PMC:4536246 / 13531-14183 JSONTXT

{"project":"TEST0","denotations":[{"id":"26272684-96-102-1511557","span":{"begin":96,"end":98},"obj":"[\"11072643\"]"},{"id":"26272684-100-106-1511558","span":{"begin":100,"end":102},"obj":"[\"9616786\"]"},{"id":"26272684-194-200-1511559","span":{"begin":194,"end":196},"obj":"[\"11166465\", \"10027765\", \"8217498\"]"},{"id":"26272684-99-105-1511560","span":{"begin":373,"end":375},"obj":"[\"21331757\"]"},{"id":"26272684-103-109-1511561","span":{"begin":377,"end":379},"obj":"[\"10526126\"]"},{"id":"26272684-107-113-1511562","span":{"begin":381,"end":383},"obj":"[\"11996533\"]"},{"id":"26272684-231-237-1511563","span":{"begin":645,"end":647},"obj":"[\"14728706\", \"24283432\", \"15182958\", \"22245521\"]"}],"text":"Strong evidence supports the idea that NO plays a pivotal role in the pathogenesis of migraine [27, 28], a disorder characterized by pain sensitization associated with cranial vascular changes [29–31], but mechanisms and modalities of NO activity are still largely unknown. Systemic GTN activates neuronal groups in selected areas of the rat brain involved in nociception [21, 32, 33] and induces spontaneous-like attacks in migraineurs via multimodal mechanisms that include GTN- induced vasodilation, peripheral sensitization induced by the increased availability of NO at the trigeminovascular level, and possibly also central sensitization [34–37]."}

{"project":"2_test","denotations":[{"id":"26272684-11072643-60565585","span":{"begin":96,"end":98},"obj":"11072643"},{"id":"26272684-9616786-60565586","span":{"begin":100,"end":102},"obj":"9616786"},{"id":"26272684-11166465-60565587","span":{"begin":194,"end":196},"obj":"11166465"},{"id":"26272684-10027765-60565587","span":{"begin":194,"end":196},"obj":"10027765"},{"id":"26272684-8217498-60565587","span":{"begin":194,"end":196},"obj":"8217498"},{"id":"26272684-21331757-60565588","span":{"begin":373,"end":375},"obj":"21331757"},{"id":"26272684-10526126-60565589","span":{"begin":377,"end":379},"obj":"10526126"},{"id":"26272684-11996533-60565590","span":{"begin":381,"end":383},"obj":"11996533"},{"id":"26272684-14728706-60565591","span":{"begin":645,"end":647},"obj":"14728706"},{"id":"26272684-24283432-60565591","span":{"begin":645,"end":647},"obj":"24283432"},{"id":"26272684-15182958-60565591","span":{"begin":645,"end":647},"obj":"15182958"},{"id":"26272684-22245521-60565591","span":{"begin":645,"end":647},"obj":"22245521"}],"text":"Strong evidence supports the idea that NO plays a pivotal role in the pathogenesis of migraine [27, 28], a disorder characterized by pain sensitization associated with cranial vascular changes [29–31], but mechanisms and modalities of NO activity are still largely unknown. Systemic GTN activates neuronal groups in selected areas of the rat brain involved in nociception [21, 32, 33] and induces spontaneous-like attacks in migraineurs via multimodal mechanisms that include GTN- induced vasodilation, peripheral sensitization induced by the increased availability of NO at the trigeminovascular level, and possibly also central sensitization [34–37]."}