ライフサイエンスコーパス: non-ischemic

1 ating the neovascularization of ischemic and non-ischemic adult mouse tissues, we utilized a hindlimb

2 necessity of urgent transplantation in both non-ischemic and ischemic HF patients (91% vs. 72%, p <

3 ion of IL-1beta protein in brain tissue from non-ischemic and ischemic mice using immunohistochemistr

4 Arterioles (60-110 microm) isolated from non-ischemic and ischemic regions of subepicardium were

5 up to 1 h (1.8-fold) post injury compared to non-ischemic and sham operated tissue.

6 seen in the control subjects (n = 3) or the non-ischemic basal ganglia of subjects undergoing 2-hour

7 Expression of tie 1 was not detected in non ischemic brain.

8 Non-ischemic cardiomyopathy (NICM) can cause left ventri

9 tor (statin) therapy on surrogate markers in non-ischemic cardiomyopathy (NICM) patients and average

10 schemic heart disease (IHD; n = 21), dilated/non-ischemic cardiomyopathy (NICM; n = 21), or hypertrop

11 Chagas disease is a leading cause of non-ischemic cardiomyopathy in endemic regions of Centra

12 The Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINI

13 ycardia Trial (MUSTT), the Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINI

14 enrolled in the DEFINITE (DEFIbrillators in Non-Ischemic cardiomyopathy Treatment Evaluation) study.

15 tertiary referral centers, 228 patients with non-ischemic cardiomyopathy without history of CHF were

16 In patients with non-ischemic cardiomyopathy without history of CHF, myoc

17 ance of myocardial fibrosis in patients with non-ischemic cardiomyopathy without history of congestiv

18 ntify a pro-fibrogenic macrophage subtype in non-ischemic cardiomyopathy, and demonstrate that WWP2 i

19 (STEMI) presentation, stress cardiomyopathy, non-ischemic cardiomyopathy, coronary spasm, or nonspeci

20 h any of the following cardiac outcomes: HF, non-ischemic cardiomyopathy, dilated cardiomyopathy (DCM

21 dictors of recovery included: age <50 years, non-ischemic cardiomyopathy, time from cardiac diagnosis

22 R implantable cardioverter defibrillator AND non-ischemic cardiomyopathy.

23 ndard angiography or from other ischemic and non-ischemic causes that may confer increased risk for f

24 mulated wound repair under both ischemic and non-ischemic conditions in young animals, although it sh

25 with hindlimb ischemia compared with that in non-ischemic control mice.

26 Anesesthetized, non-ischemic control rats (N=6) were studied.

27 ated with 3-AB at doses of 55 mg/kg; and the non-ischemic control rats.

28 ebral ischemia compared to the sham-operated non-ischemic control.

29 The other hind limb served as a non-ischemic control.

30 The ischemic group had more cell death than non-ischemic controls as assessed by Trypan Blue exclusi

31 ntly more cell death (propidium iodide) than non-ischemic controls at 24 hr and significantly more ap

32 es (n=6), while the remaining dogs served as non-ischemic controls.

33 the vehicle-treated group and contralateral non-ischemic cortex.

34 ischemic cortex was compared to that in the non-ischemic cortex.

35 t adjacent to the ischemic lesion and in the non-ischemic cortex.

36 AO), brains were dissected into ischemic and non-ischemic cortices and Western blots were employed to

37 Additionally, patients with idiopathic non-ischemic DCM were included in this study.

38 Non-ischemic dilated cardiomyopathy (DCM) has been recog

39 expression was upregulated in the hearts of non-ischemic dilated cardiomyopathy patients, and in mic

40 DS AND Ninety-nine patients with ischemic or non-ischemic dilated cardiomyopathy undergoing prophylac

41 infarction, 18 with hypertrophic and 10 with non-ischemic dilated cardiomyopathy underwent manganese-

42 rphological analysis of fibrotic scarring in non-ischemic dilated cardiomyopathy, and its relationshi

43 (ACM) constitutes up to 40% of patients with non-ischemic dilated cardiomyopathy.

44 molecules have never been analysed in human non-ischemic dilated hearts (DCM).

45 hrine was observed in brain homogenates from non-ischemic DSP-4-treated rats compared with control.

46 re also determined in brain homogenates from non-ischemic DSP-treated and control rats.

47 The introduction of BDNF into non-ischemic ears or ischemic limbs induced neoangiogene

48 ysfunction (resulting from both ischemic and non-ischemic etiologies) and symptomatic chronic heart f

49 Patients With Left Ventricular Dysfunction, Non-ischemic Etiology in Primary Prevention Treated with

50 rowth factor-B even healed more rapidly than non-ischemic excisional wounds treated with vehicle (p <

51 The study population consisted of 8 non-ischemic failing (at LVAD implant) and 8 post-LVAD h

52 cardial lipid overload was present in 30% of non-ischemic failing hearts.

53 In Group 2 animals (n = 9), the (non-ischemic) frontal pole of the ipsilateral hemisphere

54 scular disorders, dysrhythmias, ischemic and non-ischemic heart disease, pericarditis, myocarditis, h

55 Ischemic and/or non-ischemic heart diseases (IHD and/or NIHD) were detec

56 al lipid accumulation is a common feature of non-ischemic heart failure and is associated with change

57 eart tissue from 27 patients (9 female) with non-ischemic heart failure.

58 aramedian cortex and thalamus), while in the non-ischemic hemisphere all regions measured showed sign

59 Few apoptotic cells were detected in the non-ischemic hemisphere of control rats.

60 ellular cytoplasm of control rats and in the non-ischemic hemisphere of rats subjected to MCAo.

61 o ADC decreases of about 30% compared to the non-ischemic hemisphere.

62 schemic hemisphere and in the contralateral (non-ischemic) hemisphere when compared to vehicle-treate

63 perfusion in the ischemic as well as in the non-ischemic hemispheres after permanent MCAo.

64 of x-ray attenuation between ischemic versus non-ischemic hemispheres.

65 reserved ejection fraction cases, and 11,122 non-ischemic HF cases among 213,828 individuals and iden

66 roved survival in patients with ischemic and non-ischemic HF.

67 in-B levels are altered in both ischemic and non-ischemic human heart failure.

68 diomyocyte cell death following ischemic and non-ischemic injuries.

69 ity of the heart following both ischemic and non-ischemic injury.

70 g activity were observed in the ischemic and non-ischemic lesions in the mouse brain.

71 As additional controls, non-ischemic livers preserved with 6 hr of SCS or NELP a

72 increased equivalently in both ischemic and non-ischemic lobes, suggesting a more generalized role i

73 upregulated in ischemic tissue compared with non-ischemic matched pairs (p<0.001) and both TKR and VV

74 s LVDP and cardiac contractility in isolated non-ischemic murine hearts, prolongs ischemic contractur

75 ion of genetically engineered myoblasts into non-ischemic muscle led to an increase in vascular struc

76 Exposure of H(2) gas to non-ischemic neonates resulted in a significant increase

77 The fourth case underwent a non-ischemic open PN in the setting of a midpole tumor w

78 luated for a range of different ischemic and non-ischemic pathologies encountered in clinical practic

79 s in the ischemic CRVO group compared to the non-ischemic patients (P = 0.005, Fisher's exact test).

80 vels rose with exercise in both ischemic and non-ischemic patients.

81 brain edema, were measured in contralateral (non-ischemic), penumbra and densely ischemic brain regio

82 MASCs transplanted into non-ischemic pups survived but retained their astrocytic

83 nt increase in NO production was observed in non-ischemic rat hearts treated with P188, further estab

84 2 calculated for cortical areas representing non-ischemic (Region A), perifocal/penumbral (Region B)

85 the hypothesis that neurons in ischemic and non-ischemic regions died from different mechanisms; spe

86 sions were increased in the border zones and non-ischemic remote regions of the post-ischemic heart.

87 feasible in both patients with ischemic and non-ischemic scar patterns.

88 disease and no disadvantage in patients with non-ischemic scar, dark-blood LGE can be readily and wid

89 disease related gene variants are common in non-ischemic SCD but further studies are required to det

90 n (68.9 +/- 4.6% vs. 89.3 +/- 3.0% reference non-ischemic septal segments; p < 0.001).

91 es of uninjured distal ischemic and proximal non-ischemic skin were harvested at below knee amputatio

92 was compared with patient- and site-matched non-ischemic skin.

93 The contribution of genetic variants to non-ischemic sudden cardiac death (SCD) due to acquired

94 ardioverter Defibrillators] in Patients With Non-Ischemic Systolic Heart Failure on Mortality) did no

95 Assess the Efficacy of ICDs in Patients With Non-Ischemic Systolic Heart Failure on Mortality), addin

96 Assess the Efficacy of ICDs in Patients with Non-ischemic Systolic Heart Failure on Mortality).

97 Assess the Efficacy of ICDs in Patients With Non-Ischemic Systolic Heat Failure on Mortality) suggest

98 apoptosis occurs in the penumbra region and non-ischemic thalamus after cerebral ischemia.

99 elayed cell death in the ischemic cortex and non-ischemic thalamus.

100 ATP synthesis was attenuated in non-ischemic TNFalpha-Tg rats, demonstrated by reduction