ライフサイエンスコーパス: infarct area

1 regulation of neutrophil infiltration to the infarct area.

2 ocation of NFkappaB in affected cells in the infarct area.

3 ate, consequently decreasing the size of the infarct area.

4 g intracerebral bleeding thus reducing brain infarct area.

5 g and postischemic inflammation, in the peri-infarct area.

6 ume of phosphate-buffered saline in the peri-infarct area.

7 sults in the generation of dead cells in the infarcted area.

8 erized by the presence of macrophages in the infarcted area.

9 e (vehicle) along the border of the blanched infarcted area.

10 was detected when moving from healthy toward infarcted area.

11 apoptosis in cardiomyocytes adjacent to the infarcted area.

12 rganization of the collagenous matrix in the infarcted area.

13 sponse and infiltration of leukocytes to the infarcted area.

14 ligation, iPS cells were delivered to mapped infarcted areas.

15 nslocated into the nuclei of neurons in peri-infarcted areas.

16 ones, whereas no positive cells were seen in infarcted areas.

17 limitation in cell delivery into ischemic or infarcted areas.

18 uced tracer uptake; scrambled CRIP uptake in infarct area (0.74 +/- 0.17%) was similar to CRIP uptake

19 d increases in CBF around the boundary of an infarct area 1 month after ischemia.

20 receiving Ad-CXCR4 displayed an increase in infarct area (13.5% +/- 4.1%) and decreased fractional s

21 We isolated cells from the cortical peri-infarct area 3 d after stroke, and cultured them in neur

22 ntricular zone, corpus callosum and the peri-infarct area 7 days after stroke by 2.2-fold, 2.3-fold a

23 Arteriolar density increased 3-fold in the infarct area (8.4+/-0.9/mm(2) in controls versus 22.2+/-

24 from the contralateral hemisphere) toward an infarcted area (a representative CNS injury), where loca

25 In contrast, remote from the primarily infarcted areas, a marked T2(*)- hypointensity was detec

26 All rats were sacrificed for measurement of infarct area after 24 h.

27 improves microvascular flow and reduces the infarct area after coronary occlusion/reperfusion, indep

28 ects of MSCs, we injected MSCs into the peri-infarct area after ligation of the left anterior descend

29 reduction of neuronal nuclear antigen in the infarcted area, although no improvement in neurological

30 hown to promote neovascularization, decrease infarct area and attenuate left ventricular (LV) dysfunc

31 ll population predominantly increases in the infarct area and exhibits strengthened reparative abilit

32 of cerebral blood flow (CBF), prediction of infarct area and hemoglobin oxygenation over the whole m

33 l increases endogenous cardiomyocytes in the infarct area and maintains cardiac function without indu

34 number of neuroblasts migrating in the peri-infarct area and the cortical width index.

35 gnificantly increased vascularization of the infarct areas and reduced myocardial scarring in animals

36 own to extend cortical representation of the infarcted area and improve skilled motor performance.

37 , 38 miRNAs were differentially expressed in infarcted areas and 33 miRNAs were aberrantly expressed

38 ake was significantly reduced in reperfused, infarcted areas and was reflective of viability and the

39 n, lipid peroxidation and apoptosis, a large infarct area, and a decrease in left ventricular functio

40 ated with inhibition of angiogenesis, larger infarct areas, and contractile dysfunction after MI.

41 l, increased ejection fraction, reduction of infarct areas, and inhibition of cardiac apoptosis and f

42 -MI leukocyte density, residence time in the infarcted area, and exit from the infarcted injury predi

43 ession was markedly up-regulated in the peri-infarct area at 3 days after permanent focal cerebral is

44 Contrary to our hypothesis, the size of infarct area at risk was similar in the heterozygous con

45 e total infarct volume (by 52%) and cortical infarct areas at multiple coronal levels, but subcortica

46 table cortical neurons (even >1 mm into peri-infarct areas, away from the infarct core) were impaired

47 ted disease severity, evidenced by increased infarct area, blood-brain barrier dysfunction, increased

48 yocytes and inflammatory infiltrates in peri-infarct areas, but not in remote areas.

49 pression was significantly down-regulated in infarcted areas, but was up-regulated in border areas.

50 ells promoted neovascularization in the peri-infarct area by paracrine activity rather than active tr

51 rem2 is transiently induced after MI in peri-infarct area cardiomyocytes during the inflammatory phas

52 treatment group had a statistically smaller infarct area compared with the control infarct group.

53 dly reduced collagen fibril formation in the infarct area due to impaired fibroblast activation.

54 hemical HDAC inhibitors significantly reduce infarct area, even when delivered 1 h after the ischemic

55 staining was performed on brains at 24 h and infarct area fractions were measured.

56 autologous skeletal myoblasts into the peri-infarct area has been performed at bypass surgery and by

57 athy in the area immediately surrounding the infarcted area; however, the effect was transient, poten

58 ng parameters to estimate risk area (RA) and infarct area (IA) during coronary occlusion and reperfus

59 astrocyte hypertrophy were found around the infarct area in testosterone-treated rats compared with

60 mented in ventricular tissue surrounding the infarct area in the heart of rats with myocardial infarc

61 by 0.75 +/- 0.10-fold of the control in the infarct area in the mouse brains.

62 ne treated rats showed significantly reduced infarct areas in the caudoputamen compared to saline tre

63 Microvasculature in peri-infarct area, infarct size, and animal functional recove

64 The coronal infarct area (mean+/-S.E.M.) was 19.3+/-1.8% for vehicle

65 The coronal infarct area (mean+/-S.E.M.) was 9.5+/-1.0% for intact f

66 ischemia-reperfusion injury, as assessed by infarct area measurements, DNA laddering, terminal deoxy

67 c echo (ICE, 9 MHz) and grouped by location: infarct (area of akinesis by ICE), border (0.5-cm perime

68 density was significantly higher in the peri-infarct area of hSCF/tetracycline transactivator mice co

69 flow and microvascular integrity in the peri-infarct area of miR-155 inhibitor-injected mice.

70 rating decreased neuronal damage in the peri-infarct area of stroke.

71 n Cx43 (Connexin 43) was reduced in the peri-infarct area of wild-type compared with Mpo(-/-) mice.

72 nce staining) was significantly lower in the infarct areas of f/f/Cre-MI compared with f/f-MI mice.

73 rus-transduced hMSCs were injected into peri-infarct areas of the hearts of severe combined immune-de

74 The ME-labeled iCMs were injected into the infarcted area of murine heart and probed by MRI and bio

75 However, injecting the infarcted area of the adult mammalian heart with exogeno

76 blasts in fibrin glue were injected into the infarcted area of the left ventricle.

77 y decreased cell apoptosis in the border and infarcted areas of the infarcted rat hearts after treatm

78 not find evidence of new muscle cells in the infarct area, our conclusion is that G-CSF and SCF enhan

79 and their brains were evaluated to determine infarct area, oxidative stress parameters, and ET recept

80 s, with a small but significant reduction in infarct area (p = 0.038).

81 Maximum CRIP uptake was observed in the infarct area; quantitative uptake (percent injected dose

82 The quality of restoration (graft/infarct area ratio) was 45.5+/-10.8% in group I and 29.1

83 Degree of restoration (GFP-positive graft/infarct area ratio), expression of cardiac markers, host

84 erfusion, revealed AT1R up-regulation in the infarct area relative to remote myocardium, whereas rete

85 ible for the engulfment of dead cells in the infarcted area remain largely unknown.

86 ir ability to improve vascularization of the infarct area seen after transplantation.

87 Infarct area size was significantly reduced in GPI dogs

88 CT Hounsfield units (HUs) in the infarct area started to exceed those of arterial blood a

89 ase (MMP)-2 and MMP-3 expression in the peri-infarct area, suggesting decreased fibrotic remodeling o

90 O mice had less collagen accumulation in the infarcted area than did WT mice, and they showed enhance

91 ntour of the bright region exactly match the infarcted area, this level of validation does not exist

92 r, histological measurements of the ratio of infarct area to area at risk were smaller in AMD3100-tre

93 rate myocardium and improve perfusion to the infarct area to improve cardiac function but also sugges

94 th high spatial resolution spanning from the infarcted area to the remote to identify new regulators

95 cipital white matter, and at least one large infarct (area under the receiver operating characteristi

96 ional AT1R upregulation is detectable in the infarct area using (11)C-KR31173.

97 Accumulation of gadoversetamide in the infarct area was apparent after 5 minutes, and the peak

98 The elevated uptake of (11)C-KR31173 in the infarct area was detectable by small-animal PET in vivo,

99 2,3,5-triphenyltetrazolium chloride, and the infarct area was determined with a computer digitizer.

100 Less collagen I mRNA within the infarct area was found in OIM/OIM animals.

101 r reduction in gadoterate meglumine-enhanced infarct area was measured in treated animals (18.6%+/-1.

102 Additionally, the infarct area was reduced to the same extent in Lac + Hyd

103 ch were OX62(+) dendritic cells, in the peri-infarct area was significantly attenuated by HMGB1 injec

104 Infarct area was significantly reduced in G-3.

105 The down-regulation of miR-21 in the infarcted areas was inhibited by ischemic preconditionin

106 In fact, fibroblasts within the infarcted area were largely of epicardial origin.

107 vo analysis confirmed ET-A expression in the infarct area, where the signal was partially colocalized

108 TTC stain was used to mark infarct areas, which were sized using computerized digit

109 The reduction in infarct area with CSD during inhalation of 1% halothane

110 yocytes results in a significant increase in infarct area with decreased expression of the antiapopto

111 gional AT1R upregulation was detected in the infarct area, with a peak at 1-3 wk after surgery (autor