PMC:7463108 / 50858-52508 JSON TXT

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LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T505","span":{"begin":48,"end":51},"obj":"Body_part"},{"id":"T506","span":{"begin":688,"end":691},"obj":"Body_part"},{"id":"T507","span":{"begin":764,"end":771},"obj":"Body_part"},{"id":"T508","span":{"begin":845,"end":854},"obj":"Body_part"},{"id":"T509","span":{"begin":942,"end":955},"obj":"Body_part"},{"id":"T510","span":{"begin":1561,"end":1568},"obj":"Body_part"}],"attributes":[{"id":"A505","pred":"fma_id","subj":"T505","obj":"http://purl.org/sig/ont/fma/fma278683"},{"id":"A506","pred":"fma_id","subj":"T506","obj":"http://purl.org/sig/ont/fma/fma278683"},{"id":"A507","pred":"fma_id","subj":"T507","obj":"http://purl.org/sig/ont/fma/fma54527"},{"id":"A508","pred":"fma_id","subj":"T508","obj":"http://purl.org/sig/ont/fma/fma67314"},{"id":"A509","pred":"fma_id","subj":"T509","obj":"http://purl.org/sig/ont/fma/fma82760"},{"id":"A510","pred":"fma_id","subj":"T510","obj":"http://purl.org/sig/ont/fma/fma67257"}],"text":"Morphine exacerbates the excitotoxic effects of HIV Tat by mobilizing Ca2+ from ryanodine (RyR)-sensitive internal stores. (a) Tat-induced increases in [Ca2+]i were not attenuated by ryanodine, whereas ryanodine and pyruvate attenuate combined Tat and morphine-induced increases in [Ca2+]i. Nimodipine (L-type Ca2+ channel blocker) and dantrolene did not show any effects. (b) Average [Ca2+]i over 10 min indicated ryanodine significantly blocked combined Tat and morphine-induced increases in [Ca2+]i, whereas no effects were noted for nimodipine, dantrolene, or pyruvate. *p \u003c 0.05 vs. control, #p \u003c 0.05 vs. Tat 50 nM, §p \u003c 0.05 vs. TM, TM: Tat 50 nM + Morphine 500 nM. (c) Summary of HIV-1 Tat and morphine interactive neuronal injury in striatal medium spiny neurons. Combined Tat and morphine promotes structural and functional defects in dendrites via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), N-methyl-D-aspartic acid receptors (NMDAR), and MOR, causing influxes of Na+ and/or Ca2+, compensatory increases in Na+/K+-dependent ATPase activity, and a rapid loss in ATP mobilization with an inability to extrude excess Na+ via Na+/K+-ATPase caused by mitochondrial hyperpolarization. Dysregulation of [Ca2+]i homeostasis by combined Tat and morphine appears to be mediated downstream of [Na+]i at the level of calcium mobilization, which in turn appears to be regulated via ryanodine (RyR)-sensitive sites, and enhanced by morphine exposure likely via MOR-dependent stimulation of PI3-kinase and Ca2+ mobilization via the Gβγ protein subunit. (a-b) Modified and reprinted with permission from Fitting et al. (2014a)"}

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T136","span":{"begin":732,"end":738},"obj":"Disease"}],"attributes":[{"id":"A136","pred":"mondo_id","subj":"T136","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"}],"text":"Morphine exacerbates the excitotoxic effects of HIV Tat by mobilizing Ca2+ from ryanodine (RyR)-sensitive internal stores. (a) Tat-induced increases in [Ca2+]i were not attenuated by ryanodine, whereas ryanodine and pyruvate attenuate combined Tat and morphine-induced increases in [Ca2+]i. Nimodipine (L-type Ca2+ channel blocker) and dantrolene did not show any effects. (b) Average [Ca2+]i over 10 min indicated ryanodine significantly blocked combined Tat and morphine-induced increases in [Ca2+]i, whereas no effects were noted for nimodipine, dantrolene, or pyruvate. *p \u003c 0.05 vs. control, #p \u003c 0.05 vs. Tat 50 nM, §p \u003c 0.05 vs. TM, TM: Tat 50 nM + Morphine 500 nM. (c) Summary of HIV-1 Tat and morphine interactive neuronal injury in striatal medium spiny neurons. Combined Tat and morphine promotes structural and functional defects in dendrites via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), N-methyl-D-aspartic acid receptors (NMDAR), and MOR, causing influxes of Na+ and/or Ca2+, compensatory increases in Na+/K+-dependent ATPase activity, and a rapid loss in ATP mobilization with an inability to extrude excess Na+ via Na+/K+-ATPase caused by mitochondrial hyperpolarization. Dysregulation of [Ca2+]i homeostasis by combined Tat and morphine appears to be mediated downstream of [Na+]i at the level of calcium mobilization, which in turn appears to be regulated via ryanodine (RyR)-sensitive sites, and enhanced by morphine exposure likely via MOR-dependent stimulation of PI3-kinase and Ca2+ mobilization via the Gβγ protein subunit. (a-b) Modified and reprinted with permission from Fitting et al. (2014a)"}

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T596","span":{"begin":124,"end":125},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T597","span":{"begin":374,"end":375},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T598","span":{"begin":1071,"end":1079},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T599","span":{"begin":1085,"end":1086},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T600","span":{"begin":1579,"end":1580},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T601","span":{"begin":1581,"end":1582},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"}],"text":"Morphine exacerbates the excitotoxic effects of HIV Tat by mobilizing Ca2+ from ryanodine (RyR)-sensitive internal stores. (a) Tat-induced increases in [Ca2+]i were not attenuated by ryanodine, whereas ryanodine and pyruvate attenuate combined Tat and morphine-induced increases in [Ca2+]i. Nimodipine (L-type Ca2+ channel blocker) and dantrolene did not show any effects. (b) Average [Ca2+]i over 10 min indicated ryanodine significantly blocked combined Tat and morphine-induced increases in [Ca2+]i, whereas no effects were noted for nimodipine, dantrolene, or pyruvate. *p \u003c 0.05 vs. control, #p \u003c 0.05 vs. Tat 50 nM, §p \u003c 0.05 vs. TM, TM: Tat 50 nM + Morphine 500 nM. (c) Summary of HIV-1 Tat and morphine interactive neuronal injury in striatal medium spiny neurons. Combined Tat and morphine promotes structural and functional defects in dendrites via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), N-methyl-D-aspartic acid receptors (NMDAR), and MOR, causing influxes of Na+ and/or Ca2+, compensatory increases in Na+/K+-dependent ATPase activity, and a rapid loss in ATP mobilization with an inability to extrude excess Na+ via Na+/K+-ATPase caused by mitochondrial hyperpolarization. Dysregulation of [Ca2+]i homeostasis by combined Tat and morphine appears to be mediated downstream of [Na+]i at the level of calcium mobilization, which in turn appears to be regulated via ryanodine (RyR)-sensitive sites, and enhanced by morphine exposure likely via MOR-dependent stimulation of PI3-kinase and Ca2+ mobilization via the Gβγ protein subunit. (a-b) Modified and reprinted with permission from Fitting et al. (2014a)"}

LitCovid-PD-CHEBI

LitCovid-PubTator

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T90","span":{"begin":1244,"end":1255},"obj":"http://purl.obolibrary.org/obo/GO_0042592"},{"id":"T91","span":{"begin":1345,"end":1365},"obj":"http://purl.obolibrary.org/obo/GO_0051209"}],"text":"Morphine exacerbates the excitotoxic effects of HIV Tat by mobilizing Ca2+ from ryanodine (RyR)-sensitive internal stores. (a) Tat-induced increases in [Ca2+]i were not attenuated by ryanodine, whereas ryanodine and pyruvate attenuate combined Tat and morphine-induced increases in [Ca2+]i. Nimodipine (L-type Ca2+ channel blocker) and dantrolene did not show any effects. (b) Average [Ca2+]i over 10 min indicated ryanodine significantly blocked combined Tat and morphine-induced increases in [Ca2+]i, whereas no effects were noted for nimodipine, dantrolene, or pyruvate. *p \u003c 0.05 vs. control, #p \u003c 0.05 vs. Tat 50 nM, §p \u003c 0.05 vs. TM, TM: Tat 50 nM + Morphine 500 nM. (c) Summary of HIV-1 Tat and morphine interactive neuronal injury in striatal medium spiny neurons. Combined Tat and morphine promotes structural and functional defects in dendrites via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), N-methyl-D-aspartic acid receptors (NMDAR), and MOR, causing influxes of Na+ and/or Ca2+, compensatory increases in Na+/K+-dependent ATPase activity, and a rapid loss in ATP mobilization with an inability to extrude excess Na+ via Na+/K+-ATPase caused by mitochondrial hyperpolarization. Dysregulation of [Ca2+]i homeostasis by combined Tat and morphine appears to be mediated downstream of [Na+]i at the level of calcium mobilization, which in turn appears to be regulated via ryanodine (RyR)-sensitive sites, and enhanced by morphine exposure likely via MOR-dependent stimulation of PI3-kinase and Ca2+ mobilization via the Gβγ protein subunit. (a-b) Modified and reprinted with permission from Fitting et al. (2014a)"}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T732","span":{"begin":291,"end":643},"obj":"Sentence"},{"id":"T733","span":{"begin":644,"end":772},"obj":"Sentence"},{"id":"T734","span":{"begin":773,"end":1218},"obj":"Sentence"},{"id":"T735","span":{"begin":1219,"end":1650},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Morphine exacerbates the excitotoxic effects of HIV Tat by mobilizing Ca2+ from ryanodine (RyR)-sensitive internal stores. (a) Tat-induced increases in [Ca2+]i were not attenuated by ryanodine, whereas ryanodine and pyruvate attenuate combined Tat and morphine-induced increases in [Ca2+]i. Nimodipine (L-type Ca2+ channel blocker) and dantrolene did not show any effects. (b) Average [Ca2+]i over 10 min indicated ryanodine significantly blocked combined Tat and morphine-induced increases in [Ca2+]i, whereas no effects were noted for nimodipine, dantrolene, or pyruvate. *p \u003c 0.05 vs. control, #p \u003c 0.05 vs. Tat 50 nM, §p \u003c 0.05 vs. TM, TM: Tat 50 nM + Morphine 500 nM. (c) Summary of HIV-1 Tat and morphine interactive neuronal injury in striatal medium spiny neurons. Combined Tat and morphine promotes structural and functional defects in dendrites via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPAR), N-methyl-D-aspartic acid receptors (NMDAR), and MOR, causing influxes of Na+ and/or Ca2+, compensatory increases in Na+/K+-dependent ATPase activity, and a rapid loss in ATP mobilization with an inability to extrude excess Na+ via Na+/K+-ATPase caused by mitochondrial hyperpolarization. Dysregulation of [Ca2+]i homeostasis by combined Tat and morphine appears to be mediated downstream of [Na+]i at the level of calcium mobilization, which in turn appears to be regulated via ryanodine (RyR)-sensitive sites, and enhanced by morphine exposure likely via MOR-dependent stimulation of PI3-kinase and Ca2+ mobilization via the Gβγ protein subunit. (a-b) Modified and reprinted with permission from Fitting et al. (2014a)"}