Zobrazeno 1 - 10
of 107
pro vyhledávání: '"C Nassenstein"'
Publikováno v:
Journal of Allergy and Clinical Immunology. 142:1415-1422
Neuroimmune interaction has long been discussed in the pathogenesis of allergic airway diseases, such as allergic asthma. Mediators released during inflammation can alter the function of both sensory and parasympathetic neurons innervating the airway
Publikováno v:
Journal of Natural Products. 80:2953-2961
Plant pollens are strong airborne elicitors of asthma. Their proteinaceous allergens have been studied intensively, but little is known about a possible contribution of pollen secondary metabolites to the nonallergic exacerbation of asthma. Pollen sa
Publikováno v:
Planta Medica. 81:S1-S381
Akademický článek
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Publikováno v:
Pneumologie. 70
Publikováno v:
Pneumologie. 70
Publikováno v:
British Journal of Pharmacology. 154:1359-1368
Background and purpose: Clinical studies have demonstrated significant reductions in allergen-induced nasal symptoms of atopic rhinitis subjects by CysLT1 antagonists, including neuronally mediated symptoms such as sneeze, itch and reflex hypersecret
Autor:
HG Hoymann, Silke Wiegand, E Spies, C Nassenstein, Armin Braun, G Haider, Wolfgang Kummer, JH Lee
Publikováno v:
Pneumologie. 69
TRPA1 is a cation channel of the transient receptor potential channel family that is predominantly expressed in sensory C-fibers and activated by a wide variety of environmental irritants and endogenous inflammatory mediators relevant for asthma. Act
Autor:
I Jurastow, Anna Zakrzewicz, Silke Wiegand, Amir Rafiq, Wolfgang Kummer, Veronika Grau, M Bünemann, C Nassenstein, S Engel
Publikováno v:
Pneumologie. 69
Introduction: β-Nicotinamide adenine dinucleotide (β-NAD) has been reported to relax vascular and intestinal smooth muscle via purinergic P2Y1 and P2Y11 receptors, and we recently demonstrated its relaxing activity on murine and human airway smooth
Publikováno v:
International immunopharmacology. 29(1)
In addition to quantal, vesicular release of acetylcholine (ACh), there is also non-quantal release at the motor endplate which is insufficient to evoke postsynaptic responses unless acetylcholinesterase (AChE) is inhibited. We here addressed potenti