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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
6 seen in the control subjects (n = 3) or the non-ischemic basal ganglia of subjects undergoing 2-hour
8 tor (statin) therapy on surrogate markers in non-ischemic cardiomyopathy (NICM) patients and average
10 ycardia Trial (MUSTT), the Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINI
11 enrolled in the DEFINITE (DEFIbrillators in Non-Ischemic cardiomyopathy Treatment Evaluation) study.
12 tertiary referral centers, 228 patients with non-ischemic cardiomyopathy without history of CHF were
14 ance of myocardial fibrosis in patients with non-ischemic cardiomyopathy without history of congestiv
15 dictors of recovery included: age <50 years, non-ischemic cardiomyopathy, time from cardiac diagnosis
17 ndard angiography or from other ischemic and non-ischemic causes that may confer increased risk for f
18 mulated wound repair under both ischemic and non-ischemic conditions in young animals, although it sh
23 The ischemic group had more cell death than non-ischemic controls as assessed by Trypan Blue exclusi
24 ntly more cell death (propidium iodide) than non-ischemic controls at 24 hr and significantly more ap
29 AO), brains were dissected into ischemic and non-ischemic cortices and Western blots were employed to
31 DS AND Ninety-nine patients with ischemic or non-ischemic dilated cardiomyopathy undergoing prophylac
34 hrine was observed in brain homogenates from non-ischemic DSP-4-treated rats compared with control.
37 ysfunction (resulting from both ischemic and non-ischemic etiologies) and symptomatic chronic heart f
38 Patients With Left Ventricular Dysfunction, Non-ischemic Etiology in Primary Prevention Treated with
39 rowth factor-B even healed more rapidly than non-ischemic excisional wounds treated with vehicle (p <
44 al lipid accumulation is a common feature of non-ischemic heart failure and is associated with change
46 aramedian cortex and thalamus), while in the non-ischemic hemisphere all regions measured showed sign
50 schemic hemisphere and in the contralateral (non-ischemic) hemisphere when compared to vehicle-treate
57 increased equivalently in both ischemic and non-ischemic lobes, suggesting a more generalized role i
58 upregulated in ischemic tissue compared with non-ischemic matched pairs (p<0.001) and both TKR and VV
59 s LVDP and cardiac contractility in isolated non-ischemic murine hearts, prolongs ischemic contractur
60 ion of genetically engineered myoblasts into non-ischemic muscle led to an increase in vascular struc
63 s in the ischemic CRVO group compared to the non-ischemic patients (P = 0.005, Fisher's exact test).
65 brain edema, were measured in contralateral (non-ischemic), penumbra and densely ischemic brain regio
67 2 calculated for cortical areas representing non-ischemic (Region A), perifocal/penumbral (Region B)
68 the hypothesis that neurons in ischemic and non-ischemic regions died from different mechanisms; spe
69 sions were increased in the border zones and non-ischemic remote regions of the post-ischemic heart.
71 es of uninjured distal ischemic and proximal non-ischemic skin were harvested at below knee amputatio
73 ardioverter Defibrillators] in Patients With Non-Ischemic Systolic Heart Failure on Mortality) did no
74 Assess the Efficacy of ICDs in Patients With Non-Ischemic Systolic Heat Failure on Mortality) suggest
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