PMC:3681796 / 5033-6449 JSONTXT

{"project":"NEUROSES","denotations":[{"id":"T124","span":{"begin":220,"end":225},"obj":"CHEBI_30212"},{"id":"T125","span":{"begin":220,"end":225},"obj":"PATO_0000665"},{"id":"T126","span":{"begin":226,"end":230},"obj":"PATO_0000327"},{"id":"T127","span":{"begin":247,"end":252},"obj":"CHEBI_15377"},{"id":"T128","span":{"begin":247,"end":252},"obj":"CHEBI_46629"},{"id":"T129","span":{"begin":344,"end":347},"obj":"PATO_0000011"},{"id":"T130","span":{"begin":344,"end":347},"obj":"CHEBI_84123"},{"id":"T131","span":{"begin":384,"end":387},"obj":"PATO_0000308"},{"id":"T132","span":{"begin":913,"end":916},"obj":"PATO_0000308"},{"id":"T133","span":{"begin":422,"end":426},"obj":"PATO_0000384"},{"id":"T134","span":{"begin":422,"end":426},"obj":"CHEBI_30780"},{"id":"T135","span":{"begin":469,"end":479},"obj":"PATO_0002107"},{"id":"T136","span":{"begin":537,"end":541},"obj":"PATO_0000125"},{"id":"T137","span":{"begin":581,"end":585},"obj":"PATO_0000125"},{"id":"T138","span":{"begin":1324,"end":1328},"obj":"PATO_0000125"},{"id":"T139","span":{"begin":1411,"end":1415},"obj":"PATO_0000125"},{"id":"T140","span":{"begin":542,"end":550},"obj":"CHEBI_6121"},{"id":"T141","span":{"begin":618,"end":625},"obj":"PATO_0002425"},{"id":"T142","span":{"begin":618,"end":625},"obj":"PATO_0001646"},{"id":"T143","span":{"begin":708,"end":712},"obj":"PATO_0000573"},{"id":"T144","span":{"begin":972,"end":978},"obj":"CHEBI_29309"},{"id":"T145","span":{"begin":972,"end":978},"obj":"CHEBI_32875"},{"id":"T146","span":{"begin":1017,"end":1032},"obj":"CHEBI_50127"},{"id":"T147","span":{"begin":1042,"end":1051},"obj":"CHEBI_18049"},{"id":"T148","span":{"begin":1058,"end":1068},"obj":"CHEBI_30954"},{"id":"T149","span":{"begin":1152,"end":1161},"obj":"CHEBI_35222"},{"id":"T150","span":{"begin":1198,"end":1202},"obj":"CHEBI_23888"},{"id":"T151","span":{"begin":1365,"end":1369},"obj":"CHEBI_33290"}],"text":"Animals\nFVB/N males overexpressing the murine G86R SOD1 mutation [15], and C57BL/6 males knockout for the SCD1 gene (The Jackson Laboratory, Bar Harbor, ME) were maintained in our animal facility at 23°C with a 12 hours light/dark cycle. They had water and regular A04 rodent chow ad libitum. SOD1(G86R) mice were 60-, 75-, 90- and 105 days of age. SCD1 knockout mice were 4–6 months old. The corresponding non-transgenic male littermates served as controls. To induce peripheral nerve injury, mice were anesthetized with 100 mg/kg body mass ketamine chlorhydrate and 5 mg/kg body mass xylazine. The sciatic nerve was exposed at the midthigh level, and crushed with a fine forceps for 30 s or sectioned 3 mm long with microscissors. Skin incision was sutured, and mice were allowed to recover. Hind limbs contralateral to the lesion served as controls [16]. To induce SCD deficiency pharmacologically, 4–6 months old mice were fed with A04 chow ad libitum containing 3-(5-methyl-[1], [3], [4]thiadiazol-2-yl)-6-[4-(2-trifluoromethyl-phenoxy)-piperidin-1-yl]-pyridazine, or MF-438 (Prestwick Chemical, Illkirch, France), which is an orally bioavailable inhibitor of SCD enzymatic activity [17]. The drug regimen was prepared to contain 0.00625% (w/w) MF-438 (Safe, Augy, France), which provided a daily dose of 10 mg/kg body mass, as calculated on a basis of 4 g of food intake per day and 25 g of averaged body mass."}

{"project":"2_test","denotations":[{"id":"23785402-7846037-91676662","span":{"begin":66,"end":68},"obj":"7846037"},{"id":"23785402-20079427-91676663","span":{"begin":853,"end":855},"obj":"20079427"},{"id":"23785402-21296405-91676664","span":{"begin":980,"end":981},"obj":"21296405"},{"id":"23785402-19404401-91676665","span":{"begin":985,"end":986},"obj":"19404401"},{"id":"23785402-20223753-91676666","span":{"begin":990,"end":991},"obj":"20223753"},{"id":"23785402-20004097-91676667","span":{"begin":1189,"end":1191},"obj":"20004097"}],"text":"Animals\nFVB/N males overexpressing the murine G86R SOD1 mutation [15], and C57BL/6 males knockout for the SCD1 gene (The Jackson Laboratory, Bar Harbor, ME) were maintained in our animal facility at 23°C with a 12 hours light/dark cycle. They had water and regular A04 rodent chow ad libitum. SOD1(G86R) mice were 60-, 75-, 90- and 105 days of age. SCD1 knockout mice were 4–6 months old. The corresponding non-transgenic male littermates served as controls. To induce peripheral nerve injury, mice were anesthetized with 100 mg/kg body mass ketamine chlorhydrate and 5 mg/kg body mass xylazine. The sciatic nerve was exposed at the midthigh level, and crushed with a fine forceps for 30 s or sectioned 3 mm long with microscissors. Skin incision was sutured, and mice were allowed to recover. Hind limbs contralateral to the lesion served as controls [16]. To induce SCD deficiency pharmacologically, 4–6 months old mice were fed with A04 chow ad libitum containing 3-(5-methyl-[1], [3], [4]thiadiazol-2-yl)-6-[4-(2-trifluoromethyl-phenoxy)-piperidin-1-yl]-pyridazine, or MF-438 (Prestwick Chemical, Illkirch, France), which is an orally bioavailable inhibitor of SCD enzymatic activity [17]. The drug regimen was prepared to contain 0.00625% (w/w) MF-438 (Safe, Augy, France), which provided a daily dose of 10 mg/kg body mass, as calculated on a basis of 4 g of food intake per day and 25 g of averaged body mass."}