Search Results - (Author, Cooperation:M. Bloom)
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1S. K. Lathrop ; S. M. Bloom ; S. M. Rao ; K. Nutsch ; C. W. Lio ; N. Santacruz ; D. A. Peterson ; T. S. Stappenbeck ; C. S. Hsieh
Nature Publishing Group (NPG)
Published 2011Staff ViewPublication Date: 2011-09-23Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Colitis/immunology/prevention & control ; Colon/cytology/*immunology/*microbiology ; Immune System/cytology/*immunology ; Immune Tolerance/immunology ; Immunity, Mucosal/immunology ; Metagenome/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Antigen, T-Cell/immunology/metabolism ; T-Lymphocytes, Regulatory/immunology/metabolism ; Thymus Gland/cytology/immunologyPublished by: -
2J. Yan ; M. Bloom ; S. C. Bae ; E. Luijten ; S. Granick
Nature Publishing Group (NPG)
Published 2012Staff ViewPublication Date: 2012-11-23Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsPublished by: -
3Keegan, C., Krutzik, S., Schenk, M., Scumpia, P. O., Lu, J., Pang, Y. L. J., Russell, B. S., Lim, K. S., Shell, S., Prestwich, E., Su, D., Elashoff, D., Hershberg, R. M., Bloom, B. R., Belisle, J. T., Fortune, S., Dedon, P. C., Pellegrini, M., Modlin, R. L.
The American Association of Immunologists (AAI)
Published 2018Staff ViewPublication Date: 2018-04-24Publisher: The American Association of Immunologists (AAI)Print ISSN: 0022-1767Electronic ISSN: 1550-6606Topics: MedicinePublished by: -
4Staff View
Publication Date: 2018-02-09Publisher: American Association for the Advancement of Science (AAAS)Electronic ISSN: 2375-2548Topics: Natural Sciences in GeneralPublished by: -
5Liu, J., Bowman, K. W., Schimel, D., Parazoo, N. C., Jiang, Z., Lee, M., Bloom, A. A., Wunch, D., Frankenberg, C., Sun, Y., ODell, C. W., Gurney, K. R., Menemenlis, D., Gierach, M., Crisp, D., Eldering, A.
American Association for the Advancement of Science (AAAS)
Published 2018Staff ViewPublication Date: 2018-11-30Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyGeosciencesComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Atmospheric SciencePublished by: -
6Staff View
Publication Date: 2018-01-05Publisher: Genetics Society of America (GSA)Print ISSN: 0016-6731Topics: BiologyPublished by: -
7Crampette, I. ; Mainprice, B. ; Bloom, M. ; Bousauet, J. ; Campbell, A. M.
Oxford, UK : Blackwell Publishing Ltd
Published 1996Staff ViewISSN: 1398-9995Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: The mechanism of action of H1-lockers requires elucidation because they may possess properties unrelated to the blockage of histamine at its receptor level. A study was performed with enzymatically dispersed cells obtained from nasal polyps to examine the effect of terfenadine (0.1–10 μmol) on the release of leukotrienes (LT) (LTC4/D4 and LTB4) after stimulation by anti-IgE, and on the spontaneous release of cytokines (granulocyte/macrophage-colony stimulating factor [GM-CSF] and tumor necrosis factor-alpha [TNF-α]) released from cells cultured for 6 h. Terfenadine inhibited significantly, and in a dose-dependent manner, the release of LTC4/D4, LTB4, TNF-α, and GM-CSF. IC50 values were determined for LTC4/D, (8 μmol), LTB4 (9.9 μmol), TNF-α (6.1 μmol), and GM-CSF (4 μmol). Terfenadine was found to possess new antiallergic properties with a novel in vitro model which mimics more closely inflammatory cells of allergic rhinitis or asthma.Type of Medium: Electronic ResourceURL: -
8Staff View
ISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Mink persistently infected with Aleutian disease virus (ADV) develop hypergammaglobulinaemia and immune complex disease. Radiolabelled antibodies from mink infected with ADV-G, DK, Pullman, and Utah I strains of ADV were reacted against all four ADV strains in radioimmunoassay (RIA). The amount of anti-ADV antibody in two equally hypergammaglobulinaemic serum pools varied from 13% (anti-Pullman) to 57% (anti-Utah I). Serum pools from two other sources (anti-DK and anti-ADV-G), although less hypergammaglobulinaemic, had 5% and 13%, respectively, indicating that 43–95% of the Ig in the sera of mink with AD was not specific antibody to ADV structural antigens. The possibility of a general polyclonal activation of the humoral immune system is being discussed. Comparison of plateau RIA binding levels for the four serum pools against the four viral antigens suggested three patterns of reactivity: DK and Utah I reacted similarly, but Pullman and ADV-G reacted serologically different.Type of Medium: Electronic ResourceURL: -
9Staff View
ISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Mink persistently infected with Aleutian disease virus (ADV) develop plasmacytosis (hypergammaglobulinaemia) and immune complex disease. Mink of different colour phases were infected with different strains of ADV and bled at different times after infection. The average antibody affinities (Kav) were measured in the sera and found to fall in the range of 2×109−2 × 1010 M−1, thus indicating good-quality antibodies. In sera of non-Aleutian genotype mink a decline in Kav during development of plasmacytosis was observed. Moreover, the antibody heterogeneity (a values) tended to decrease during the disease progress. In contrast. the Kav values in sera of infected Aleutian genotype mink remained relatively high alter hypergammaglobulinaemia developed, and the antibody heterogeneity for certain of the mink sera indicated restricted heterogeneity (high α values). In agreement with the clonal selection theory, low virus burden (for instance, during infection with a low-virulence ADV strain (generated relatively higher affinity antibodies than a high virus burden (for instance, the highly virulent Utah I strain of ADV), Furthermore, antibodies present in low concentration were of higher affinity than antibodies present in high concentrations. The relatively high affinity antibodies found in this study indicate that if the immune complex disease seen in AD is caused by virus-anti-virus antibodies, good-quality antibodies are likely to be responsible for the pathological findings.Type of Medium: Electronic ResourceURL: -
10BENLOUNES, N. ; DUPONT, C. ; CANDALH, C. ; BLATON, M.-A. ; BLOOM, M. ; HEYMAN, M.
Oxford, UK : Blackwell Publishing Ltd
Published 1997Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background In infants with cow's milk allergy and intestinal symptotns, peripheral blood mononuclear cells stimulated in vitro with cow's milk proteins, secrete large amounts of the proinflammatory cytokine TNFα thus altering intestinal barrier capacity. Terfenadine, an antihistaminic drug, inhibits the release of several inflammatory mediators, including histamine, prostaglandins and leukotrienes.Objectives To test the potential ability of terfenadine to inhibit TNFα secretion by mononuclear cells from infants with cow's milk allergy.Methods Mononuclear cells from infants allergic to cow's milk proteins were stimulated in vitro for 6 days by a mixture of milk proteins (β-lactoglobulin, α-lactalbumin and casein) with or without terfenadine (0.1 –1 μM) and culture supernatants were assayed for TNFα by enzyme immunoassay. The effect of culture supernatants on intestinal barrier capacity was evaluated by measuring the electrical resistance (index of integrity) of filter-grown HT29–19 A intestinal cells in Ussing chambers.Results During active cow's milk allergy, mononuclear cells stimulated with cow's milk proteins secreted large amounts of TNFα which significantly reduced the electrical resistance of HT29–19 A intestinal cells. There was a dose-dependent decrease in TNFα secretion in the presence of terfenadine, with a maximal inhibition of 62% of this secretion at 1 μM. Accordingly, terfenadine-treated mononuclear cells supernatants did not alter the electrical resistance of intestinal HT29. 19 A cells.Conclusion These results indicate that in infants with intestinal dysfunction due to cow's milk allergy, terfenadine is a potent inhibitor of the TNFα secretion induced by sensitizing milk protein antigens. This inhibition prevents the degradation of intestinal function as measured in an intestinal cell line, in vitro.Type of Medium: Electronic ResourceURL: -
11Campbell, A. M. ; Chanez, P. ; Marty-Ané, C. ; Albat, B. ; Bloom, M. ; Michel, F. B. ; Godard, P. ; Bousquet, J.
Oxford, UK : Blackwell Publishing Ltd
Published 1993Staff ViewISSN: 1398-9995Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Terfenadine is an H1-blocker that may have antiallergic properties. A study was carried out to examine the ability of terfenadine to inhibit the release of histamine and arachidonic-acid-derived mediators from human lung cells. Cells were dispersed from fresh human lung tissue obtained from tour accident victims whose hearts were donated for transplantation and four lung cancer resections. Cells were dispersed by enzymatic digestion with type XIV protease and chymopapain, and this resulted in a cell population containing approximately 5% mast cells. The remaining cells were mainly macrophages. The cells were challenged with anti-IgE at a 1/1000 dilution. Cells were challenged without terfenadine and after a preincubation of 0.1, 1, and 10 umol terfenadine. The release of PGD2 and LTC4/D4 was assessed with an EIA. Histamine was assayed by RIA with a monoclonal antibody against acylated histamine.A release of both eicosanoids and histamine was observed m all experiments. An inhibition of eicosanoids was observed at both 1 and 10 μmol terfenadine (median percentage of inhibition of PGD2: 38.00 ± 15.65 and 56,00 ± 13,12; median percentage of inhibition of LTC4/D4: 37.5 ± 19,80 and 52.5 ± 26.8). On the other hand, histamine release was not blocked by terfenadine.Terfenadine inhibits, in a dose-dependent manner, the release of eicosanoids after challenge of dispersed lung cells by anti-IgE, and this effect may have some clinical relevance.Type of Medium: Electronic ResourceURL: -
12Staff View
ISSN: 0005-2736Keywords: (Human) ; Erythrocyte membrane ; Fluidity ; Low temperature ; ^2H-NMRSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyMedicinePhysicsType of Medium: Electronic ResourceURL: -
13Staff View
ISSN: 0005-2736Keywords: Dimyristoylphosphatidylcholine ; Membrane protein ; Membrane reconstitution ; Rhodopsin ; ^1H-NMRSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyMedicinePhysicsType of Medium: Electronic ResourceURL: -
14Staff View
ISSN: 0005-2736Keywords: (A. laidlawii membrane) ; Cholesterol ; Molecular order ; Temperature dependence ; ^2H-NMRSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyMedicinePhysicsType of Medium: Electronic ResourceURL: -
15Staff View
ISSN: 0009-3084Keywords: Correlation time ; Length scale ; Nuclear magnetic resonance (NMR) ; Time scaleSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
16Staff View
ISSN: 0009-3084Keywords: bilayer thickness ; lipid ; multilamellar dispersion ; phase diagramSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
17Staff View
ISSN: 0009-3084Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
18Mackay, A.L. ; Burnell, E.E. ; Nichol, C.P. ; Weeks, G. ; Bloom, M. ; Valic, M.I.
Amsterdam : ElsevierStaff ViewISSN: 0014-5793Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
19Staff View
ISSN: 0014-5793Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
20Staff View
ISSN: 0022-2364Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: PhysicsType of Medium: Electronic ResourceURL: