PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21356304-1	2011	Cytokine-induced stimulation of p38 mitogen activated protein kinase (MAPK) has been shown to influence behaviorally-relevant pathophysiologic pathways including monoamine neurotransmission and neuroendocrine function and thus may contribute to behavioral changes that occur during chronic administration of the innate immune cytokine, interferon (IFN)-alpha.	monoamine	162-171	interferon alpha 1	Homo sapiens	336-358	
15927336-10	2005	Tissue monoamine analysis revealed that chronic IFN-alpha reduced DA levels in prefrontal cortex, and decreased 5-HT levels and increased 5-HT turnover in amygdala.	monoamine	7-16	interferon alpha 1	Homo sapiens	48-57	
18793712-3	2009	Using administration of interferon (IFN)-alpha as a tool to unravel these mechanisms, we have expanded upon findings from the basic science literature implicating cytokine-induced changes in monoamine metabolism as a primary pathway to depression.	monoamine	191-200	interferon alpha 1	Homo sapiens	24-46	
12788515-0	2003	The non-steroidal anti-inflammatory drug diclofenac sodium attenuates IFN-alpha induced alterations to monoamine turnover in prefrontal cortex and hippocampus.	monoamine	103-112	interferon alpha 1	Homo sapiens	70-79	
12788515-3	2003	To investigate this possibility further, we sought to determine the effect of the NSAID diclofenac sodium on monoamine turnover in brain induced by acute IFN-alpha exposure.	monoamine	109-118	interferon alpha 1	Homo sapiens	154-163	
12910630-4	2003	Impaired neuroendocine function, fronto-striatal dysfunction and decreased monoamine were found to contribute to the pathophysiology of core symptoms of IFN-alpha-induced depression, including symptoms of mood alterations, cognitive dysfunction, anhedonia and psychomotor retardation.	monoamine	75-84	interferon alpha 1	Homo sapiens	153-162