PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18702818-5	2008	The acute injury phase after Cl2 exposure (< or = 24 hrs post-exposure) was characterized by airway epithelial cell apoptosis (increased TUNEL staining) and sloughing, elevated protein in bronchoalveolar lavage fluid, and a modest increase in airway responses to methacholine.	Methacholine Chloride	266-278	doublecortin-like kinase 2	Mus musculus	29-32	
27226094-5	2016	CysLT1R-deficient (CysLTr1(-/-)) mice that were exposed to Cl2 demonstrated airway hyperresponsiveness to inhaled methacholine significantly greater than in WT BALB/c mice.	Methacholine Chloride	114-126	doublecortin-like kinase 2	Mus musculus	59-62	
20925946-7	2010	RESULTS: Mice exposed to Cl2 had airway hyperresponsiveness to MCh compared to control animals pre-treated and post-treated with DMTU.	Methacholine Chloride	63-66	doublecortin-like kinase 2	Mus musculus	25-28	
18702818-9	2008	We conclude that a single exposure of mice to Cl2 gas causes acute changes in lung function, including pulmonary responsiveness to methacholine challenge, associated with airway damage, followed by subsequent repair and airway remodelling.	Methacholine Chloride	131-143	doublecortin-like kinase 2	Mus musculus	46-49	
17343743-7	2007	RESULTS: Wild type mice developed a greater degree of airway hyperresponsiveness to MCh at 1 day post exposure to Cl2 compared with TCR-delta-/- mice.	Methacholine Chloride	84-87	doublecortin-like kinase 2	Mus musculus	114-117