Search Results - (Author, Cooperation:M. Lowman)
-
1C. Beck ; K. Klemow ; J. Paulson ; A. Bernstein ; M. Lam ; G. Middendorf ; J. Reynolds ; K. Belanger ; C. Cardelus ; C. Cid ; S. Doshi ; N. Gerardo ; L. Jablonski ; H. Kimmel ; M. Lowman ; A. Macrae-Crerar ; B. Pohlad ; J. de Roode ; C. Thomas
American Association for the Advancement of Science (AAAS)
Published 2012Staff ViewPublication Date: 2012-03-17Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: *Curriculum ; *Education, Premedical ; *Educational Status ; *School Admission Criteria ; *Schools, MedicalPublished by: -
2L. A. Rocha ; A. Aleixo ; G. Allen ; F. Almeda ; C. C. Baldwin ; M. V. Barclay ; J. M. Bates ; A. M. Bauer ; F. Benzoni ; C. M. Berns ; M. L. Berumen ; D. C. Blackburn ; S. Blum ; F. Bolanos ; R. C. Bowie ; R. Britz ; R. M. Brown ; C. D. Cadena ; K. Carpenter ; L. M. Ceriaco ; P. Chakrabarty ; G. Chaves ; J. H. Choat ; K. D. Clements ; B. B. Collette ; A. Collins ; J. Coyne ; J. Cracraft ; T. Daniel ; M. R. de Carvalho ; K. de Queiroz ; F. Di Dario ; R. Drewes ; J. P. Dumbacher ; A. Engilis, Jr. ; M. V. Erdmann ; W. Eschmeyer ; C. R. Feldman ; B. L. Fisher ; J. Fjeldsa ; P. W. Fritsch ; J. Fuchs ; A. Getahun ; A. Gill ; M. Gomon ; T. Gosliner ; G. R. Graves ; C. E. Griswold ; R. Guralnick ; K. Hartel ; K. M. Helgen ; H. Ho ; D. T. Iskandar ; T. Iwamoto ; Z. Jaafar ; H. F. James ; D. Johnson ; D. Kavanaugh ; N. Knowlton ; E. Lacey ; H. K. Larson ; P. Last ; J. M. Leis ; H. Lessios ; J. Liebherr ; M. Lowman ; D. L. Mahler ; V. Mamonekene ; K. Matsuura ; G. C. Mayer ; H. Mays, Jr. ; J. McCosker ; R. W. McDiarmid ; J. McGuire ; M. J. Miller ; R. Mooi ; R. D. Mooi ; C. Moritz ; P. Myers ; M. W. Nachman ; R. A. Nussbaum ; D. O. Foighil ; L. R. Parenti ; J. F. Parham ; E. Paul ; G. Paulay ; J. Perez-Eman ; A. Perez-Matus ; S. Poe ; J. Pogonoski ; D. L. Rabosky ; J. E. Randall ; J. D. Reimer ; D. R. Robertson ; M. O. Rodel ; M. T. Rodrigues ; P. Roopnarine ; L. Ruber ; M. J. Ryan ; F. Sheldon ; G. Shinohara ; A. Short ; W. B. Simison ; W. F. Smith-Vaniz ; V. G. Springer ; M. Stiassny ; J. G. Tello ; C. W. Thompson ; T. Trnski ; P. Tucker ; T. Valqui ; M. Vecchione ; E. Verheyen ; P. C. Wainwright ; T. A. Wheeler ; W. T. White ; K. Will ; J. T. Williams ; G. Williams ; E. O. Wilson ; K. Winker ; R. Winterbottom ; C. C. Witt
American Association for the Advancement of Science (AAAS)
Published 2014Staff ViewPublication Date: 2014-05-24Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Biology/*methods ; Classification/*methods ; *Endangered Species ; *Extinction, BiologicalPublished by: -
3OKAYAMA, Y. ; BENYON, R. C. ; REES, P. H. ; LOWMAN, M. A. ; HILLIER, K. ; CHURCH, M. K.
Oxford, UK : Blackwell Publishing Ltd
Published 1992Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: We have studied an aspect of the functional heterogeneity of human mast cells, namely responsiveness to the inhibitory effects of sodium cromoglycate and nedocromil sodium. The effects of these drugs were examined on the release of histamine and PGD2 from mast cells of human skin, lung, tonsils, adenoids and intestine. A high concentration, 1000 μM, of sodium cromoglycate was required to significantly inhibit histamine release from lung and tonsillar mast cells. Nedocromil sodium, 1000 μM, was more effective than sodium cromoglycate against histamine release from lung, tonsillar and adenoidal cells. Both compounds showed tachyphylaxis in lung and tonsillar mast cells but not in adenoidal and intestinal mast cells. In contrast, in intestinal mast cells, the effect of nedocromil sodium was weaker and more variable than sodium cromoglycate. Skin mast cells differed from mast cells of the other anatomical sites in being unresponsive to sodium cromoglycate and nedocromil sodium. Our results confirm that high concentrations of sodium cromoglycate and nedocromil sodium are required to achieve even modest inhibition of mediator release from human mast cells under in vitro conditions. Notwithstanding this, the results also indicate that differences exist among skin, lung, tonsillar, adenoidal and intestinal mast cells with respect to their sensitivity to sodium cromoglycate and nedocromil sodium, thus extending our knowledge of functional heterogeneity within the human mast cell populations.Type of Medium: Electronic ResourceURL: -
4Okayama, Y. ; Benyon, R. C. ; Lowman, M. A. ; Church, M. K.
Oxford, UK : Blackwell Publishing Ltd
Published 1994Staff ViewISSN: 1398-9995Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Mast cells from different anatomic sites differ in cytochemistry and response to various secretory stimuli. We have investigated whether responsiveness to the second-generation H1-receptor antagonists, which are important first-line drugs for the relief of symptoms in patients with chronic urticaria and allergic rhinoconjunctivitis, also differs according to the site of origin of mast cells. The effects of terfenadine, ketotifen, and cetirizine were therefore examined in relation to the IgE-dependent release of histamine and prostaglandin D2 (PGD2) from dispersed human lung, tonsil, and skin mast cells. Terfenadine had a biphasic effect on lung and skin mast cells: at low concentrations, a concentration-dependent inhibition of histamine release from lung and skin mast cells was observed, whereas at higher concentrations the drug stimulated mediator release. Even at a high concentration, terfenadine inhibited mediator release from tonsil mast cells. Ketotifen had low potency as an inhibitor of mediator release from lung and tonsil mast cells. In skin mast cells, no inhibition of mediator release was observed below 1.0 μM, and above that concentration it induced mediator release. Cetirizine, a much less lipophilic drug than the others tested, did not induce mediator release from mast cells even at concentrations up to 100 μM. This drug showed concentration-dependent inhibition of IgE-dependent mediator release from lung and tonsil mast cells only. Our results show that human mast cells are heterogeneous with respect to modulation of mediator release by these H1-antihistamines. In particular, differences were observed between skin mast cells and those dispersed from lung and tonsils.Type of Medium: Electronic ResourceURL: -
5Church, M. K. ; Benyon, R. C. ; Lowman, M. A. ; Hutson, P. A. ; Holgate, S. T.
Springer
Published 1989Staff ViewISSN: 1420-908XSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract This short review examines two examples of studies into the mechanisms of allergic responses which have particular relevance to inflammation research. The first is the ability of human skin mast cells, but not those derived from lung, adenoids, tonsils or intestine, to release histamine in response to stimulation by neuropeptides including substance P, vasoactive intestinal polypeptide (VIP) and somatostatin. The neuropeptide activation site does not appear to be a classical tachykinin receptor but rather a binding site of low affinity and low specificity capable of interacting with neuropeptides and compounds with similar physicochemical characteristics. In contrast to IgE-dependent activation, neuropeptide stimulation of skin mast cells induces a rapid release of histamine with minimal generation of PGD2 and LTC4. This pseudo-allergic reaction is thought to underlie the weal and flare response in the skin and may have a role in urticaria. The second example describes studies to elucidate the mechanisms of the late asthmatic response by use of a guinea-pig model. As in man, both early and late phase responses in the guinea-pig are inhibited by sodium cromoglycate whereas only the early response is inhibited by theβ-adrenoceptor stimulant drug salbutamol. Examination of bronchoalveolar fluid has shown a temporal relationship between an airways neutrophilia and the late response. However, pharmacological manipulation and the use of an anti-neutrophil serum has shown that these events are not interdependent. The role of the airways eosinophilia requires further investigation.Type of Medium: Electronic ResourceURL: -
6Staff View
ISSN: 1420-908XSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Conclusions We have demonstrated that, unlike mast cells of the lung, adenoids, tonsils and intestine, whose primary role is thought to be IgE-mediated host defence, human skin mast cells respond to neuropeptide stimulation with a rapid release of histamine and minimal generation of PGD2 and LTC4. This ability of skin mast cells to release mediators in response to neuropeptide stimulation is evidence in favour of a neuro-immune interaction within human skin which may have evolved to promote angiogenesis [70] or control cutaneous blood flow [71]. In this context, it is interesting to note that mast cells are found in particularly high numbers in the blush areas of the neck and face [72]. A knowledge of the functional heterogeneity of human mast cells, and of their responsiveness to neuropeptides in particular, will prove to be of great importance to our understanding of the role of mast cells in health and disease. Enhanced responsiveness of skin mast cells to neuropeptides may contribute to the aetiology of some forms of urticaria as suggested by the presence of enhanced weal responses of patients with chronic idiopathic urticaria to various non-immunological stimuli [73–76]. Furthermore, the high ratios of histamine to PGD2 (〉1000∶1) [31, 32] in the venous effluent of thermally-challenged limbs of patients with heat- or cold-induced urticaria suggests mast cell activation by a neuropeptide rather than an immunological stimulus. However, the caveat applies that these two mediators may have been metabolised to different extents before reaching the sampling site.Type of Medium: Electronic ResourceURL: -
7Staff View
ISSN: 1618-2650Source: Springer Online Journal Archives 1860-2000Topics: Chemistry and PharmacologyType of Medium: Electronic ResourceURL: