PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10351919-1 1999 Short-acting beta2-agonists provide greater protection against bronchoconstriction induced by adenosine 5"-monophosphate (AMP) than by direct-acting bronchoconstrictors such as histamine and methacholine. Methacholine Chloride 191-203 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 13-18 10329815-2 1999 OBJECTIVES: The primary aim of this study was to evaluate whether there is a potential in vivo interaction between long- and short-acting beta2-agonists in the presence of increased airway tone induced by methacholine. Methacholine Chloride 205-217 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 138-143 10378545-4 1999 RESULTS: Inhalation of the beta2-agonist was associated with an increase in provocative concentration causing a 20% decrease in FEV1 (PC20) values (geometric mean) from 1.01+/-2.76 to 20.54+/-6.24 mg/mL for methacholine and from 2.29+/-2.26 to 19.82+/-5.93 mg/mL for histamine. Methacholine Chloride 207-219 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 27-32 9310023-2 1997 With short-acting beta 2-agonists, this is more readily demonstrable using indirectly acting agents such as adenosine monophosphate (AMP), which may act via mast cell degranulation, than using methacholine (MCh), implying more rapid mast cell than smooth muscle desensitization. Methacholine Chloride 207-210 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 18-24 9412548-2 1997 Because AMP produces bronchoconstriction through release of mediators from mast cells, and methacholine directly constricts airway smooth muscle, this suggests that beta(2)-agonists stabilize mast cells in vivo. Methacholine Chloride 91-103 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 165-171 9139768-1 1997 After complete abstinence, regular use of short-acting beta 2-agonists results in an increase in early and late asthmatic (allergen) response, exercise-induced bronchoconstriction, and nonspecific airways responsiveness (methacholine). Methacholine Chloride 221-233 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 55-61 9139768-2 1997 Regular use of long-acting beta 2-agonists also results in increased nonspecific airways responsiveness (methacholine) with or without concomitant inhaled corticosteroids and attenuates the response to escalating doses of inhaled short-acting beta 2-agonists such as might be used in an acute exacerbation. Methacholine Chloride 105-117 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 27-33 8568137-1 1996 BACKGROUND: Two adverse effects of inhaled beta 2-agonists are increased airway responsiveness to allergen and tolerance to the bronchoprotective effect of beta 2-agonists versus bronchoconstrictors (e.g., methacholine). Methacholine Chloride 206-218 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 43-49 1673830-0 1991 Prolonged protection against methacholine-induced bronchoconstriction by the inhaled beta 2-agonist formoterol. Methacholine Chloride 29-41 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 85-91 7582281-0 1995 Interaction of inhaled beta 2 agonist and inhaled corticosteroid on airway responsiveness to allergen and methacholine. Methacholine Chloride 106-118 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 23-29 7750333-0 1995 The reversibility of airway obstruction to an inhaled beta 2-adrenergic agent is less satisfactory after methacholine testing in asthmatic subjects. Methacholine Chloride 105-117 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 54-60 7750333-1 1995 AIMS: The aim of this work was to compare the response to an inhaled beta 2-adrenergic agent in two situations: (1) spontaneous airway obstruction in asthmatic subjects who had withheld treatment with the medication for more than 12 hs; and (2) after methacholine-induced airway obstruction once airway caliber had recovered to the premethacholine test value. Methacholine Chloride 251-263 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 69-75 7750333-7 1995 CONCLUSION: After a methacholine test, the reversibility of an inhaled beta 2 agent is not significantly different from a placebo and is less satisfactory than in a situation of spontaneous airway obstruction. Methacholine Chloride 20-32 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 71-77 8296255-0 1993 Changes in methacholine induced bronchoconstriction with the long acting beta 2 agonist salmeterol in mild to moderate asthmatic patients. Methacholine Chloride 11-23 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 73-79 8296255-1 1993 BACKGROUND: Beta-2 agonists protect against non-specific bronchoconstricting agents such as methacholine, but it has been suggested that the protection afforded by long acting beta 2 agonists wanes rapidly with regular treatment. Methacholine Chloride 92-104 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 12-18 8104272-1 1993 Regular inhaled beta 2 agonist causes tolerance to the acute protective effect of beta 2 agonist against bronchoconstriction induced by chemical stimuli such as AMP, histamine, and methacholine. Methacholine Chloride 181-193 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 16-22 8104272-1 1993 Regular inhaled beta 2 agonist causes tolerance to the acute protective effect of beta 2 agonist against bronchoconstriction induced by chemical stimuli such as AMP, histamine, and methacholine. Methacholine Chloride 181-193 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 82-88 8099699-6 1993 Single doses of long-acting beta 2-agonists give a prolonged protection against methacholine- and histamine-induced airway sensitivity of at least 12 hours. Methacholine Chloride 80-92 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 28-34 2566160-0 1989 [Effectiveness of a new beta 2-agonist (broxaterol) on bronchospasm induced by methacholine (blind study versus salbutamol)]. Methacholine Chloride 79-91 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 24-30 15338791-0 2004 Relief of dyspnoea by beta2-agonists after methacholine-induced bronchoconstriction. Methacholine Chloride 43-55 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 22-27 21923426-0 2011 Methacholine challenge as a clinical bioassay of pulmonary delivery of a long-acting beta2-adrenergic agonist. Methacholine Chloride 0-12 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 85-90 21923426-1 2011 STUDY OBJECTIVE: To determine whether the methacholine challenge method used for albuterol can be applied to assess long-acting beta2-adrenergic agonist (LABA) bioequivalence, which would require a sufficiently steep dose-response curve. Methacholine Chloride 42-54 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 128-133 12640377-6 2003 The only significant relationship between asthma severity and height percentile was with methacholine bronchoprovocation in girls (beta 2.98, P =.019, covariate multiple regression). Methacholine Chloride 89-101 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 131-137