ライフサイエンスコーパス: triphenyltetrazolium

1 .9%) than true infarction as demonstrated by triphenyltetrazolium chloride (TTC) (24.6+/-1.4%, P<0.00

2 weeks), the lesion was assessed using 2,3,5-triphenyltetrazolium chloride (TTC) or hematoxylin and e

3 Necrosis was assessed with triphenyltetrazolium chloride (TTC) staining and a trans

4 Triphenyltetrazolium chloride (TTC) staining demonstrate

5 ) and to compare 99mTc-sestamibi imaging and triphenyltetrazolium chloride (TTC) staining for reliabi

6 ly to the rat, and often paired with 2, 3, 5-triphenyltetrazolium chloride (TTC) staining for stroke

7 ed at 24 h after acute coronary occlusion by triphenyltetrazolium chloride (TTC) staining in wild-typ

8 Triphenyltetrazolium chloride (TTC) staining indicated t

9 e relationship of infarct size determined by triphenyltetrazolium chloride (TTC) staining versus (99m

10 Postmortem triphenyltetrazolium chloride (TTC) staining was used to

11 Cell death was visualized by 2,3,5-triphenyltetrazolium chloride (TTC) staining, hematoxyli

12 wed by infarct volumes measurements by 2,3,5-triphenyltetrazolium chloride (TTC) staining.

13 maging, microsphere blood flow analysis, and triphenyltetrazolium chloride (TTC) staining.

14 24-h post-ischaemia by histology with 2,3,5-triphenyltetrazolium chloride (TTC) staining.

15 Histochemical staining with triphenyltetrazolium chloride (TTC) was used to confirm

16 Triphenyltetrazolium chloride (TTC) was used to delineat

17 Heart slices were imaged, then stained with triphenyltetrazolium chloride (TTC), and tissues were we

18 d with microsphere-determined blood flow and triphenyltetrazolium chloride (TTC)-stained tissue sampl

19 into coronal slices and stained with 2, 3, 5-triphenyltetrazolium chloride (TTC).

20 )Na MRI correlated best with infarct size by triphenyltetrazolium chloride and contrast-enhanced (1)H

21 farct size, determined by dual staining with triphenyltetrazolium chloride and phthalocyanine blue dy

22 farct size, determined by dual staining with triphenyltetrazolium chloride and phthalocyanine blue dy

23 compared with normal remote regions, without triphenyltetrazolium chloride evidence of necrosis.

24 both models despite normal perfusion and no triphenyltetrazolium chloride evidence of necrosis.

25 The brains were removed and stained with triphenyltetrazolium chloride for infarct volume determi

26 Triphenyltetrazolium chloride infarcts among animals wit

27 Infarcted regions were defined as 2,3,5 triphenyltetrazolium chloride negative regions.

28 hin 24 h after reperfusion and compared with triphenyltetrazolium chloride pathology.

29 Assessment of necrosis by histology or triphenyltetrazolium chloride showed 40+/-5% multifocal

30 tion (IF) for each segment was determined by triphenyltetrazolium chloride stain.

31 8.5% +/- 0.9 vs 11.3% +/- 0.9, P = .048) and triphenyltetrazolium chloride staining (9.4% +/- 1.5 vs

32 MDCT infarct volume compared well with triphenyltetrazolium chloride staining (acute infarcts 2

33 with infarct volumes as determined by 2,3,5-triphenyltetrazolium chloride staining (R(2) = 0.692, P

34 red by in vivo 23Na MRI correlated well with triphenyltetrazolium chloride staining (r=0.87, y=0.92x+

35 -dependent brain damage as revealed by 2,3,5-triphenyltetrazolium chloride staining (severe > moderat

36 In nonbeating hearts and at triphenyltetrazolium chloride staining at 1 week, microi

37 s assessed by serial echocardiography, 2,3,5-triphenyltetrazolium chloride staining determined infarc

38 echo time 8 ms, 2-tesla system), followed by triphenyltetrazolium chloride staining for infarct detec

39 and histology (thioflavin for area at risk, triphenyltetrazolium chloride staining for MI size).

40 after MI as assessed by echocardiography and triphenyltetrazolium chloride staining of live tissue.

41 ion in infarct volumes (P < 0.001), based on triphenyltetrazolium chloride staining of serial cerebra

42 Postmortem 2,3,5-triphenyltetrazolium chloride staining quantified SEMI.

43 Triphenyltetrazolium chloride staining showed that infar

44 sessed by echocardiography couple with 2,3,5-Triphenyltetrazolium chloride staining to measure MI siz

45 was compared with pathological (exclusion of triphenyltetrazolium chloride staining) and ICE measurem

46 iated with a decreased infarct volume (2,3,5-triphenyltetrazolium chloride staining) in the striatum

47 Infarct size (triphenyltetrazolium chloride staining) was comparable b

48 With triphenyltetrazolium chloride staining, anatomic infarct

49 Infarct size was determined by 2,3,5-triphenyltetrazolium chloride staining, and creatine kin

50 y, magnetic resonance imaging, hemodynamics, triphenyltetrazolium chloride staining, and histological

51 Infarct size (IS) was measured by triphenyltetrazolium chloride staining, and iNOS express

52 Myocardial infarct size was measured through triphenyltetrazolium chloride staining, and polymorphonu

53 Infarct size was determined by triphenyltetrazolium chloride staining, and the activity

54 tion of cerebral infarct volumes measured by triphenyltetrazolium chloride staining, as well as impro

55 imaging results were confirmed by postmortem triphenyltetrazolium chloride staining, elastica van Gie

56 Ischemic lesion was evaluated by 2,3,5-triphenyltetrazolium chloride staining, hematoxylin and

57 Infarcted, reperfused regions, identified by triphenyltetrazolium chloride staining, showed a signifi

58 -activated cell sorting and hearts for 2,3,5-triphenyltetrazolium chloride staining.

59 hibitor cucurbitacin I (JSI-124) using 2,3,5-triphenyltetrazolium chloride staining.

60 CAO, and infarct volume was determined using triphenyltetrazolium chloride staining.

61 MA and Gd-DTPA and were confirmed by ex vivo triphenyltetrazolium chloride staining.

62 ts were free of infarction, as detected with triphenyltetrazolium chloride staining.

63 s were defined by anti-myoglobin antibody or triphenyltetrazolium chloride staining.

64 erfusion, and infarct size was quantified by triphenyltetrazolium chloride staining.

65 fluorescent particles and infarct size with triphenyltetrazolium chloride staining.

66 extent of necrosis (TEN) (%) was measured by triphenyltetrazolium chloride staining.

67 extent of the infarct was assessed by 2,3,5 triphenyltetrazolium chloride staining.

68 measured at 22 hrs of reperfusion with 2,3,5-triphenyltetrazolium chloride staining.

69 nd infarct volume was assessed after 48 h by triphenyltetrazolium chloride staining.

70 Infarct size was determined by triphenyltetrazolium chloride staining.

71 (left ventricular pressure-volume curves; 1% triphenyltetrazolium chloride staining; creatine kinase

72 ated as the primary outcome measure by using triphenyltetrazolium chloride vital staining.

73 The infarction size defined by using triphenyltetrazolium chloride was 13% +/- 4 smaller than

74 ompared with postmortem myocardial staining (triphenyltetrazolium chloride) and microsphere blood flo

75 The effect on infarct size (triphenyltetrazolium chloride) of acute ethanol exposure

76 ), less decline in +/-dP/dt, and smaller MI (triphenyltetrazolium chloride, 21+/-11% versus 3+/-8%; P

77 characterized by magnetic resonance imaging, triphenyltetrazolium chloride, and hemotoxylin and eosin

78 brains were sectioned and stained with 2,3,5-triphenyltetrazolium chloride, and the infarct area was

79 itially using the cell viability stain 2,3,5-triphenyltetrazolium chloride, but was determined in sub

80 obstruction (thioflavin S) and infarct size (triphenyltetrazolium chloride, TTC).

81 abnormal time constants correlated well with triphenyltetrazolium chloride-determined infarct size (r

82 ined by quantitative image analysis of 2,3,5-triphenyltetrazolium chloride-stained brain sections.

83 tion of the pattern of dye staining on 2,3,5-triphenyltetrazolium chloride-stained heart slices agree

84 ined by threshold analysis and compared with triphenyltetrazolium chloride-stained sections of the ex

85 Ablation size was visualized by using 2% triphenyltetrazolium chloride.

86 measurement of formazan produced from 2,3,5-triphenyltetrazolium chloride.

87 troxyl reduction was confirmed using EPR and triphenyltetrazolium chloride.

88 dium was stained with thioflavin-S and 2,3,5-triphenyltetrazolium chloride.

89 reperfusion, infarct size was measured with triphenyltetrazolium chloride.

90 Postmortem infarct size was measured with triphenyltetrazolium chloride.

91 ea infarcted was determined by staining with triphenyltetrazolium chloride.

92 ricle, 2.2+/-0.5% versus 5.4+/-1.5%, P=0.04; triphenyltetrazolium chloride: anterior wall, 10.3+/-4.6

93 Triphenyltetrazolium-determined injury volume of the ips

94 nt of the area at risk (AAR) was measured by triphenyltetrazolium stain.

95 Myocardial infarct size was determined by triphenyltetrazolium staining and expressed as a percent

96 We used triphenyltetrazolium staining to determine the amount of

97 Triphenyltetrazolium staining was used to assess the ext

98 nscription polymerase chain reaction, ELISA, triphenyltetrazolium staining, colorimetric/fluorometric

99 of the area at risk (AAR) was determined by triphenyltetrazolium staining.

100 ffect of treatment being evaluated by 2,3, 5-triphenyltetrazolium (TTC) staining after 3 days of reco

101 , hemorrhages are adjacent to areas of 2,3,5-triphenyltetrazolium (TTC)-negative tissue, normally ass

102 ermined by staining slices of the heart with triphenyltetrazolium, was significantly reduced in PC co