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(2014). https://www.sciencedirect.com/science/article/abs/pii/S0006291X14006482 DOI: 10.1016/j.bbrc.2014.04.017","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Cultured astrocytes","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"nutrient_deficiency","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"98f62d83-fb98-55b6-81d7-ddc5c4b5aea6","evidence_kind":"source_excerpt","locator":"Lines 1325-1337","start_line":1325,"end_line":1337,"excerpt":"### thiamine-def-nfkb-inhibition-glt1b\nNF-kappa-B inhibition attenuated GLT-1b loss in astrocytes exposed to the thiamine-disruption protocol.\nCondition category: nutrient_deficiency\nnutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Suppressing the inflammatory pathway helped preserve this particular glutamate-transporter isoform.\norganism: Rattus norvegicus\ntissue_or_cell_type: Cultured astrocytes\nexperimental_model: Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors.\nlimitations: Pharmacological inhibition is not isoform-specific genetic proof; the accessible record does not establish efficacy in intact human brain.\nevidence_location: Abstract; NF-kappa-B inhibitor experiment\nevidence_span: ameliorated the decrease in GLT-1b\nexposure: Thiamine-free medium plus pyrithiamine in cultured newborn-rat astrocytes\n[jhala-2014-astrocyte-inflammatory-signaling] Thiamine deficiency results in release of soluble factors that disrupt mitochondrial membrane potential and downregulate the glutamate transporter splice-variant GLT-1b in cultured astrocytes. 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