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stringclasses
7 values
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1 value
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stringlengths
3
9
predicat@headOffset
stringlengths
3
9
predicat@id
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206 values
predicat@text
stringlengths
2
124
predicat@type
stringclasses
29 values
predicat@charOffsetMin
int64
0
3.96k
predicat@charOffsetMax
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6
3.97k
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stringclasses
1 value
subject@charOffset
stringlengths
3
9
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stringlengths
3
9
subject@id
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197 values
subject@text
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2
49
subject@type
stringclasses
72 values
subject@charOffsetMin
int64
0
3.98k
subject@charOffsetMax
int64
3
4k
object@xml:space
stringclasses
1 value
object@charOffset
stringlengths
3
9
object@headOffset
stringlengths
3
9
object@id
stringclasses
198 values
object@text
stringlengths
2
53
object@type
stringclasses
73 values
object@charOffsetMin
int64
0
3.93k
object@charOffsetMax
int64
4
3.94k
id
stringclasses
58 values
raw_sent_text
stringlengths
20
749
sent_charOffset
stringlengths
4
9
sent_charOffsetMin
int64
0
3.88k
sent_charOffsetMax
int64
26
4.2k
formated_sentence
stringlengths
34
768
Fact
preserve
168-288
201-211
T18
aldosterone are not always fully suppressed during chronic angiotensin converting enzyme (ACE) inhibitor treatment
ISA
168
288
preserve
143-157
143-154
T11
Angiotensin II
AminoAcidPeptideOrProtein
143
157
preserve
279-288
279-288
T17
treatment
TherapeuticOrPreventiveProcedure
279
288
A11
OBJECTIVE: Angiotensin II (AII) and aldosterone are not always fully suppressed during chronic angiotensin converting enzyme (ACE) inhibitor treatment.
132-289
132
289
OBJECTIVE: @SUBJECT$ (AII) and @PREDICAT$ @OBJECT$ .
Fact
preserve
1785-1789
1785-1789
T118
with
PART_OF
1,785
1,789
preserve
1802-1805
1802-1805
T112
ACE
AminoAcidPeptideOrProtein
1,802
1,805
preserve
1776-1784
1776-1784
T110
patients
PatientOrDisabledGroup
1,776
1,784
A12
In patients with high plasma ACE concentrations, non-compliance should be considered along with inadequate dose titration.
1773-1907
1,773
1,907
In @OBJECT$ @PREDICAT$ high plasma @SUBJECT$ concentrations, non-compliance should be considered along with inadequate dose titration.
Fact
preserve
102-111
102-111
T10
treatment
TREATS
102
111
preserve
88-101
92-101
T6
ACE inhibitor
PharmacologicSubstance
88
101
preserve
115-130
123-130
T8
cardiac failure
DiseaseOrSyndrome
115
130
A16
How often are angiotensin II and aldosterone concentrations raised during chronic ACE inhibitor treatment in cardiac failure?
0-131
0
131
How often are angiotensin II and aldosterone concentrations raised during chronic @SUBJECT$ @PREDICAT$ in @OBJECT$ ?
Fact
preserve
2242-2249
2242-2249
T151
treated
TREATS
2,242
2,249
preserve
2258-2271
2262-2271
T148
ACE inhibitor
PharmacologicSubstance
2,258
2,271
preserve
2214-2227
2220-2227
T146
heart failure
DiseaseOrSyndrome
2,214
2,227
A17
It is important to establish the cause of detectable or increased AII concentrations in a heart failure patient treated with an ACE inhibitor.
2118-2272
2,118
2,272
It is important to establish the cause of detectable or increased AII concentrations in a @OBJECT$ patient @PREDICAT$ with an @SUBJECT$ .
Fact
preserve
2093-2097
2093-2097
T140
than
compared_with
2,093
2,097
preserve
2035-2046
2035-2046
T134
aldosterone
Hormone
2,035
2,046
preserve
2098-2101
2098-2101
T138
AII
AminoAcidPeptideOrProtein
2,098
2,101
A18
Raised aldosterone concentrations appear to be more common than AII "reactivation".
2028-2117
2,028
2,117
Raised @SUBJECT$ concentrations appear to be more common @PREDICAT$ @OBJECT$ "reactivation".
Fact
preserve
1920-1924
1920-1924
T130
with
PART_OF
1,920
1,924
preserve
1936-1939
1936-1939
T122
ACE
AminoAcidPeptideOrProtein
1,936
1,939
preserve
1911-1919
1911-1919
T119
patients
PatientOrDisabledGroup
1,911
1,919
A19
In patients with low plasma ACE and high AII concentrations, non-ACE mediated production of AII may be operative.
1908-2027
1,908
2,027
In @OBJECT$ @PREDICAT$ low plasma @SUBJECT$ and high AII concentrations, non-ACE mediated production of AII may be operative.
Fact
preserve
792-823
814-823
T53
ACE inhibitors (enalapril
ISA
792
823
preserve
825-835
825-835
T49
lisinopril
AminoAcidPeptideOrProtein
825
835
preserve
792-806
796-806
T47
ACE inhibitors
PharmacologicSubstance
792
806
A20
A representative range of ACE inhibitors (enalapril, lisinopril, captopril, perindopril, and fosinopril) was examined.
766-890
766
890
A representative range of @OBJECT$ @PREDICAT$ , @SUBJECT$ , captopril, perindopril, and fosinopril) was examined.
Fact
preserve
1284-1294
1284-1294
T84
correlated
COEXISTS_WITH
1,284
1,294
preserve
1246-1249
1246-1249
T78
AII
AminoAcidPeptideOrProtein
1,246
1,249
preserve
1318-1321
1318-1321
T80
ACE
AminoAcidPeptideOrProtein
1,318
1,321
A21
AII concentrations were significantly correlated (p < 0.001) with ACE but not with aldosterone concentrations.
1246-1362
1,246
1,362
@SUBJECT$ concentrations were significantly @PREDICAT$ (p < 0.001) with @OBJECT$ but not with aldosterone concentrations.
Fact
preserve
88-111
102-111
T9
ACE inhibitor treatment
USES
88
111
preserve
102-111
102-111
T7
treatment
TherapeuticOrPreventiveProcedure
102
111
preserve
88-101
92-101
T6
ACE inhibitor
PharmacologicSubstance
88
101
A22
How often are angiotensin II and aldosterone concentrations raised during chronic ACE inhibitor treatment in cardiac failure?
0-131
0
131
How often are angiotensin II and aldosterone concentrations raised during chronic @OBJECT$ @PREDICAT$ @SUBJECT$ in cardiac failure?
Fact
preserve
2242-2249
2242-2249
T151
treated
TREATS
2,242
2,249
preserve
2258-2271
2262-2271
T148
ACE inhibitor
PharmacologicSubstance
2,258
2,271
preserve
2234-2241
2234-2241
T147
patient
PatientOrDisabledGroup
2,234
2,241
A23
It is important to establish the cause of detectable or increased AII concentrations in a heart failure patient treated with an ACE inhibitor.
2118-2272
2,118
2,272
It is important to establish the cause of detectable or increased AII concentrations in a heart failure @OBJECT$ @PREDICAT$ with an @SUBJECT$ .
Fact
preserve
168-288
201-211
T18
aldosterone are not always fully suppressed during chronic angiotensin converting enzyme (ACE) inhibitor treatment
ISA
168
288
preserve
168-179
168-179
T12
aldosterone
Hormone
168
179
preserve
279-288
279-288
T17
treatment
TherapeuticOrPreventiveProcedure
279
288
A24
OBJECTIVE: Angiotensin II (AII) and aldosterone are not always fully suppressed during chronic angiotensin converting enzyme (ACE) inhibitor treatment.
132-289
132
289
OBJECTIVE: Angiotensin II (AII) and @SUBJECT$ @PREDICAT$ @OBJECT$ .
Fact
preserve
2214-2241
2234-2241
T149
heart failure patient
PROCESS_OF
2,214
2,241
preserve
2214-2227
2220-2227
T146
heart failure
DiseaseOrSyndrome
2,214
2,227
preserve
2234-2241
2234-2241
T147
patient
PatientOrDisabledGroup
2,234
2,241
A25
It is important to establish the cause of detectable or increased AII concentrations in a heart failure patient treated with an ACE inhibitor.
2118-2272
2,118
2,272
It is important to establish the cause of detectable or increased AII concentrations in a @SUBJECT$ @PREDICAT$ @OBJECT$ treated with an ACE inhibitor.
Fact
preserve
792-823
814-823
T53
ACE inhibitors (enalapril
ISA
792
823
preserve
848-859
848-859
T51
perindopril
OrganicChemical
848
859
preserve
792-806
796-806
T47
ACE inhibitors
PharmacologicSubstance
792
806
A27
A representative range of ACE inhibitors (enalapril, lisinopril, captopril, perindopril, and fosinopril) was examined.
766-890
766
890
A representative range of @OBJECT$ @PREDICAT$ , lisinopril, captopril, @SUBJECT$ , and fosinopril) was examined.
Fact
preserve
233-288
279-288
T20
angiotensin converting enzyme (ACE) inhibitor treatment
USES
233
288
preserve
279-288
279-288
T17
treatment
TherapeuticOrPreventiveProcedure
279
288
preserve
233-278
269-278
T16
angiotensin converting enzyme (ACE) inhibitor
PharmacologicSubstance
233
278
A28
OBJECTIVE: Angiotensin II (AII) and aldosterone are not always fully suppressed during chronic angiotensin converting enzyme (ACE) inhibitor treatment.
132-289
132
289
OBJECTIVE: Angiotensin II (AII) and aldosterone are not always fully suppressed during chronic @OBJECT$ @PREDICAT$ @SUBJECT$ .
Fact
preserve
1929-1939
1936-1939
T129
plasma ACE
LOCATION_OF
1,929
1,939
preserve
1929-1935
1929-1935
T121
plasma
BodySubstance
1,929
1,935
preserve
1936-1939
1936-1939
T122
ACE
AminoAcidPeptideOrProtein
1,936
1,939
A29
In patients with low plasma ACE and high AII concentrations, non-ACE mediated production of AII may be operative.
1908-2027
1,908
2,027
In patients with low @SUBJECT$ @PREDICAT$ @OBJECT$ and high AII concentrations, non-ACE mediated production of AII may be operative.
Fact
preserve
1813-1820
1813-1820
T117
therapy
TREATS
1,813
1,820
preserve
1771-1782
1771-1782
T102
Naratriptan
OrganicChemical
1,771
1,782
preserve
1831-1839
1831-1839
T108
migraine
DiseaseOrSyndrome
1,831
1,839
A1
CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat patients who poorly tolerate other triptan therapies or have longer duration migraine headaches.
1758-1975
1,758
1,975
CONCLUSIONS: @SUBJECT$ is a promising new oral @PREDICAT$ for acute @OBJECT$ ; it may successfully treat patients who poorly tolerate other triptan therapies or have longer duration migraine headaches.
Fact
preserve
1908-1925
1916-1925
T115
triptan therapies
ISA
1,908
1,925
preserve
1908-1915
1908-1915
T111
triptan
OrganicChemical
1,908
1,915
preserve
1916-1925
1916-1925
T112
therapies
TherapeuticOrPreventiveProcedure
1,916
1,925
A2
CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat patients who poorly tolerate other triptan therapies or have longer duration migraine headaches.
1758-1975
1,758
1,975
CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat patients who poorly tolerate other @SUBJECT$ @PREDICAT$ @OBJECT$ or have longer duration migraine headaches.
Fact
preserve
850-859
850-859
T54
treatment
TREATS
850
859
preserve
925-936
925-936
T49
sumatriptan
OrganicChemical
925
936
preserve
863-871
863-871
T47
migraine
DiseaseOrSyndrome
863
871
A3
DATA SYNTHESIS: The treatment of migraine has been dramatically improved with the use of sumatriptan, other triptans, and serotonin-receptor subtype 1B and 1D agonists.
830-1010
830
1,010
DATA SYNTHESIS: The @PREDICAT$ of @OBJECT$ has been dramatically improved with the use of @SUBJECT$ , other triptans, and serotonin-receptor subtype 1B and 1D agonists.
Fact
preserve
1147-1217
1177-1185
T67
Naratriptan has been recently approved for acute oral migraine therapy
ISA
1,147
1,217
preserve
1147-1158
1147-1158
T61
Naratriptan
OrganicChemical
1,147
1,158
preserve
1210-1217
1210-1217
T66
therapy
TherapeuticOrPreventiveProcedure
1,210
1,217
A4
Naratriptan has been recently approved for acute oral migraine therapy.
1147-1218
1,147
1,218
@SUBJECT$ @PREDICAT$ @OBJECT$ .
Fact
preserve
1929-1933
1929-1933
T119
have
PROCESS_OF
1,929
1,933
preserve
1950-1974
1965-1974
T114
migraine headaches
DiseaseOrSyndrome
1,950
1,974
preserve
1867-1875
1867-1875
T109
patients
PatientOrDisabledGroup
1,867
1,875
A5
CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat patients who poorly tolerate other triptan therapies or have longer duration migraine headaches.
1758-1975
1,758
1,975
CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat @OBJECT$ who poorly tolerate other triptan therapies or @PREDICAT$ longer duration @SUBJECT$ .
Fact
preserve
1258-1266
1258-1266
T82
compared
compared_with
1,258
1,266
preserve
1246-1257
1246-1257
T71
naratriptan
OrganicChemical
1,246
1,257
preserve
1272-1279
1272-1279
T72
placebo
MedicalDevice
1,272
1,279
A6
In two Phase III trials of naratriptan compared with placebo, relief at four hours was obtained in 60% and 68% of patients using the 2.5-mg dose, with recurrence of headache in 24 hours in 27% and 28% of patients.
1219-1444
1,219
1,444
In two Phase III trials of @SUBJECT$ @PREDICAT$ with @OBJECT$ , relief at four hours was obtained in 60% and 68% of patients using the 2.5-mg dose, with recurrence of headache in 24 hours in 27% and 28% of patients.
Fact
preserve
850-859
850-859
T54
treatment
TREATS
850
859
preserve
944-952
944-952
T50
triptans
OrganicChemical
944
952
preserve
863-871
863-871
T47
migraine
DiseaseOrSyndrome
863
871
A9
DATA SYNTHESIS: The treatment of migraine has been dramatically improved with the use of sumatriptan, other triptans, and serotonin-receptor subtype 1B and 1D agonists.
830-1010
830
1,010
DATA SYNTHESIS: The @PREDICAT$ of @OBJECT$ has been dramatically improved with the use of sumatriptan, other @SUBJECT$ , and serotonin-receptor subtype 1B and 1D agonists.
Fact
preserve
28-31
28-31
T4
for
TREATS
28
31
preserve
0-11
0-11
T1
Naratriptan
OrganicChemical
0
11
preserve
32-40
32-40
T3
migraine
DiseaseOrSyndrome
32
40
A13
Naratriptan: an alternative for migraine.
0-41
0
41
@SUBJECT$ : an alternative @PREDICAT$ @OBJECT$ .
Fact
preserve
1771-1820
1813-1820
T116
Naratriptan is a promising new oral therapy
ISA
1,771
1,820
preserve
1771-1782
1771-1782
T102
Naratriptan
OrganicChemical
1,771
1,782
preserve
1813-1820
1813-1820
T106
therapy
TherapeuticOrPreventiveProcedure
1,813
1,820
A14
CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat patients who poorly tolerate other triptan therapies or have longer duration migraine headaches.
1758-1975
1,758
1,975
CONCLUSIONS: @SUBJECT$ @PREDICAT$ @OBJECT$ for acute migraine; it may successfully treat patients who poorly tolerate other triptan therapies or have longer duration migraine headaches.
Fact
preserve
1210-1217
1210-1217
T68
therapy
TREATS
1,210
1,217
preserve
1147-1158
1147-1158
T61
Naratriptan
OrganicChemical
1,147
1,158
preserve
1201-1209
1201-1209
T65
migraine
DiseaseOrSyndrome
1,201
1,209
A16
Naratriptan has been recently approved for acute oral migraine therapy.
1147-1218
1,147
1,218
@SUBJECT$ has been recently approved for acute oral @OBJECT$ @PREDICAT$ .
Fact
preserve
1908-1925
1916-1925
T118
triptan therapies
USES
1,908
1,925
preserve
1916-1925
1916-1925
T112
therapies
TherapeuticOrPreventiveProcedure
1,916
1,925
preserve
1908-1915
1908-1915
T111
triptan
OrganicChemical
1,908
1,915
A18
CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat patients who poorly tolerate other triptan therapies or have longer duration migraine headaches.
1758-1975
1,758
1,975
CONCLUSIONS: Naratriptan is a promising new oral therapy for acute migraine; it may successfully treat patients who poorly tolerate other @OBJECT$ @PREDICAT$ @SUBJECT$ or have longer duration migraine headaches.
Fact
preserve
1370-1377
1370-1377
T88
treated
TREATS
1,370
1,377
preserve
1397-1411
1397-1411
T85
beclomethasone
Hormone
1,397
1,411
preserve
1361-1369
1361-1369
T83
patients
PatientOrDisabledGroup
1,361
1,369
A4
PImax as an absolute value was significantly lower in steroid-dependent asthmatics than in patients treated with inhaled beclomethasone and controls (p < 0.01).
1264-1436
1,264
1,436
PImax as an absolute value was significantly lower in steroid-dependent asthmatics than in @OBJECT$ @PREDICAT$ with inhaled @SUBJECT$ and controls (p < 0.01).
Fact
preserve
643-661
653-661
T44
asthmatic patients
PROCESS_OF
643
661
preserve
643-652
643-652
T40
asthmatic
DiseaseOrSyndrome
643
652
preserve
653-661
653-661
T41
patients
PatientOrDisabledGroup
653
661
A7
OBJECTIVE: We aimed to evaluate the effects of long-term moderate dose of systemic corticosteroids and high-dose inhaled beclomethasone on maximal inspiratory and expiratory pressures (PImax and PEmax, respectively) in two groups of asthmatic patients exhibiting comparable levels of hyperinflation.
392-709
392
709
OBJECTIVE: We aimed to evaluate the effects of long-term moderate dose of systemic corticosteroids and high-dose inhaled beclomethasone on maximal inspiratory and expiratory pressures (PImax and PEmax, respectively) in two groups of @SUBJECT$ @PREDICAT$ @OBJECT$ exhibiting comparable levels of hyperinflation.
Fact
preserve
104-106
104-106
T7
in
COEXISTS_WITH
104
106
preserve
88-103
95-103
T4
muscle weakness
Finding
88
103
preserve
107-113
107-113
T5
asthma
DiseaseOrSyndrome
107
113
A9
Inhaled and systemic corticosteroid therapies: Do they contribute to inspiratory muscle weakness in asthma?
0-114
0
114
Inhaled and systemic corticosteroid therapies: Do they contribute to inspiratory @SUBJECT$ @PREDICAT$ @OBJECT$ ?
Fact
preserve
1664-1682
1674-1682
T102
asthmatic patients
PROCESS_OF
1,664
1,682
preserve
1664-1673
1664-1673
T100
asthmatic
DiseaseOrSyndrome
1,664
1,673
preserve
1674-1682
1674-1682
T101
patients
PatientOrDisabledGroup
1,674
1,682
A10
A significant correlation was found between %PImax and hyperinflation assessed by %RV, %FRC, %FRC/TLC (p < 0.05) in all asthmatic patients.
1532-1683
1,532
1,683
A significant correlation was found between %PImax and hyperinflation assessed by %RV, %FRC, %FRC/TLC (p < 0.05) in all @SUBJECT$ @PREDICAT$ @OBJECT$ .
Fact
preserve
21-45
36-45
T6
corticosteroid therapies
USES
21
45
preserve
12-45
36-45
T2
systemic corticosteroid therapies
TherapeuticOrPreventiveProcedure
12
45
preserve
21-35
21-35
T1
corticosteroid
Hormone
21
35
A11
Inhaled and systemic corticosteroid therapies: Do they contribute to inspiratory muscle weakness in asthma?
0-114
0
114
Inhaled and @SUBJECT$ @OBJECT$ @PREDICAT$ : Do they contribute to inspiratory muscle weakness in asthma?
Fact
preserve
136-140
136-140
T17
with
PROCESS_OF
136
140
preserve
141-147
141-147
T9
asthma
DiseaseOrSyndrome
141
147
preserve
127-135
127-135
T8
Patients
PatientOrDisabledGroup
127
135
A13
BACKGROUND: Patients with asthma incur the risk of steroid-induced myopathy, which is a well-known side effect of treatment with corticosteroids.
115-266
115
266
BACKGROUND: @OBJECT$ @PREDICAT$ @SUBJECT$ incur the risk of steroid-induced myopathy, which is a well-known side effect of treatment with corticosteroids.
Fact
preserve
1370-1377
1370-1377
T88
treated
TREATS
1,370
1,377
preserve
1397-1411
1397-1411
T85
beclomethasone
Hormone
1,397
1,411
preserve
1342-1352
1342-1352
T82
asthmatics
DiseaseOrSyndrome
1,342
1,352
A14
PImax as an absolute value was significantly lower in steroid-dependent asthmatics than in patients treated with inhaled beclomethasone and controls (p < 0.01).
1264-1436
1,264
1,436
PImax as an absolute value was significantly lower in steroid-dependent @OBJECT$ than in patients @PREDICAT$ with inhaled @SUBJECT$ and controls (p < 0.01).
Fact
preserve
2141-2168
2160-2168
T132
inspiratory muscle function
PROCESS_OF
2,141
2,168
preserve
2141-2152
2141-2152
T127
inspiratory
OrganOrTissueFunction
2,141
2,152
preserve
2153-2168
2160-2168
T128
muscle function
OrganOrTissueFunction
2,153
2,168
A16
CONCLUSIONS: We believe that hyperinflation plays a major role in inspiratory muscle dysfunction in asthma, but the finding of significantly decreased PImax values in steroid-dependent asthmatics when compared with patients on high-dose inhaled beclomethasone with a comparable level of hyperinflation points to a deleterious effect of long-term, moderate-dose systemic corticosteroid but not high-dose beclomethasone on inspiratory muscle function in asthmatics.
1684-2183
1,684
2,183
CONCLUSIONS: We believe that hyperinflation plays a major role in inspiratory muscle dysfunction in asthma, but the finding of significantly decreased PImax values in steroid-dependent asthmatics when compared with patients on high-dose inhaled beclomethasone with a comparable level of hyperinflation points to a deleterious effect of long-term, moderate-dose systemic corticosteroid but not high-dose beclomethasone on @SUBJECT$ @PREDICAT$ @OBJECT$ in asthmatics.
Fact
preserve
1034-1046
1034-1046
T62
attributable
CAUSES
1,034
1,046
preserve
1050-1072
1063-1072
T54
occupational exposures
InjuryOrPoisoning
1,050
1,072
preserve
1020-1026
1020-1026
T53
asthma
DiseaseOrSyndrome
1,020
1,026
A1
The risk of asthma attributable to occupational exposures is probably underappreciated due to underreporting and to inappropriate use of narrow definitions of exposure in epidemiologic studies of attributable risk.
1008-1241
1,008
1,241
The risk of @OBJECT$ @PREDICAT$ to @SUBJECT$ is probably underappreciated due to underreporting and to inappropriate use of narrow definitions of exposure in epidemiologic studies of attributable risk.
Possible
preserve
539-543
539-543
T32
risk
PREDISPOSES
539
543
preserve
602-613
602-613
T29
isocyanates
OrganicChemical
602
613
preserve
547-553
547-553
T27
asthma
DiseaseOrSyndrome
547
553
A3
Painters may have an increased risk of asthma due to exposure to a variety of agents, such as isocyanates, alkyd resins, and chromates.
502-649
502
649
Painters may have an increased @PREDICAT$ of @OBJECT$ due to exposure to a variety of agents, such as @SUBJECT$ , alkyd resins, and chromates.
Possible
preserve
539-543
539-543
T32
risk
PREDISPOSES
539
543
preserve
639-648
639-648
T31
chromates
InorganicChemical
639
648
preserve
547-553
547-553
T27
asthma
DiseaseOrSyndrome
547
553
A4
Painters may have an increased risk of asthma due to exposure to a variety of agents, such as isocyanates, alkyd resins, and chromates.
502-649
502
649
Painters may have an increased @PREDICAT$ of @OBJECT$ due to exposure to a variety of agents, such as isocyanates, alkyd resins, and @SUBJECT$ .
Fact
preserve
43-45
43-45
T6
in
PROCESS_OF
43
45
preserve
0-19
13-19
T1
Occupational asthma
DiseaseOrSyndrome
0
19
preserve
48-61
54-61
T3
spray painter
ProfessionalOrOccupationalGroup
48
61
A5
Occupational asthma and contact dermatitis in a spray painter after introduction of an aziridine cross-linker.
0-117
0
117
@SUBJECT$ and contact dermatitis @PREDICAT$ a @OBJECT$ after introduction of an aziridine cross-linker.
Fact
preserve
43-45
43-45
T6
in
PROCESS_OF
43
45
preserve
24-42
32-42
T2
contact dermatitis
DiseaseOrSyndrome
24
42
preserve
48-61
54-61
T3
spray painter
ProfessionalOrOccupationalGroup
48
61
A6
Occupational asthma and contact dermatitis in a spray painter after introduction of an aziridine cross-linker.
0-117
0
117
Occupational asthma and @SUBJECT$ @PREDICAT$ a @OBJECT$ after introduction of an aziridine cross-linker.
Fact
preserve
208-221
208-221
T18
characterized
COEXISTS_WITH
208
221
preserve
231-250
239-250
T14
airways obstruction
DiseaseOrSyndrome
231
250
preserve
179-207
197-207
T12
respiratory difficulty
SignOrSymptom
179
207
A7
A 23-year-old spray painter developed contact dermatitis and respiratory difficulty characterized by small airways obstruction shortly after the polyfunctional aziridine cross-linker CX-100 began to be used in his workplace as a paint activator.
118-381
118
381
A 23-year-old spray painter developed contact dermatitis and @OBJECT$ @PREDICAT$ by small @SUBJECT$ shortly after the polyfunctional aziridine cross-linker CX-100 began to be used in his workplace as a paint activator.
Possible
preserve
539-543
539-543
T32
risk
PREDISPOSES
539
543
preserve
627-633
627-633
T30
resins
OrganicChemical
627
633
preserve
547-553
547-553
T27
asthma
DiseaseOrSyndrome
547
553
A8
Painters may have an increased risk of asthma due to exposure to a variety of agents, such as isocyanates, alkyd resins, and chromates.
502-649
502
649
Painters may have an increased @PREDICAT$ of @OBJECT$ due to exposure to a variety of agents, such as isocyanates, alkyd @SUBJECT$ , and chromates.
Fact
preserve
1494-1498
1494-1498
T92
have
PROCESS_OF
1,494
1,498
preserve
1499-1522
1515-1522
T87
coronary artery disease
DiseaseOrSyndrome
1,499
1,522
preserve
1448-1456
1448-1456
T84
patients
PatientOrDisabledGroup
1,448
1,456
A1
In addition to the studies completed in patients with MI, there are ongoing studies evaluating whether or not ACE inhibitors can reduce myocardial ischemic events in patients without a prior infarction who have coronary artery disease or hypertension and preserved LV function.
1270-1571
1,270
1,571
In addition to the studies completed in patients with MI, there are ongoing studies evaluating whether or not ACE inhibitors can reduce myocardial ischemic events in @OBJECT$ without a prior infarction who @PREDICAT$ @SUBJECT$ or hypertension and preserved LV function.
Fact
preserve
1778-1782
1778-1782
T108
have
PROCESS_OF
1,778
1,782
preserve
1783-1797
1786-1797
T104
LV dysfunction
PathologicFunction
1,783
1,797
preserve
1758-1767
1758-1767
T102
survivors
PatientOrDisabledGroup
1,758
1,767
A2
There is also growing evidence that concomitant therapy with a beta-blocker and an ACE inhibitor may reduce mortality rates beyond that observed with ACE inhibitors alone in survivors of MI who have LV dysfunction.
1572-1798
1,572
1,798
There is also growing evidence that concomitant therapy with a beta-blocker and an ACE inhibitor may reduce mortality rates beyond that observed with ACE inhibitors alone in @OBJECT$ of MI who @PREDICAT$ @SUBJECT$ .
Fact
preserve
1325-1329
1325-1329
T90
with
PROCESS_OF
1,325
1,329
preserve
1330-1332
1330-1332
T78
MI
DiseaseOrSyndrome
1,330
1,332
preserve
1316-1324
1316-1324
T77
patients
PatientOrDisabledGroup
1,316
1,324
A3
In addition to the studies completed in patients with MI, there are ongoing studies evaluating whether or not ACE inhibitors can reduce myocardial ischemic events in patients without a prior infarction who have coronary artery disease or hypertension and preserved LV function.
1270-1571
1,270
1,571
In addition to the studies completed in @OBJECT$ @PREDICAT$ @SUBJECT$ , there are ongoing studies evaluating whether or not ACE inhibitors can reduce myocardial ischemic events in patients without a prior infarction who have coronary artery disease or hypertension and preserved LV function.
Fact
preserve
1755-1757
1755-1757
T107
in
TREATS
1,755
1,757
preserve
1734-1748
1738-1748
T101
ACE inhibitors
PharmacologicSubstance
1,734
1,748
preserve
1758-1767
1758-1767
T102
survivors
PatientOrDisabledGroup
1,758
1,767
A4
There is also growing evidence that concomitant therapy with a beta-blocker and an ACE inhibitor may reduce mortality rates beyond that observed with ACE inhibitors alone in survivors of MI who have LV dysfunction.
1572-1798
1,572
1,798
There is also growing evidence that concomitant therapy with a beta-blocker and an ACE inhibitor may reduce mortality rates beyond that observed with @SUBJECT$ alone @PREDICAT$ @OBJECT$ of MI who have LV dysfunction.
Fact
preserve
966-970
966-970
T55
with
PROCESS_OF
966
970
preserve
971-991
980-991
T50
LV dysfunction
PathologicFunction
971
991
preserve
957-965
957-965
T49
patients
PatientOrDisabledGroup
957
965
A5
It appears from the findings of recent studies that the greatest benefit from beta-blocker therapy is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both).
709-1016
709
1,016
It appears from the findings of recent studies that the greatest benefit from beta-blocker therapy is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, @OBJECT$ @PREDICAT$ @SUBJECT$ or arrhythmias or both).
Fact
preserve
966-970
966-970
T55
with
PROCESS_OF
966
970
preserve
995-1006
995-1006
T51
arrhythmias
PathologicFunction
995
1,006
preserve
957-965
957-965
T49
patients
PatientOrDisabledGroup
957
965
A7
It appears from the findings of recent studies that the greatest benefit from beta-blocker therapy is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both).
709-1016
709
1,016
It appears from the findings of recent studies that the greatest benefit from beta-blocker therapy is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, @OBJECT$ @PREDICAT$ LV dysfunction or @SUBJECT$ or both).
Fact
preserve
1062-1069
1062-1069
T74
treated
TREATS
1,062
1,069
preserve
1075-1089
1079-1089
T60
ACE inhibitors
PharmacologicSubstance
1,075
1,089
preserve
1042-1055
1048-1055
T59
heart failure
DiseaseOrSyndrome
1,042
1,055
A8
Patients with class I-IV heart failure treated with ACE inhibitors have fewer recurrent infarctions, a lower incidence of severe congestive heart failure, and a reduced incidence of total cardiovascular death and sudden cardiac death.
1017-1269
1,017
1,269
Patients with class I-IV @OBJECT$ @PREDICAT$ with @SUBJECT$ have fewer recurrent infarctions, a lower incidence of severe congestive heart failure, and a reduced incidence of total cardiovascular death and sudden cardiac death.
Fact
preserve
360-364
360-364
T23
with
PROCESS_OF
360
364
preserve
374-382
374-382
T17
symptoms
SignOrSymptom
374
382
preserve
351-359
351-359
T15
patients
PatientOrDisabledGroup
351
359
A9
beta-Blockers reduce cardiovascular death and reinfarction in patients with a history of myocardial infarction (MI), and angiotensin-converting enzyme (ACE) inhibitors provide an overall survival benefit in patients with signs or symptoms of left ventricular (LV) dysfunction and a history of acute MI.
132-452
132
452
beta-Blockers reduce cardiovascular death and reinfarction in patients with a history of myocardial infarction (MI), and angiotensin-converting enzyme (ACE) inhibitors provide an overall survival benefit in @OBJECT$ @PREDICAT$ signs or @SUBJECT$ of left ventricular (LV) dysfunction and a history of acute MI.
Fact
preserve
832-834
832-834
T53
in
TREATS
832
834
preserve
812-819
812-819
T40
therapy
TherapeuticOrPreventiveProcedure
812
819
preserve
885-893
885-893
T45
patients
PatientOrDisabledGroup
885
893
A11
It appears from the findings of recent studies that the greatest benefit from beta-blocker therapy is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both).
709-1016
709
1,016
It appears from the findings of recent studies that the greatest benefit from beta-blocker @SUBJECT$ is achieved @PREDICAT$ patients who are more than 60 years of age and in @OBJECT$ at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both).
Fact
preserve
832-834
832-834
T53
in
TREATS
832
834
preserve
812-819
812-819
T40
therapy
TherapeuticOrPreventiveProcedure
812
819
preserve
835-843
835-843
T41
patients
PatientOrDisabledGroup
835
843
A12
It appears from the findings of recent studies that the greatest benefit from beta-blocker therapy is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both).
709-1016
709
1,016
It appears from the findings of recent studies that the greatest benefit from beta-blocker @SUBJECT$ is achieved @PREDICAT$ @OBJECT$ who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both).
Fact
preserve
1628-1632
1628-1632
T105
with
USES
1,628
1,632
preserve
1620-1627
1620-1627
T97
therapy
TherapeuticOrPreventiveProcedure
1,620
1,627
preserve
1661-1674
1665-1674
T99
ACE inhibitor
PharmacologicSubstance
1,661
1,674
A15
There is also growing evidence that concomitant therapy with a beta-blocker and an ACE inhibitor may reduce mortality rates beyond that observed with ACE inhibitors alone in survivors of MI who have LV dysfunction.
1572-1798
1,572
1,798
There is also growing evidence that concomitant @SUBJECT$ @PREDICAT$ a beta-blocker and an @OBJECT$ may reduce mortality rates beyond that observed with ACE inhibitors alone in survivors of MI who have LV dysfunction.
Fact
preserve
1090-1094
1090-1094
T75
have
PROCESS_OF
1,090
1,094
preserve
1111-1122
1111-1122
T63
infarctions
PathologicFunction
1,111
1,122
preserve
1017-1025
1017-1025
T57
Patients
PatientOrDisabledGroup
1,017
1,025
A16
Patients with class I-IV heart failure treated with ACE inhibitors have fewer recurrent infarctions, a lower incidence of severe congestive heart failure, and a reduced incidence of total cardiovascular death and sudden cardiac death.
1017-1269
1,017
1,269
@OBJECT$ with class I-IV heart failure treated with ACE inhibitors @PREDICAT$ fewer recurrent @SUBJECT$ , a lower incidence of severe congestive heart failure, and a reduced incidence of total cardiovascular death and sudden cardiac death.
Fact
preserve
146-152
146-152
T21
reduce
DISRUPTS
146
152
preserve
132-145
132-145
T6
beta-Blockers
PharmacologicSubstance
132
145
preserve
168-173
168-173
T7
death
OrganismFunction
168
173
A18
beta-Blockers reduce cardiovascular death and reinfarction in patients with a history of myocardial infarction (MI), and angiotensin-converting enzyme (ACE) inhibitors provide an overall survival benefit in patients with signs or symptoms of left ventricular (LV) dysfunction and a history of acute MI.
132-452
132
452
@SUBJECT$ @PREDICAT$ cardiovascular @OBJECT$ and reinfarction in patients with a history of myocardial infarction (MI), and angiotensin-converting enzyme (ACE) inhibitors provide an overall survival benefit in patients with signs or symptoms of left ventricular (LV) dysfunction and a history of acute MI.
Fact
preserve
360-364
360-364
T23
with
PROCESS_OF
360
364
preserve
365-370
365-370
T16
signs
SignOrSymptom
365
370
preserve
351-359
351-359
T15
patients
PatientOrDisabledGroup
351
359
A19
beta-Blockers reduce cardiovascular death and reinfarction in patients with a history of myocardial infarction (MI), and angiotensin-converting enzyme (ACE) inhibitors provide an overall survival benefit in patients with signs or symptoms of left ventricular (LV) dysfunction and a history of acute MI.
132-452
132
452
beta-Blockers reduce cardiovascular death and reinfarction in patients with a history of myocardial infarction (MI), and angiotensin-converting enzyme (ACE) inhibitors provide an overall survival benefit in @OBJECT$ @PREDICAT$ @SUBJECT$ or symptoms of left ventricular (LV) dysfunction and a history of acute MI.
Fact
preserve
1026-1030
1026-1030
T73
with
PROCESS_OF
1,026
1,030
preserve
1042-1055
1048-1055
T59
heart failure
DiseaseOrSyndrome
1,042
1,055
preserve
1017-1025
1017-1025
T57
Patients
PatientOrDisabledGroup
1,017
1,025
A20
Patients with class I-IV heart failure treated with ACE inhibitors have fewer recurrent infarctions, a lower incidence of severe congestive heart failure, and a reduced incidence of total cardiovascular death and sudden cardiac death.
1017-1269
1,017
1,269
@OBJECT$ @PREDICAT$ class I-IV @SUBJECT$ treated with ACE inhibitors have fewer recurrent infarctions, a lower incidence of severe congestive heart failure, and a reduced incidence of total cardiovascular death and sudden cardiac death.
Fact
preserve
793-819
812-819
T52
beta-blocker therapy
USES
793
819
preserve
812-819
812-819
T40
therapy
TherapeuticOrPreventiveProcedure
812
819
preserve
793-805
793-805
T39
beta-blocker
PharmacologicSubstance
793
805
A21
It appears from the findings of recent studies that the greatest benefit from beta-blocker therapy is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both).
709-1016
709
1,016
It appears from the findings of recent studies that the greatest benefit from @OBJECT$ @PREDICAT$ @SUBJECT$ is achieved in patients who are more than 60 years of age and in patients at moderate or high risk for reinfarction and death (eg, patients with LV dysfunction or arrhythmias or both).
Fact
preserve
1628-1632
1628-1632
T105
with
USES
1,628
1,632
preserve
1620-1627
1620-1627
T97
therapy
TherapeuticOrPreventiveProcedure
1,620
1,627
preserve
1641-1653
1641-1653
T98
beta-blocker
PharmacologicSubstance
1,641
1,653
A22
There is also growing evidence that concomitant therapy with a beta-blocker and an ACE inhibitor may reduce mortality rates beyond that observed with ACE inhibitors alone in survivors of MI who have LV dysfunction.
1572-1798
1,572
1,798
There is also growing evidence that concomitant @SUBJECT$ @PREDICAT$ a @OBJECT$ and an ACE inhibitor may reduce mortality rates beyond that observed with ACE inhibitors alone in survivors of MI who have LV dysfunction.
Fact
preserve
1494-1498
1494-1498
T92
have
PROCESS_OF
1,494
1,498
preserve
1526-1538
1526-1538
T88
hypertension
DiseaseOrSyndrome
1,526
1,538
preserve
1448-1456
1448-1456
T84
patients
PatientOrDisabledGroup
1,448
1,456
A23
In addition to the studies completed in patients with MI, there are ongoing studies evaluating whether or not ACE inhibitors can reduce myocardial ischemic events in patients without a prior infarction who have coronary artery disease or hypertension and preserved LV function.
1270-1571
1,270
1,571
In addition to the studies completed in patients with MI, there are ongoing studies evaluating whether or not ACE inhibitors can reduce myocardial ischemic events in @OBJECT$ without a prior infarction who @PREDICAT$ coronary artery disease or @SUBJECT$ and preserved LV function.
Counterfact
preserve
766-777
774-777
T47
smoking men
PROCESS_OF
766
777
preserve
766-773
766-773
T45
smoking
IndividualBehavior
766
773
preserve
774-777
774-777
T46
men
PopulationGroup
774
777
A1
All subjects were non-smoking men.
744-778
744
778
All subjects were non- @SUBJECT$ @PREDICAT$ @OBJECT$ .
Fact
preserve
1486-1488
1486-1488
T83
in
COEXISTS_WITH
1,486
1,488
preserve
1458-1485
1473-1485
T72
chronic airway inflammation
PathologicFunction
1,458
1,485
preserve
1495-1505
1495-1505
T73
bronchitis
DiseaseOrSyndrome
1,495
1,505
A3
These results indicate that cough sensitivity is potentiated by chronic airway inflammation in bronchitis but not in asthma, and suggest that cough sensitivity and bronchial responsiveness may be independently potentiated by different mechanisms resulting from chronic airway inflammation.
1388-1701
1,388
1,701
These results indicate that cough sensitivity is potentiated by @SUBJECT$ @PREDICAT$ @OBJECT$ but not in asthma, and suggest that cough sensitivity and bronchial responsiveness may be independently potentiated by different mechanisms resulting from chronic airway inflammation.
Fact
preserve
97-99
97-99
T11
in
TREATS
97
99
preserve
84-96
84-96
T7
methacholine
IndicatorReagentOrDiagnosticAid
84
96
preserve
100-109
100-109
T8
asthmatic
DiseaseOrSyndrome
100
109
A4
Airway cough sensitivity to inhaled capsaicin and bronchial responsiveness to methacholine in asthmatic and bronchitic subjects.
0-134
0
134
Airway cough sensitivity to inhaled capsaicin and bronchial responsiveness to @SUBJECT$ @PREDICAT$ @OBJECT$ and bronchitic subjects.
Fact
preserve
13-24
13-24
T10
sensitivity
AFFECTS
13
24
preserve
36-45
36-45
T4
capsaicin
Lipid
36
45
preserve
7-12
7-12
T1
cough
SignOrSymptom
7
12
A5
Airway cough sensitivity to inhaled capsaicin and bronchial responsiveness to methacholine in asthmatic and bronchitic subjects.
0-134
0
134
Airway @OBJECT$ @PREDICAT$ to inhaled @SUBJECT$ and bronchial responsiveness to methacholine in asthmatic and bronchitic subjects.
Fact
preserve
390-397
390-397
T36
treated
TREATS
390
397
preserve
429-436
429-436
T30
placebo
MedicalDevice
429
436
preserve
352-378
369-378
T28
impaired glucose tolerance
Finding
352
378
A1
METHODS: Nineteen obese patients with impaired glucose tolerance (IGT) were treated with either metformin or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
308-511
308
511
METHODS: Nineteen obese patients with @OBJECT$ (IGT) were @PREDICAT$ with either metformin or @SUBJECT$ in a randomized, double-blind, placebo-controlled, cross-over study.
Fact
preserve
390-397
390-397
T36
treated
TREATS
390
397
preserve
416-425
416-425
T29
metformin
OrganicChemical
416
425
preserve
352-378
369-378
T28
impaired glucose tolerance
Finding
352
378
A2
METHODS: Nineteen obese patients with impaired glucose tolerance (IGT) were treated with either metformin or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
308-511
308
511
METHODS: Nineteen obese patients with @OBJECT$ (IGT) were @PREDICAT$ with either @SUBJECT$ or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
Fact
preserve
332-346
338-346
T34
obese patients
PROCESS_OF
332
346
preserve
332-337
332-337
T26
obese
DiseaseOrSyndrome
332
337
preserve
338-346
338-346
T27
patients
PatientOrDisabledGroup
338
346
A3
METHODS: Nineteen obese patients with impaired glucose tolerance (IGT) were treated with either metformin or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
308-511
308
511
METHODS: Nineteen @SUBJECT$ @PREDICAT$ @OBJECT$ with impaired glucose tolerance (IGT) were treated with either metformin or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
Fact
preserve
347-351
347-351
T35
with
PROCESS_OF
347
351
preserve
352-378
369-378
T28
impaired glucose tolerance
Finding
352
378
preserve
338-346
338-346
T27
patients
PatientOrDisabledGroup
338
346
A5
METHODS: Nineteen obese patients with impaired glucose tolerance (IGT) were treated with either metformin or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
308-511
308
511
METHODS: Nineteen obese @OBJECT$ @PREDICAT$ @SUBJECT$ (IGT) were treated with either metformin or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
Fact
preserve
120-124
120-124
T14
with
PROCESS_OF
120
124
preserve
125-151
142-151
T10
impaired glucose tolerance
Finding
125
151
preserve
111-119
111-119
T9
patients
PatientOrDisabledGroup
111
119
A6
Metformin treatment leads to an increase in basal, but not insulin-stimulated, glucose disposal in obese patients with impaired glucose tolerance.
0-152
0
152
Metformin treatment leads to an increase in basal, but not insulin-stimulated, glucose disposal in obese @OBJECT$ @PREDICAT$ @SUBJECT$ .
Fact
preserve
390-397
390-397
T36
treated
TREATS
390
397
preserve
429-436
429-436
T30
placebo
MedicalDevice
429
436
preserve
338-346
338-346
T27
patients
PatientOrDisabledGroup
338
346
A7
METHODS: Nineteen obese patients with impaired glucose tolerance (IGT) were treated with either metformin or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
308-511
308
511
METHODS: Nineteen obese @OBJECT$ with impaired glucose tolerance (IGT) were @PREDICAT$ with either metformin or @SUBJECT$ in a randomized, double-blind, placebo-controlled, cross-over study.
Fact
preserve
1464-1478
1464-1478
T100
administration
ADMINISTERED_TO
1,464
1,478
preserve
1454-1463
1454-1463
T91
metformin
OrganicChemical
1,454
1,463
preserve
1482-1490
1482-1490
T92
patients
PatientOrDisabledGroup
1,482
1,490
A8
CONCLUSIONS: These results indicate that metformin administration to patients with IGT is associated with enhanced glucose disposal at baseline insulin concentrations and a fall in blood pressure.
1406-1622
1,406
1,622
CONCLUSIONS: These results indicate that @SUBJECT$ @PREDICAT$ to @OBJECT$ with IGT is associated with enhanced glucose disposal at baseline insulin concentrations and a fall in blood pressure.
Fact
preserve
212-231
222-231
T24
metformin treatment
USES
212
231
preserve
222-231
222-231
T20
treatment
TherapeuticOrPreventiveProcedure
222
231
preserve
212-221
212-221
T19
metformin
OrganicChemical
212
221
A9
AIMS: This study was initiated to test the hypothesis that metformin treatment leads to enhanced glucose disposal at ambient insulin concentrations.
153-307
153
307
AIMS: This study was initiated to test the hypothesis that @OBJECT$ @PREDICAT$ @SUBJECT$ leads to enhanced glucose disposal at ambient insulin concentrations.
Fact
preserve
105-119
111-119
T12
obese patients
PROCESS_OF
105
119
preserve
105-110
105-110
T8
obese
DiseaseOrSyndrome
105
110
preserve
111-119
111-119
T9
patients
PatientOrDisabledGroup
111
119
A11
Metformin treatment leads to an increase in basal, but not insulin-stimulated, glucose disposal in obese patients with impaired glucose tolerance.
0-152
0
152
Metformin treatment leads to an increase in basal, but not insulin-stimulated, glucose disposal in @SUBJECT$ @PREDICAT$ @OBJECT$ with impaired glucose tolerance.
Fact
preserve
1724-1743
1734-1743
T110
metformin treatment
USES
1,724
1,743
preserve
1734-1743
1734-1743
T106
treatment
TherapeuticOrPreventiveProcedure
1,734
1,743
preserve
1724-1733
1724-1733
T105
metformin
OrganicChemical
1,724
1,733
A12
In contrast, neither glucose oxidation nor glucose disposal were increased in association with metformin treatment under conditions of physiological hyperinsulinaemia.
1623-1802
1,623
1,802
In contrast, neither glucose oxidation nor glucose disposal were increased in association with @OBJECT$ @PREDICAT$ @SUBJECT$ under conditions of physiological hyperinsulinaemia.
Fact
preserve
0-19
10-19
T11
Metformin treatment
USES
0
19
preserve
10-19
10-19
T2
treatment
TherapeuticOrPreventiveProcedure
10
19
preserve
0-9
0-9
T1
Metformin
OrganicChemical
0
9
A15
Metformin treatment leads to an increase in basal, but not insulin-stimulated, glucose disposal in obese patients with impaired glucose tolerance.
0-152
0
152
@OBJECT$ @PREDICAT$ @SUBJECT$ leads to an increase in basal, but not insulin-stimulated, glucose disposal in obese patients with impaired glucose tolerance.
Fact
preserve
390-397
390-397
T36
treated
TREATS
390
397
preserve
416-425
416-425
T29
metformin
OrganicChemical
416
425
preserve
338-346
338-346
T27
patients
PatientOrDisabledGroup
338
346
A17
METHODS: Nineteen obese patients with impaired glucose tolerance (IGT) were treated with either metformin or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
308-511
308
511
METHODS: Nineteen obese @OBJECT$ with impaired glucose tolerance (IGT) were @PREDICAT$ with either @SUBJECT$ or placebo in a randomized, double-blind, placebo-controlled, cross-over study.
Fact
preserve
1491-1495
1491-1495
T101
with
PROCESS_OF
1,491
1,495
preserve
1496-1499
1496-1499
T93
IGT
Finding
1,496
1,499
preserve
1482-1490
1482-1490
T92
patients
PatientOrDisabledGroup
1,482
1,490
A19
CONCLUSIONS: These results indicate that metformin administration to patients with IGT is associated with enhanced glucose disposal at baseline insulin concentrations and a fall in blood pressure.
1406-1622
1,406
1,622
CONCLUSIONS: These results indicate that metformin administration to @OBJECT$ @PREDICAT$ @SUBJECT$ is associated with enhanced glucose disposal at baseline insulin concentrations and a fall in blood pressure.
Possible
preserve
1678-1685
1678-1685
T104
benefit
TREATS
1,678
1,685
preserve
1696-1706
1696-1706
T103
pranlukast
OrganicChemical
1,696
1,706
preserve
1591-1601
1591-1601
T98
asthmatics
DiseaseOrSyndrome
1,591
1,601
A2
Severe asthmatics (FEV1.0 < 80%) who deteriorate after reduction of inhaled steroid may benefit most from pranlukast.
1584-1707
1,584
1,707
Severe @OBJECT$ (FEV1.0 < 80%) who deteriorate after reduction of inhaled steroid may @PREDICAT$ most from @SUBJECT$ .
Fact
preserve
251-267
257-267
T20
adult asthmatics
PROCESS_OF
251
267
preserve
257-267
257-267
T18
asthmatics
DiseaseOrSyndrome
257
267
preserve
251-256
251-256
T17
adult
AgeGroup
251
256
A3
We undertook a community based case-control study to measure the effect of pranlukast on the reduction of inhaled steroid in adult asthmatics.
120-268
120
268
We undertook a community based case-control study to measure the effect of pranlukast on the reduction of inhaled steroid in @OBJECT$ @PREDICAT$ @SUBJECT$ .
Fact
preserve
655-662
655-662
T48
receive
ADMINISTERED_TO
655
662
preserve
670-680
670-680
T43
pranlukast
OrganicChemical
670
680
preserve
616-624
616-624
T42
Patients
PatientOrDisabledGroup
616
624
A5
Patients were then randomized to receive either pranlukast with 400 microgram of BDP or 400 microgram alone for 8 weeks.
616-748
616
748
@OBJECT$ were then randomized to @PREDICAT$ either @SUBJECT$ with 400 microgram of BDP or 400 microgram alone for 8 weeks.
Fact
preserve
101-117
107-117
T9
adult asthmatics
PROCESS_OF
101
117
preserve
107-117
107-117
T8
asthmatics
DiseaseOrSyndrome
107
117
preserve
101-106
101-106
T7
adult
AgeGroup
101
106
A7
[Pranlukast allows reduction of inhaled steroid dose without deterioration in lung function in adult asthmatics].
0-119
0
119
[Pranlukast allows reduction of inhaled steroid dose without deterioration in lung function in @OBJECT$ @PREDICAT$ @SUBJECT$ ].
Fact
preserve
185-191
185-191
T19
effect
INTERACTS_WITH
185
191
preserve
240-247
240-247
T16
steroid
Steroid
240
247
preserve
201-211
201-211
T14
pranlukast
OrganicChemical
201
211
A8
We undertook a community based case-control study to measure the effect of pranlukast on the reduction of inhaled steroid in adult asthmatics.
120-268
120
268
We undertook a community based case-control study to measure the @PREDICAT$ of @OBJECT$ on the reduction of inhaled @SUBJECT$ in adult asthmatics.
Fact
preserve
625-629
625-629
T38
with
USES
625
629
preserve
617-624
617-624
T34
therapy
TherapeuticOrPreventiveProcedure
617
624
preserve
636-676
666-676
T35
angiotensin-converting enzyme inhibitors
PharmacologicSubstance
636
676
A1
Long-term therapy with angiotensin-converting enzyme inhibitors should be continued in patients with systolic dysfunction.
607-741
607
741
Long-term @SUBJECT$ @PREDICAT$ @OBJECT$ should be continued in patients with systolic dysfunction.
Fact
preserve
709-713
709-713
T39
with
PROCESS_OF
709
713
preserve
720-740
729-740
T37
systolic dysfunction
PathologicFunction
720
740
preserve
700-708
700-708
T36
patients
PatientOrDisabledGroup
700
708
A2
Long-term therapy with angiotensin-converting enzyme inhibitors should be continued in patients with systolic dysfunction.
607-741
607
741
Long-term therapy with angiotensin-converting enzyme inhibitors should be continued in @OBJECT$ @PREDICAT$ @SUBJECT$ .
Fact
preserve
437-441
437-441
T29
with
PROCESS_OF
437
441
preserve
442-480
473-480
T23
atherosclerotic cardiovascular disease
DiseaseOrSyndrome
442
480
preserve
428-436
428-436
T22
patients
PatientOrDisabledGroup
428
436
A3
All patients with atherosclerotic cardiovascular disease should be considered for lipid lowering therapy, antiplatelet agents, beta-blockers, and control of hypertension.
424-606
424
606
All @OBJECT$ @PREDICAT$ @SUBJECT$ should be considered for lipid lowering therapy, antiplatelet agents, beta-blockers, and control of hypertension.
Fact
preserve
178-182
178-182
T12
with
PROCESS_OF
178
182
preserve
189-205
198-205
T10
coronary disease
DiseaseOrSyndrome
189
205
preserve
169-177
169-177
T8
patients
PatientOrDisabledGroup
169
177
A6
Compelling evidence from clinical trials confirms the benefits of secondary prevention for patients with known coronary disease.
72-206
72
206
Compelling evidence from clinical trials confirms the benefits of secondary prevention for @OBJECT$ @PREDICAT$ known @SUBJECT$ .
Fact
preserve
165-168
165-168
T11
for
TREATS
165
168
preserve
138-164
154-164
T7
secondary prevention
TherapeuticOrPreventiveProcedure
138
164
preserve
169-177
169-177
T8
patients
PatientOrDisabledGroup
169
177
A7
Compelling evidence from clinical trials confirms the benefits of secondary prevention for patients with known coronary disease.
72-206
72
206
Compelling evidence from clinical trials confirms the benefits of @SUBJECT$ @PREDICAT$ @OBJECT$ with known coronary disease.
Fact
preserve
165-168
165-168
T11
for
TREATS
165
168
preserve
138-164
154-164
T7
secondary prevention
TherapeuticOrPreventiveProcedure
138
164
preserve
189-205
198-205
T10
coronary disease
DiseaseOrSyndrome
189
205
A8
Compelling evidence from clinical trials confirms the benefits of secondary prevention for patients with known coronary disease.
72-206
72
206
Compelling evidence from clinical trials confirms the benefits of @SUBJECT$ @PREDICAT$ patients with known @OBJECT$ .
Possible
preserve
1930-1937
1930-1937
T128
promote
PREDISPOSES
1,930
1,937
preserve
1810-1816
1810-1816
T112
leptin
AminoAcidPeptideOrProtein
1,810
1,816
preserve
1938-1943
1938-1943
T121
tumor
NeoplasticProcess
1,938
1,943
A1
The elevated levels of aromatase activity may contribute to increase circulating estrogen levels in certain obese women and suggest that elevated leptin concentrations in obese women may cause locally elevated estrogen concentrations in the breast and thereby promote tumor formation.
1652-1960
1,652
1,960
The elevated levels of aromatase activity may contribute to increase circulating estrogen levels in certain obese women and suggest that elevated @SUBJECT$ concentrations in obese women may cause locally elevated estrogen concentrations in the breast and thereby @PREDICAT$ @OBJECT$ formation.
Fact
preserve
1832-1834
1832-1834
T126
in
LOCATION_OF
1,832
1,834
preserve
1841-1846
1841-1846
T115
women
PopulationGroup
1,841
1,846
preserve
1810-1816
1810-1816
T112
leptin
AminoAcidPeptideOrProtein
1,810
1,816
A2
The elevated levels of aromatase activity may contribute to increase circulating estrogen levels in certain obese women and suggest that elevated leptin concentrations in obese women may cause locally elevated estrogen concentrations in the breast and thereby promote tumor formation.
1652-1960
1,652
1,960
The elevated levels of aromatase activity may contribute to increase circulating estrogen levels in certain obese women and suggest that elevated @OBJECT$ concentrations @PREDICAT$ obese @SUBJECT$ may cause locally elevated estrogen concentrations in the breast and thereby promote tumor formation.
Counterfact
preserve
1143-1149
1143-1149
T74
effect
AFFECTS
1,143
1,149
preserve
1039-1045
1039-1045
T65
Leptin
AminoAcidPeptideOrProtein
1,039
1,045
preserve
1153-1171
1163-1171
T73
aromatase activity
MolecularFunction
1,153
1,171
A3
Leptin concentrations in the physiological range of normal weight or thin women (10 ng/ml) had no effect on aromatase activity.
1039-1172
1,039
1,172
@SUBJECT$ concentrations in the physiological range of normal weight or thin women (10 ng/ml) had no @PREDICAT$ on @OBJECT$ .
Fact
preserve
1333-1335
1333-1335
T86
in
ASSOCIATED_WITH
1,333
1,335
preserve
1251-1256
1251-1256
T81
obese
DiseaseOrSyndrome
1,251
1,256
preserve
1336-1354
1346-1354
T85
aromatase activity
MolecularFunction
1,336
1,354
A4
In 2 of 8 abdominal fat cultures and 1 of 2 breast fat cultures, a high obese concentration of leptin (100 ng/ml) stimulated a significant increase in aromatase activity.
1173-1355
1,173
1,355
In 2 of 8 abdominal fat cultures and 1 of 2 breast fat cultures, a high @SUBJECT$ concentration of leptin (100 ng/ml) stimulated a significant increase @PREDICAT$ @OBJECT$ .
Fact
preserve
326-328
326-328
T32
in
LOCATION_OF
326
328
preserve
337-356
351-356
T24
stromal cells
Cell
337
356
preserve
302-311
302-311
T22
aromatase
AminoAcidPeptideOrProtein
302
311
A6
The aromatase gene promoter in adipose stromal cells contains a functional STAT binding region, leading to the hypothesis that leptin may regulate aromatase activity in fat tissue.
298-490
298
490
The @OBJECT$ gene promoter @PREDICAT$ adipose @SUBJECT$ contains a functional STAT binding region, leading to the hypothesis that leptin may regulate aromatase activity in fat tissue.
Fact
preserve
756-768
762-768
T52
human leptin
PART_OF
756
768
preserve
762-768
762-768
T51
leptin
AminoAcidPeptideOrProtein
762
768
preserve
756-761
756-761
T50
human
Human
756
761
A7
MATERIALS AND METHODS: The cells were treated for three days with increasing concentrations of recombinant human leptin.
643-769
643
769
MATERIALS AND METHODS: The cells were treated for three days with increasing concentrations of recombinant @OBJECT$ @PREDICAT$ @SUBJECT$ .
Fact
preserve
1835-1846
1841-1846
T125
obese women
PROCESS_OF
1,835
1,846
preserve
1835-1840
1835-1840
T114
obese
DiseaseOrSyndrome
1,835
1,840
preserve
1841-1846
1841-1846
T115
women
PopulationGroup
1,841
1,846
A10
The elevated levels of aromatase activity may contribute to increase circulating estrogen levels in certain obese women and suggest that elevated leptin concentrations in obese women may cause locally elevated estrogen concentrations in the breast and thereby promote tumor formation.
1652-1960
1,652
1,960
The elevated levels of aromatase activity may contribute to increase circulating estrogen levels in certain obese women and suggest that elevated leptin concentrations in @SUBJECT$ @PREDICAT$ @OBJECT$ may cause locally elevated estrogen concentrations in the breast and thereby promote tumor formation.
Uncommitted
preserve
7-17
7-17
T7
regulation
AFFECTS
7
17
preserve
0-6
0-6
T1
Leptin
AminoAcidPeptideOrProtein
0
6
preserve
21-39
31-39
T3
aromatase activity
MolecularFunction
21
39
A11
Leptin regulation of aromatase activity in adipose stromal cells from regularly cycling women.
0-100
0
100
@SUBJECT$ @PREDICAT$ of @OBJECT$ in adipose stromal cells from regularly cycling women.
Fact
preserve
277-283
277-283
T21
within
LOCATION_OF
277
283
preserve
284-296
291-296
T20
target cells
Cell
284
296
preserve
257-276
268-276
T19
STAT proteins
AminoAcidPeptideOrProtein
257
276
A13
Leptin causes the activation of STAT proteins within target cells.
225-297
225
297
Leptin causes the activation of @OBJECT$ @PREDICAT$ @SUBJECT$ .
Fact
preserve
1766-1777
1772-1777
T123
obese women
PROCESS_OF
1,766
1,777
preserve
1766-1771
1766-1771
T109
obese
DiseaseOrSyndrome
1,766
1,771
preserve
1772-1777
1772-1777
T110
women
PopulationGroup
1,772
1,777
A14
The elevated levels of aromatase activity may contribute to increase circulating estrogen levels in certain obese women and suggest that elevated leptin concentrations in obese women may cause locally elevated estrogen concentrations in the breast and thereby promote tumor formation.
1652-1960
1,652
1,960
The elevated levels of aromatase activity may contribute to increase circulating estrogen levels in certain @SUBJECT$ @PREDICAT$ @OBJECT$ and suggest that elevated leptin concentrations in obese women may cause locally elevated estrogen concentrations in the breast and thereby promote tumor formation.
Possible
preserve
448-456
448-456
T33
regulate
AFFECTS
448
456
preserve
437-443
437-443
T29
leptin
AminoAcidPeptideOrProtein
437
443
preserve
457-475
467-475
T30
aromatase activity
MolecularFunction
457
475
A15
The aromatase gene promoter in adipose stromal cells contains a functional STAT binding region, leading to the hypothesis that leptin may regulate aromatase activity in fat tissue.
298-490
298
490
The aromatase gene promoter in adipose stromal cells contains a functional STAT binding region, leading to the hypothesis that @SUBJECT$ may @PREDICAT$ @OBJECT$ in fat tissue.
Fact
preserve
1467-1557
1524-1534
T68
occupational asthma are directly applicable to the evaluation of diisocyanate asthma
ISA
1,467
1,557
preserve
1467-1486
1480-1486
T66
occupational asthma
DiseaseOrSyndrome
1,467
1,486
preserve
1551-1557
1551-1557
T67
asthma
DiseaseOrSyndrome
1,551
1,557
A1
CONCLUSIONS: Published diagnostic guidelines for occupational asthma are directly applicable to the evaluation of diisocyanate asthma.
1418-1558
1,418
1,558
CONCLUSIONS: Published diagnostic guidelines for @SUBJECT$ @PREDICAT$ @OBJECT$ .
Fact
preserve
364-373
364-373
T27
diagnosis
DIAGNOSES
364
373
preserve
507-524
519-524
T24
immunologic tests
DiagnosticProcedure
507
524
preserve
390-396
390-396
T19
asthma
DiseaseOrSyndrome
390
396
A2
The accurate diagnosis of diisocyanate asthma requires a systematic approach that combines information obtained from the occupational history, immunologic tests and physiologic studies.
351-549
351
549
The accurate @PREDICAT$ of diisocyanate @OBJECT$ requires a systematic approach that combines information obtained from the occupational history, @SUBJECT$ and physiologic studies.