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1 ed post-MI, giving rise to a 'neural sensory border zone'.
2 rimary prevention ICD by quantifying the LGE border zone.
3 proliferation and synaptogenesis in the ICH border zone.
4 arrhythmia susceptibility in the healed scar border zone.
5 ar or mesenchymal stem cells) in LV scar and border zone.
6 M-derived cell incorporation in the ischemic border zone.
7 ce had fewer progenitor cells in the infarct border zone.
8 lood flow (MBF), particularly in the infarct border zone.
9 d increased in vivo proliferation within the border zone.
10 ger in the central ischemic zone than in the border zone.
11 th factor (VEGF), or MSCs +HGF/VEGF into the border zone.
12 animals, rising higher in the MI + MR-group border zone.
13 rcts also had marked TSP-1 deposition in the border zone.
14 on site was consistently located in the scar border zone.
15 types of therapeutic interest in the infarct border zone.
16 the presence of nerve fibers in the infarct border zone.
17 and large sinusoidal vascular canals in the border zone.
18 apoptosis, including myocytes in the infarct border zone.
19 e more viable cardiomyocytes within the scar/border zone.
20 FLT3 ligand (FL) or vehicle into the infarct border zone.
21 f resting perfusion in either the MI core or border zone.
22 gradients in cellular properties across the border zone.
23 e ions and carbon dioxide across an ischemic border zone.
24 increased neovascularization of the infarct border zone.
25 r conduction velocity in the anterior-septal border zone.
26 that were mainly located in the infarct and border zones.
27 cular function observed in either infarct or border zones.
28 in alone (sham) was injected into epicardial border zones.
29 idized fatty acid production in the ischemic border zones.
30 TESI was guided to 10 sites in infarct-border zones.
31 sed the T-tubule integrity at the remote and border zones.
32 tients, with no difference in the transition/border zone (11.4% [Q1-Q3, 9.5%-13.2%] versus 16.6% [Q1-
34 % CI, -2.78 to 1.34), and wall motion in the border zone (16.0 to 16.6 mm vs 16.1 to 19.3 mm; between
35 re run: (1) single injection to the anterior border zone; (2) therapeutic multiple border zone inject
36 ation of inflammatory cells into the infarct border zone 24 hours after ischemia/reperfusion injury,
37 g factor enhancement pathways in the infarct border zone 24 hours after MI, leading to decreased card
38 69+/-41 478 pixels(2)), intermediate in scar border zone (255 979+/-36 016 pixels(2)), and highest in
39 n of surviving myocardium within the infarct border zone, (4) reduced magnitudes of EGM negative deri
40 re within bipolar voltage-defined scar (7%), border zone (57%), and areas of normal voltage (36%), bu
41 ant, capillary density was 30% higher in the border zone (908.1+/-99.7/mm(2) in control versus 1209.0
42 nctional capillary network at the remote and border zone, accompanied by reduced scar extension, pres
45 tensity, a priori information and a weighted border zone algorithm, were compared with a modified ful
48 an important therapeutic target of peri-scar border zone and a promising therapeutic potential for us
49 ak Ecc than did noninducible patients in the border zone and adjacent and infarcted regions (P < .001
51 ng of the epicardium was also performed, and border zone and dense scar surface area and late potenti
52 c(hi) monocytes infiltrated into the infarct border zone and differentiated into mature Ly6c(lo) phag
56 able T-tubule remodeling near the infarction border zone and moderate LV remodeling remote from the M
57 ), nuclear Yap1 was found selectively in the border zone and not in the remote area of the heart.
59 ular potassium was found to have the largest border zone and this was attributed to the voltage depen
60 in-walled, dilated neovessels in the infarct border zone and was accompanied by decreased expression
63 and WISP1 expressions were increased in the border zones and non-ischemic remote regions of the post
65 isual characteristics of normal tissue, scar border zone, and dense scar in vivo with the use of a no
68 ed intensity, a priori information, weighted border zone, and modified full-width half-maximum algori
71 nce of the VT, 4 originated from an ischemic border zone, and the origin of 2 could not be determined
72 cute infarcts along the internal or anterior border zones, and 2 patients showed microembolic signals
73 in vivo testing, CLG-4 application decreased border zone area (21.3+/-14.3 to 17.1+/-11.1 mm(2), P=0.
74 of the reentrant circuits in the epicardial border zone associated with each morphology indicated tw
75 increase AZ7379 availability in the infarct/border zone at 24h post-injection as compared with free
76 iomyocyte cell cycle activity at the infarct border zone at 4 weeks after permanent coronary artery o
78 < or = 50% that without repair in remote and border zones at 3 months, and the matrix metalloproteina
79 on) left ventricular function in infarct and border zones at 6 months measured by cardiac magnetic re
82 (wall motion) LV function in the infarct and border zone between baseline and 6 months, measured by c
85 9 Hz resulted in wavebreak at the interface (border zone) between infected and non-infected regions;
93 ell-treatment group, P<0.05) in the periscar border zone (BZ), which was accompanied by improvements
95 es targeting these cell types in the infarct border zone can improve cardiac function but are limited
96 mice with recombinant Emc10 enhanced infarct border-zone capillarization and exerted a sustained bene
97 Shh) also reduced infarct size and increased border zone capillary density compared with unmodified C
98 r zone induces multiple local effects in the border zone cardiac myocytes resulting in beneficial ven
100 DCs lead to cardiomyocyte hyperplasia in the border zone, consistent with the observed stimulation of
101 l significantly different from the values in border zone cortex, and in cortex contralateral to ische
104 amyocardial injection of FL into the infarct border zone decreased infarct size and ameliorated post-
107 nts for weak acid (e.g., CO(2)) occur across border zones during regional myocardial ischemia, raisin
111 ap-junctional distribution in the epicardial border zone (EBZ) of healing canine infarcts define the
113 tricular fibrillation (VF) in the epicardial border zone (EBZ) of hearts with chronic myocardial infa
114 ax in myocytes dispersed from the epicardial border zone (EBZ) of the 5-day infarcted canine heart (m
115 in the remodeled substrate of the epicardial border zone (EBZ) of the 5-day infarcted canine heart.
116 ct Na+ channels of cells from the epicardial border zone (EBZ) of the 5-day infarcted heart different
118 was measured in arrhythmogenic subepicardial border zone (EBZ) tissue overlying the infarct and from
119 tanding of the mechanisms underlying infarct border zone electrogram fractionation may be helpful to
123 volume (approximately 4.5%) reduce elevated border zone fiber stresses from mean end-systole levels
124 erated remodeling and hypertrophy, increased border zone fibrosis, augmented NF-kappaB and p38 mitoge
126 significant disparities in the width of the border zone for each ionic species, with intracellular s
127 cortex contralateral to ischemic cortex and border zone (for all samples n=60, mean wet weight 2.037
131 decreased in culture media-treated rats, and border-zone function was preserved in ESC-treated animal
135 ish a cellular basis for hyperfluorescent GA border zones, histologic autofluorescence (HAF) was meas
138 dial injection of 6 mug ephrinA1-Fc into the border zone immediately after permanent coronary artery
141 nction correlated with less apoptosis in the border zone in those animals that received AdVEGF-165 ex
143 io at the ventral posterior nucleus-pulvinar border zone indicates that this area is crucial in the p
144 the delivery of GATA4 locally to the infarct border zone induces multiple local effects in the border
145 terior border zone; (2) therapeutic multiple border zone injections; and (3) injection of material to
146 stress may prevent the incorporation of the border zone into the infarct, decreasing infarct size an
147 eceptors decreased in the hippocampus in the border zone ipsilateral to the injury while there was an
150 have an apparent thickening of the anterior border zone; it remains to be established whether this i
151 icular with late gadolinium-enhanced infarct border zone mass (r=0.84, P<0.0001) and with peak tropon
152 re 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-width at
153 evious studies suggest that the peri-infarct border zone may be an important arrhythmogenic substrate
155 catecholamine handling in the viable infarct border zone may play an important role in ventricular re
156 ndogenous expression of TSP-1 in the infarct border zone may serve as a "barrier," limiting expansion
157 6.0%; interquartile range [IQR], 4.1%-8.0%), border zone (median, 8.4%; IQR, 6.4%-10.2%), and remote
158 ed in alleviation of abnormalities including border zone myocardial perfusion, contractile dysfunctio
159 tein connexin 43 (Cx43) occurs in epicardial border zone myocytes following myocardial infarction (MI
161 al muscle Na(+) channel (SkM1) to epicardial border zones normalizes conduction and reduces induction
163 maps of reentrant circuits in the epicardial border zone of 4-day old infarcted dog hearts with the c
166 ed us, in an earlier study, to inject in the border zone of acute infarcts Lin(-) c-kit(POS) BMC from
167 addition, human CDCs were injected into the border zone of acute myocardial infarcts in immunodefici
168 GF)-beta/Smad3 signaling is activated in the border zone of healing infarcts and induces fibrotic rem
171 ned from cloned embryos were injected in the border zone of infarcted mice to induce tissue reconstit
172 oth muscle coverage in the neovessels of the border zone of infarcted myocardium are severely impaire
177 endothelial growth factor (phVEGF165) in the border zone of myocardial infarct tissue in rat hearts w
179 into the infarct, and there was a continuous border zone of neutrophil infiltration that overlapped a
181 h muscle cells (VSMC) were injected into the border zone of subacute infarcted syngeneic Fischer rat
182 nd capillary density, was observed in the MI border zone of Tbx20(OE) hearts compared with controls.
183 2-isoketals were generated in the epicardial border zone of the canine healing infarct, an arrhythmog
186 s and decreased myofibroblast density in the border zone of the infarct support the beneficial effect
187 tion in reentrant circuits in the epicardial border zone of the infarct was mapped using 192 to 312 b
189 trant circuits were mapped in the epicardial border zone of the infarcts with a multielectrode array
192 early reperfusion is primarily in the viable border zone of the myocardium where myocyte ICAM-1 mRNA
196 nt) for sIL-1ra, were implanted into infarct border zones of female nude mice immediately after left
198 re placed in a linear fashion traversing the border zones of infarcted and normal tissue (mean of 3.4
201 ere transplanted (n=12) to cover infarct and border zones of recipient rat hearts 1 month after ische
203 release of Fa to and from Cp in the aqueous border zones on both sides of the cell membranes form th
205 initiated by extrasystoles arising from the border zone or unidirectional conduction block of paced
206 in MI; P = 0.03), creating a 'neural sensory border zone', or heterogeneity in afferent information.
207 e profile of ionic concentrations across the border zone play a significant role in determining cellu
208 patients with primary prophylactic ICD, LGE border zone predicted ICD therapy in univariable and mul
210 grammed electrical stimulation of epicardial border zones, QRS duration in cMSC/SkM1 was shorter than
211 y increased capillary density in the infarct border zone, reduced cardiac dilatation, ventricular wal
215 ssion of early commitment markers within the border zone relative to combinatorial and individual cel
216 uates the effects of gap junction epicardial border zone remodeling (i.e., Gj reduction and Cx43 late
217 ical medicine is whether infarction size and border zone remodeling of the heart can be influenced by
220 Inducible patients had more infarcted and border zone sectors and a shorter time to peak Ecc than
221 associated neovascularization in the infarct border zone (see the related article beginning on page 1
222 th seizure onset were located over metabolic border zones significantly more frequently than over hyp
223 olar electrograms were acquired from infarct border zone sites in 10 canine heart experiments 3 to 5
224 ession in murine heart tissue in the infarct border zone suggesting that ER stress may play a role in
226 ctions may assume clinical importance in the border zone surrounding an infarction, where local prote
231 mic areas, particularly in the inner infarct border zone (the penumbra), of the bid-deficient brains.
232 As a fraction of the geographic atrophy border zone, the mean new GA was 0.44+/-0.20, and the me
234 In depolarized myocardial infarct epicardial border zones, the cardiac sodium channel (SCN5A) is larg
235 In depolarized myocardial infarct epicardial border zones, the cardiac sodium channel is largely inac
238 heterogeneity by measuring infarct core and border zones through CMR might have a higher association
239 nalysis was also conducted with a 500-microm border zone to determine the predictive value of proximi
241 on, preserved cardiac function, and enhanced border zone wall thickening, was observed in Akt1(-/-) m
242 /-0.7 versus control 14.4+/-0.4 mm, P<0.001; border-zone wall thickness 1.59+/-0.11 versus control 1.
245 echocardiography, and sonomicrometry of the border zone was compared with the normal left ventricle
246 ys after MI, MMP-9 expression in the infarct border zone was higher in OIM/OIM than in WT/WT animals.
247 MI, however, capillarization of the infarct border zone was impaired in KO mice, and the animals dev
249 -1.8; P=0.03) incorporated into the ischemic border zone was reduced as compared with wild-type (WT)
250 ular tachycardia occurring in the epicardial border zone was used in 54 experiments (25 canine hearts
251 ery thromboembolism with impaired washout at border zones was a common mechanism in stroke recurrence
252 ip, defined as a lead tip positioned on scar/border zone, was determined by overlaying fluoroscopic p
253 ct Cx43 lateralization within the epicardial border zone, we performed Western blot, immunoprecipitat
254 o identify peptides specific for the infarct/border zone, we used in vivo phage display methods and a
257 st-derived inflammatory cells in the infarct border zone, whereas intracoronary BM cell injection pro
258 the medically managed patients had a larger border zone, whereas there was no difference between bor
259 stained multinuclear myotubes were found in border zones, whereas no positive cells were seen in inf
260 moderately enhanced patchy microinfarcts in border zones, which represent different degrees of contr
261 nt ventricular tachycardia in the epicardial border zone with a figure 8 pattern of conduction was us
262 nt ventricular tachycardia in the epicardial border zone with a figure-8 pattern of conduction was us
263 y monomorphic PVCs originating from the scar border zone with preceding PLPs; targeting these PVCs ma
264 was due to intermediate levels of CollBF in border zones within the risk area that had escaped necro
265 ory IL-1 receptor antagonist (sIL-1ra) at MI border zones would specifically attenuate adverse remode
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