesi, A.
- Published
- 1976
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256. Membrane Ig on MPC11 myeloma cells: correlation between the expression of membrane Ig, a receptor for Ig and the process of secretion.
- Author
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Corte, G., Risso, Angela, Ferrarini, M., and Bargellesi, A.
- Published
- 1976
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257. Expression of a receptor for IgM by human T cells in vitro.
- Author
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Moretta, L., Ferrarini, M., Durante, Maria Laura, and Mingari, Maria Cristina
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- 1975
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258. Lymphocyte membrane receptors in human lymphoid leukemias.
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Ferrarini, M., Tonda, G. P., Risso, Angela, and Viale, Giovanna
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- 1975
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259. Complement Receptor Distinguishes between Two Subsets of Large Granular Lymphocytes with Different Natural Killer Activity and Cytochemical and Ultrastructural Features.
- Author
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Nocera, A., Montesoro, E., Balbo, P., Ferrarini, M., Leprini, A., Zicca, A., and Grossi, C. E.
- Subjects
BLOOD cells ,LYMPHOCYTES ,CELL receptors ,CYTOPLASMIC granules ,HYDROLASES ,ENZYMES - Abstract
Human peripheral blood large granular lymphocytes (LGL)--that is, cells with intracytoplasmic azurophilic (electron-dense) granules, with a positivity for the cytochemical localization of certain acid hydrolases, and with avid surface receptors for the Fc portion of IgG--have been purified on Percoll density gradients. Approximately 30% of these cells expressed receptors for the third complement component (C3R). They were separated into C3R-positive and C3R-negative cells. C3R
+ cells had a significantly greater natural killer (NK) activity against K562 target cells than C3R+ cells. This difference was unrelated to the presence in the C3R+ cells of a contaminant cell type incapable of NK activity, since cytochemical and ultrastructural analysis revealed that C3R+ and C3R- fractions contained comparable LGL numbers. Agarose cytotoxicity assays at the single-cell level demonstrated that C3R+ LGL contained a large number of cells that bound to but did not lyse the target. The remaining fully cytotoxic C3R+ LGL had, however, the same killing and recycling properties as the cells from the C3R- fraction. Electron microscopy and cytochemical studies showed that C3R+ cells had fewer electron-dense granules than C3R- cells and stained more faintly for the localization of alpha-naphtyl acetate esterase. In contrast to C3R- cells, C3R+ LGL displayed morphological features suggesting that an active process of granule formation was taking place. Taken together, the data indicate that C3R+ cells represent a discrete subset or a maturational stage of LGL. [ABSTRACT FROM AUTHOR]- Published
- 1983
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260. Receptors for the Third Complement Component on a Proportion of Large Granular Lymphocytes from Human Peripheral Blood.
- Author
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Nocera, A., Cadoni, A., Zicca, A., Di Primio, R., Leprini, A., and Ferrarini, M.
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CELLS ,ERYTHROCYTES ,BLOOD cells ,B cells ,T cells - Abstract
Large granular lymphocytes (LGL) are nonadherent cells with cytoplasmic azurophitic granules, avid receptors for the Fc portion of lgG, and a paranuclear localization of alpha-naphthyl acid esterase or acid phosphatase. LGL constitute the bulk of T
G cells (cells wish receptors for sheep erythrocytes and for IGC molecules) and null cells (non-T, non-B cells). In the present study we demonstrate that 20-33% of the circulating human LGL express receptors (or the third complement component (C3R). When TG or null cell fractions from normal individuals or non-T cells from a patient with infantile agammaglobulinaemia (which contained almost exclusively LGL) were rosetted with erythrocytes coated with antibody and complement, a variable number of C3R-bearing cells were detected. Such cells were isolated and analysed further; the great majority of them displayed she cytochemical and ultrastructural features of LGL. [ABSTRACT FROM AUTHOR]- Published
- 1982
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261. In vitro selective expansion of allergen specific T cells from atopic patients.
- Author
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Lanzavecchia, A., Santini, Pierina, Maggi, E., Prete, G. F. Del, Falagiani, P., Romagnani, S., and Ferrarini, M.
- Subjects
T cells ,ALLERGENS ,LYMPHOCYTES ,IMMUNOGLOBULINS ,ANTIGENS ,CELL lines - Abstract
Peripheral blood mononuclear cells from atopic donors were stimulated in vitro with allergens (Rye group I or Dermatophagoides pteronyssinus). T cell lines were originated and maintained in long term culture using lL-2 and periodical restimulations with allergen. The lines were antigen specific (i.e. responded to the allergen used to raise them and not to other antigens) and required that the antigen was presented by autologous cells (i.e. they were restricted). The restriction elements were probably at the level of HLA-DR antigens since the proliferative response was specifically blocked by anti-HLA-DR antibodies. Surface marker analysis revealed that the lines comprised mainly cells with an helper/inducer phenotype, although cells with markers of the suppressor/cytotoxic T cells were also present. The lines could be cloned by limiting dilution and clones with the same restriction and specificity as the parental line were isolated. These studies demonstrate the possibility of obtaining a large number of allergen specific human T cells that can be used for further in vitro studies on the regulation of the IgE response. [ABSTRACT FROM AUTHOR]
- Published
- 1983
262. Antigen-Binding Cells Following Contact-Sensitization Detected by Rosette-Formation.
- Author
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Ferrarini, M., Munro, A., Kent, S.P., Gurner, B., and Coombs, R.R.A.
- Published
- 1973
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263. Distribution of Immunoglobulin Determinants and Antigen Receptors on the Surface of Rabbit Lymphoid Cells as Shown by Peroxidase-Labelled Antibody and Cell Rosetting Techniques.
- Author
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Kent, S.P., Ferrarini, M., Coombs, R.R.A., and Hockaday, A.H.
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- 1972
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264. An Enzyme Histochemical Study of Antibody Production by Single Cells.
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Governa, M., Scelsi, R., and Ferrarini, M.
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- 1971
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265. An Artificial Model for Double Mixed Agglutination Reaction.
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Ferrarini, M. and Kelus, A.S.
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- 1970
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266. Cytophilic antibody: correlation of its distribution with activation of basophils and macrophages.
- Author
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Ferrarini, M., Munro, A., and Wilson, Anne B.
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- 1973
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267. Allotypic determinants on the surface of rosette-forming cells in the rabbit.
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Ferrarini, M., Kent, S. P., Munro, A., Kelus, A. S., Catty, D., and Coombs, R. R. A.
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- 1973
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268. The detection of Θ antigen on cells by immunofluorescence: Failure to detect Θ antigen on rosette-forming cells.
- Author
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Russell, S. M., Ferrarini, M., Munro, A., and Lachmann, P. J.
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- 1972
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269. A somatic and germline mosaic mutation in MPZ/P0mimics recessive inheritance of CMT1B
- Author
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Fabrizi, G. M., Ferrarini, M., Cavallaro, T., Jarre, L., Polo, A., and Rizzuto, N.
- Abstract
To identify the molecular basis of a demyelinating Charcot–Marie–Tooth disease type 1 (CMT1) with presumed autosomal recessive inheritance.
- Published
- 2001
270. Maturation of B cells; correlation between the capacity of responding to T cell factors in vitro and the stage of maturation reached in vivo
- Author
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RUBARTELLI A., GROSSI C. E., FERRARINI M., SITIA , ROBERTO, Rubartelli, A., Sitia, Roberto, Grossi, C. E., and Ferrarini, M.
- Published
- 1985
271. Differentiation of chronic lymphocytic leukaemia cells: correlation between the synthesis and secretion of immunoglobulin and the ultrastructure of the malignant cells
- Author
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RUBARTELLI A., ZICCA A., GROSSI C. E., FERRARINI M., SITIA , ROBERTO, Rubartelli, A., Sitia, Roberto, Zicca, A., Grossi, C. E., and Ferrarini, M.
- Published
- 1983
272. Differentiation of Chronic Lymphocytic Leukemia Cells: Correlation Between the Synthesis and Secretion of Immunoglobulins and the Ultrastructure of the Malignant Cells
- Author
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Rubartelli, A., Sitia, R., Zicca, A., Grossi, C.E., and Ferrarini, M.
- Abstract
The capacity of synthesizing and secreting Ig molecules was studied in 11 patients with B-cell chronic lymphocytic leukemia (B-CLL) whose cells expressed surface IgM, in 3 patients with surface IgG-bearing cells, and in 2 IgM prolymphocyte leukemias (IgM-PLL). Three types of μchains were detected by SDS-polyacrylamide gel electrophoresis analysis of the endogenously labeled molecules isolated by specific immunoprecipitation. Two of them were isolated from the cell lysates and were identified as the membrane μchain and the precursor of the secreted molecules, respectively. The latter also possibly contained precursors of the membrane molecules. The third type of molecule was detected only in the culture medium and was identified as secretory μchain. Not all of the malignant clones possessed the three types of μchains. Only of the IgM-bearing malignant cell clones were capable of secretion, whereas the remaining synthesized the secretory μchains but degraded them intracellularly. Two types of molecules (membrane and secreted) were found in the IgG-bearing CLL cells from three patients. In all of them, secretion was detected. Ultrastructural analysis demonstrated that cells from the secreting clones had the features of more mature lymphocytes than the cells from nonsecreting clones. These features were represented by a developed Golgi apparatus, various types of vesicles (smooth and coated), and strands of the rough endoplasmic reticulum. A certain heterogeneity of the degree of maturation of the cells was observed within these clones. The data are consistent with the hypothesis that CLL clones are heterogeneous and can be distinguished through the different degrees of maturation of their cell components.
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- 1983
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273. Large Granular Lymphocytes Have a Promoting Activity on Human Peripheral Blood Erythroid Burst-Forming Units
- Author
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Pistoia, V., Ghio, R., Nocera, A., Leprini, A., Perata, Angela, and Ferrarini, M.
- Abstract
Peripheral blood mononuclear cells were fractionated according to the expression of a variety of surface markers, and the fractions obtained were tested for erythroid burst-forming unit (BFU-E) colony formation. BFU-Es were detected in the HLA-DR+non-T cell fraction, but gave rise to optimum colony numbers only in the presence of a nonadherent, relatively radioresistant cell. This accessory cell was found among the HLA-DR−non-T, non-B cells, a fraction that was particularly enriched in large granular lymphocytes (LGLs). Experiments carried out to assess directly the surface markers of the accessory cell revealed an FcR+, OKM1+, Leu 7+, Leu 11+, OKT4−, OKT8−surface phenotype, which is consistent with that of the majority of LGLs. Peripheral blood LGLs, purified by Percoll density gradient, proved very efficient in promoting optimal BFU-E colony formation. All of these results indicate that LGLs have a potent erythroid burst-promoting activity. Such activity is probably mediated through the release of soluble factors, as shown by the observation that LGL culture supernatants were as effective as LGLs in sustaining colony formation. © 1985 by Grune & Stratton, Inc.
- Published
- 1985
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274. Production of colony-stimulating activity by human natural killer cells: analysis of the conditions that influence the release and detection of colony-stimulating activity
- Author
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Pistoia, V, Zupo, S, Corcione, A, Roncella, S, Matera, L, Ghio, R, and Ferrarini, M
- Abstract
Highly purified natural killer (NK) cell suspensions were tested for their capacity to release colony-stimulating activity (CSA) in vitro. NK cell suspensions comprised primarily CD16+ cells and were devoid of CD3+ T cells, CD15+ monocytes, and of B cells. CSA was detected in the NK cell supernatants and sustained the growth of myeloid colonies from both normal peripheral blood and bone marrow. CSA could be in part inhibited by pretreating NK cell culture supernatants with a specific goat anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antiserum. The inhibition, however, was never complete, a finding that suggests that additional factors were responsible for CSA. Incubation of NK cells with K562 cells (an NK-sensitive target) or with normal bone marrow cells resulted in the appearance of a strong colony- inhibiting activity (CIA) in the culture supernatants. Such CIA was demonstrable in an experimental system where bone marrow or peripheral blood progenitors were induced to form myeloid colonies in the presence of conditioned medium by CSA-producing giant cell tumor (GCT) cells. Stimulation of NK cells with NK-insensitive targets failed to induce CIA production. Neutralizing antitumor necrosis factor (TNF) monoclonal antibodies (MoAbs) were found capable of inhibiting CIA present in the supernatants of NK cells stimulated with K562 cells. Following treatment with anti-TNF antibodies, CSA was again detectable in the same supernatants. This finding indicates that induction of TNF production did not concomitantly switch off CSA production by NK cells. Pretreatment of NK cells with recombinant interleukin-2 (rIL-2) or gamma interferon (r gamma IFN) did not change the amount of CSA released. However, treatment with rIL-2 caused the appearance of a factor in the NK cell supernatants capable of sustaining the formation of colonies of a larger size.
- Published
- 1989
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275. Production of colony-stimulating activity by normal and neoplastic human B lymphocytes
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Pistoia, V, Ghio, R, Roncella, S, Cozzolino, F, Zupo, S, and Ferrarini, M
- Abstract
Normal human B cells were purified from peripheral blood or tonsils and tested for their ability to release colony-stimulating activity (CSA) in short-term cultures. The target cells used in the CSA assays were from peripheral blood or bone marrow. Unstimulated B cells produced CSA in amounts similar to those present in the GCT-conditioned medium used as a positive control. The B cell-derived CSA predominantly promoted the growth of colonies that contained macrophages alone or macrophages and granulocytes. CSA eluted in a single peak from a G-75 Sephadex column with an approximate molecular weight (mw) of 65 to 70 kilodaltons (kd). Fractionation of tonsil B lymphocytes on Percoll density gradients showed that large B cells, probably already activated in vivo, were the main source of CSA. By contrast, small, resting B cells recovered from a different fraction of the Percoll gradient released minimum amounts or no CSA. However, these B cells became CSA producers following stimulation with Staphylococcus aureus Cowan (SAC) in vitro. B cells purified from the peripheral blood of nine out of 12 patients with B-cell chronic lymphocytic leukemia (B-CLL) also released CSA in vitro in the absence of stimuli. These findings suggest that by releasing CSA, B cells may have a role in the regulation of hematopoiesis and in the control of the inflammatory process.
- Published
- 1987
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276. Acid hydrolases as markers of maturation in B-cell chronic lymphocytic leukemia
- Author
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Grossi, CE, Zicca, A, Leprini, A, Cadoni, A, Pistoia, V, and Ferrarini, M
- Abstract
Malignant lymphocytes from 30 B-cell chronic lymphocytic leukemia (B- CLL) patients were studied for the cytochemical localization of two acid hydrolases, alpha-naphthyl acetate esterase (ANAE) and acid phosphatase (AT). The large majority of the cells stained for both ANAE and AP in 7 cases, for AP only in 18 cases, and were negative for both the enzymes in 5 cases. Ultrastructural analysis revealed that the cells that displayed more mature morphological features, such as well developed smooth and rough membrane compartments, were those positive for acid hydrolases. That ANAE and AP are expressed by B cells at late stage of maturation was confirmed by the finding that some lymphocytes and all of the plasmacytoid lymphocytes and plasma cells from Walderstrom's macroglobulinemia, from mixed cryoglobulinemia, and from multiple myeloma patients stained strongly for both ANAE and AP. Using the expression of acid hydrolases and certain ultrastructural features as markers of cell differentiation, it was possible to demonstrate a process of maturation within the single B-CLL clones with accumulation of the cells at stages that differed in the various cases.
- Published
- 1982
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277. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain
- Author
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Harms, L., Bock, A., JÄnisch, W., Valdueza, J., Weber, J., Link, I., De Keyser, J., Goossens, A., Wilczak, N., Vedeler, C., Bjorge, L., Uvestad, E., Conti, G., Williams, K., Ginsberg, L., Rafique, S., Rapoport, S. I., Gershfeld, N. L., De La Meilleure, G., Crevits, L., Faiss, J. H., Heye, N., Blanke, J., Sackmann, A., Kastrup, O., Doornbos, R., van der Worp, H. B., Kappelle, L. J., Bar, P. R., Davie, C. A., Barker, G. J., Brenton, D., Miller, D. H., Thompson, A. J., Block, F., Schwarz, M., Delodovici, L., Baruzzi, F., Bonaldi, G., Dario, A., Marra, A., Mercuri, A., Dworzak, F., Cavallari, P., Confalonieri, P., Zuffi, M., Antozzi, C., Cornelio, F., Baldissera, F., Chassande, B., Ameri, A., Eymard, B., Poisson, M., Vérier, A., Brunet, P., Congia, S., Murgia, P. L., Cannas, A., Borghero, G., Uselli, S., Mellino, G., Ferrai, R., Lampis, R., Massa, R., Muzzetto, B., Giannini, F., Rossi, S., Cioni, R., d'Aniello, C., Guarneri, A., Battistini, N., Ceriani, F., Del Santo, A., Poloni, M., Campo, J. F., Iglesias, F., Guitera, M. V., Farinas, C., Pascual, J., Leno, C., Berciano, J., Thorpe, I. W., Kendall, B. E., McDonald, W. I., Moulignier, A., Dromer, F., Baudrimont, M., Dupont, B., Gozlan, J., El Amrani, M., Petit, J. C., Roullet, E., Sterzi, R., Causaran, R., Protti, A., Riva, M., Erminio, F., Arena, O., Villa, F., Maccagnano, E., Miletta, M., Spinelli, F., Ben-Hur, T., Weidenfeldl, J., Rao, N. S., Chari, C. C., Laforet, P., Matheron, S., Adams, D., Chemouilli, Ph., Desi, M., Said, G., Davous, P., Lionnet, F., Pulik, M., Genet, P., Rozenberg, F., Cartier, L. M., Castillo, J. L., Cea, J. G., Villagra, R., de Saint Martin, L., Mahieux, F., Manifacier, M. J., Mattos, K., Queiros, C., Publio, L., Vinhas, V., PeÇanha-Martins, A. C., Melo, A., Liska, U., Zifko, U., Budka, H., Drlicek, M., Grisold, W., Kaufmann, R., Kaiser, R., Czygan, M., Gomes, I., Jones, N., Cunha, S., EmbiruÇu, E. Katiane, Vieira, V., Araujo, I., Alexandra, M., Ferreira, A., Goes, J., Chemouilli, P., Israel-Biet, Masson, H., Lacroix, C., Gasnault, J., Hildebrandt-Müller, B., Oschmann, P., Krack, P., Willems, W. R., Dorndorf, W., Freitas, V., Bittencourt, A., Fernandes, D., Nascimento, M. H., Severo, M., Moraes, D., Muller, M., Hasert, K., Merkelbach, S., Schimrigk, K., van Oosten, B. W., Lai, M., Polman, C. H., Bertelsmann, F. W., Hodgkinson, S., Cabre, P. H., Volpe, L., Smadja, D., Vernant, J. P., Villaroya, H., Violleau, K., Younes-Chennoufi, A. Ben, Baumann, N., Villanueva-Hemandez, P., Ballabriga, J., Basart, E., Arbizu, T. X., Perez-Serra, J., Vinuels, F., Giron, J. M., Castilla, J. M., Redondo, L., Izquierdo, G., Lauer, K., Henneberg, A., Bittmann, N., Link, D., Wollinsky, K. H., Mobner, R., Fassbender, K., Kuhnen, J., Schwartz, A., Hennerici, M., Miller, A., Lider, O., Abramsky, O., Weiner, H. L., Offner, H., Vanderbark, A. A., Paoino, E., Fainardi, E., Addonizio, M. C., Ruppi, P., Tola, M. R., Granieri, E., Carreras, M., Sazdovitch, V., Joutel, A., Verdier-taillefer, M. H., Heinzlef, O., Radder, C., Tournier-Lasserve, E., Brenner, R. E., Munro, P. M. G., Williams, S. C. R., Bell, J. D., Hawkins, C. P., Filippi, M., Campi, A., Dousset, V., Canal, N., Comi, G., Zhu, J., Weber, F., Retska, R., List, J., Zhang, L., Brock, M., Taphoorn, M. J. B., Heimans, J. J., van der Veen, E. A., Karim, A. B. M. F., Sarazin, M., Argentino, N., Delattre, J. Y., Derkinderen, P., Buchwald, B., Schroter, G., Serve, G., Franke, C. H., Conrad, B., Kitchen, N. D., Thomas, D. G. T., Forman, A. D., Ang, Kie- Kian, Price, R., Stephens, C., Salmaggi, A., Nermni, R., Silvani, A., Forno, M. G., Luksch, R., Boiardi, A., Grzelec, H., Fryze, C., Nowacki, P., Zdziarska, B., Sanson, M., Merel, P., Richard, S., Rouleau, G., Thomas, G., Olsen, N. K., Pfeiffer, P., Egund, N., Bentzen, S. M., Johannesen, L., Mondrup, K., Rose, C., Zyluk, B., Wondrusch, E., Berger, O., Fast, N., Jellinger, K., Lindner, K., Urman, A., Thibault, J. L., Duyckaerts, Ch., Strik, H., Muller, B., Richter, E., Krauseneck, P., Steinbrecher, A., Schabet, M., Hess, C., Bamberg, M., Dichgans, J., Counsell, C. E., McLeod, M., Grant, R., Creel, G. B., Claus, D., Sieber, E., Engelhardt, A., Rechlin, T., Thierauf, P., Neubauer, U., Peresson, M., Di Giovacchino, G., Romani, G. L., Di Silverio, F., Danek, A., Kuffner, M., Hoermann, R., Schopohl, J., Laska, M., Heye, B., Zangaladze, A. T., Valls-SoIè, J., Cammarota, A., Alvarez, R., Tolosa, E., Hallett, M., Ulbricht, D., Ganslandt, O., Kober, H., Vieth, J., Grummich, P., Pongratz, H., Brigel, C., Fahlbusch, R., Serra, F. P., Palma, V., Nolfe, G., Buscaino, G. A., Rothstein, T. L., Gibson, J. M., Morrison, P. M., Collins, A. D., Eiselt, M., Wagnur, H., Zwiener, U., Schindler, T., Efendi, H., Ertekin, C., Erfas, M., Larsson, L. E., Sirin, H., AraÇ, N., Toygar, A., Demir, Y., Seddigh, S., Vogt, T. H., Hundemer, H., Visbeck, A., Pastena, L., Faralli, F., Mainardi, G., Gagliardi, R., Linden, D., Berlit, P., Lopez, O. L., Becker, J. T., Jungreis, C., Brenner, R., Rezek, D., Dekesky, S. T., Estol, C., Boller, F., Fernandez, J. M., Mederer, S., Batlle, J., Turon, A., Codina, A., Hitzenberger, P., Vila, N., Valls-SolÇ, J., Chamorro, A., Pouget, J., Schmied, A., Morin, D., Azulay, J. Ph., Vedel, J. P., Montalt, J., Escudero, J., Barona, R., Campos, A., Varli, K., Ertem, E., Uludag, B., Yagiz, A., Privorkin, Z., Steinvil, Y., Kott, E., Combarros, O., Sanchez-Pernaute, R., Orizaola, P., Mokrusch, Th., Kutluaye, E., Selcuki, D., Ertikin, C., Zettl, U., Gold, R., Harvey, G. K., Hartung, H. P., Toyka, K. V., Wokke, J. H. J., Oey, P. L., Ippel, P. F., Jansen, G. H., Franssen, H., Toyooka, K., Fujimura, H., Ueno, S., Yoshikawa, H., Yorifuji, S., Yanagihara, T., Talamon, C., Tzourio, C., Kiefer, R., Jung, S., Toyka, K., Ruolt, I., Tranchant, C., Mohr, M., Warter, J. M., Younger, D. S., Rosoklija, G., Hays, A. P., Kurita, R., Hasegawa, O., Matsumto, M., Komiyama, A., Nara, Y., Oueslati, S., Belal, S., Turki, I., Ben Hamida, C., Hentati, F., Ben Hamida, M., Kwiecinski, H., Krolicki, L., Domzal-Stryga, A., Dellemijn, P. L. I., van Deventer, P., van Moll, B., Drogendijk, T., Vecht, Ch. J., Nemni, S., Amadio, Fazio, R., Galardin, G., Delodovici, M. L., Peghi, E., Monticelli, M. L., Sessa, A., Viguera, M. L., Palomar, M., Gamez, J., Cervera, C., Navarro, C., Serena, J., Duran, I., Fernandez, A. L., Comabella, M., Nos, C., Rio, J., Montalban, J., Navarro, X., Verdu, E., Darbra, S., Buti, M., Mrabet, A., Fredj, M., Gouider, R., Tounsi, H., Khalfallah, N., Haddad, A., Dbaiss, T., Ghnassia, R., Rouillet, E., Chedru, F., Porsche, H., Strenge, H., Li, S. W., Young, Y. P., Garcia, A. A., Baron, P., Scarpini, E., Bianchi, R., Conti, A., Livraghi, S., Rees, J. H., Gregson, N. A., Hughes, R. A. C., Sedano, M. J., Calleja, J., Canga, E., Bahou, Y., Biary, N., Al Deeb, S. M., Guern, E. L. E., Gugenheim, M., Tardieu, S., Aisonobe, T. M., Agid, Y., Bouche, P., Brice, A., Rautenstrauss, B., Nelis, E., Grehl, H., Van Broeckhoven, C., Pfeiffer, R. A., Liehr, T., Ganzmann, E., Gehring, C., Neundörfer, B., Geremia, L., Doronzo, R., Sacilotto, G., Sergi, P., Pastorino, G. C., Scarlato, G., Planté-Bordeneuve, V., Mantel, A., Baas, F., Moser, H., Antonini, A., Psylla, M., Günther, I., Vontobell, P., Beer, H. F., Leenders, K. L., Chaudhuri, K. Ray, Parker, J., Pye, I. F., Millac, P. A. H., Abbott, R. J., Sutter, M., Albani, C., de Rijk, M. C., Breteler, M. M. B., Graveland, G. A., van der Mechè, F. G. A., Hofman, A., Keipes, M., Hilger, Ch., Diederich, N., Metz, H., Hentges, F., Pollak, P., Benabid, A. L., Limousin, P., Hoffmann, D., Benazzouz, A., Perret, J., Laihinen, A., Rinne, J. O., Ruottinen, H., Nagren, K., Lehikoinen, P., Oikonen, V., Ruotsalainen, U., Rinne, U. K., Cocozza, S., Pizzuti, A., Cavalcanti, F., Monticelli, A., Pianese, L., Redolfi, E., Paiau, F., Di Donato, S., Pandolfo, M., Palau, F., Monros, E., De Michele, G., Smeyers, P., Lopez-ArLandis, J., Uilchez, J., Filla, A., Genis, D., Matilla, T., Volpini, V., Blanchs, M. I., Davalos, A., Molins, A., Rosell, J., Estivill, X., De Jonghe, P., Smeyers, G., Krols, L., Mercelis, R., Hazan, J., Weissenbach, J., Martin, J. J., Warner, T. A. T., Williams, L., Orb, A. S., Harding, A. E., Giunti, P., Sweeney, M. G., Spadaro, M., Jodice, C., Novelletto, A., Malaspina, P., Frontali, M., Salmon, E., Gregoire, Fiore, Del, Comar, Franck, G., Scheltens, P. H., Siegfried, K., Dartigues, E., De Deyn, P., Horn, R., Nelson, I., Hanna, M. G., Morgan-Hughes, J. A., Collinge, J., Palmer, M. S., Campbell, T., Mahal, S., Sidle, K., Humphreys, C., Tavitian, B., Pappata, S., Jobert, A., Crouzel, A. M., DiGiamberardino, L., Steimetz, G., Barbanti, P., Fabbrini, G., Salvatore, M., Buzzi, M. G., Di Piero, V., Petraroli, R., Sbriccoli, A., Pocchiari, M., Macchi, G., Lenzi, G. L., Spiegel, R., Maguire, P., Schmid, W., Ott, A., Bots, M. L., Grobbe, D. E., Hofman, A., Howard, R. S., Russell, S., Losseff, N., Hirsch, N. P., Couderc, R., Bailleul, S., Nargeot, M. C., Touchon, J., Picot, M. C., Rizzo, M., Watson, G., McGehee, D., Dingus, T., Kappos, L., Radü, E. W., Haas, J., Hartard, C. H., Spuler, S., Yousry, T., Voltz, R., Scheller, A., Holler, E., Hohlfeld, R., Scolding, N. J., Sussman, J., Kolar, O. J., Farlow, M. R., Rice, P. H., Zipp, F., Sotgiu, S., Weiss, E. H., Wekerle, H., Chalmers, R., Robertson, N., Compston, D. A. S., Martino, G., Clementi, E., Brambilla, E., Moiola, L., Martinelli, V., Colombo, B., Poggi, A., Rovaris, M., Grimaldi, L. M. E., Roth, M. P., Descoins, P., Ballivet, S., Ruidavets, J. B., Waubant, E., Nogueira, L., Cambon-Thomsen, A., Clanet, M., Leppert, D., Hauser, S., Lugaresi, A., Tartaro, A., D'aurelio, P., Befalo, L. L. O., Thomas, A., Malatesta, G., Gambi, D., Benedikz, J. E. G., Magnusson, H., Poser, C. M., Guomundsson, G., Bates, T. E., Davies, S. E. C., Clark, J. B., Landon, D. N., ùther, J. R., Rautenberg, W., Overgaard, K., Sereghy, T., Pedersen, H., Boysen, G., Diez-Tejedor, E., Carceller, F., Gutierrez, M., Lopez-Pajares, R., Roda, J. M., Chandra, B., Ricart, W., Gonzalez-Huix, F., Molina, A., Rundek, T., Demarin, V., De Reuck, J., Boon, P., Decoq, D., Strijckmans, K., Goethals, P., Lemahieu, I., Nibbio, A., Chabriat, H., Vahedi, K., Nagy, T., Verin, M., Mas, J. L., Julien, J., Ducrocq, X., Iba-Zizen, M. T., Cabanis, E. A., Bousser, M. G., Rolland, Y., Landgraf, F., Bompais, B., Lemaitre, M. H., Edan, G., Vorstrup, S., Knudsen, L., Olsen, K. Skovgaard, Videbaek, C., Schroeder, T., van Gijn, J., Jansen, H. M. L., Pruim, J., Paans, A. M. J., Willemsen, A. T. M., Hew, J. M., vd Vliet, A. M., Haaxma, R., Vaalburg, W., Minderhoud, J. M., Korf, J., Soudain, S. E., Ho, T. W., Mishu, B., Li, C. Y., Nachainkin, I., Gao, C. Y., Cornblath, D. R., Griffin, J. W., Asbury, A. K., Blaser, M. J., McKhann, G. M., Ho, T., Macko, C., Xue, P., Stadlan, E. M., Ramos-Alvarez, M., Valenciano, L., Visser, L. H., van der Meché, F. G. A., van Darn, P. A., Meulstee, J., Schmitz, P. I. M., Jacobs, B., Oomes, P. G., Kleyweg, R. P., Jacobs, B. C., Endtz, H. P., van Doorn, P. A., van der Mech, F. G. A., Van den Berg, L. H., Mollee, I., Logtenberg, T., Thomas, P. K., Plant, G., Baxter, P. J., Luis, R. Santiago, Matsumoto, M., Notermans, N. C., Wokke, J. H. J., Lokhorst, H. M., van der Graaf, Y., Jennekens, F. G. I., Azulay, J. P., Bille-Turg, F., Valentin, P., Farnarier, G. G., Pellissier, J. F., Serratrice, G., Quasthoff, S., Schneider, U., Grafe, P., Hilkens, P. H. E., Moll, J. W. B., van der Burg, M. E. L., Planting, A. S. T., van Putten, W. L. J., van den Bent, M. J., Birklein, F., Spitzer, A., Lang, E., Neundorfer, B., Diehl, R. R., Lücke, D., Smith, G. D. P., Mathias, C. J., Serra, J., Campera, M., Ochoa, J. L., Ray Chaudhuri, K., Pavitt, D., Alam, M., Handwerker, H. O., Bleasdale-Barr, K., Smith, G., Murray, N. M. F., Hawkins, P., Pepys, M., Gellera, C., DiDonato, S., Taroni, F., Uncini, A., Di Muzio, A., Servidei, S., Silvestri, G., Lodi, R., Iotti, S., Barbiroli, B., Morrissey, S. P., Borruat, F. X., Francis, D., Mosely, I., Hansen, H. C., Helmke, K., Kunze, K., Sadzot, B., Maquet, P., Lemaire, Plenevaux, Damhaut, Sommer, C., Myers, R. R., Berta, E., Mantegazza, R., Argov, Z., Shapira, Y., Wirguin, I., Beuuer, J., Franke, C., Roberts, M., Willison, H., Vincent, A., Newsom-Davis, J., Morrison, K. E., Damels, R., Francis, M., Campbell, L., Davies, K. E., Kohler, W., Bucka, C., Hertel, G., Kanovsky, P., Auer, D., Ackermann, H., Klose, U., Naegele, Th., Bien, S., Voigt, K., Fink, G. R., Stephan, K. M., Wise, R. J. S., Mullatti, N., Hewer, L., Frackowiak, R. S. J., Weiller, C. S., Rijnites, M., Jueptner, M., Bauermann, T., Krams, M., Diener, H. C., van Walderveen, M. A. A., Barkhof, F., Hommes, O. R., Valk, J., Willmer, J. P., Guzman, D. A., Passingham, R. E., Silbersweig, D., Ceballos-Baumann, A., Frith, C. D., Frackowiak, R., Lucas, C. H., Goullard, L., Marchau, M. J., Godefroy, O., Rondepierre, P. H., Chamas, E., Mounier-Vehier, F., Leys, D., Renato, J., Verdugo, M. S. C., Campero, M., Jose, L., Ochoa, D. S. C., Vivancos, F., Tejedor, E. Diez, Martinez, N., Roda, J., Frank, A., Barreiro, P., Satoh, Y., Nagata, K., Maeda, T., Hirata, Y., YalÇinerner, B., Ozkara, C., Ozer, F., Ozer, S., Hanoglu, L., Zunker, P., Pozo, J. L., Oberwittler, C., Schick, A., Buschmann, H. -Ch., Ringelstein, E. Bernd, Lara, M., Anzola, G. P., Magoni, M., Volta, G. Dalla, Tarasov, A., Feigin, V., Beaudry, M. G., Carrier, S., Chicoutimi, Henriques, I. L., Bogoussslavsky, J., van Melle, G., Mathieu, J., Perusse, L., Allard, P., Prevost, C., Cantin, L., Bouchard, J. M., De Braekeleer, M., Agbo, C., Neau, J. P., Tantot, A. M., Dary-Auriol, M., Ingrand, P., Gil, R., Baltadjiev, D., Zekin, D., Sabey, K., Gennaula, C. P., Pope, B. A., Caparros-Lefebvre, D., Girard-Buttaz, I., Pruvo, J. P., Petit, H., Hipola, D., Martin, M., Giménez-Roldan, S., Ivanez, V., Japaridze, G., Carrasco, J. L., Picomell, I., Herranz, J. L., Macias, J. A., Nieto, M., Noya, M., Oller, L., Kiteva-Trencevska, G., Delgado, M. R., Liu, H., Luengo, A., Parra, J., Colas, J., Fernandez, M. J., Manzanares, R., Kornhuber, M. E., Malashkhia, V., Orkodashili, G., Martinez, M., Bonaventura, I., Porta, G., Martinez, I., Fernandez, A., Aguilar, M., Masnou, P., Drouet, A., Dreyfus, M., Cartron, J., Morel-Kopp, M. C., Tchernia, G., Kaplan, C., Lammers, M. W., Hekster, Y. A., Keyser, A., Meinardi, H., Renier, W. O., Boon, P. A. J. M., Have, M. D., Kint, B., Cruz, P., Cadilha, A., Almeida, R., Goncalves, M., Pimenta, M., Ramos, L. M. P., Polder, T. W., Broere, C. A., Polman, L., Rother, I., Rother, M., Schlaug, G., Arnold, S., Holthausen, H., Wunderlich, G., Ebner, A., Luders, H., Witte, O. W., Seitz, R. J., Serra, L. L., Gallicchio, B., Rotondi, F., Wieshmann, U., Meierkord, H., Sabev, K., Di Carlo, V., Gueguen, B., Derouesné, Ch., Ancri, D., Bourdel, M. C., Guillou, S., Aliaga, R., Chornet, M. A., Rodrigo, A., Pascual, A. Pascual -Leone, Catala, M. D., Pascual-Leone, A., Benbadis, S. R., Dinner, D. S., Chelune, G. J., Lüders, H. O., Piedmonte, M. R., Blanco, T., Lopez, M. P., Romero, B., Deltoro, A., Pascual, A., Pascual, Leone, Bolgert, F., Josse, M. O., Tassan, P., Touze, E., Laplane, D., Godenberg, F., Brizioli, E., Del Gobbo, M., Pelliccioni, G., Scarpino, O., Durak, H., Damlacik, G., Tunca, Z., Fidaner, H., Yurekli, Y., Yemez, B., Kaygisiz, A., Anllo, E. A., Esperet, E., Giovagnoli, A. R., Casazza, M., Spreafico, R., Avanzini, G., Mascheroni, S., Vecchio, I., Tornali, C., Antonuzzo, A., Grasso, A. A., Bella, R., Pennisi, G., Raffaele, R., Broeckx, J., Schildermans, F., Hospers, W., Deberdt, W., Carney, J. M., Aksenova, M., Chen, M. S., Juncadella, M., Busquets, N., De la Fuente, I., Rodriguez, A., Rubio, F., Soler, R., Khati, C., Pillon, B., Deweer, B., Malapani, C., Malichard, N., Dubois, B., Rancurel, G., Lopez, D. L., Jungreia, G., DeKosky, S. T., Boiler, F., Weiller, C., Rijntjes, M., Mueller, S. P., Maguire, E. A., Burke, E. T., Staunton, H., Phillips, J., Rousseaux, M., Pena, J., Bertran, I., Santacruz, P., Lopez, R., Catafau, A., Lomena, F., Blesa, R., Rampello, L., Nicoletti, A., Cabaret, M., Lesoin, F., Steinling, M., Tournev, I., Maier-Hauff, K., Schroeder, M., Wolf, A., Cochin, J. P., Noel, I., Augustin, P., Auzou, P., Hannequin, D., Maria, V., Lopez-Bresnahan, Danielle, D. M., Antin-Ozerkis, B. A., Bartels, E., Rodiek, S. O., Flugel, K. A., Campos, D. M., Salas-Puig, J., Del Rio, J. Sanhez, Vidal, J. A., Lahoz, C. H., Eraksoy, M., Barlas, O., Barlas, M., Bayindir, C., Ozcan, H., Birbamer, G., Gerstenbrand, F., Felber, S., Luz, G., Aichner, F., Seidel, G., Kaps, M., Hutzelmann, A., Gerriets, T., Kruggel, F., Martin, P. J., Gaunt, M. E., Abbot, R. J., Naylor, A. R., Meary, E., Dilouya, A., Meder, J. F., De Recondo, J., Lebtahi, R., Neff, K. W., Meairs, S., Viola, S., Matta, E., Aquilone, L., Rise, I. R., Authier, F. J., Kondo, H., Ghnassia, R. T., Degos, J. D., Gherardi, R. K., Bardoni, A., Ciafaloni, E., Comi, G. P., Bresolin, N., Robotti, M., Moggio, M., Rigoletto, C., Roses, A., Scarlato, G., Castelli, E., Turconi, A., Bresolin, N., Perani, D., Felisari, G., Chariot, P., de Pinieux, G., Astier, A., Jacotot, B., Gherardi, R., Fischer-Gagnepain, V., Louboutin, J. P., Crespo, F., Florea-Strat, A., Fromont, G., Sabourin, J. -C., Gonano, E. -F., Moroni, I., Prelle, A., Iannaccone, S., Quattrini, A., deRino, F., Sessa, M., Golzi, V., Smirne, S., Nemni, R., Turpin, J. C., Lucotte, G., Jacobs, S. C. J. M., Willems, P. W. A., Bootsma, A. L., Lasa, A., Calaf, M., Baiget, M., Gallano, B., Fichter-Gagnepain, V., Mazzucchelli, F., D'Angelo, M. G., Velicogna, M., Bet, L., Comi, G. P., Bordoni, A., Gonano, E. F., Bazzi, P., Rapuzzi, S., Moggio, M., Fagiolari, G., Ciscato, P., Messina, A., Battistel, A., Ryniewicz, B., Sangla, I., Desnuelle, C., Paquis, V., Cozzone, P. J., Bendahan, D., Sturenburg, H. J., Kohncke, G., Castellli, E., Linssen, W., Stegeman, D., Binkhorst, R., Notermans, S., Jaspert, A., Fahsold, R., de Munain, A. Lopez, Cobo, A., Martorell, L., Poza, J. J., Navarrete Palau, D., Emparanza, J. I., Sanchez-Roy, R., Vilchez, J. J., Hernandez, M., Tena, J. Garcia, Perla, C., Koutroumanidis, M., Papathanasopoulos, P., Papadimitriou, A., Papapetropoulos, T. H., Divari, R., Hadjigeorgiou, G. M., Anastasopoulos, I., Sansone, V., Rotondo, G., Meola, G., Rigoletto, C., Messina, S., Szwabowska-Orzeszko, E., Jozwiak, S., Michalowicz, R., Szaplyko, W., Petrella, M. A., Della Marca, G., Masullo, G., Mennuni, G. F., Kompf, D., Wascher, E., Verleger, R., Kaido, M., Soga, F., Toyooka, H., Bayon, C., Rubio, J., Carlomagno, S., Parlato, V., Santoro, A., Lavarone, A., Bonavita, V., Pentore, R., Venneri, A., Pasquier, F., Lebert, F., Grymonprez, L., Lefebvre, C., Van der Linden, M., Derouesné, C., Renault, B., Lacomblez, L., Homeyer, P., Ouss, L., Neuman, E., Malbezin, M., Barrandon, S., Guez, D., Stevens, M., van Swieten, J. C., Franke, C. L., Sanchez, A., Castellvirel, S., Mila, M., Jimenez, D., Pallesta, F., Ruiz, P. J. Garcia, Barrio, A., Barroso, T., Benitez, J., de Yebenes, J. Garcia, Manubens, J. M., Martinez-Lage, J. M., Larumbe, R., Muruzabal, J., Lacruz, F., Quesada, Pedro, Gallego, J., Ferini-Strambi, L., Marcone, A., Garancini, P., Tedesi, B., Jacob, B., Rozewicz, L., Langdon, D., Davie, C., Ron, M., Thompson, A., Koepp, M. J., Hansen, M. L., Guldin, B., Pressler, R. M., Ried, S., Scholz, C., Monaco, F., Gianelli, M., Schiavalla, M. P., Naldi, P., Cantello, R., Torta, R., Verze, L., Mutani, R., Knott, H., Ferbert, A., Schulze-Bonhage, A., Aust, W., Di Mascio, R., Marchioli, R., Vitullo, F., Di Pasquale, A., Sciulli, L., Kramer, V., Tognoni, G., Santacruz, P., Lopez, R., Marti, M. J., Charques, I., Catafau, A., Lomeila, F., Peila, J., Bertran, I., Blesa, R., Krendel, D. A., Costiga, D. A., Koeppen, S., Korn, W. M., Brugge, S., Schmitz, D., Scheulen, M. E., King, R. H. M., Robertson, A. M., Thomas, P. K., Kerkhofs, A., Vermersch, P., Dereeper, O., Daems Monpeun, C., Parent, M., Deplanque, D., Petit, H., Campero, M., Serra, J., Ochoa, J. L., Martinez-Matos, J. A., Montero, J., Olivé, M., Rene, R., Vidaller, A., Gugenheim, M., Gouider, R., Le Guern, E., Brice, A., Agid, Y., Bouche, P., Grisold, W., Ziflo, U., Drlicek, M., Budka, H., Jellinger, K., Zielinski, C. H., Ginsberg, L., King, R. H. M., Workman, J., Platts, A. D., Thomas, P. K., Gherardi, R. K., Florea-Strat, A., Poron, F., Sabourin, J. -C., Fazio, R., Nemni, R., Franceschi, M., Lorenzetti, I., Rinaldi, L., Canal, N., Weilbach, F. X., Sennlaub, A., Jung, S., Gold, R., Toyka, K. V., Hartung, H. P., Giegerich, G., Ellie, E., Vital, A., Steck, A. J., Vital, C., Julien, J., Doneda, P., Pizzul, S., Scarpini, E., Chiodi, P., Ramacci, M. T., Livraghi, S., Maimone, D., Annunziata, P., Salvadori, C., Guazzi, G. C., Arne-Bes, M. C., Delisle, M. B., Fabre, N., Hurtevent, J. F., Bes, A., Baudoin-Martin, D., Laborde, E., Viallet, F., Creisson, C., Crespi, V., Bogliun, G., Marzorati, L., Zincone, A., D'Angelo, L., Liberani, A., Merlini, M., Rivolta, R., Creange, A., Sabourin, J. -C., Theodorou, I., Gherardi, R. K., Conti, A. M., Malosio, M. L., Baron, P. L., Scarlato, G., Chorao, R., Rosas, M. J., Leite, I., Callea, L., Donati, E., Bargnani, C., Bud, M., Verdu, E., Navarro, X., Braun, S., Einius, S., Poindron, P., Warier, J. M., Bradley, J., Bekkelund, S. I., Torbergsen, T., Mellgren, S. I., Carlomagno, S., Parlato, V., Santoro, A., Lavarone, A., Boller, F., Bonavita, V., Engelhardt, A., Lörler, H., Robeck, S., Kluglein, C., Comi, G., Avoledo, V., Locatelli, T., Leocani, L., Galardi, G., Magnani, G., Medaglini, S., Chkhikvishvili, T. S., Zangaladze, A., Bratoeva, M., Kovachev, P., Chavdarov, D., Artemis, N., Karacostas, D., Milonas, I., Arpa, J., Lopez-Pajares, R., Cruz-Matinez, A., Sarria, J., Palomo, F., Alonso, M., Rodriguez-Al-barino, A., Lacasa, T., Nos, J., Barreiro, P., Martinez, A. Cruz, Villoslada, C., Alons, M., Taghavy, A., Hamer, H., Kratzer, A., Dethy, S., Pauwels, T., Monclus, M., Luxen, A., Goldman, S., Ziegler, M., Crambes, O., Ragueneau, I., Arnaud, F., Zappia, M., Montesanti, R., Colao, R., Palmieri, A., Branca, D., Nicoletti, G., Rizzo, M., Parlato, G., Quattrone, A., Vanacore, N., Zuchegna, P., Bonifati, V., Meco, G., Scholz, J., Friedrich, H. -J., Rohl, A., Ulm, G., Vieregge, P., Savettieri, G., Rocca, W. 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Martin, Fernandez, J., Mares, R., Torre, L., Mayayo, E., Lossos, A., Gomori, M., Libson, E., Goldfarb, A., Seigal, T., de Louw, A., Praamstra, P., Horstink, M., Cools, A., Tarrats, E. Basart, Calopa, M., Martinez, S., Ballabrina, J., Taussig, D., Marion, M. -H., Mallecourt, J., Ranoux, D., Gasser, T., Kabus, C., Ozelius, L., Wenzel, R., Breakefield, X. O., Boot, H., Poublon, R. M. L., Bogaard, J. M., GinaÏ, A. Z., Cabezas, C., Scholz, J., Nitschke, N., Vieregge, P., Wirk, B., Hochberg, F. H., Hefter, H., Kessler, K., Wirrwar, A., Stocklin, G., Tournier-Lasserves, E., Agundez, J. Garcia, Ruiz, E., Li, X. P., Hedlund, P. B., Fuxe, K., Kulisevsky, J., Avila, A., Berthier, M. L., Gerard, J. -M., Cambier, J., Caucheteur, C., Deuschl, G., Köster, B., Scheidt, C., Lücking, C. H., Mena, M. A., Chedru, F., Oubary, P., Rondot, P., Anagnostou, C. N., Panagopoulos, C. P., Ziogas, D. E., Vermersch, P., Robitaille, Y., Gauvreau, D., Destée, A., Delacourte, A., Ficola, U., Marozzi, P., Piccoli, F., Janelidze, M., Shakarishvili, R., Gagoshidze, T., Vashadze, T., Tsiskaridze, A., Djannelidze, M., Trullen, J. M. Perez, Pardo, P. J. Modrego, Vazquez-Andre, M. L., Bail, L., Naccache, L., Gauvrit, J. L., Panisset, M., Boller, A. F., Giannini, M., Zanette, E., Di Cesare, S., Altieri, M., Maloteaux, J. M., Delwaide, C., Sciaky, M., Newman, S. K., Kennedy, A. M., Frackowiack, R. S. J., Warrington, E. K., Rossor, M. N., Martinez-Lage, Pablo, Martinez Lage, J. Manuel, Manubens, JosÇ M., Lacruz, Francisco, Larumbe, Rosa, Muruzabal, Javier, Locatelli, T., Cursi, M., Mauri, M., Liberati, D., Fornada, C., Iriarte, L. M., Lopez, M., Grilo, A., Repeto, M., Brasic, J. R., Barnett, J. Y., Sheitman, B. B., Young, J. G., Shalit, F., Brodie, C., Sredni, B., Engelien, A., Stern, E., Huber, W., Frith, C., Miralles, F., Albadalejo, M. D., Antem, M., Pastor, I., Estelies, M. A., Del Ser, T., Ochoa, H. Severo, Munoz, D., Hachinski, V., Cucinotta, D., Senin, U., Girardello, R., Crepaldi, G., Croria, F., Schens, D. B., Vigo-Pelfrey, C., SempereE, A. P., Ortega, M. P., Bava, L., Magni, E., Aronovich, B. D., Treves, T. A., Bornstein, N. M., Van Blercom, N., Blecic, S., Violon, Ph., Hildebrand, J., Zamboni, M., Ambrosoli, L., Poli, A., Kuehnen, J., Tilgner, C., Raltzig, M., Moering, B., Faiss, J., Deeb, S. M. Al, Daif, A., Sharif, H., Tatay, J., Caroeller, F., Avendano, C., Vinogradova, T., Pinto, A. N., Canhao, P., Neau, J. -Ph., Pacquereau, J., Meurice, J. -C., Schwab, M., Bauer, R., Deeb, M. AL, Tjan, T. J., Aabed, M., Berges, S., Crepin-Leblond, T., Chavot, D., Cattin, F., Snidaro, M. H., Chopard, J. L., Ley, C. Oliveras, Alameda, F., Alfonso, S., Podobnik-Sarkanji, S., Pniewski, J., Torbicki, A., Mieszkowski, J., Plaza, I., Petrunjashev, V., Velcheva, I., Hadjiev, D., Yancheva, S., Petrov, L., Karakaneva, S., Petkov, A., Nikolov, E., Niehaus, L., Sacchetti, M. L., Toni, D., Fiorelli, M., Gori, C., Argentino, C., Lyrer, Ph., Radu, E. W., Gratzl, O., Rondepierre, Ph., Leclerc, X., Marchau, M., Scheltens, Ph., Hamon, M., Janssens, E., Henon, H., Lucas, C., KuÇukoglu, H., Baybas, S., Dervis, A., YalÇiner, B., Yilmaz, N., Ozturk, M., Arpaci, B., Navarro, J. A., Arenas, J., Perez-Sempere, A., Egido, J. A., Soriano-Soriano, C., Beau, P., Gergaud, J. -M., Coudero, C., Dierckx, R. A., Dobbeleir, A., Timmermans, E., Vandevivere, J., Lucas, C. H., Gomez, M., Aguirre, J., Berenguer, A., Duran, C., Parrilla, J., Gonzalez, F., Gironell, A., Rey, A., Marti-Vilalta, J. L., de Lecinana, M. Alonso, Federico, F., Conte, C., Simone, I. L., Giannini, P., Liguori, M., Lucivero, V., Picciola, E., Tortorella, C., Drislane, F., Wang, A. Ming, Di Mascio, R., Marchioli, R., Vitullo, F., Di Pasquale, A., Sciulli, L., Kramer, V., Tognoni, G., Levivier, M., del Olmo, A., Caballero, E., Degaey, I., de Bruijn, S. F. T. M., Tchaoussoglou, I., Bastianello, S., Pozzilli, C., Cervello, A., Catala, N., Koskas, F., Kieffer, E., Botia, E., Vivancos, J., Leon, T., Segura, T., Ramo, C., Lopez, F., Karepov, V. G., Gur, A. J., Berlanga, B., Gracia, V., Fiol, C., Kurtel, H., Ozkutlu, U., Yegen, B., Grau, A. J., Buggle, F., Heindle, S., Steichen-Wiehn, C., Banerjee, T., Maiwald, M., Becher, H., Villafana, W., Medina, F., Fernandez-Real, J. M., Soler, S., Planas, E., Iceman, E., Doganer, I., Badlan, G., Genc, B., Yulug, K., Ideman, E., Dural, H., Kutlul, K., Damalik, G., Baklan, Y., Metin, B., Tekinsoy, E., Iriarte, I., Subira, M. L., Crockar, A. D., Treacy, M., McNell, T. A., Grazzi, L., Ediboglu, N., Bilgin, H., Ertas, S., Goument, J. -P., Basset, C., Campos, Y., Garcia-Silva, T., Cabello, A., Bussaglia, E., Tizzano, E., Colomer, J., Gimbergues, P., Campagne, D., Bommelaer, C., Delaguillaume, B., Ramtami, H., Ait-Kaci-Ahmed, M., Pascual, L. F., Fernandez, T., Hortells, M., Sanz, C., Morales, F., Lauritzen, L., Picard, F., Sellal, F., Collard, M., Avramidis, T., Alexiou, E., Anastopoulos, T., Frongillo, D., Delfino, F. A., Cannata, M., Calo, L., Vichi, R., Antonini, G., Fragola, V., Cannata, D., Salas, M., Ruiz, C., Angelard, B., Lacau, J., Guily, St., Sendtner, M., Goadsby, Peter J., Quin, N. P., Gadian, D. G., Roland, P. E., Seitz, Rudiger J., Frackowiak, Richard S. J., Becker, G., Krone, A., Schmidt, K., Hofmann, E., Bogdahn, U., Rosenfeld, M. R., Meneses, P., Kaplitt, M. G., Dalmau, J., Posner, J., Cordon-Cardon, C., Hoang-Xuan, K., Vega, F., Nishisho, I., Moisan, J. P., Theillet, C., Delattre, O., Zhu, Jiahong, Walther, W., Posner, J. B., Roelcke, U., von Ammon, K., Pellikka, R., Lucking, C. H., Walon, C., Boucquey, D., -Van Rijckevorsel, K. Harmant, Lannoy, N., Verellen-Dunoulin, Ch., Liszka, U., Cavaletti, G., Casati, B., Kolig, C., Bogliun, G., Marzorati, L., Johannsen, L., Chio, A., Ruda, R., Vigliani, M. C., Sciolla, R., Seliak, D., Hoang-Xuang, K., Villanueva, J. A., Montalban, X., Arboix, A., Colosimo, C., Albanese, A., Hughes, A. J., de Bruin, V., Lees, A. J., Kowalski, J. W., Banfi, S., Santoro, L., Perretti, A., Castaldo, I., Barbieri, F., Campanella, G., Bhatia, K. P., Mardsen, C. D., de Bruin, V. S., Machedo, C., Ceballos-Baumann, D., Marsden, C. D., Brooks, D. B. J., Wennlng, G. K., Quinn, N., McDonald, W. l., Warner, T. T., Bain, P. C., Davis, M. B., Conway, D., Shaunak, S., O'Sullivan, E., Crawford, T., Lawden, M., Blunt, S., Rapoport, A., Sarova-Pinchas, I., de Beyl, D. Zegers, Mavroudakis, N., Blanc, S., Godinot, C., Lenoir, G., Barkhof, M. S. F., Tas, M. W., Baron, P. L., Constantin, C., Cassatella, M. A., Langdon, D. W., Webb, S., Gasparini, P., Zeviani, A., Kidd, D., Mammi, S., Cahalon, L., Hershkoviz, R., Lahat, N., Wallach, D., Annunziata, P., Martino, T., Maimone, D., Guazzi, G. C., Porrini, A. M., Dell'Arciprete, L., Rothwell, P. M., Stewart, R. R. C., Cull, R. E., Willmes, K., Poeck, K., Russell, D., Braekken, S. K., Brucher, R., Svennevig, J., Hermesl, M., Bruckmann, H., Biraben, A., Sliwka, U., Meyer, B., Schondube, F., Noth, J., Lavenu, I., Lammers, C., Waldecker, B., Haberbosch, W., Stam, J., Schneider, R., Gautier, J. C., Berlit, T. P., Fauser, B., Kuhne, D., Geraud, G., Danielli, A., Larrue, V., Bes, A., Timmerman, E., Bono, F., Bruni, A. C., Valalentino, P., Montesi, M. P., Talerico, G., Zappia, M., Sabatelli, M., Quattrone, A., Pareyson, D., Lorenzetti, D., Sghirlanzoni, A., Castellotti, B., Lupski, J. R., Archidiacono, N., Antonacci, R., Marzella, R., Rocchi, M., Samuel, D., Goulon-Goeau, C., Costa, P. P., Bismuth, H., Said, G., De Jongh, P., Lofgren, A., Timmerman, V., Vance, J. M., Van Broeckhoven, C., Martin, J. -J., Martinez, A. Cruz, Bort, S., Arpa, J., Misra, P., King, R. H. M., Badhia, K., Anderson, M., Caballo, A., Vichez, J., Gabriel, J. M., Erne, B., Miescher, G. C., Ulrich, J., Vital, A., Vital, C., Steck, A., Petry, K., Labatut, I., Hilmi, S., Ellie, E., Ferrini-Strambi, L., Zucconl, M., Marchettini, P., Palazzi, S., Oehlschlager, M., Pepinsky, R. B., Gemignani, F., Marbini, A., Pavesi, G., Di Vittorio, S., Manganelli, P., Mancia, D., Vermersh, P., Roche, J., Durocher, A. M., Dewailly, Ph., Dettmers, C., Fink, G., Lemon, R., Stephan, K., Passingham, D., Weder, B., Knorr, U., Huang, Y., Butterfield, D. A., Peris, M. L., Peiro, C., Pascual, A. Pascual-Leone, Bottini, G., Folnegovic-Smalc, V., Knezevic, S., Bokonjic, R., Ersmark, B., Torres, M. Gonzalez, Guiraud-Chaumeil, B., Haugaard, K., Jovicic, A., Chr, Lang, Levic, Z., Parra, C. Martinez, Ochoa, J. Patrignani, Titlbach, O., Wikkelso, C., Caparros-Lefevre, D., Debachy, B., Verier, A., Cantinho, G., Santos, A. I., Godinho, F., Bagunya, J., Roig, T., Ensenyat, A., Santiag, O., Trabucchi, H., De Leo, D., Koch, Ch., Zeumer, H., Matkovic, Z., Morris, P., Donaghy, M., Köhler, W., Kammer, T., Röther, J., Navon, R., Fontaine, B., Wu, Y., Capdevila, A., Guardiola, M. J., van Dijk, G. W., Notermans, N. C., Kruize, A. A., Kater, L., Bertelt, C., Hesse, S., Friedrich, H., Mauritz, K. -H., Giron, L. T., Watanabe, I. S., Ewing, D., Koepp, M., Lempert, T., Sander, B., Kauerz, U., Mehdorn, H. M., Hezel, J., Eickhoff, W., Kryst, T., Timsit, S., Gardeur, D., Reis, Mitermayer Galvao dos, Secor, E., Filho, A. Andrade, Silva, M. Cardoso, Santos, S. R. Silveira, Vasilaski, G., Reis, E. A. dos, Velupillai, P., Harn, D. A., Tigera, J. Garcia, Dreke, R. Martinez, Crespo, R. Piedra, Besses, C., Acin, P., Massons, J., Florensa, L., Oliveres, M., Sans-Sabrafen, J., Wicklein, E. M., Pleiffer, G., Kunre, K., Dieterich, M., Brandt, Th., Guarino, M., Stracciari, A., Pazzaglia, P., D'Alessandro, R., Santilli, I., and Donato, M.
- Published
- 1994
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278. Large granular lymphocytes from patients with expanded LGL populations acquire cytotoxic functions and release lymphokines upon in vitro activation
- Author
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Pistoia, V, Prasthofer, EF, Tilden, AB, Barton, JC, Ferrarini, M, Grossi, CE, and Zuckerman, K
- Abstract
The phenotypic and functional features of purified large granular lymphocytes (LGL) from ten patients with LGL population expansions and cytopenias are described. The predominant LGL phenotypes were T3+, T8+, Leu-11+/-; however, in two patients, LGL expressed a T3-, Leu-11+ phenotype. Variable combinations of other LGL markers (OKM1, Leu-7), and HLA-DR were detected in individual cases. In nine of ten cases, freshly isolated LGL did not exert cytolytic activity for K562 target cells, but purified LGL cultured in the presence of recombinant interleukin 2 (rIL2) acquired potent cytotoxic activity in all cases tested. LGL did not proliferate in response to phytohemagglutinin (PHA). However, LGL released variable amounts of IL2 and gamma- interferon (gamma-IFN) after PHA stimulation. In some cases, stimulation of fresh LGL with recombinant IL2 induced production of gamma-IFN. No correlation was found between the functional capabilities and the original phenotype of the expanded LGL populations.
- Published
- 1986
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279. Large granular lymphocytes in human peripheral blood: ultrastructural and cytochemical characterization of the granules
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Grossi, CE, Cadoni, A, Zicca, A, Leprini, A, and Ferrarini, M
- Abstract
Large granular lymphocytes (LGL) are defined as nonadherent mononuclear cells with cytoplasmic azurophilic granules, avid receptors for the Fc portion of IgG, and cytotoxic functions (NK or ADCC activities). In the present study, the granules of LGL isolated from human peripheral blood have been analyzed by enzyme cytochemistry and electron microscopy. It had been found that: (1) in the single cells, granules at different stages of maturation could be detected: in addition, packaging of the granules took place in the proximity of the Golgi apparatus, which is similar to that seen in secretory cell types. (2) Acid phosphatase (AP) was observed within the granules and the vesicles located in the Golgi area: the Golgi apparatus identified through its thiamine pyrophosphatase-positivity was consistently negative for AP. (3) Alpha naphthyl-acetate esterase (ANAE) activity was localized in the granules as well as on the membrane of LGL and monocytes. (4) The ANAE activity of LGL was of the monocytic and not of the lymphocytic type, as shown by NaF inhibition. (5) The LGL granules, although identifiable as primary lysosomes, were not involved in the process of phagocytosis, since LGL failed consistently to ingest latex particles or opsonized red cells.
- Published
- 1982
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280. Autocrine nitric oxide modulates CD95-induced apoptosis in gammadelta T lymphocytes.
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Sciorati, C, Rovere, P, Ferrarini, M, Heltai, S, Manfredi, A A, and Clementi, E
- Abstract
Gammadelta T lymphocytes play an important early role in the defense against pathogens. Their function is terminated by acquisition of susceptibility to CD95-triggered apoptosis. Here we show that the regulation of this process depends on the activity of the endothelial NO synthase expressed by gammadelta T lymphocytes, which is modulated in an activation-dependent way. The effects of nitric oxide thus generated, mediated via cGMP generation, are exerted at at least two sites along the CD95 signaling cascade: one at, or upstream, and the other downstream of ceramide generation. At either site, nitric oxide/cGMP action is sufficient for protection from apoptosis. The effect of NO is selective for apoptosis induced by CD95 cross-linking, since it does not affect apoptotic program triggered by other stimuli. The evidence here reported demonstrates a new physiological role for nitric oxide, acting as a survival factor for T lymphocytes.
- Published
- 1997
281. Anti-lymphocyte globulin stimulates normal human T cells to proliferate and to release lymphokines in vitro. A study at the clonal level
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Barbano, GC, Schenone, A, Roncella, S, Ghio, R, Corcione, A, Mori, PG, Ferrarini, M, and Pistoia, V
- Abstract
Human peripheral blood mononuclear cells (PBMC) were stimulated in vitro with anti-lymphocyte globulin (ALG), and the phenotypic and functional properties of the blasts obtained were investigated. When stained with monoclonal antibodies (MoAbs), all of the blasts were identified as T cells that expressed predominantly the CD4 phenotype (70% of the cells). The remaining blasts were CD8+. These findings demonstrate that ALG stimulates both helper-inducer and cytotoxic- suppressor cells at random since the CD4 to CD8 ratio in the stimulated blasts was the same as in resting PBMC. This ratio is different from that observed in short-term cultures of T cells stimulated with phytohemagglutinin (PHA) under the same conditions (CD4 to CD8 ratio less than 1). ALG-stimulated T cells were cloned by limiting dilution in the presence of recombinant Interleukin-2 (rIL-2). The clones obtained were expanded and maintained in long term cultures with rIL-2. Thirty-two clones were tested for their capacity of producing colony stimulating activity (CSA) or burst promoting activity (BPA). Twenty- eight of them produced CSA and 12 produced BPA. No correlation was found between the surface phenotype and the ability of the clones to produce CSA or BPA (ie, both the CD4+ and CD8+ clones released the cytokines). When 16 of the same clones were tested for II-2 and gamma interferon (gamma IFN) production, 12 were found to be gamma INF and IL- 2 producers. All of the gamma IFN producers also released IL-2, whereas in the single clones no correlation was found with the capacity of releasing BPA and CSA. Supernatants from selected T-cell clones were also tested for hematopoietic growth factor activities in the presence of neutralizing antisera to human granulocyte-macrophage colony stimulating factor (GM-CSF) or to Interleukin-3 (IL-3). It was found that most CSA was attributable to GM-CSF, whereas BPA was mainly related to the presence of IL-3.
- Published
- 1988
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282. Characterization of cells from invaded lymph nodes in patients with solid tumors. Lymphokine requirement for tumor-specific lymphoproliferative response.
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Cozzolino, F, Torcia, M, Carossino, A M, Giordani, R, Selli, C, Talini, G, Reali, E, Novelli, A, Pistoia, V, and Ferrarini, M
- Abstract
The specific immune response against the malignant cells was investigated in patients with urinary bladder or larynx cancer. Lymphocytes from lymph nodes that drain the tumor site were tested for their proliferative and cytotoxic capacities against autologous malignant cells isolated from the primary tumor. In no occasion was a proliferative or a cytotoxic response observed. However, when the lymph node cell suspensions were depleted of cells expressing both OKM1 and Leu-7 markers by rosetting with the appropriate mAbs, a proliferative response could be observed. The lymphocytes responded to autologous tumor cells only if IL-2 was added to the cultures. IL-2 alone induced some cell proliferation, which was not, however, comparable to that observed in response to both IL-2 and tumor cells. A panel of allogeneic tumor cells consistently failed to stimulate OKM1-, Leu-7- cells in vitro. Response to autologous tumor cells was not caused by HLA-encoded molecules, as occurs in the autologous mixed lymphocyte reaction, since OKM1-, Leu-7- cells failed to be stimulated by autologous non-T cells. A proliferative response was observed only with cells from lymph nodes that had been classified as invaded by malignant cells according to histopathologic criteria. Cells from noninvaded lymph nodes consistently failed to respond. Cells stimulated with autologous tumor cells could be expanded in short-term lines by continuous addition of IL-2 and malignant cells. One of these lines, which comprised mainly T8+ cells, was stimulated to proliferate only by autologous tumor cells, and its proliferative response was inhibitable by anti-class I and not by anti-class II mAbs. This line showed lytic capacities against autologous malignant targets, while it was inefficient against all of the other allogeneic cells tested. In another set of experiments, the mechanisms whereby exogenous IL-2 had to be added to the cultures to sustain a proliferative response against neoplastic cells were investigated. When cocultured with autologous malignant cells, OKM1-, Leu-7- lymphocytes expressed IL-2 receptors, as could be assessed by anti-Tac fluorescent staining. Under these culture conditions, these cells did not produce IL-2, and no proliferation was observed. Addition of purified IL-1 to the cultures induced IL-2 production and cell proliferation. It is concluded that metastatic lymph nodes contain a T cell population that can be detected in a proliferative assay when both suppressor cells are removed and the appropriate molecular signals are supplied.
- Published
- 1987
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283. Presence of T-cell subset abnormalities in newly diagnosed cases of multiple sclerosis and relationship with short-term clinical activity
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Eoli, M., Ferrarini, M., Dufour, A., Heltaj, S., Bevilacqua, L., Comi, G., Cosi, V., Filippini, G., Martinelli, V., Milanese, C., LaMantia, L., and Salmaggi, A.
- Abstract
Abnormalities of T-cell subsets in patients with multiple sclerosis are well known; in order to assess whether immunological abnormalities are relevant in the pathogenesis of the disease after its clinical onset, peripheral blood lymphocyte subsets (CD3
+ , CD4+ , CD4+ CD45RA+ , CD4+ CD45RA- , CD8+ , CD8+ CD57+ , CD57+ , CD25+ ) were analysed serially in 25 patients at the first clinical episode suggestive of inflammatory demyelinating disease and in an equal number of age- and sex-matched controls. During the follow-up period (12–18 months, mean 14) 6 of 25 patients presented new relapses: in this subgroup of patients, significant changes in CD4+ ratio (% CD4+ CD45RA- /%CD4+ CD45RA- ) were detected in comparison both with healthy controls and with clinically stable patients. Patients clinically stable at follow-up did not display immunological abnormalities, regardless of the presence or absence of cerebrospinal fluid and/or magnetic resonance imaging alterations consistent with multiple sclerosis. These findings suggest a possible prognostic role of early T-cell subset imbalance in multiple sclerosis.- Published
- 1993
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284. Lamproitic rocks from Cabezo Negro de Zeneta: Brown micas as a record of magma mixing
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Toscani, L., Contini, S., and Ferrarini, M.
- Abstract
Summary Phlogopite and biotite coexist in the ultrapotassic rocks from Cabezo Negro de Zeneta (SE Spain). The compositional range of the early crystallizing phlogopite is comparable to other Spanish lamproitic occurrences, except that it is higher in Al
2 O3 , probably reflecting the higher Al2 O3 and/or different oxygen fugacity of the Zeneta magma. Magmatic Al-rich and metamorphic Al-poor biotites also occur in these rocks. The magmatic biotite probably crystallised from intermediate to silicic peraluminous magma(s), whereas the metamorphic type comes from crustal relics of metapelitic rocks entrained and dismembered into the lamproitic melt. It is concluded that the melt of Zeneta was generated through the mixing of a Mg-rich lamproitic component, quantitatively dominant, with a crustal-derived anatectic component, both already partially crystallised before mixing. The “mixed” melt attained chemical homogenization as suggested by the development of late overgrowths of similar composition on the two micas.- Published
- 1995
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285. Establishment of Tac-negative, interleukin-2-dependent cytotoxic cell lines from large granular lymphocytes (LGL) of patients with expanded LGL populations
- Author
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Pistoia, V., Carroll, A. J., Prasthofer, E. F., Tilden, A. B., Zuckerman, K. S., Ferrarini, M., and Grossi, C. E.
- Abstract
Cell lines were established from purified large granular lymphocites (LGL) isolated from the peripheral blood of seven patients with phenotypically homogeneous LGL expansions. LGL were stimulated with phytohemagglutinin (PHA) or recombinant interleukin-2 (rIL-2) and further expandedin vitro in IL-2-containing media. The surface phenotype of LGL, as assessed by monoclonal antibody staining, was T3
+ T8+ in five patients, T3- T8- in one, and T3+ T8- in another patient. The cells also expressed Leu 7, Leu 11, and/or OKM 1 markers in various proportions and were identifiable as LGL by their morphological and cytochemical features. The original surface phenotype of the unstimulated LGL was retained in the IL-2-dependent cell lines from each individual patient, i.e., T3+ T8+ cells originated T3+ T8+ cell lines and T3- T8- cells originated T3- T8- cell lines. Other markers, such as Leu 11 and OKM 1, were generally lost in culture. LGL proliferated in response to rIL-2 but did not express detectable IL-2 receptors, even after prolonged periods of culture. All cell lines from each individual patient had the same surface phenotype, and within the single lines, all of the cells expressed the same markers. Cell lines from two patients consistently displayed chromosomal abnormalities. Although different in the two patients, the abnormalities were identical in all of the lines from the same patient and detectable in most of the cells examined, suggesting a clonal origin for the abnormally expanded LGL populations. Freshly isolated LGL did not exert NK activity. However, the IL-2-dependent LGL lines acquired the ability to kill K562 target cells and to produce gamma interferon (?-IFN). No direct correlation was observed between these two properties.- Published
- 1986
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286. Chromogranin A is preferentially cleaved into pro-angiogenic peptides in the bone marrow of multiple myeloma patients
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Bianco M, Am, Gasparri, BARBARA COLOMBO, Curnis F, Girlanda S, Ponzoni M, Mt, Bertilaccio, Calcinotto A, Sacchi A, Ferrero E, Ferrarini M, Chesi M, Pl, Bergsagel, Bellone M, Tonon G, Ciceri F, Marcatti M, Caligaris Cappio F, Corti A, Bianco, M, Gasparri, Am, Colombo, B, Curnis, F, Girlanda, S, Ponzoni, M, Bertilaccio, Mt, Calcinotto, A, Sacchi, A, Ferrero, E, Ferrarini, M, Chesi, M, Bergsagel, Pl, Bellone, Tonon M, G., Ciceri, Fabio, Marcatti, M, Caligaris Cappio, F, and Corti, Angelo
287. A GENOMIC APPROACH TO IDENTIFY NEW GENES RESPONSIBLE FOR INHERITED MOTOR AND CMT2 NEUROPATHIES: A COLLABORATIVE STUDY
- Author
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Previtali, S. C., Fabrizi, G. M., Manganelli, F., Mazzeo, A., Davide Pareyson, Schenone, A., Taroni, F., Vita, G., Bellone, E., Ferrarini, M., Magri, S., Scarlato, M., Riva, N., Lunetta, C., Carrera, P., Bucci, G., Mandich, P., Penco, S., Lazarevic, D., Cittaro, D., Jordanova, A., Reilly, M. M., Casari, G., Ferrari, M., Comi, G., Bolino, A., Previtali, Sc, Fabrizi, Gm, Manganelli, F, Mazzeo, A, Pareyson, D, Schenone, A, Taroni, F, Vita, G, Bellone, E, Ferrarini, M, Magri, S, Scarlato, M, Riva, N, Lunetta, C, Carrera, P, Bucci, G, Mandich, P, Penco, S, Lazarevic, D, Cittaro, D, Jordanova, A, Reilly, Mm, Casari, GIORGIO NEVIO, Ferrari, M, Comi, Giancarlo, and Bolino, A.
288. Serum-associated inhibition of neutrophil Fc receptors in cancer patients
- Author
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Patrone, F., FRANCO DALLEGRI, Gremmo, A., Bonvini, E., Migliorini, P., Cantarella, S., Ferrarini, M., and Sacchetti, C.
- Published
- 1981
289. A study of immunoglobulin classes present on the membrane and in the cytoplasm of human tonsil plasma cells
- Author
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Ferrarini, M, Viale, G, Risso, Angela, and Pernis, B.
- Subjects
immunoglobulin ,human tonsil - Published
- 1976
290. Receptors for IgG molecules on human lymphocytes forming spontaneous rosettes with sheep red cells.
- Author
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Ferrarini, M., Moretta, L., Abrile, Roberte, and Durnte, Maria Laura
- Published
- 1975
- Full Text
- View/download PDF
291. Adeno-associated virus-mediated transduction of VEGF165 markedly improves functional recovery of infarcted myocardium in chronically instrumented dogs
- Author
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Ferrarini, M., Arsic, N., Recchia, F.A., Zentilin, L., Zacchigna, S., Kinugawa, S., Glauber, M., Giacca, M., and Hintze, T.H.
- Published
- 2004
- Full Text
- View/download PDF
292. Chronic lymphocytic leukemia: a proliferation of B cells at two distinct stages of differentiation
- Author
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Rn, Damle, FRANCO FAIS, Ghiotto F, Valetto A, Albesiano E, Wasil T, Fm, Batliwalla, Sl, Allen, Schulman P, Vp, Vinciguerra, Kr, Rai, Pk, Gregersen, Ferrarini M, and Chiorazzi N
- Subjects
DNA Replication ,Embryonal Carcinoma Stem Cells ,B-Lymphocyte Subsets ,Gene Rearrangement, B-Lymphocyte, Heavy Chain ,Immunoglobulin Variable Region ,CD5 Antigens ,Lymphocyte Activation ,NAD+ Nucleosidase ,Antigens, CD ,Antigens, Neoplasm ,Humans ,ADP-ribosyl Cyclase ,Membrane Glycoproteins ,Genes, Immunoglobulin ,Cell Differentiation ,DNA, Neoplasm ,Telomere ,Germinal Center ,ADP-ribosyl Cyclase 1 ,Antigens, Differentiation ,Leukemia, Lymphocytic, Chronic, B-Cell ,Cell Transformation, Neoplastic ,Neoplastic Stem Cells ,Immunoglobulin Joining Region ,Immunoglobulin Heavy Chains ,Cell Division
293. Characterization of EBV-positive lymphoblastoid cell lines obtained from HIV seropositive patients with or without lymphomas
- Author
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Roncella, S., Francia Di Celle, P., Giovanna Cutrona, Carbone, A., Sessarego, M., Dodi, F., Foa, R., Rowe, M., and Ferrarini, M.
294. PRODUCTION OF GRANULOCYTE-COLONY STIMULATING FACTOR (G-CSF) BY NORMAL AND MALIGNANT HUMAN B-LYMPHOCYTES
- Author
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Corcione, A., Baldi, L., Dono, M., simona zupo, Dagostino, R., Ferrarini, M., and Pistoia, V.
295. QUANTITATIVE ANALYSIS OF REPETITIVE ELEMENTS METHYLATION IN B-CELL CHRONIC LYMPHOCYTIC LEUKEMIA
- Author
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Fabris, A., Motta, V., Bollati, V., Pegoraro, V., Giovanna Cutrona, Mosca, L., Matis, S., Ronchetti, D., Colombo, M., Gentile, M., Spirano, M., Callea, V., Festini, G., Molica, S., Cortelezzi, A., Deliliers, G. Lambertenghi, Morabito, F., Ferrarini, M., Bertazzi, P. A., Baccarelli, A., and Neri, A.
296. Morphological and phenotypical changes in EBV positive lymphoblastoid cells infected by HIV-1
- Author
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Rossi, A., Calabro, M. L., D Andrea, E., Panozzo, M., Saggiori, D., Fabrizio Mammano, Roncella, S., Ferrarini, M., and Chieco-Bianchi, L.
- Subjects
Adenosine Triphosphatases ,B-Lymphocytes ,Herpesvirus 4, Human ,Receptors, IgE ,Apyrase ,SYNDROME AIDS ,HTLV-III ,HIV Infections ,RETROVIRUS ,Receptors, Fc ,Antigens, Differentiation, B-Lymphocyte ,Tumor Virus Infections ,Phenotype ,Antigens, CD ,HUMAN-IMMUNODEFICIENCY-VIRUS ,LYMPHOMA-CELLS ,DNA, Viral ,HIV-1 ,EPSTEIN-BARR VIRUS ,Humans ,EPSTEIN-BARR VIRUS, HUMAN-IMMUNODEFICIENCY-VIRUS, LYMPHOMA-CELLS, SYNDROME AIDS, HTLV-III, RETROVIRUS ,Virus Activation ,Cells, Cultured - Abstract
Human Immunodeficiency Virus type 1 (HIV-1) infects CD4+ T lymphocytes and various other cell types, including B cells. Since HIV-1 seropositive individuals have high numbers of B cells carrying Epstein-Barr Virus (EBV), and are at high risk for development of EBV-associated lymphoproliferative diseases, we studied the mode of HIV-1 infection in four EBV-positive lymphoblastoid B-cell lines (LCLs) as well as some molecular and biological features of the B cells infected by both viruses. We found that LCL cells were successfully infected in vitro by HIV-1, despite the lack of CD4 antigen expression on the cell membrane. LCL cells displayed a persistent, productive, and non-cytopathic infection. Moreover, HIV-1 infection induced reactivation of EBV latent genomes in one cell line. Following HIV-1 infection, LCL cells showed a decrease in B-cell activation markers CD23 and CD39, and an increase in CD10 immature B-cell antigen. Not all cells in each LCL expressed HIV-1 antigens, but all CD10+ cells also co-expressed the HIV-1 envelope protein gp 120. Furthermore, HIV-1 infected LCL cells grew as disperse suspensions, and formed more agar colonies than control, non-HIV-1-infected LCLs. These findings raise the possibility that HIV-1 might play a role in EBV reactivation, and in B-cell lymphoma pathogenesis in AIDS patients.
297. PRODUCTION OF GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR BUT NOT IL-3 BY NORMAL AND NEOPLASTIC HUMAN LYMPHOCYTES-B
- Author
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Zupo, S., Perussia, B., Baldi, L., Anna Corcione, Dono, M., Ferrarini, M., and Pistoia, V.
298. IDENTIFICATION OF B-LYMPHOCYTE POPULATIONS WITH DIFFERENT FUNCTIONAL E-PHENOTYPIC CHARACTERISTICS
- Author
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simona zupo, Dono, M., Massara, R., Augliera, A., Rugari, E., and Ferrarini, M.
299. ABNORMAL IMMUNOGLOBULIN SERUM FREE LIGHT CHAINS RATIO IS ASSOCIATED WITH UNFAVORABLE PROGNOSTIC MARKERS AND IS A PREDICTOR OF TREATMENT FREE SURVIVAL IN CHRONIC LYMPHOCYTIC LEUKEMIA
- Author
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Morabito, F., Filippi, R., Gentile, M., Iaccarino, G., Attolico, I., Giovanna Cutrona, Neri, A., Ferrarini, M., Amoroso, B., Molica, S., Del Poeta, G., and Pinto, A.
300. Selective expansion of cytotoxic T lymphocytes with a CD4+CD56+ surface phenotype and a T helper type 1 profile of cytokine secretion in the liver of patients chronically infected with hepatitis B virus
- Author
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Barnaba, V., Franco, A., Marino PAROLI, Benvenuto, R., Petrillo, G., Burgio, V. L., Santilio, I., Balsano, C., Bonavita, M. S., Cappelli, G., Colizzi, V., Cutrona, G., and Ferrarini, M.
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