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<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"alpha-methyldopa"/ induces disease /"hypotensive"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Naloxone reverses the antihypertensive effect of clonidine.
- Abstract: In unanesthetized, spontaneously hypertensive rats the decrease in blood pressure and heart rate produced by intravenous clonidine, 5 to 20 micrograms/kg, was inhibited or reversed by nalozone, 0.2 to 2 mg/kg. The /"hypotensive"/ effect of 100 mg/kg /"alpha-methyldopa"/ was also partially reversed by naloxone. Naloxone alone did not affect either blood pressure or heart rate. In brain membranes from spontaneously hypertensive rats clonidine, 10(-8) to 10(-5) M, did not influence stereoselective binding of [3H]-naloxone (8 nM), and naloxone, 10(-8) to 10(-4) M, did not influence clonidine-suppressible binding of [3H]-dihydroergocryptine (1 nM). These findings indicate that in spontaneously hypertensive rats the effects of central alpha-adrenoceptor stimulation involve activation of opiate receptors. As naloxone and clonidine do not appear to interact with the same receptor site, the observed functional antagonism suggests the release of an endogenous opiate by clonidine or /"alpha-methyldopa"/ and the possible role of the opiate in the central control of sympathetic tone.
Question: Does chemical /"alpha-methyldopa"/ induce disease /"hypotensive"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Naloxone reverses the antihypertensive effect of clonidine. | In unanesthetized, spontaneously hypertensive rats the decrease in blood pressure and heart rate produced by intravenous clonidine, 5 to 20 micrograms/kg, was inhibited or reversed by nalozone, 0.2 to 2 mg/kg. The /"hypotensive"/ effect of 100 mg/kg /"alpha-methyldopa"/ was also partially reversed by naloxone. Naloxone alone did not affect either blood pressure or heart rate. In brain membranes from spontaneously hypertensive rats clonidine, 10(-8) to 10(-5) M, did not influence stereoselective binding of [3H]-naloxone (8 nM), and naloxone, 10(-8) to 10(-4) M, did not influence clonidine-suppressible binding of [3H]-dihydroergocryptine (1 nM). These findings indicate that in spontaneously hypertensive rats the effects of central alpha-adrenoceptor stimulation involve activation of opiate receptors. As naloxone and clonidine do not appear to interact with the same receptor site, the observed functional antagonism suggests the release of an endogenous opiate by clonidine or /"alpha-methyldopa"/ and the possible role of the opiate in the central control of sympathetic tone. | alpha-methyldopa | {
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],
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"text": [
"alpha-methyldopa"
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"type": "Chemical"
} | hypotensive | {
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{
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"db_name": "MESH"
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],
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274,
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],
"text": [
"hypotensive"
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"type": "Disease"
} | [
{
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"text": [
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"type": "Chemical"
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{
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878,
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"text": [
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"text": [
"hypertensive"
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750,
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"text": [
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] | Naloxone reverses the antihypertensive effect of clonidine. | In unanesthetized, spontaneously hypertensive rats the decrease in blood pressure and heart rate produced by intravenous clonidine, 5 to 20 micrograms/kg, was inhibited or reversed by nalozone, 0.2 to 2 mg/kg. The hypotensive effect of 100 mg/kg alpha-methyldopa was also partially reversed by naloxone. Naloxone alone did not affect either blood pressure or heart rate. In brain membranes from spontaneously hypertensive rats clonidine, 10(-8) to 10(-5) M, did not influence stereoselective binding of [3H]-naloxone (8 nM), and naloxone, 10(-8) to 10(-4) M, did not influence clonidine-suppressible binding of [3H]-dihydroergocryptine (1 nM). These findings indicate that in spontaneously hypertensive rats the effects of central alpha-adrenoceptor stimulation involve activation of opiate receptors. As naloxone and clonidine do not appear to interact with the same receptor site, the observed functional antagonism suggests the release of an endogenous opiate by clonidine or alpha-methyldopa and the possible role of the opiate in the central control of sympathetic tone. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"clonidine"/ induces disease /"hypotensive"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Naloxone reverses the antihypertensive effect of /"clonidine"/.
- Abstract: In unanesthetized, spontaneously hypertensive rats the decrease in blood pressure and heart rate produced by intravenous /"clonidine"/, 5 to 20 micrograms/kg, was inhibited or reversed by nalozone, 0.2 to 2 mg/kg. The /"hypotensive"/ effect of 100 mg/kg alpha-methyldopa was also partially reversed by naloxone. Naloxone alone did not affect either blood pressure or heart rate. In brain membranes from spontaneously hypertensive rats /"clonidine"/, 10(-8) to 10(-5) M, did not influence stereoselective binding of [3H]-naloxone (8 nM), and naloxone, 10(-8) to 10(-4) M, did not influence /"clonidine"/-suppressible binding of [3H]-dihydroergocryptine (1 nM). These findings indicate that in spontaneously hypertensive rats the effects of central alpha-adrenoceptor stimulation involve activation of opiate receptors. As naloxone and /"clonidine"/ do not appear to interact with the same receptor site, the observed functional antagonism suggests the release of an endogenous opiate by /"clonidine"/ or alpha-methyldopa and the possible role of the opiate in the central control of sympathetic tone.
Question: Does chemical /"clonidine"/ induce disease /"hypotensive"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Naloxone reverses the antihypertensive effect of /"clonidine"/. | In unanesthetized, spontaneously hypertensive rats the decrease in blood pressure and heart rate produced by intravenous /"clonidine"/, 5 to 20 micrograms/kg, was inhibited or reversed by nalozone, 0.2 to 2 mg/kg. The /"hypotensive"/ effect of 100 mg/kg alpha-methyldopa was also partially reversed by naloxone. Naloxone alone did not affect either blood pressure or heart rate. In brain membranes from spontaneously hypertensive rats /"clonidine"/, 10(-8) to 10(-5) M, did not influence stereoselective binding of [3H]-naloxone (8 nM), and naloxone, 10(-8) to 10(-4) M, did not influence /"clonidine"/-suppressible binding of [3H]-dihydroergocryptine (1 nM). These findings indicate that in spontaneously hypertensive rats the effects of central alpha-adrenoceptor stimulation involve activation of opiate receptors. As naloxone and /"clonidine"/ do not appear to interact with the same receptor site, the observed functional antagonism suggests the release of an endogenous opiate by /"clonidine"/ or alpha-methyldopa and the possible role of the opiate in the central control of sympathetic tone. | clonidine | {
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{
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}
],
"offsets": [
[
49,
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]
],
"text": [
"clonidine"
],
"type": "Chemical"
} | hypotensive | {
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{
"db_id": "D007022",
"db_name": "MESH"
}
],
"offsets": [
[
274,
285
]
],
"text": [
"hypotensive"
],
"type": "Disease"
} | [
{
"id": "3",
"normalized": [
{
"db_id": "D009270",
"db_name": "MESH"
}
],
"offsets": [
[
0,
8
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],
"text": [
"Naloxone"
],
"type": "Chemical"
},
{
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{
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"db_name": "MESH"
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],
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49,
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"text": [
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"text": [
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"type": "Chemical"
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"offsets": [
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"text": [
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"type": "Chemical"
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{
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354,
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"text": [
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],
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1039,
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"text": [
"alpha-methyldopa"
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"type": "Chemical"
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{
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{
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"db_name": "MESH"
}
],
"offsets": [
[
93,
105
]
],
"text": [
"hypertensive"
],
"type": "Disease"
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{
"id": "8",
"normalized": [
{
"db_id": "D007022",
"db_name": "MESH"
}
],
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[
274,
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"text": [
"hypotensive"
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"type": "Disease"
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{
"id": "12",
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{
"db_id": "D006973",
"db_name": "MESH"
}
],
"offsets": [
[
469,
481
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"text": [
"hypertensive"
],
"type": "Disease"
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{
"id": "18",
"normalized": [
{
"db_id": "D006973",
"db_name": "MESH"
}
],
"offsets": [
[
750,
762
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],
"text": [
"hypertensive"
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"type": "Disease"
}
] | Naloxone reverses the antihypertensive effect of clonidine. | In unanesthetized, spontaneously hypertensive rats the decrease in blood pressure and heart rate produced by intravenous clonidine, 5 to 20 micrograms/kg, was inhibited or reversed by nalozone, 0.2 to 2 mg/kg. The hypotensive effect of 100 mg/kg alpha-methyldopa was also partially reversed by naloxone. Naloxone alone did not affect either blood pressure or heart rate. In brain membranes from spontaneously hypertensive rats clonidine, 10(-8) to 10(-5) M, did not influence stereoselective binding of [3H]-naloxone (8 nM), and naloxone, 10(-8) to 10(-4) M, did not influence clonidine-suppressible binding of [3H]-dihydroergocryptine (1 nM). These findings indicate that in spontaneously hypertensive rats the effects of central alpha-adrenoceptor stimulation involve activation of opiate receptors. As naloxone and clonidine do not appear to interact with the same receptor site, the observed functional antagonism suggests the release of an endogenous opiate by clonidine or alpha-methyldopa and the possible role of the opiate in the central control of sympathetic tone. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"Lidocaine"/ induces disease /"cardiac asystole"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Lidocaine"/-induced /"cardiac asystole"/.
- Abstract: Intravenous administration of a single 50-mg bolus of /"lidocaine"/ in a 67-year-old man resulted in profound depression of the activity of the sinoatrial and atrioventricular nodal pacemakers. The patient had no apparent associated conditions which might have predisposed him to the development of bradyarrhythmias; and, thus, this probably represented a true idiosyncrasy to /"lidocaine"/.
Question: Does chemical /"Lidocaine"/ induce disease /"cardiac asystole"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | /"Lidocaine"/-induced /"cardiac asystole"/. | Intravenous administration of a single 50-mg bolus of /"lidocaine"/ in a 67-year-old man resulted in profound depression of the activity of the sinoatrial and atrioventricular nodal pacemakers. The patient had no apparent associated conditions which might have predisposed him to the development of bradyarrhythmias; and, thus, this probably represented a true idiosyncrasy to /"lidocaine"/. | Lidocaine | {
"id": "28",
"normalized": [
{
"db_id": "D008012",
"db_name": "MESH"
}
],
"offsets": [
[
0,
9
]
],
"text": [
"Lidocaine"
],
"type": "Chemical"
} | cardiac asystole | {
"id": "29",
"normalized": [
{
"db_id": "D006323",
"db_name": "MESH"
}
],
"offsets": [
[
18,
34
]
],
"text": [
"cardiac asystole"
],
"type": "Disease"
} | [
{
"id": "28",
"normalized": [
{
"db_id": "D008012",
"db_name": "MESH"
}
],
"offsets": [
[
0,
9
]
],
"text": [
"Lidocaine"
],
"type": "Chemical"
},
{
"id": "30",
"normalized": [
{
"db_id": "D008012",
"db_name": "MESH"
}
],
"offsets": [
[
90,
99
]
],
"text": [
"lidocaine"
],
"type": "Chemical"
},
{
"id": "33",
"normalized": [
{
"db_id": "D008012",
"db_name": "MESH"
}
],
"offsets": [
[
409,
418
]
],
"text": [
"lidocaine"
],
"type": "Chemical"
}
] | [
{
"id": "29",
"normalized": [
{
"db_id": "D006323",
"db_name": "MESH"
}
],
"offsets": [
[
18,
34
]
],
"text": [
"cardiac asystole"
],
"type": "Disease"
},
{
"id": "31",
"normalized": [
{
"db_id": "D003866",
"db_name": "MESH"
}
],
"offsets": [
[
142,
152
]
],
"text": [
"depression"
],
"type": "Disease"
},
{
"id": "32",
"normalized": [
{
"db_id": "D001919",
"db_name": "MESH"
}
],
"offsets": [
[
331,
347
]
],
"text": [
"bradyarrhythmias"
],
"type": "Disease"
}
] | Lidocaine-induced cardiac asystole. | Intravenous administration of a single 50-mg bolus of lidocaine in a 67-year-old man resulted in profound depression of the activity of the sinoatrial and atrioventricular nodal pacemakers. The patient had no apparent associated conditions which might have predisposed him to the development of bradyarrhythmias; and, thus, this probably represented a true idiosyncrasy to lidocaine. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"Lidocaine"/ induces disease /"depression"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Lidocaine"/-induced cardiac asystole.
- Abstract: Intravenous administration of a single 50-mg bolus of /"lidocaine"/ in a 67-year-old man resulted in profound /"depression"/ of the activity of the sinoatrial and atrioventricular nodal pacemakers. The patient had no apparent associated conditions which might have predisposed him to the development of bradyarrhythmias; and, thus, this probably represented a true idiosyncrasy to /"lidocaine"/.
Question: Does chemical /"Lidocaine"/ induce disease /"depression"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | /"Lidocaine"/-induced cardiac asystole. | Intravenous administration of a single 50-mg bolus of /"lidocaine"/ in a 67-year-old man resulted in profound /"depression"/ of the activity of the sinoatrial and atrioventricular nodal pacemakers. The patient had no apparent associated conditions which might have predisposed him to the development of bradyarrhythmias; and, thus, this probably represented a true idiosyncrasy to /"lidocaine"/. | Lidocaine | {
"id": "28",
"normalized": [
{
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"db_name": "MESH"
}
],
"offsets": [
[
0,
9
]
],
"text": [
"Lidocaine"
],
"type": "Chemical"
} | depression | {
"id": "31",
"normalized": [
{
"db_id": "D003866",
"db_name": "MESH"
}
],
"offsets": [
[
142,
152
]
],
"text": [
"depression"
],
"type": "Disease"
} | [
{
"id": "28",
"normalized": [
{
"db_id": "D008012",
"db_name": "MESH"
}
],
"offsets": [
[
0,
9
]
],
"text": [
"Lidocaine"
],
"type": "Chemical"
},
{
"id": "30",
"normalized": [
{
"db_id": "D008012",
"db_name": "MESH"
}
],
"offsets": [
[
90,
99
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],
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],
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409,
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"text": [
"lidocaine"
],
"type": "Chemical"
}
] | [
{
"id": "29",
"normalized": [
{
"db_id": "D006323",
"db_name": "MESH"
}
],
"offsets": [
[
18,
34
]
],
"text": [
"cardiac asystole"
],
"type": "Disease"
},
{
"id": "31",
"normalized": [
{
"db_id": "D003866",
"db_name": "MESH"
}
],
"offsets": [
[
142,
152
]
],
"text": [
"depression"
],
"type": "Disease"
},
{
"id": "32",
"normalized": [
{
"db_id": "D001919",
"db_name": "MESH"
}
],
"offsets": [
[
331,
347
]
],
"text": [
"bradyarrhythmias"
],
"type": "Disease"
}
] | Lidocaine-induced cardiac asystole. | Intravenous administration of a single 50-mg bolus of lidocaine in a 67-year-old man resulted in profound depression of the activity of the sinoatrial and atrioventricular nodal pacemakers. The patient had no apparent associated conditions which might have predisposed him to the development of bradyarrhythmias; and, thus, this probably represented a true idiosyncrasy to lidocaine. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"Suxamethonium"/ induces disease /"fasciculations"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Suxamethonium"/ infusion rate and observed /"fasciculations"/. A dose-response study.
- Abstract: /"Suxamethonium chloride"/ (/"Sch"/) was administered i.v. to 36 adult males at six rates: 0.25 mg s-1 to 20 mg s-1. The infusion was discontinued either when there was no muscular response to tetanic stimulation of the ulnar nerve or when /"Sch"/ 120 mg was exceeded. Six additional patients received a 30-mg i.v. bolus dose. /"Fasciculations"/ in six areas of the body were scored from 0 to 3 and summated as a total /"fasciculation"/ score. The times to first /"fasciculation"/, twitch suppression and tetanus suppression were inversely related to the infusion rates. /"Fasciculations"/ in the six areas and the total /"fasciculation"/ score were related directly to the rate of infusion. Total /"fasciculation"/ scores in the 30-mg bolus group and the 5-mg s-1 and 20-mg s-1 infusion groups were not significantly different.
Question: Does chemical /"Suxamethonium"/ induce disease /"fasciculations"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | /"Suxamethonium"/ infusion rate and observed /"fasciculations"/. A dose-response study. | /"Suxamethonium chloride"/ (/"Sch"/) was administered i.v. to 36 adult males at six rates: 0.25 mg s-1 to 20 mg s-1. The infusion was discontinued either when there was no muscular response to tetanic stimulation of the ulnar nerve or when /"Sch"/ 120 mg was exceeded. Six additional patients received a 30-mg i.v. bolus dose. /"Fasciculations"/ in six areas of the body were scored from 0 to 3 and summated as a total /"fasciculation"/ score. The times to first /"fasciculation"/, twitch suppression and tetanus suppression were inversely related to the infusion rates. /"Fasciculations"/ in the six areas and the total /"fasciculation"/ score were related directly to the rate of infusion. Total /"fasciculation"/ scores in the 30-mg bolus group and the 5-mg s-1 and 20-mg s-1 infusion groups were not significantly different. | Suxamethonium | {
"id": "40",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
0,
13
]
],
"text": [
"Suxamethonium"
],
"type": "Chemical"
} | fasciculations | {
"id": "41",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
41,
55
]
],
"text": [
"fasciculations"
],
"type": "Disease"
} | [
{
"id": "40",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
0,
13
]
],
"text": [
"Suxamethonium"
],
"type": "Chemical"
},
{
"id": "42",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
80,
102
]
],
"text": [
"Suxamethonium chloride"
],
"type": "Chemical"
},
{
"id": "43",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
104,
107
]
],
"text": [
"Sch"
],
"type": "Chemical"
},
{
"id": "45",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
312,
315
]
],
"text": [
"Sch"
],
"type": "Chemical"
}
] | [
{
"id": "41",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
41,
55
]
],
"text": [
"fasciculations"
],
"type": "Disease"
},
{
"id": "44",
"normalized": [
{
"db_id": "D013746",
"db_name": "MESH"
}
],
"offsets": [
[
265,
272
]
],
"text": [
"tetanic"
],
"type": "Disease"
},
{
"id": "46",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
395,
409
]
],
"text": [
"Fasciculations"
],
"type": "Disease"
},
{
"id": "47",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
483,
496
]
],
"text": [
"fasciculation"
],
"type": "Disease"
},
{
"id": "48",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
523,
536
]
],
"text": [
"fasciculation"
],
"type": "Disease"
},
{
"id": "49",
"normalized": [
{
"db_id": "D013746",
"db_name": "MESH"
}
],
"offsets": [
[
538,
544
]
],
"text": [
"twitch"
],
"type": "Disease"
},
{
"id": "50",
"normalized": [
{
"db_id": "D013746",
"db_name": "MESH"
}
],
"offsets": [
[
561,
568
]
],
"text": [
"tetanus"
],
"type": "Disease"
},
{
"id": "51",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
627,
641
]
],
"text": [
"Fasciculations"
],
"type": "Disease"
},
{
"id": "52",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
673,
686
]
],
"text": [
"fasciculation"
],
"type": "Disease"
},
{
"id": "53",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
746,
759
]
],
"text": [
"fasciculation"
],
"type": "Disease"
}
] | Suxamethonium infusion rate and observed fasciculations. A dose-response study. | Suxamethonium chloride (Sch) was administered i.v. to 36 adult males at six rates: 0.25 mg s-1 to 20 mg s-1. The infusion was discontinued either when there was no muscular response to tetanic stimulation of the ulnar nerve or when Sch 120 mg was exceeded. Six additional patients received a 30-mg i.v. bolus dose. Fasciculations in six areas of the body were scored from 0 to 3 and summated as a total fasciculation score. The times to first fasciculation, twitch suppression and tetanus suppression were inversely related to the infusion rates. Fasciculations in the six areas and the total fasciculation score were related directly to the rate of infusion. Total fasciculation scores in the 30-mg bolus group and the 5-mg s-1 and 20-mg s-1 infusion groups were not significantly different. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"Suxamethonium"/ induces disease /"tetanic"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Suxamethonium"/ infusion rate and observed fasciculations. A dose-response study.
- Abstract: /"Suxamethonium chloride"/ (/"Sch"/) was administered i.v. to 36 adult males at six rates: 0.25 mg s-1 to 20 mg s-1. The infusion was discontinued either when there was no muscular response to /"tetanic"/ stimulation of the ulnar nerve or when /"Sch"/ 120 mg was exceeded. Six additional patients received a 30-mg i.v. bolus dose. Fasciculations in six areas of the body were scored from 0 to 3 and summated as a total fasciculation score. The times to first fasciculation, /"twitch"/ suppression and /"tetanus"/ suppression were inversely related to the infusion rates. Fasciculations in the six areas and the total fasciculation score were related directly to the rate of infusion. Total fasciculation scores in the 30-mg bolus group and the 5-mg s-1 and 20-mg s-1 infusion groups were not significantly different.
Question: Does chemical /"Suxamethonium"/ induce disease /"tetanic"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | /"Suxamethonium"/ infusion rate and observed fasciculations. A dose-response study. | /"Suxamethonium chloride"/ (/"Sch"/) was administered i.v. to 36 adult males at six rates: 0.25 mg s-1 to 20 mg s-1. The infusion was discontinued either when there was no muscular response to /"tetanic"/ stimulation of the ulnar nerve or when /"Sch"/ 120 mg was exceeded. Six additional patients received a 30-mg i.v. bolus dose. Fasciculations in six areas of the body were scored from 0 to 3 and summated as a total fasciculation score. The times to first fasciculation, /"twitch"/ suppression and /"tetanus"/ suppression were inversely related to the infusion rates. Fasciculations in the six areas and the total fasciculation score were related directly to the rate of infusion. Total fasciculation scores in the 30-mg bolus group and the 5-mg s-1 and 20-mg s-1 infusion groups were not significantly different. | Suxamethonium | {
"id": "40",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
0,
13
]
],
"text": [
"Suxamethonium"
],
"type": "Chemical"
} | tetanic | {
"id": "44",
"normalized": [
{
"db_id": "D013746",
"db_name": "MESH"
}
],
"offsets": [
[
265,
272
]
],
"text": [
"tetanic"
],
"type": "Disease"
} | [
{
"id": "40",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
0,
13
]
],
"text": [
"Suxamethonium"
],
"type": "Chemical"
},
{
"id": "42",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
80,
102
]
],
"text": [
"Suxamethonium chloride"
],
"type": "Chemical"
},
{
"id": "43",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
104,
107
]
],
"text": [
"Sch"
],
"type": "Chemical"
},
{
"id": "45",
"normalized": [
{
"db_id": "D013390",
"db_name": "MESH"
}
],
"offsets": [
[
312,
315
]
],
"text": [
"Sch"
],
"type": "Chemical"
}
] | [
{
"id": "41",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
41,
55
]
],
"text": [
"fasciculations"
],
"type": "Disease"
},
{
"id": "44",
"normalized": [
{
"db_id": "D013746",
"db_name": "MESH"
}
],
"offsets": [
[
265,
272
]
],
"text": [
"tetanic"
],
"type": "Disease"
},
{
"id": "46",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
395,
409
]
],
"text": [
"Fasciculations"
],
"type": "Disease"
},
{
"id": "47",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
483,
496
]
],
"text": [
"fasciculation"
],
"type": "Disease"
},
{
"id": "48",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
523,
536
]
],
"text": [
"fasciculation"
],
"type": "Disease"
},
{
"id": "49",
"normalized": [
{
"db_id": "D013746",
"db_name": "MESH"
}
],
"offsets": [
[
538,
544
]
],
"text": [
"twitch"
],
"type": "Disease"
},
{
"id": "50",
"normalized": [
{
"db_id": "D013746",
"db_name": "MESH"
}
],
"offsets": [
[
561,
568
]
],
"text": [
"tetanus"
],
"type": "Disease"
},
{
"id": "51",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
627,
641
]
],
"text": [
"Fasciculations"
],
"type": "Disease"
},
{
"id": "52",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
673,
686
]
],
"text": [
"fasciculation"
],
"type": "Disease"
},
{
"id": "53",
"normalized": [
{
"db_id": "D005207",
"db_name": "MESH"
}
],
"offsets": [
[
746,
759
]
],
"text": [
"fasciculation"
],
"type": "Disease"
}
] | Suxamethonium infusion rate and observed fasciculations. A dose-response study. | Suxamethonium chloride (Sch) was administered i.v. to 36 adult males at six rates: 0.25 mg s-1 to 20 mg s-1. The infusion was discontinued either when there was no muscular response to tetanic stimulation of the ulnar nerve or when Sch 120 mg was exceeded. Six additional patients received a 30-mg i.v. bolus dose. Fasciculations in six areas of the body were scored from 0 to 3 and summated as a total fasciculation score. The times to first fasciculation, twitch suppression and tetanus suppression were inversely related to the infusion rates. Fasciculations in the six areas and the total fasciculation score were related directly to the rate of infusion. Total fasciculation scores in the 30-mg bolus group and the 5-mg s-1 and 20-mg s-1 infusion groups were not significantly different. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"scopolamine"/ induces disease /"overdosage"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Galanthamine hydrobromide, a longer acting anticholinesterase drug, in the treatment of the central effects of /"scopolamine"/ (/"Hyoscine"/).
- Abstract: Galanthamine hydrobromide, an anticholinesterase drug capable of penetrating the blood-brain barrier, was used in a patient demonstrating central effects of /"scopolamine"/ (/"hyoscine"/) /"overdosage"/. It is longer acting than physostigmine and is used in anaesthesia to reverse the non-depolarizing neuromuscular block. However, studies into the dose necessary to combating /"scopolamine"/ intoxication are indicated.
Question: Does chemical /"scopolamine"/ induce disease /"overdosage"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Galanthamine hydrobromide, a longer acting anticholinesterase drug, in the treatment of the central effects of /"scopolamine"/ (/"Hyoscine"/). | Galanthamine hydrobromide, an anticholinesterase drug capable of penetrating the blood-brain barrier, was used in a patient demonstrating central effects of /"scopolamine"/ (/"hyoscine"/) /"overdosage"/. It is longer acting than physostigmine and is used in anaesthesia to reverse the non-depolarizing neuromuscular block. However, studies into the dose necessary to combating /"scopolamine"/ intoxication are indicated. | scopolamine | {
"id": "86",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
111,
122
]
],
"text": [
"scopolamine"
],
"type": "Chemical"
} | overdosage | {
"id": "91",
"normalized": [
{
"db_id": "D062787",
"db_name": "MESH"
}
],
"offsets": [
[
315,
325
]
],
"text": [
"overdosage"
],
"type": "Disease"
} | [
{
"id": "85",
"normalized": [
{
"db_id": "D005702",
"db_name": "MESH"
}
],
"offsets": [
[
0,
25
]
],
"text": [
"Galanthamine hydrobromide"
],
"type": "Chemical"
},
{
"id": "86",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
111,
122
]
],
"text": [
"scopolamine"
],
"type": "Chemical"
},
{
"id": "87",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
124,
132
]
],
"text": [
"Hyoscine"
],
"type": "Chemical"
},
{
"id": "88",
"normalized": [
{
"db_id": "D005702",
"db_name": "MESH"
}
],
"offsets": [
[
135,
160
]
],
"text": [
"Galanthamine hydrobromide"
],
"type": "Chemical"
},
{
"id": "89",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
292,
303
]
],
"text": [
"scopolamine"
],
"type": "Chemical"
},
{
"id": "90",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
305,
313
]
],
"text": [
"hyoscine"
],
"type": "Chemical"
},
{
"id": "92",
"normalized": [
{
"db_id": "D010830",
"db_name": "MESH"
}
],
"offsets": [
[
352,
365
]
],
"text": [
"physostigmine"
],
"type": "Chemical"
},
{
"id": "93",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
500,
511
]
],
"text": [
"scopolamine"
],
"type": "Chemical"
}
] | [
{
"id": "91",
"normalized": [
{
"db_id": "D062787",
"db_name": "MESH"
}
],
"offsets": [
[
315,
325
]
],
"text": [
"overdosage"
],
"type": "Disease"
}
] | Galanthamine hydrobromide, a longer acting anticholinesterase drug, in the treatment of the central effects of scopolamine (Hyoscine). | Galanthamine hydrobromide, an anticholinesterase drug capable of penetrating the blood-brain barrier, was used in a patient demonstrating central effects of scopolamine (hyoscine) overdosage. It is longer acting than physostigmine and is used in anaesthesia to reverse the non-depolarizing neuromuscular block. However, studies into the dose necessary to combating scopolamine intoxication are indicated. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"physostigmine"/ induces disease /"overdosage"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Galanthamine hydrobromide, a longer acting anticholinesterase drug, in the treatment of the central effects of scopolamine (Hyoscine).
- Abstract: Galanthamine hydrobromide, an anticholinesterase drug capable of penetrating the blood-brain barrier, was used in a patient demonstrating central effects of scopolamine (hyoscine) /"overdosage"/. It is longer acting than /"physostigmine"/ and is used in anaesthesia to reverse the non-depolarizing neuromuscular block. However, studies into the dose necessary to combating scopolamine intoxication are indicated.
Question: Does chemical /"physostigmine"/ induce disease /"overdosage"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Galanthamine hydrobromide, a longer acting anticholinesterase drug, in the treatment of the central effects of scopolamine (Hyoscine). | Galanthamine hydrobromide, an anticholinesterase drug capable of penetrating the blood-brain barrier, was used in a patient demonstrating central effects of scopolamine (hyoscine) /"overdosage"/. It is longer acting than /"physostigmine"/ and is used in anaesthesia to reverse the non-depolarizing neuromuscular block. However, studies into the dose necessary to combating scopolamine intoxication are indicated. | physostigmine | {
"id": "92",
"normalized": [
{
"db_id": "D010830",
"db_name": "MESH"
}
],
"offsets": [
[
352,
365
]
],
"text": [
"physostigmine"
],
"type": "Chemical"
} | overdosage | {
"id": "91",
"normalized": [
{
"db_id": "D062787",
"db_name": "MESH"
}
],
"offsets": [
[
315,
325
]
],
"text": [
"overdosage"
],
"type": "Disease"
} | [
{
"id": "85",
"normalized": [
{
"db_id": "D005702",
"db_name": "MESH"
}
],
"offsets": [
[
0,
25
]
],
"text": [
"Galanthamine hydrobromide"
],
"type": "Chemical"
},
{
"id": "86",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
111,
122
]
],
"text": [
"scopolamine"
],
"type": "Chemical"
},
{
"id": "87",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
124,
132
]
],
"text": [
"Hyoscine"
],
"type": "Chemical"
},
{
"id": "88",
"normalized": [
{
"db_id": "D005702",
"db_name": "MESH"
}
],
"offsets": [
[
135,
160
]
],
"text": [
"Galanthamine hydrobromide"
],
"type": "Chemical"
},
{
"id": "89",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
292,
303
]
],
"text": [
"scopolamine"
],
"type": "Chemical"
},
{
"id": "90",
"normalized": [
{
"db_id": "D012601",
"db_name": "MESH"
}
],
"offsets": [
[
305,
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] | Galanthamine hydrobromide, a longer acting anticholinesterase drug, in the treatment of the central effects of scopolamine (Hyoscine). | Galanthamine hydrobromide, an anticholinesterase drug capable of penetrating the blood-brain barrier, was used in a patient demonstrating central effects of scopolamine (hyoscine) overdosage. It is longer acting than physostigmine and is used in anaesthesia to reverse the non-depolarizing neuromuscular block. However, studies into the dose necessary to combating scopolamine intoxication are indicated. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"lithium"/ induces disease /"hypertension"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Effects of uninephrectomy and high protein feeding on /"lithium"/-induced chronic renal failure in rats.
- Abstract: Rats with /"lithium"/-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a /"lithium"/-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-/"lithium"/ pretreated groups were generated. When comparing all /"lithium"/ treated versus non-/"lithium"/-treated groups, /"lithium"/ caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or /"lithium"/ clearance. Consequently, /"lithium"/ pretreatment caused a fall in filtration fraction and an increase in fractional /"Li"/ excretion. /"Lithium"/ also caused proteinuria and systolic /"hypertension"/ in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in /"lithium"/ pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in /"Li"/-pretreated rats. The results indicate that /"Li"/-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic /"hypertension"/. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Question: Does chemical /"lithium"/ induce disease /"hypertension"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Effects of uninephrectomy and high protein feeding on /"lithium"/-induced chronic renal failure in rats. | Rats with /"lithium"/-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a /"lithium"/-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-/"lithium"/ pretreated groups were generated. When comparing all /"lithium"/ treated versus non-/"lithium"/-treated groups, /"lithium"/ caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or /"lithium"/ clearance. Consequently, /"lithium"/ pretreatment caused a fall in filtration fraction and an increase in fractional /"Li"/ excretion. /"Lithium"/ also caused proteinuria and systolic /"hypertension"/ in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in /"lithium"/ pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in /"Li"/-pretreated rats. The results indicate that /"Li"/-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic /"hypertension"/. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) | lithium | {
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] | Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats. | Rats with lithium-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"lithium"/ induces disease /"proteinuria"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Effects of uninephrectomy and high protein feeding on /"lithium"/-induced chronic renal failure in rats.
- Abstract: Rats with /"lithium"/-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a /"lithium"/-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-/"lithium"/ pretreated groups were generated. When comparing all /"lithium"/ treated versus non-/"lithium"/-treated groups, /"lithium"/ caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or /"lithium"/ clearance. Consequently, /"lithium"/ pretreatment caused a fall in filtration fraction and an increase in fractional /"Li"/ excretion. /"Lithium"/ also caused /"proteinuria"/ and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in /"lithium"/ pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in /"Li"/-pretreated rats. The results indicate that /"Li"/-induced nephropathy, even when the GFR is only modestly reduced, is associated with /"proteinuria"/ and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Question: Does chemical /"lithium"/ induce disease /"proteinuria"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Effects of uninephrectomy and high protein feeding on /"lithium"/-induced chronic renal failure in rats. | Rats with /"lithium"/-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a /"lithium"/-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-/"lithium"/ pretreated groups were generated. When comparing all /"lithium"/ treated versus non-/"lithium"/-treated groups, /"lithium"/ caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or /"lithium"/ clearance. Consequently, /"lithium"/ pretreatment caused a fall in filtration fraction and an increase in fractional /"Li"/ excretion. /"Lithium"/ also caused /"proteinuria"/ and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in /"lithium"/ pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in /"Li"/-pretreated rats. The results indicate that /"Li"/-induced nephropathy, even when the GFR is only modestly reduced, is associated with /"proteinuria"/ and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) | lithium | {
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] | Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats. | Rats with lithium-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"lithium"/ induces disease /"chronic renal failure"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Effects of uninephrectomy and high protein feeding on /"lithium"/-induced /"chronic renal failure"/ in rats.
- Abstract: Rats with /"lithium"/-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a /"lithium"/-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-/"lithium"/ pretreated groups were generated. When comparing all /"lithium"/ treated versus non-/"lithium"/-treated groups, /"lithium"/ caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or /"lithium"/ clearance. Consequently, /"lithium"/ pretreatment caused a fall in filtration fraction and an increase in fractional /"Li"/ excretion. /"Lithium"/ also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in /"lithium"/ pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in /"Li"/-pretreated rats. The results indicate that /"Li"/-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of /"chronic renal failure"/ the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Question: Does chemical /"lithium"/ induce disease /"chronic renal failure"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Effects of uninephrectomy and high protein feeding on /"lithium"/-induced /"chronic renal failure"/ in rats. | Rats with /"lithium"/-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a /"lithium"/-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-/"lithium"/ pretreated groups were generated. When comparing all /"lithium"/ treated versus non-/"lithium"/-treated groups, /"lithium"/ caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or /"lithium"/ clearance. Consequently, /"lithium"/ pretreatment caused a fall in filtration fraction and an increase in fractional /"Li"/ excretion. /"Lithium"/ also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in /"lithium"/ pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in /"Li"/-pretreated rats. The results indicate that /"Li"/-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of /"chronic renal failure"/ the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) | lithium | {
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] | Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats. | Rats with lithium-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"lithium"/ induces disease /"glomerulosclerosis"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Effects of uninephrectomy and high protein feeding on /"lithium"/-induced chronic renal failure in rats.
- Abstract: Rats with /"lithium"/-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a /"lithium"/-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-/"lithium"/ pretreated groups were generated. When comparing all /"lithium"/ treated versus non-/"lithium"/-treated groups, /"lithium"/ caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or /"lithium"/ clearance. Consequently, /"lithium"/ pretreatment caused a fall in filtration fraction and an increase in fractional /"Li"/ excretion. /"Lithium"/ also caused proteinuria and systolic hypertension in absence of /"glomerulosclerosis"/. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in /"lithium"/ pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in /"Li"/-pretreated rats. The results indicate that /"Li"/-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Question: Does chemical /"lithium"/ induce disease /"glomerulosclerosis"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Effects of uninephrectomy and high protein feeding on /"lithium"/-induced chronic renal failure in rats. | Rats with /"lithium"/-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a /"lithium"/-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-/"lithium"/ pretreated groups were generated. When comparing all /"lithium"/ treated versus non-/"lithium"/-treated groups, /"lithium"/ caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or /"lithium"/ clearance. Consequently, /"lithium"/ pretreatment caused a fall in filtration fraction and an increase in fractional /"Li"/ excretion. /"Lithium"/ also caused proteinuria and systolic hypertension in absence of /"glomerulosclerosis"/. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in /"lithium"/ pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in /"Li"/-pretreated rats. The results indicate that /"Li"/-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) | lithium | {
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] | Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats. | Rats with lithium-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"creatinine"/ induces disease /"renal failure"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats.
- Abstract: Rats with lithium-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of /"renal failure"/. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of /"renal failure"/ and in fact tended to increase GFR and decrease plasma /"creatinine"/ levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Question: Does chemical /"creatinine"/ induce disease /"renal failure"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats. | Rats with lithium-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of /"renal failure"/. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of /"renal failure"/ and in fact tended to increase GFR and decrease plasma /"creatinine"/ levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) | creatinine | {
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] | Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats. | Rats with lithium-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"creatinine"/ induces disease /"nephropathy"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats.
- Abstract: Rats with lithium-induced /"nephropathy"/ were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma /"creatinine"/ levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced /"nephropathy"/, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
Question: Does chemical /"creatinine"/ induce disease /"nephropathy"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats. | Rats with lithium-induced /"nephropathy"/ were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma /"creatinine"/ levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced /"nephropathy"/, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) | creatinine | {
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"nephropathy"
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"proteinuria"
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"hypertension"
],
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{
"db_id": "D007676",
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}
],
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],
"text": [
"chronic renal failure"
],
"type": "Disease"
}
] | Effects of uninephrectomy and high protein feeding on lithium-induced chronic renal failure in rats. | Rats with lithium-induced nephropathy were subjected to high protein (HP) feeding, uninephrectomy (NX) or a combination of these, in an attempt to induce glomerular hyperfiltration and further progression of renal failure. Newborn female Wistar rats were fed a lithium-containing diet (50 mmol/kg) for 8 weeks and then randomized to normal diet, HP diet (40 vs. 19%), NX or HP+NX for another 8 weeks. Corresponding non-lithium pretreated groups were generated. When comparing all lithium treated versus non-lithium-treated groups, lithium caused a reduction in glomerular filtration rate (GFR) without significant changes in effective renal plasma flow (as determined by a marker secreted into the proximal tubules) or lithium clearance. Consequently, lithium pretreatment caused a fall in filtration fraction and an increase in fractional Li excretion. Lithium also caused proteinuria and systolic hypertension in absence of glomerulosclerosis. HP failed to accentuante progression of renal failure and in fact tended to increase GFR and decrease plasma creatinine levels in lithium pretreated rats. NX caused an additive deterioration in GFR which, however, was ameliorated by HP. NX+HP caused a further rise in blood pressure in Li-pretreated rats. The results indicate that Li-induced nephropathy, even when the GFR is only modestly reduced, is associated with proteinuria and arterial systolic hypertension. In this model of chronic renal failure the decline in GFR is not accompanied by a corresponding fall in effective renal plasma flow, which may be the functional expression of the formation of nonfiltrating atubular glomeruli. The fractional reabsorption of tubular fluid by the proximal tubules is reduced, leaving the distal delivery unchanged.(ABSTRACT TRUNCATED AT 250 WORDS) |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"fusidic acid"/ induces disease /"nausea"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Treatment of Crohn's disease with /"fusidic acid"/: an antibiotic with immunosuppressive properties similar to cyclosporin.
- Abstract: Fusidic acid is an antibiotic with T-cell specific immunosuppressive effects similar to those of cyclosporin. Because of the need for the development of new treatments for Crohn's disease, a pilot study was undertaken to estimate the pharmacodynamics and tolerability of /"fusidic acid"/ treatment in chronic active, therapy-resistant patients. Eight Crohn's disease patients were included. /"Fusidic acid"/ was administered orally in a dose of 500 mg t.d.s. and the treatment was planned to last 8 weeks. The disease activity was primarily measured by a modified individual grading score. Five of 8 patients (63%) improved during /"fusidic acid"/ treatment: 3 at two weeks and 2 after four weeks. There were no serious clinical side effects, but dose reduction was required in two patients because of /"nausea"/. Biochemically, an increase in alkaline phosphatases was noted in 5 of 8 cases (63%), and the greatest increases were seen in those who had elevated levels prior to treatment. All reversed to pre-treatment levels after cessation of treatment. The results of this pilot study suggest that /"fusidic acid"/ may be of benefit in selected chronic active Crohn's disease patients in whom conventional treatment is ineffective. Because there seems to exist a scientific rationale for the use of /"fusidic acid"/ at the cytokine level in inflammatory bowel disease, we suggest that the role of this treatment should be further investigated.
Question: Does chemical /"fusidic acid"/ induce disease /"nausea"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Treatment of Crohn's disease with /"fusidic acid"/: an antibiotic with immunosuppressive properties similar to cyclosporin. | Fusidic acid is an antibiotic with T-cell specific immunosuppressive effects similar to those of cyclosporin. Because of the need for the development of new treatments for Crohn's disease, a pilot study was undertaken to estimate the pharmacodynamics and tolerability of /"fusidic acid"/ treatment in chronic active, therapy-resistant patients. Eight Crohn's disease patients were included. /"Fusidic acid"/ was administered orally in a dose of 500 mg t.d.s. and the treatment was planned to last 8 weeks. The disease activity was primarily measured by a modified individual grading score. Five of 8 patients (63%) improved during /"fusidic acid"/ treatment: 3 at two weeks and 2 after four weeks. There were no serious clinical side effects, but dose reduction was required in two patients because of /"nausea"/. Biochemically, an increase in alkaline phosphatases was noted in 5 of 8 cases (63%), and the greatest increases were seen in those who had elevated levels prior to treatment. All reversed to pre-treatment levels after cessation of treatment. The results of this pilot study suggest that /"fusidic acid"/ may be of benefit in selected chronic active Crohn's disease patients in whom conventional treatment is ineffective. Because there seems to exist a scientific rationale for the use of /"fusidic acid"/ at the cytokine level in inflammatory bowel disease, we suggest that the role of this treatment should be further investigated. | fusidic acid | {
"id": "216",
"normalized": [
{
"db_id": "D005672",
"db_name": "MESH"
}
],
"offsets": [
[
34,
46
]
],
"text": [
"fusidic acid"
],
"type": "Chemical"
} | nausea | {
"id": "224",
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{
"db_id": "D009325",
"db_name": "MESH"
}
],
"offsets": [
[
910,
916
]
],
"text": [
"nausea"
],
"type": "Disease"
} | [
{
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{
"db_id": "D005672",
"db_name": "MESH"
}
],
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[
34,
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]
],
"text": [
"fusidic acid"
],
"type": "Chemical"
},
{
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{
"db_id": "D016572",
"db_name": "MESH"
}
],
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[
107,
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]
],
"text": [
"cyclosporin"
],
"type": "Chemical"
},
{
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{
"db_id": "D016572",
"db_name": "MESH"
}
],
"offsets": [
[
217,
228
]
],
"text": [
"cyclosporin"
],
"type": "Chemical"
},
{
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{
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}
],
"offsets": [
[
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"text": [
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"text": [
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"text": [
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] | [
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{
"db_id": "D003424",
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}
],
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[
13,
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],
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],
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{
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],
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"text": [
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{
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}
],
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"text": [
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}
] | Treatment of Crohn's disease with fusidic acid: an antibiotic with immunosuppressive properties similar to cyclosporin. | Fusidic acid is an antibiotic with T-cell specific immunosuppressive effects similar to those of cyclosporin. Because of the need for the development of new treatments for Crohn's disease, a pilot study was undertaken to estimate the pharmacodynamics and tolerability of fusidic acid treatment in chronic active, therapy-resistant patients. Eight Crohn's disease patients were included. Fusidic acid was administered orally in a dose of 500 mg t.d.s. and the treatment was planned to last 8 weeks. The disease activity was primarily measured by a modified individual grading score. Five of 8 patients (63%) improved during fusidic acid treatment: 3 at two weeks and 2 after four weeks. There were no serious clinical side effects, but dose reduction was required in two patients because of nausea. Biochemically, an increase in alkaline phosphatases was noted in 5 of 8 cases (63%), and the greatest increases were seen in those who had elevated levels prior to treatment. All reversed to pre-treatment levels after cessation of treatment. The results of this pilot study suggest that fusidic acid may be of benefit in selected chronic active Crohn's disease patients in whom conventional treatment is ineffective. Because there seems to exist a scientific rationale for the use of fusidic acid at the cytokine level in inflammatory bowel disease, we suggest that the role of this treatment should be further investigated. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"fusidic acid"/ induces disease /"inflammatory bowel disease"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Treatment of Crohn's disease with /"fusidic acid"/: an antibiotic with immunosuppressive properties similar to cyclosporin.
- Abstract: Fusidic acid is an antibiotic with T-cell specific immunosuppressive effects similar to those of cyclosporin. Because of the need for the development of new treatments for Crohn's disease, a pilot study was undertaken to estimate the pharmacodynamics and tolerability of /"fusidic acid"/ treatment in chronic active, therapy-resistant patients. Eight Crohn's disease patients were included. /"Fusidic acid"/ was administered orally in a dose of 500 mg t.d.s. and the treatment was planned to last 8 weeks. The disease activity was primarily measured by a modified individual grading score. Five of 8 patients (63%) improved during /"fusidic acid"/ treatment: 3 at two weeks and 2 after four weeks. There were no serious clinical side effects, but dose reduction was required in two patients because of nausea. Biochemically, an increase in alkaline phosphatases was noted in 5 of 8 cases (63%), and the greatest increases were seen in those who had elevated levels prior to treatment. All reversed to pre-treatment levels after cessation of treatment. The results of this pilot study suggest that /"fusidic acid"/ may be of benefit in selected chronic active Crohn's disease patients in whom conventional treatment is ineffective. Because there seems to exist a scientific rationale for the use of /"fusidic acid"/ at the cytokine level in /"inflammatory bowel disease"/, we suggest that the role of this treatment should be further investigated.
Question: Does chemical /"fusidic acid"/ induce disease /"inflammatory bowel disease"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Treatment of Crohn's disease with /"fusidic acid"/: an antibiotic with immunosuppressive properties similar to cyclosporin. | Fusidic acid is an antibiotic with T-cell specific immunosuppressive effects similar to those of cyclosporin. Because of the need for the development of new treatments for Crohn's disease, a pilot study was undertaken to estimate the pharmacodynamics and tolerability of /"fusidic acid"/ treatment in chronic active, therapy-resistant patients. Eight Crohn's disease patients were included. /"Fusidic acid"/ was administered orally in a dose of 500 mg t.d.s. and the treatment was planned to last 8 weeks. The disease activity was primarily measured by a modified individual grading score. Five of 8 patients (63%) improved during /"fusidic acid"/ treatment: 3 at two weeks and 2 after four weeks. There were no serious clinical side effects, but dose reduction was required in two patients because of nausea. Biochemically, an increase in alkaline phosphatases was noted in 5 of 8 cases (63%), and the greatest increases were seen in those who had elevated levels prior to treatment. All reversed to pre-treatment levels after cessation of treatment. The results of this pilot study suggest that /"fusidic acid"/ may be of benefit in selected chronic active Crohn's disease patients in whom conventional treatment is ineffective. Because there seems to exist a scientific rationale for the use of /"fusidic acid"/ at the cytokine level in /"inflammatory bowel disease"/, we suggest that the role of this treatment should be further investigated. | fusidic acid | {
"id": "216",
"normalized": [
{
"db_id": "D005672",
"db_name": "MESH"
}
],
"offsets": [
[
34,
46
]
],
"text": [
"fusidic acid"
],
"type": "Chemical"
} | inflammatory bowel disease | {
"id": "228",
"normalized": [
{
"db_id": "D015212",
"db_name": "MESH"
}
],
"offsets": [
[
1440,
1466
]
],
"text": [
"inflammatory bowel disease"
],
"type": "Disease"
} | [
{
"id": "216",
"normalized": [
{
"db_id": "D005672",
"db_name": "MESH"
}
],
"offsets": [
[
34,
46
]
],
"text": [
"fusidic acid"
],
"type": "Chemical"
},
{
"id": "217",
"normalized": [
{
"db_id": "D016572",
"db_name": "MESH"
}
],
"offsets": [
[
107,
118
]
],
"text": [
"cyclosporin"
],
"type": "Chemical"
},
{
"id": "218",
"normalized": [
{
"db_id": "D016572",
"db_name": "MESH"
}
],
"offsets": [
[
217,
228
]
],
"text": [
"cyclosporin"
],
"type": "Chemical"
},
{
"id": "220",
"normalized": [
{
"db_id": "D005672",
"db_name": "MESH"
}
],
"offsets": [
[
391,
403
]
],
"text": [
"fusidic acid"
],
"type": "Chemical"
},
{
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{
"db_id": "D005672",
"db_name": "MESH"
}
],
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[
507,
519
]
],
"text": [
"Fusidic acid"
],
"type": "Chemical"
},
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{
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],
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"fusidic acid"
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"type": "Chemical"
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{
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}
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"fusidic acid"
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{
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}
],
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[
1402,
1414
]
],
"text": [
"fusidic acid"
],
"type": "Chemical"
}
] | [
{
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{
"db_id": "D003424",
"db_name": "MESH"
}
],
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[
13,
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]
],
"text": [
"Crohn's disease"
],
"type": "Disease"
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{
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}
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292,
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"text": [
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{
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{
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}
],
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[
910,
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]
],
"text": [
"nausea"
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"type": "Disease"
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{
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"db_name": "MESH"
}
],
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[
1263,
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]
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"text": [
"Crohn's disease"
],
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{
"db_id": "D015212",
"db_name": "MESH"
}
],
"offsets": [
[
1440,
1466
]
],
"text": [
"inflammatory bowel disease"
],
"type": "Disease"
}
] | Treatment of Crohn's disease with fusidic acid: an antibiotic with immunosuppressive properties similar to cyclosporin. | Fusidic acid is an antibiotic with T-cell specific immunosuppressive effects similar to those of cyclosporin. Because of the need for the development of new treatments for Crohn's disease, a pilot study was undertaken to estimate the pharmacodynamics and tolerability of fusidic acid treatment in chronic active, therapy-resistant patients. Eight Crohn's disease patients were included. Fusidic acid was administered orally in a dose of 500 mg t.d.s. and the treatment was planned to last 8 weeks. The disease activity was primarily measured by a modified individual grading score. Five of 8 patients (63%) improved during fusidic acid treatment: 3 at two weeks and 2 after four weeks. There were no serious clinical side effects, but dose reduction was required in two patients because of nausea. Biochemically, an increase in alkaline phosphatases was noted in 5 of 8 cases (63%), and the greatest increases were seen in those who had elevated levels prior to treatment. All reversed to pre-treatment levels after cessation of treatment. The results of this pilot study suggest that fusidic acid may be of benefit in selected chronic active Crohn's disease patients in whom conventional treatment is ineffective. Because there seems to exist a scientific rationale for the use of fusidic acid at the cytokine level in inflammatory bowel disease, we suggest that the role of this treatment should be further investigated. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"cocaine"/ induces disease /"myocardial infarction"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized /"cocaine"/ abusers.
- Abstract: The electrocardiograms (ECG) of 99 /"cocaine"/-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the /"cocaine"/ abusers and none of the controls had ECG evidence of significant myocardial injury defined as /"myocardial infarction"/, ischemia, and bundle branch block.
Question: Does chemical /"cocaine"/ induce disease /"myocardial infarction"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized /"cocaine"/ abusers. | The electrocardiograms (ECG) of 99 /"cocaine"/-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the /"cocaine"/ abusers and none of the controls had ECG evidence of significant myocardial injury defined as /"myocardial infarction"/, ischemia, and bundle branch block. | cocaine | {
"id": "239",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
83,
90
]
],
"text": [
"cocaine"
],
"type": "Chemical"
} | myocardial infarction | {
"id": "244",
"normalized": [
{
"db_id": "D009203",
"db_name": "MESH"
}
],
"offsets": [
[
334,
355
]
],
"text": [
"myocardial infarction"
],
"type": "Disease"
} | [
{
"id": "239",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
83,
90
]
],
"text": [
"cocaine"
],
"type": "Chemical"
},
{
"id": "240",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
135,
142
]
],
"text": [
"cocaine"
],
"type": "Chemical"
},
{
"id": "242",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
232,
239
]
],
"text": [
"cocaine"
],
"type": "Chemical"
}
] | [
{
"id": "238",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
33,
50
]
],
"text": [
"myocardial injury"
],
"type": "Disease"
},
{
"id": "241",
"normalized": [
{
"db_id": "D012559",
"db_name": "MESH"
}
],
"offsets": [
[
194,
207
]
],
"text": [
"schizophrenic"
],
"type": "Disease"
},
{
"id": "243",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
305,
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]
],
"text": [
"myocardial injury"
],
"type": "Disease"
},
{
"id": "244",
"normalized": [
{
"db_id": "D009203",
"db_name": "MESH"
}
],
"offsets": [
[
334,
355
]
],
"text": [
"myocardial infarction"
],
"type": "Disease"
},
{
"id": "245",
"normalized": [
{
"db_id": "D007511",
"db_name": "MESH"
}
],
"offsets": [
[
357,
365
]
],
"text": [
"ischemia"
],
"type": "Disease"
},
{
"id": "246",
"normalized": [
{
"db_id": "D002037",
"db_name": "MESH"
}
],
"offsets": [
[
371,
390
]
],
"text": [
"bundle branch block"
],
"type": "Disease"
}
] | Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized cocaine abusers. | The electrocardiograms (ECG) of 99 cocaine-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the cocaine abusers and none of the controls had ECG evidence of significant myocardial injury defined as myocardial infarction, ischemia, and bundle branch block. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"cocaine"/ induces disease /"bundle branch block"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized /"cocaine"/ abusers.
- Abstract: The electrocardiograms (ECG) of 99 /"cocaine"/-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the /"cocaine"/ abusers and none of the controls had ECG evidence of significant myocardial injury defined as myocardial infarction, ischemia, and /"bundle branch block"/.
Question: Does chemical /"cocaine"/ induce disease /"bundle branch block"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized /"cocaine"/ abusers. | The electrocardiograms (ECG) of 99 /"cocaine"/-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the /"cocaine"/ abusers and none of the controls had ECG evidence of significant myocardial injury defined as myocardial infarction, ischemia, and /"bundle branch block"/. | cocaine | {
"id": "239",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
83,
90
]
],
"text": [
"cocaine"
],
"type": "Chemical"
} | bundle branch block | {
"id": "246",
"normalized": [
{
"db_id": "D002037",
"db_name": "MESH"
}
],
"offsets": [
[
371,
390
]
],
"text": [
"bundle branch block"
],
"type": "Disease"
} | [
{
"id": "239",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
83,
90
]
],
"text": [
"cocaine"
],
"type": "Chemical"
},
{
"id": "240",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
135,
142
]
],
"text": [
"cocaine"
],
"type": "Chemical"
},
{
"id": "242",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
232,
239
]
],
"text": [
"cocaine"
],
"type": "Chemical"
}
] | [
{
"id": "238",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
33,
50
]
],
"text": [
"myocardial injury"
],
"type": "Disease"
},
{
"id": "241",
"normalized": [
{
"db_id": "D012559",
"db_name": "MESH"
}
],
"offsets": [
[
194,
207
]
],
"text": [
"schizophrenic"
],
"type": "Disease"
},
{
"id": "243",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
305,
322
]
],
"text": [
"myocardial injury"
],
"type": "Disease"
},
{
"id": "244",
"normalized": [
{
"db_id": "D009203",
"db_name": "MESH"
}
],
"offsets": [
[
334,
355
]
],
"text": [
"myocardial infarction"
],
"type": "Disease"
},
{
"id": "245",
"normalized": [
{
"db_id": "D007511",
"db_name": "MESH"
}
],
"offsets": [
[
357,
365
]
],
"text": [
"ischemia"
],
"type": "Disease"
},
{
"id": "246",
"normalized": [
{
"db_id": "D002037",
"db_name": "MESH"
}
],
"offsets": [
[
371,
390
]
],
"text": [
"bundle branch block"
],
"type": "Disease"
}
] | Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized cocaine abusers. | The electrocardiograms (ECG) of 99 cocaine-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the cocaine abusers and none of the controls had ECG evidence of significant myocardial injury defined as myocardial infarction, ischemia, and bundle branch block. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"cocaine"/ induces disease /"ischemia"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized /"cocaine"/ abusers.
- Abstract: The electrocardiograms (ECG) of 99 /"cocaine"/-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the /"cocaine"/ abusers and none of the controls had ECG evidence of significant myocardial injury defined as myocardial infarction, /"ischemia"/, and bundle branch block.
Question: Does chemical /"cocaine"/ induce disease /"ischemia"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized /"cocaine"/ abusers. | The electrocardiograms (ECG) of 99 /"cocaine"/-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the /"cocaine"/ abusers and none of the controls had ECG evidence of significant myocardial injury defined as myocardial infarction, /"ischemia"/, and bundle branch block. | cocaine | {
"id": "239",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
83,
90
]
],
"text": [
"cocaine"
],
"type": "Chemical"
} | ischemia | {
"id": "245",
"normalized": [
{
"db_id": "D007511",
"db_name": "MESH"
}
],
"offsets": [
[
357,
365
]
],
"text": [
"ischemia"
],
"type": "Disease"
} | [
{
"id": "239",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
83,
90
]
],
"text": [
"cocaine"
],
"type": "Chemical"
},
{
"id": "240",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
135,
142
]
],
"text": [
"cocaine"
],
"type": "Chemical"
},
{
"id": "242",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
232,
239
]
],
"text": [
"cocaine"
],
"type": "Chemical"
}
] | [
{
"id": "238",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
33,
50
]
],
"text": [
"myocardial injury"
],
"type": "Disease"
},
{
"id": "241",
"normalized": [
{
"db_id": "D012559",
"db_name": "MESH"
}
],
"offsets": [
[
194,
207
]
],
"text": [
"schizophrenic"
],
"type": "Disease"
},
{
"id": "243",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
305,
322
]
],
"text": [
"myocardial injury"
],
"type": "Disease"
},
{
"id": "244",
"normalized": [
{
"db_id": "D009203",
"db_name": "MESH"
}
],
"offsets": [
[
334,
355
]
],
"text": [
"myocardial infarction"
],
"type": "Disease"
},
{
"id": "245",
"normalized": [
{
"db_id": "D007511",
"db_name": "MESH"
}
],
"offsets": [
[
357,
365
]
],
"text": [
"ischemia"
],
"type": "Disease"
},
{
"id": "246",
"normalized": [
{
"db_id": "D002037",
"db_name": "MESH"
}
],
"offsets": [
[
371,
390
]
],
"text": [
"bundle branch block"
],
"type": "Disease"
}
] | Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized cocaine abusers. | The electrocardiograms (ECG) of 99 cocaine-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the cocaine abusers and none of the controls had ECG evidence of significant myocardial injury defined as myocardial infarction, ischemia, and bundle branch block. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"cocaine"/ induces disease /"myocardial injury"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Electrocardiographic evidence of /"myocardial injury"/ in psychiatrically hospitalized /"cocaine"/ abusers.
- Abstract: The electrocardiograms (ECG) of 99 /"cocaine"/-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the /"cocaine"/ abusers and none of the controls had ECG evidence of significant /"myocardial injury"/ defined as myocardial infarction, ischemia, and bundle branch block.
Question: Does chemical /"cocaine"/ induce disease /"myocardial injury"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Electrocardiographic evidence of /"myocardial injury"/ in psychiatrically hospitalized /"cocaine"/ abusers. | The electrocardiograms (ECG) of 99 /"cocaine"/-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the /"cocaine"/ abusers and none of the controls had ECG evidence of significant /"myocardial injury"/ defined as myocardial infarction, ischemia, and bundle branch block. | cocaine | {
"id": "239",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
83,
90
]
],
"text": [
"cocaine"
],
"type": "Chemical"
} | myocardial injury | {
"id": "238",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
33,
50
]
],
"text": [
"myocardial injury"
],
"type": "Disease"
} | [
{
"id": "239",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
83,
90
]
],
"text": [
"cocaine"
],
"type": "Chemical"
},
{
"id": "240",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
135,
142
]
],
"text": [
"cocaine"
],
"type": "Chemical"
},
{
"id": "242",
"normalized": [
{
"db_id": "D003042",
"db_name": "MESH"
}
],
"offsets": [
[
232,
239
]
],
"text": [
"cocaine"
],
"type": "Chemical"
}
] | [
{
"id": "238",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
33,
50
]
],
"text": [
"myocardial injury"
],
"type": "Disease"
},
{
"id": "241",
"normalized": [
{
"db_id": "D012559",
"db_name": "MESH"
}
],
"offsets": [
[
194,
207
]
],
"text": [
"schizophrenic"
],
"type": "Disease"
},
{
"id": "243",
"normalized": [
{
"db_id": "D009202",
"db_name": "MESH"
}
],
"offsets": [
[
305,
322
]
],
"text": [
"myocardial injury"
],
"type": "Disease"
},
{
"id": "244",
"normalized": [
{
"db_id": "D009203",
"db_name": "MESH"
}
],
"offsets": [
[
334,
355
]
],
"text": [
"myocardial infarction"
],
"type": "Disease"
},
{
"id": "245",
"normalized": [
{
"db_id": "D007511",
"db_name": "MESH"
}
],
"offsets": [
[
357,
365
]
],
"text": [
"ischemia"
],
"type": "Disease"
},
{
"id": "246",
"normalized": [
{
"db_id": "D002037",
"db_name": "MESH"
}
],
"offsets": [
[
371,
390
]
],
"text": [
"bundle branch block"
],
"type": "Disease"
}
] | Electrocardiographic evidence of myocardial injury in psychiatrically hospitalized cocaine abusers. | The electrocardiograms (ECG) of 99 cocaine-abusing patients were compared with the ECGs of 50 schizophrenic controls. Eleven of the cocaine abusers and none of the controls had ECG evidence of significant myocardial injury defined as myocardial infarction, ischemia, and bundle branch block. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"Sulpiride"/ induces disease /"tardive dystonia"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Sulpiride"/-induced /"tardive dystonia"/.
- Abstract: /"Sulpiride"/ is a selective D2-receptor antagonist with antipsychotic and antidepressant properties. Although initially thought to be free of extrapyramidal side effects, /"sulpiride"/-induced tardive dyskinesia and parkinsonism have been reported occasionally. We studied a 37-year-old man who developed persistent segmental /"dystonia"/ within 2 months after starting /"sulpiride"/ therapy. We could not find any previous reports of /"sulpiride"/-induced /"tardive dystonia"/.
Question: Does chemical /"Sulpiride"/ induce disease /"tardive dystonia"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | /"Sulpiride"/-induced /"tardive dystonia"/. | /"Sulpiride"/ is a selective D2-receptor antagonist with antipsychotic and antidepressant properties. Although initially thought to be free of extrapyramidal side effects, /"sulpiride"/-induced tardive dyskinesia and parkinsonism have been reported occasionally. We studied a 37-year-old man who developed persistent segmental /"dystonia"/ within 2 months after starting /"sulpiride"/ therapy. We could not find any previous reports of /"sulpiride"/-induced /"tardive dystonia"/. | Sulpiride | {
"id": "256",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
0,
9
]
],
"text": [
"Sulpiride"
],
"type": "Chemical"
} | tardive dystonia | {
"id": "257",
"normalized": [
{
"db_id": "D004421",
"db_name": "MESH"
}
],
"offsets": [
[
18,
34
]
],
"text": [
"tardive dystonia"
],
"type": "Disease"
} | [
{
"id": "256",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
0,
9
]
],
"text": [
"Sulpiride"
],
"type": "Chemical"
},
{
"id": "258",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
36,
45
]
],
"text": [
"Sulpiride"
],
"type": "Chemical"
},
{
"id": "259",
"normalized": [
{
"db_id": "D000928",
"db_name": "MESH"
}
],
"offsets": [
[
107,
121
]
],
"text": [
"antidepressant"
],
"type": "Chemical"
},
{
"id": "260",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
204,
213
]
],
"text": [
"sulpiride"
],
"type": "Chemical"
},
{
"id": "264",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
395,
404
]
],
"text": [
"sulpiride"
],
"type": "Chemical"
},
{
"id": "265",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
456,
465
]
],
"text": [
"sulpiride"
],
"type": "Chemical"
}
] | [
{
"id": "257",
"normalized": [
{
"db_id": "D004421",
"db_name": "MESH"
}
],
"offsets": [
[
18,
34
]
],
"text": [
"tardive dystonia"
],
"type": "Disease"
},
{
"id": "261",
"normalized": [
{
"db_id": "D004409",
"db_name": "MESH"
}
],
"offsets": [
[
222,
240
]
],
"text": [
"tardive dyskinesia"
],
"type": "Disease"
},
{
"id": "262",
"normalized": [
{
"db_id": "D010302",
"db_name": "MESH"
}
],
"offsets": [
[
245,
257
]
],
"text": [
"parkinsonism"
],
"type": "Disease"
},
{
"id": "263",
"normalized": [
{
"db_id": "D004421",
"db_name": "MESH"
}
],
"offsets": [
[
355,
363
]
],
"text": [
"dystonia"
],
"type": "Disease"
},
{
"id": "266",
"normalized": [
{
"db_id": "D004421",
"db_name": "MESH"
}
],
"offsets": [
[
474,
490
]
],
"text": [
"tardive dystonia"
],
"type": "Disease"
}
] | Sulpiride-induced tardive dystonia. | Sulpiride is a selective D2-receptor antagonist with antipsychotic and antidepressant properties. Although initially thought to be free of extrapyramidal side effects, sulpiride-induced tardive dyskinesia and parkinsonism have been reported occasionally. We studied a 37-year-old man who developed persistent segmental dystonia within 2 months after starting sulpiride therapy. We could not find any previous reports of sulpiride-induced tardive dystonia. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"Sulpiride"/ induces disease /"parkinsonism"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Sulpiride"/-induced tardive dystonia.
- Abstract: /"Sulpiride"/ is a selective D2-receptor antagonist with antipsychotic and antidepressant properties. Although initially thought to be free of extrapyramidal side effects, /"sulpiride"/-induced tardive dyskinesia and /"parkinsonism"/ have been reported occasionally. We studied a 37-year-old man who developed persistent segmental dystonia within 2 months after starting /"sulpiride"/ therapy. We could not find any previous reports of /"sulpiride"/-induced tardive dystonia.
Question: Does chemical /"Sulpiride"/ induce disease /"parkinsonism"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | /"Sulpiride"/-induced tardive dystonia. | /"Sulpiride"/ is a selective D2-receptor antagonist with antipsychotic and antidepressant properties. Although initially thought to be free of extrapyramidal side effects, /"sulpiride"/-induced tardive dyskinesia and /"parkinsonism"/ have been reported occasionally. We studied a 37-year-old man who developed persistent segmental dystonia within 2 months after starting /"sulpiride"/ therapy. We could not find any previous reports of /"sulpiride"/-induced tardive dystonia. | Sulpiride | {
"id": "256",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
0,
9
]
],
"text": [
"Sulpiride"
],
"type": "Chemical"
} | parkinsonism | {
"id": "262",
"normalized": [
{
"db_id": "D010302",
"db_name": "MESH"
}
],
"offsets": [
[
245,
257
]
],
"text": [
"parkinsonism"
],
"type": "Disease"
} | [
{
"id": "256",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
0,
9
]
],
"text": [
"Sulpiride"
],
"type": "Chemical"
},
{
"id": "258",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
36,
45
]
],
"text": [
"Sulpiride"
],
"type": "Chemical"
},
{
"id": "259",
"normalized": [
{
"db_id": "D000928",
"db_name": "MESH"
}
],
"offsets": [
[
107,
121
]
],
"text": [
"antidepressant"
],
"type": "Chemical"
},
{
"id": "260",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
204,
213
]
],
"text": [
"sulpiride"
],
"type": "Chemical"
},
{
"id": "264",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
395,
404
]
],
"text": [
"sulpiride"
],
"type": "Chemical"
},
{
"id": "265",
"normalized": [
{
"db_id": "D013469",
"db_name": "MESH"
}
],
"offsets": [
[
456,
465
]
],
"text": [
"sulpiride"
],
"type": "Chemical"
}
] | [
{
"id": "257",
"normalized": [
{
"db_id": "D004421",
"db_name": "MESH"
}
],
"offsets": [
[
18,
34
]
],
"text": [
"tardive dystonia"
],
"type": "Disease"
},
{
"id": "261",
"normalized": [
{
"db_id": "D004409",
"db_name": "MESH"
}
],
"offsets": [
[
222,
240
]
],
"text": [
"tardive dyskinesia"
],
"type": "Disease"
},
{
"id": "262",
"normalized": [
{
"db_id": "D010302",
"db_name": "MESH"
}
],
"offsets": [
[
245,
257
]
],
"text": [
"parkinsonism"
],
"type": "Disease"
},
{
"id": "263",
"normalized": [
{
"db_id": "D004421",
"db_name": "MESH"
}
],
"offsets": [
[
355,
363
]
],
"text": [
"dystonia"
],
"type": "Disease"
},
{
"id": "266",
"normalized": [
{
"db_id": "D004421",
"db_name": "MESH"
}
],
"offsets": [
[
474,
490
]
],
"text": [
"tardive dystonia"
],
"type": "Disease"
}
] | Sulpiride-induced tardive dystonia. | Sulpiride is a selective D2-receptor antagonist with antipsychotic and antidepressant properties. Although initially thought to be free of extrapyramidal side effects, sulpiride-induced tardive dyskinesia and parkinsonism have been reported occasionally. We studied a 37-year-old man who developed persistent segmental dystonia within 2 months after starting sulpiride therapy. We could not find any previous reports of sulpiride-induced tardive dystonia. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"desferrioxamine"/ induces disease /"pigmentary retinal deposits"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Ocular and auditory toxicity in hemodialyzed patients receiving /"desferrioxamine"/.
- Abstract: During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and /"pigmentary retinal deposits"/. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible.
Question: Does chemical /"desferrioxamine"/ induce disease /"pigmentary retinal deposits"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Ocular and auditory toxicity in hemodialyzed patients receiving /"desferrioxamine"/. | During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and /"pigmentary retinal deposits"/. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. | desferrioxamine | {
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] | Ocular and auditory toxicity in hemodialyzed patients receiving desferrioxamine. | During an 18-month period of study 41 hemodialyzed patients receiving desferrioxamine (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. Desferrioxamine withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of desferrioxamine or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving desferrioxamine. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"desferrioxamine"/ induces disease /"Ocular and auditory toxicity"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Ocular and auditory toxicity"/ in hemodialyzed patients receiving /"desferrioxamine"/.
- Abstract: During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of /"audiovisual toxicity"/. 6 patients presented clinical symptoms of /"visual or auditory toxicity"/. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that /"audiovisual toxicity"/ is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible.
Question: Does chemical /"desferrioxamine"/ induce disease /"Ocular and auditory toxicity"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | /"Ocular and auditory toxicity"/ in hemodialyzed patients receiving /"desferrioxamine"/. | During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of /"audiovisual toxicity"/. 6 patients presented clinical symptoms of /"visual or auditory toxicity"/. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that /"audiovisual toxicity"/ is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. | desferrioxamine | {
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"text": [
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] | Ocular and auditory toxicity in hemodialyzed patients receiving desferrioxamine. | During an 18-month period of study 41 hemodialyzed patients receiving desferrioxamine (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. Desferrioxamine withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of desferrioxamine or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving desferrioxamine. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"desferrioxamine"/ induces disease /"Ocular"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Ocular"/ and auditory /"Ocular"/ in hemodialyzed patients receiving /"desferrioxamine"/.
- Abstract: During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of /"visual"/ or auditory /"visual"/. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. /"Visual toxicity"/ was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with /"a loss of visual acuity"/ and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible.
Question: Does chemical /"desferrioxamine"/ induce disease /"Ocular"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | /"Ocular"/ and auditory /"Ocular"/ in hemodialyzed patients receiving /"desferrioxamine"/. | During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of /"visual"/ or auditory /"visual"/. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. /"Visual toxicity"/ was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with /"a loss of visual acuity"/ and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. | desferrioxamine | {
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] | Ocular and auditory toxicity in hemodialyzed patients receiving desferrioxamine. | During an 18-month period of study 41 hemodialyzed patients receiving desferrioxamine (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. Desferrioxamine withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of desferrioxamine or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving desferrioxamine. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"desferrioxamine"/ induces disease /"neurosensorial hearing loss"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Ocular and auditory toxicity in hemodialyzed patients receiving /"desferrioxamine"/.
- Abstract: During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency /"neurosensorial hearing loss"/ and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible.
Question: Does chemical /"desferrioxamine"/ induce disease /"neurosensorial hearing loss"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | Ocular and auditory toxicity in hemodialyzed patients receiving /"desferrioxamine"/. | During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency /"neurosensorial hearing loss"/ and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. | desferrioxamine | {
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] | Ocular and auditory toxicity in hemodialyzed patients receiving desferrioxamine. | During an 18-month period of study 41 hemodialyzed patients receiving desferrioxamine (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. Desferrioxamine withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of desferrioxamine or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving desferrioxamine. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"desferrioxamine"/ induces disease /"toxicity"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Ocular and auditory toxicity in hemodialyzed patients receiving /"desferrioxamine"/.
- Abstract: During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This /"toxicity"/ appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible.
Question: Does chemical /"desferrioxamine"/ induce disease /"toxicity"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Ocular and auditory toxicity in hemodialyzed patients receiving /"desferrioxamine"/. | During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This /"toxicity"/ appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. | desferrioxamine | {
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] | Ocular and auditory toxicity in hemodialyzed patients receiving desferrioxamine. | During an 18-month period of study 41 hemodialyzed patients receiving desferrioxamine (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. Desferrioxamine withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of desferrioxamine or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving desferrioxamine. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"desferrioxamine"/ induces disease /"hearing loss"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Ocular and auditory toxicity in hemodialyzed patients receiving /"desferrioxamine"/.
- Abstract: During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of /"hearing loss"/ in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible.
Question: Does chemical /"desferrioxamine"/ induce disease /"hearing loss"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Ocular and auditory toxicity in hemodialyzed patients receiving /"desferrioxamine"/. | During an 18-month period of study 41 hemodialyzed patients receiving /"desferrioxamine"/ (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. /"Desferrioxamine"/ withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of /"hearing loss"/ in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of /"desferrioxamine"/ or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving /"desferrioxamine"/. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. | desferrioxamine | {
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] | Ocular and auditory toxicity in hemodialyzed patients receiving desferrioxamine. | During an 18-month period of study 41 hemodialyzed patients receiving desferrioxamine (10-40 mg/kg BW/3 times weekly) for the first time were monitored for detection of audiovisual toxicity. 6 patients presented clinical symptoms of visual or auditory toxicity. Moreover, detailed ophthalmologic and audiologic studies disclosed abnormalities in 7 more asymptomatic patients. Visual toxicity was of retinal origin and was characterized by a tritan-type dyschromatopsy, sometimes associated with a loss of visual acuity and pigmentary retinal deposits. Auditory toxicity was characterized by a mid- to high-frequency neurosensorial hearing loss and the lesion was of the cochlear type. Desferrioxamine withdrawal resulted in a complete recovery of visual function in 1 patient and partial recovery in 3, and a complete reversal of hearing loss in 3 patients and partial recovery in 3. This toxicity appeared in patients receiving the higher doses of desferrioxamine or coincided with the normalization of ferritin or aluminium serum levels. The data indicate that audiovisual toxicity is not an infrequent complication in hemodialyzed patients receiving desferrioxamine. Periodical audiovisual monitoring should be performed on hemodialyzed patients receiving the drug in order to detect adverse effects as early as possible. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"magnesium"/ induces disease /"Myasthenia gravis"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: /"Myasthenia gravis"/ presenting as weakness after /"magnesium"/ administration.
- Abstract: We studied a patient with no prior history of neuromuscular disease who became virtually quadriplegic after parenteral /"magnesium"/ administration for preeclampsia. The serum /"magnesium"/ concentration was 3.0 mEq/L, which is usually well tolerated. The /"magnesium"/ was stopped and she recovered over a few days. While she was weak, 2-Hz repetitive stimulation revealed a decrement without significant facilitation at rapid rates or after exercise, suggesting postsynaptic neuromuscular blockade. After her strength returned, repetitive stimulation was normal, but single fiber EMG revealed increased jitter and blocking. Her acetylcholine receptor antibody level was markedly elevated. Although paralysis after /"magnesium"/ administration has been described in patients with known /"myasthenia gravis"/, it has not previously been reported to be the initial or only manifestation of the disease. Patients who are unusually sensitive to the neuromuscular effects of /"magnesium"/ should be suspected of having an underlying disorder of neuromuscular transmission.
Question: Does chemical /"magnesium"/ induce disease /"Myasthenia gravis"/ according to this article? Respond with "Yes" or "No" only. [/INST] Yes. </s> | Yes | /"Myasthenia gravis"/ presenting as weakness after /"magnesium"/ administration. | We studied a patient with no prior history of neuromuscular disease who became virtually quadriplegic after parenteral /"magnesium"/ administration for preeclampsia. The serum /"magnesium"/ concentration was 3.0 mEq/L, which is usually well tolerated. The /"magnesium"/ was stopped and she recovered over a few days. While she was weak, 2-Hz repetitive stimulation revealed a decrement without significant facilitation at rapid rates or after exercise, suggesting postsynaptic neuromuscular blockade. After her strength returned, repetitive stimulation was normal, but single fiber EMG revealed increased jitter and blocking. Her acetylcholine receptor antibody level was markedly elevated. Although paralysis after /"magnesium"/ administration has been described in patients with known /"myasthenia gravis"/, it has not previously been reported to be the initial or only manifestation of the disease. Patients who are unusually sensitive to the neuromuscular effects of /"magnesium"/ should be suspected of having an underlying disorder of neuromuscular transmission. | magnesium | {
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{
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}
],
"offsets": [
[
47,
56
]
],
"text": [
"magnesium"
],
"type": "Chemical"
} | Myasthenia gravis | {
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{
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}
],
"offsets": [
[
0,
17
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],
"text": [
"Myasthenia gravis"
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"type": "Disease"
} | [
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47,
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"text": [
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] | Myasthenia gravis presenting as weakness after magnesium administration. | We studied a patient with no prior history of neuromuscular disease who became virtually quadriplegic after parenteral magnesium administration for preeclampsia. The serum magnesium concentration was 3.0 mEq/L, which is usually well tolerated. The magnesium was stopped and she recovered over a few days. While she was weak, 2-Hz repetitive stimulation revealed a decrement without significant facilitation at rapid rates or after exercise, suggesting postsynaptic neuromuscular blockade. After her strength returned, repetitive stimulation was normal, but single fiber EMG revealed increased jitter and blocking. Her acetylcholine receptor antibody level was markedly elevated. Although paralysis after magnesium administration has been described in patients with known myasthenia gravis, it has not previously been reported to be the initial or only manifestation of the disease. Patients who are unusually sensitive to the neuromuscular effects of magnesium should be suspected of having an underlying disorder of neuromuscular transmission. |
<s> [INST] <<SYS>>
Your task is to analyse the following medical article to determine whether chemical /"acetylcholine"/ induces disease /"preeclampsia"/. You only need to answer Yes or No, nothing else.
<</SYS>>
- Title: Myasthenia gravis presenting as weakness after magnesium administration.
- Abstract: We studied a patient with no prior history of neuromuscular disease who became virtually quadriplegic after parenteral magnesium administration for /"preeclampsia"/. The serum magnesium concentration was 3.0 mEq/L, which is usually well tolerated. The magnesium was stopped and she recovered over a few days. While she was weak, 2-Hz repetitive stimulation revealed a decrement without significant facilitation at rapid rates or after exercise, suggesting postsynaptic neuromuscular blockade. After her strength returned, repetitive stimulation was normal, but single fiber EMG revealed increased jitter and blocking. Her /"acetylcholine"/ receptor antibody level was markedly elevated. Although paralysis after magnesium administration has been described in patients with known myasthenia gravis, it has not previously been reported to be the initial or only manifestation of the disease. Patients who are unusually sensitive to the neuromuscular effects of magnesium should be suspected of having an underlying disorder of neuromuscular transmission.
Question: Does chemical /"acetylcholine"/ induce disease /"preeclampsia"/ according to this article? Respond with "Yes" or "No" only. [/INST] No. </s> | No | Myasthenia gravis presenting as weakness after magnesium administration. | We studied a patient with no prior history of neuromuscular disease who became virtually quadriplegic after parenteral magnesium administration for /"preeclampsia"/. The serum magnesium concentration was 3.0 mEq/L, which is usually well tolerated. The magnesium was stopped and she recovered over a few days. While she was weak, 2-Hz repetitive stimulation revealed a decrement without significant facilitation at rapid rates or after exercise, suggesting postsynaptic neuromuscular blockade. After her strength returned, repetitive stimulation was normal, but single fiber EMG revealed increased jitter and blocking. Her /"acetylcholine"/ receptor antibody level was markedly elevated. Although paralysis after magnesium administration has been described in patients with known myasthenia gravis, it has not previously been reported to be the initial or only manifestation of the disease. Patients who are unusually sensitive to the neuromuscular effects of magnesium should be suspected of having an underlying disorder of neuromuscular transmission. | acetylcholine | {
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{
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}
],
"offsets": [
[
691,
704
]
],
"text": [
"acetylcholine"
],
"type": "Chemical"
} | preeclampsia | {
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{
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}
],
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[
221,
233
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"text": [
"preeclampsia"
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"text": [
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"text": [
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"offsets": [
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1024,
1033
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],
"text": [
"magnesium"
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] | [
{
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{
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"db_name": "MESH"
}
],
"offsets": [
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0,
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],
"text": [
"Myasthenia gravis"
],
"type": "Disease"
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{
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],
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119,
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"text": [
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},
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"db_id": "D011782",
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],
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],
"text": [
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"type": "Disease"
},
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"id": "365",
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{
"db_id": "D011225",
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],
"offsets": [
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221,
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"text": [
"preeclampsia"
],
"type": "Disease"
},
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"id": "368",
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"db_id": "D009468",
"db_name": "MESH"
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],
"text": [
"postsynaptic neuromuscular blockade"
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"normalized": [
{
"db_id": "D010243",
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}
],
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"text": [
"paralysis"
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}
],
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"text": [
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"id": "374",
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1078,
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"text": [
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"type": "Disease"
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] | Myasthenia gravis presenting as weakness after magnesium administration. | We studied a patient with no prior history of neuromuscular disease who became virtually quadriplegic after parenteral magnesium administration for preeclampsia. The serum magnesium concentration was 3.0 mEq/L, which is usually well tolerated. The magnesium was stopped and she recovered over a few days. While she was weak, 2-Hz repetitive stimulation revealed a decrement without significant facilitation at rapid rates or after exercise, suggesting postsynaptic neuromuscular blockade. After her strength returned, repetitive stimulation was normal, but single fiber EMG revealed increased jitter and blocking. Her acetylcholine receptor antibody level was markedly elevated. Although paralysis after magnesium administration has been described in patients with known myasthenia gravis, it has not previously been reported to be the initial or only manifestation of the disease. Patients who are unusually sensitive to the neuromuscular effects of magnesium should be suspected of having an underlying disorder of neuromuscular transmission. |
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