ライフサイエンスコーパス: infarct border zone

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

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

3 ted with increased neovascularization of the infarct border zone.

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

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

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

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

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

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

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

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

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

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

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

15 Larger infarct border zone and its percentage of myocardium wer

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

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

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

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

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

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

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

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

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

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

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

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

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

29 Ventricular infarct border zone is characterized by abnormal cellula

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

31 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

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

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

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

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

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

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

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

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

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

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

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

43 In the infarct border zone, secretoneurin induced coronary angi

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

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

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

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

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

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

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

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

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