PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31095747-2	2019	Currently, four genetic defects have been described causing impairment of thiamine transport and metabolism: SLC19A2 dysfunction leads to diabetes mellitus, megaloblastic anemia and sensory-neural hearing loss, whereas SLC19A3, SLC25A19, and TPK1-related disorders result in recurrent encephalopathy, basal ganglia necrosis, generalized dystonia, severe disability, and early death.	Thiamine	74-82	solute carrier family 19 member 3	Homo sapiens	219-226	
31095747-4	2019	SLC19A3 patients present a profound decrease of free-thiamine in cerebrospinal fluid (CSF) and fibroblasts.	Thiamine	53-61	solute carrier family 19 member 3	Homo sapiens	0-7	
31095747-7	2019	In a significant number of patients with SLC19A3, thiamine improves clinical outcome and survival, and prevents further metabolic crisis.	Thiamine	50-58	solute carrier family 19 member 3	Homo sapiens	41-48	
31095747-9	2019	Moreover, thiamine supplementation leads to normal concentrations of free-thiamine in the CSF of SLC19A3 patients.	Thiamine	10-18	solute carrier family 19 member 3	Homo sapiens	97-104	
31095747-9	2019	Moreover, thiamine supplementation leads to normal concentrations of free-thiamine in the CSF of SLC19A3 patients.	Thiamine	74-82	solute carrier family 19 member 3	Homo sapiens	97-104