ライフサイエンスコーパス: infarct region

1 re was an intermediate quantity of TG in the infarct region.

2 response observed histologically in the peri-infarct region.

3 ells or polymers, alter the mechanics of the infarct region.

4 droitinase ABC did not neuroprotect the peri-infarct region.

5 angiopoietin-2 (Ang-2) increased in the peri-infarct region.

6 perfusion caused marked p21 induction in the infarct region.

7 ctions; and (3) injection of material to the infarct region.

8 infarction through bulking or stiffening the infarct region.

9 n=35) or Ad-null (control; n=15) at the peri-infarct region.

10 6) myoblasts were injected directly into the infarct region.

11 eased exclusively in neurons within the peri-infarct region.

12 ally uncoupling viable cardiomyocytes in the infarct region.

13 infarction is usually due to reentry in the infarct region.

14 en diameter, and red blood cell flux in peri-infarct regions.

15 iomyocyte apoptosis was measured in the peri-infarct regions.

16 thelial growth factor receptor type 2 in the infarcted region.

17 endogenous c-Kit(+) progenitor cells to the infarcted region.

18 sion coefficient (ADC), decreases within the infarcted region.

19 d nullified conduction delay in adjacent non-infarcted regions.

20 issue from preserved myocardial regions into infarcted regions.

21 n survival of neurones, particularly in peri-infarcted regions.

22 activity predominantly coregistered with the infarcted regions.

23 he survival of neurons, particularly in peri-infarcted regions.

24 mechanical load, or mechanical tethering to infarcted regions.

25 Afferent inputs were attenuated from the infarcted region (19% in control vs. 7% in MI; P = 0.03)

26 aerobic and aerobic metabolism of an acutely infarcting region; (2) define changes in anaerobic glyco

27 10 [9] SD micromol/g wet weight) than in non-infarcted regions (26 [11] micromol/g, p=0.001) of myoca

28 39K MR image intensity was reduced in infarcted regions (51.7+/-4.8% of remote; P<0.001).

29 Eight weeks later, the chronically infarcted region again hyperenhanced (253+/-54% of norma

30 lectroanatomic mapping system to measure the infarct region and ablation lines.

31 Further examination revealed that the infarct region and apoptotic as well as necrotic injurie

32 expression was limited to the immediate peri-infarct region and was absent from remote areas of the l

33 mia by increasing the level of Bcl-2 in peri-infarct regions and that estrogen-induced bcl-2 gene exp

34 vation, and TUNEL-positive cells in the peri-infarct region, and suppresses autophagic cell death com

35 eability, loss of synaptic structure in peri-infarct regions, and improved recovery of forepaw functi

36 yzed both globally and regionally, excluding infarcted regions, and a mismatch score, defined as the

37 ence between contours of T2-hyperintense and infarcted regions, and the transmural-extent of these re

38 own to correspond well with noninfarcted and infarcted regions as detected by delayed enhancement car

39 ease in myocardial radiotracer uptake in the infarct region associated with histological evidence of

40 diomyocytes were found primarily in the peri-infarct region at a prevalence of around 0.02% and were

41 In contrast, in the infarcted region, at four weeks after infarction, fracti

42 t size and divided it into the core and peri-infarct regions based on signal-intensity thresholds (>3

43 emia while triggering remodeling in the peri-infarct region by means of perceived hyperoxia.

44 ntense regions with the intricate contour of infarcted regions by delayed-enhancement MRI.

45 d the wall thickness in the apex and basilar infarct regions compared with the control infarct.

46 ram wet weight) in the control, at-risk, and infarct regions confirmed the 1H NMR measurements.

47 le dose at three different sites of the peri-infarct region consisting, respectively, of DNA enzyme E

48 motes cellular hypertrophy in the border and infarcted regions coupled with an upregulation of hypert

49 mage intensity were correlated with those of infarcted regions defined histologically (r=0.97 and r=0

50 provement in wall thickening was observed in infarcted regions during NTG infusion, dobutamine infusi

51 After MI, FBzBMS uptake was preserved in the infarct region from day 1 to month 6, whereas the perfus

52 Infarct regions from wild-type and MMP-9 null mice (n=8

53 Compared with remote regions, in acutely infarcted regions, Gd was increased (235+/-24%, P<0.005)

54 Similarly, in chronically infarcted regions, Gd was increased (472+/-78%, P<0.001)

55 emote regions, tissue analysis revealed that infarcted regions had reduced 39K concentration (by MR s

56 xide synthase expression in peri-infarct and infarct regions in the hearts of constitutive HIF-1alpha

57 apillaries, and arterioles were noted in the infarcted region in cytokine-treated chimeric mice treat

58 injection of bone marrow-derived cells into infarcted regions in animal models.

59 oint (p < 0.01), and ESLV wall stress in the infarcted regions increased with time (25.1 +/- 5.9 vs.

60 mimicking the mechanical environment of the infarct region induces a synthetic phenotype with elevat

61 Infarct region, infarct-related artery, male sex, and RV

62 ptosis of hypertrophied myocytes in the peri-infarct region, long-term salvage and survival of viable

63 sinus rhythm, slow conduction through an old infarct region may depolarize tissue after the end of th

64 nce of microvascular obstruction (MO) within infarcted regions may adversely influence left ventricul

65 Peak hyperenhancement of infarcted regions occurred approximately 5 minutes after

66 ificantly less blood vessel formation in the infarct region of disrupted mice; by day 14, echocardiog

67 p62 indicated an impaired mitophagy in peri-infarct regions of LV in T2DM mice compared with control

68 rdiomyocytes and cardiac macrophages in peri-infarct regions of LV in T2DM mice.

69 lular matrix proteins were attenuated in the infarct regions of MMP-28(-/-) mice, indicating reduced

70 HLA were identified in the infarct and peri-infarct regions of the mouse hearts.

71 nism that inhibits collagen synthesis in the infarcted region of Agtr2-/Y mice.

72 closely related miRNAs, is regulated in the infarcted region of the heart in response to ischemia-re

73 Emc10 protein abundance was increased in the infarcted region of the left ventricle and in the circul

74 inflammatory cells from both stroke and peri-infarcted regions of the brain.

75 d over the entire slice (P=0.038) and in the infarcted region (P=0.0086) was significantly higher in

76 increase of microvasculature density in the infarcted region (P=0.0105 versus vehicle).

77 patients in the border zone and adjacent and infarcted regions (P < .001).

78 lysis showed increased OPN expression in the infarcted region, peaking 3 days after MI and gradually

79 tensity appeared to be identical to those of infarcted regions (r=0.97, y=0.92x+1.52, P<0.001).

80 colony stimulating factor, would home to the infarcted region, replicate, differentiate, and ultimate

81 -fold and approximately 7-fold in remote and infarcted regions, respectively, of WT hearts after MI b

82 sity and preserved cardiomyocyte size in the infarcted regions suggesting CCs role in protective para

83 ng gap junctions were incorporated into both infarct regions, the periinfarct zone (PZ) and the scar;

84 ts, the LV was remodeled by plication of the infarct region to reduce myocardial bulging, without mus

85 Afferent neural signals from the infarcted region to IC neurons are attenuated, while tho

86 y redistribution of myocardial work from the infarcted region to the viable tissue.

87 owed by 24-hour reperfusion, showed that the infarct region-to-risk region ratio was 8.1+/-1.1% in TG

88 In infarcted regions, total tissue [Na+] was elevated (89+/

89 in part, to enhanced neoangiogenesis in the infarcted region via upregulation of the ER target gene

90 nt of large, thin-walled vessels at the peri-infarct region was accompanied by induction of prolifera

91 fusion-induced up-regulation of Acta2 in the infarct region was completely abrogated in p21-deficient

92 e time of acute PTCA to follow-up PET in the infarct region was significant (p = 0.005).

93 Hearts were explanted and the infarcted region was restored using collagen matrix (CM)

94 Myocardial work in infarcted regions was zero.

95 henyltetrazolium chloride staining, anatomic infarct regions were delineated, dissected, and weighed.

96 In 11 patients, 13 confluent low-voltage infarct regions were present.

97 Infarcted regions were defined as 2,3,5 triphenyltetrazo

98 Infarcted regions were defined by anti-myoglobin antibod

99 erfusion was preserved and flow estimates in infarcted regions were differentiated more easily from n

100 Strains in infarcted regions were greatly impaired compared with re

101 ly unexcitable scar (EUS) within low-voltage infarct regions will locate reentry circuit isthmuses by

102 IRF imaging of MMP activity increased in the infarct region, with maximal expression at 1 to 2 weeks,