ライフサイエンスコーパス: infarct border zone

1 pling and myofibroblast proliferation in the infarct border zone.

2 to cell types of therapeutic interest in the infarct border zone.

3 onfirmed the presence of nerve fibers in the infarct border zone.

4 reduced apoptosis, including myocytes in the infarct border zone.

5 tion of FLT3 ligand (FL) or vehicle into the infarct border zone.

6 ted with increased neovascularization of the infarct border zone.

7 eated mice had fewer progenitor cells in the infarct border zone.

8 ardial blood flow (MBF), particularly in the infarct border zone.

9 xpressing endothelial cell population in the infarct border zone.

10 TESI was guided to 10 sites in infarct-border zones.

11 and migration of inflammatory cells into the infarct border zone 24 hours after ischemia/reperfusion

12 ctivating factor enhancement pathways in the infarct border zone 24 hours after MI, leading to decrea

13 ctivation of surviving myocardium within the infarct border zone, (4) reduced magnitudes of EGM negat

14 um, and a subset of mononuclear cells of the infarct border zone after 5 to 28 days of reperfusion.

15 pansion and cardiac myocyte apoptosis in the infarct border zone after myocardial infarction.

16 ture Ly6c(hi) monocytes infiltrated into the infarct border zone and differentiated into mature Ly6c(

17 dysfunction, and accentuated fibrosis in the infarct border zone and in the papillary muscles.

18 Larger infarct border zone and its percentage of myocardium wer

19 round thin-walled, dilated neovessels in the infarct border zone and was accompanied by decreased exp

20 ic LV regions can be described after MI: the infarct, border zone, and remote regions.

21 the delivery vehicle was injected around the infarct border zone area.

22 of cardiomyocyte cell cycle activity at the infarct border zone at 4 weeks after permanent coronary

23 -buffered saline; n=5) was injected into the infarct border zones at 14 days after MI.

24 aped H9c2 cells were found integrated in the infarct border zones at day 28.

25 able to increase AZ7379 availability in the infarct/border zone at 24h post-injection as compared wi

26 After myocardial infarction, the infarct border zone (BZ) is the dominant source of life-

27 Therapies targeting these cell types in the infarct border zone can improve cardiac function but are

28 Infarct border zone capillarization was impaired, scar s

29 g FVB/N mice with recombinant Emc10 enhanced infarct border-zone capillarization and exerted a sustai

30 infarction released Vegfa from HS, enhanced infarct border-zone capillarization, and exerted sustain

31 Residual ischaemia in the peri-infarct border zone causes further cardiomyocyte damage,

32 The intramyocardial injection of FL into the infarct border zone decreased infarct size and ameliorat

33 d understanding of the mechanisms underlying infarct border zone electrogram fractionation may be hel

34 genic electrophysiological remodeling at the infarct border zone (IBZ) compared to young rabbits.

35 majority of VTs late post-MI arise from the infarct border zone (IBZ).

36 s, ablation with PFA or RFA was performed at infarct border zones identified by abnormal electrograms

37 sels showed improved vascular density in the infarct border zone in captopril treated mice in compari

38 o-2'-deoxyuridine+) myocytes detected at the infarct border zone in fixed tissues.

39 te that the delivery of GATA4 locally to the infarct border zone induces multiple local effects in th

40 Ventricular infarct border zone is characterized by abnormal cellula

41 in particular with late gadolinium-enhanced infarct border zone mass (r=0.84, P<0.0001) and with pea

42 farct core mass was 21.7 g (4.4-45.9 g), and infarct border zone mass was 29.8 g (3.9-60.2 g) (full-w

43 Previous studies suggest that the peri-infarct border zone may be an important arrhythmogenic s

44 The infarct border zone may be capable of modulating the hea

45 mpaired catecholamine handling in the viable infarct border zone may play an important role in ventri

46 ective endogenous expression of TSP-1 in the infarct border zone may serve as a "barrier," limiting e

47 In the viable infarct border zone, neuronal vesicular catecholamine st

48 Increased granulocyte infiltration into the infarct border zone occurred in OIM/OIM animals.

49 When injected into the infarct border zone of immunodeficient mice 1 week after

50 sing (cont) for sIL-1ra, were implanted into infarct border zones of female nude mice immediately aft

51 e myocardium bound by the scar tissue at the infarct border zone or over the infarct.

52 e, injecting cMSC-conditioned media into the infarct border zone reduced apoptotic cardiomyocytes > 7

53 ificantly increased capillary density in the infarct border zone, reduced cardiac dilatation, ventric

54 6, and 8 days) enhanced angiogenesis in the infarct border zone, reduced scar size, and attenuated l

55 In the infarct border zone, SAHA increased autophagic flux, ass

56 In the infarct border zone, secretoneurin induced coronary angi

57 nes and associated neovascularization in the infarct border zone (see the related article beginning o

58 del, bipolar electrograms were acquired from infarct border zone sites in 10 canine heart experiments

59 RB3 expression in murine heart tissue in the infarct border zone suggesting that ER stress may play a

60 he ischemic areas, particularly in the inner infarct border zone (the penumbra), of the bid-deficient

61 cide with sharp thin-to-thick transitions in infarct border zone thickness.

62 At 2 days after MI, MMP-9 expression in the infarct border zone was higher in OIM/OIM than in WT/WT

63 After MI, however, capillarization of the infarct border zone was impaired in KO mice, and the ani

64 To identify peptides specific for the infarct/border zone, we used in vivo phage display metho

65 lated host-derived inflammatory cells in the infarct border zone, whereas intracoronary BM cell injec

66 of 11 PFA and 15 RFA lesions were created at infarct border zones with heterogeneous scar.