PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24489087-10	2014	These data demonstrate that the primary mechanism by which pioglitazone protects against polymicrobial sepsis is through the impairment of MyD88 responses.	Pioglitazone	59-71	myeloid differentiation primary response gene 88	Mus musculus	139-144	
32665906-10	2020	Results: We show that activation of PPARgamma by its agonist, pioglitazone, reduces cell proliferation, Tlr-4, Myd-88, Nf-kb mRNA expression, and tumor necrosis factor-alpha (TNF-alpha) production but not interleukin-1 beta (IL-1beta) in B16F10 LPS-stimulated cells in vitro.	Pioglitazone	62-74	myeloid differentiation primary response gene 88	Mus musculus	111-117	
31509504-10	2019	RESULTS: We observed that activation of PPARgamma by its agonist, pioglitazone, reduces tumor volume, Tlr-4, Myd-88, Nf-kb1 mRNA expression, TLR4 protein expression and TNF-alpha production in melanoma tumor especially in groups that were injected with LPS -stimulated cells.	Pioglitazone	66-78	myeloid differentiation primary response gene 88	Mus musculus	109-115