PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2809211-7	1989	Peak SAP mRNA concentrations were observed 8 h after thioglycollate and 12 to 18 h after azocasein injection; by 36 h concentrations were close to preinflammatory levels.	Thioglycolates	53-67	amyloid P component, serum	Mus musculus	5-8	
2809211-8	1989	All mRNA species studied (SAP, SAA and the complement components C3, C5 and factor B) were induced more rapidly by the thioglycollate stimulus and reached higher peak concentrations.	Thioglycolates	119-133	amyloid P component, serum	Mus musculus	26-29	
2809211-9	1989	SAP mRNA levels were correlated with other parameters of inflammation: infiltration of peritoneal exudate cells (PEC) into the peritoneum after thioglycollate injection, and serum concentrations of SAP after azocasein injection.	Thioglycolates	144-158	amyloid P component, serum	Mus musculus	0-3	
2809211-11	1989	The highest numbers of PEC were present 24 h after the thioglycollate stimulus, i.e. 16 h after the maximum SAP mRNA concentration, indicating the continuation of an active local inflammation many hours after one aspect of the systemic response has ceased.	Thioglycolates	55-69	amyloid P component, serum	Mus musculus	108-111	
6600258-4	1983	The endogenous SAP levels of all strains increased to 180 to 230 micrograms/ml 24 h after an inflammatory stimulus of either thioglycollate (TG) or lipopolysaccharide (LPS).	Thioglycolates	125-139	amyloid P component, serum	Mus musculus	15-18	
6600258-4	1983	The endogenous SAP levels of all strains increased to 180 to 230 micrograms/ml 24 h after an inflammatory stimulus of either thioglycollate (TG) or lipopolysaccharide (LPS).	Thioglycolates	141-143	amyloid P component, serum	Mus musculus	15-18	
6806378-5	1982	SAP levels increased five-fold by 24 hr after challenge with lipopolysaccharide (LPS) or thioglycollate.	Thioglycolates	89-103	amyloid P component, serum	Mus musculus	0-3