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1 ipitates into cardiac insulin resistance and contractile dysfunction.
2 h mechanical ventilation-induced atrophy and contractile dysfunction.
3 c weakness attributable to fiber atrophy and contractile dysfunction.
4 cal ventilation-induced myofiber atrophy and contractile dysfunction.
5 ess resulting from both myofiber atrophy and contractile dysfunction.
6 lation can promote diaphragmatic atrophy and contractile dysfunction.
7 ve cardiomyocyte and cardiac hypertrophy and contractile dysfunction.
8 cyte hypertrophy, interstitial fibrosis, and contractile dysfunction.
9 y transitioned to ventricular dilatation and contractile dysfunction.
10 lation is also associated with diaphragmatic contractile dysfunction.
11 rsing maladaptive hypertrophy, fibrosis, and contractile dysfunction.
12 and substrate utilization may contribute to contractile dysfunction.
13 cerol (TAG) metabolism in the development of contractile dysfunction.
14 xibility and render the heart susceptible to contractile dysfunction.
15 of p38 mitogen-activated protein kinase, and contractile dysfunction.
16 denced by reduced hypertrophy, fibrosis, and contractile dysfunction.
17 Its overexpression results in contractile dysfunction.
18 and calsequestrin but resulted in no obvious contractile dysfunction.
19 t (CA) and reperfusion and may contribute to contractile dysfunction.
20 otilin mutations promote aggregate-dependent contractile dysfunction.
21 atinib-treated mice develop left ventricular contractile dysfunction.
22 endotoxin-induced cardiac mitochondrial and contractile dysfunction.
23 ac activity, ischemic myocardial damage, and contractile dysfunction.
24 the change in its expression contributes to contractile dysfunction.
25 reatic beta-cell dysfunction, and myocardial contractile dysfunction.
26 loading of Na+/Ca2+, and produced myocardial contractile dysfunction.
27 de (BNP) are sensitive biomarkers of cardiac contractile dysfunction.
28 in gene expression that are associated with contractile dysfunction.
29 mice were protected against S aureus-induced contractile dysfunction.
30 des within cardiomyocytes is associated with contractile dysfunction.
31 ust induction of the fetal gene program, and contractile dysfunction.
32 lation-induced diaphragmatic proteolysis and contractile dysfunction.
33 omplex phenomenon not simply attributable to contractile dysfunction.
34 impaired systolic strain indicating a subtle contractile dysfunction.
35 lum calcium pump (SERCA), contribute to this contractile dysfunction.
36 dative stress and subsequent proteolysis and contractile dysfunction.
37 tial to limit the extent of resultant MI and contractile dysfunction.
38 ular and lipid metabolic changes, as well as contractile dysfunction.
39 but appear unlikely to contribute to chronic contractile dysfunction.
40 uced injury together with the development of contractile dysfunction.
41 oved ischemia/reperfusion-induced myocardial contractile dysfunction.
42 was first ascribed to papillary muscle (PM) contractile dysfunction.
43 resulted in a reduction of ischemia-induced contractile dysfunction.
44 tic impairment during AF could contribute to contractile dysfunction.
45 ne model of hypovascular nonnecrotic cardiac contractile dysfunction.
46 play a role in the subsequent development of contractile dysfunction.
47 , resulting in abnormal calcium handling and contractile dysfunction.
48 isolated from these hearts did not manifest contractile dysfunction.
49 yocardial hypertrophy, cardiac fibrosis, and contractile dysfunction.
50 a response associated with profound cardiac contractile dysfunction.
51 is primarily due to intrinsic cardiomyocyte contractile dysfunction.
52 ve LV dilation, LV pump failure, and myocyte contractile dysfunction.
53 tial strain (Ecc) at 12 months, a measure of contractile dysfunction.
54 al ventilation-induced diaphragm atrophy and contractile dysfunction.
55 otective intervention to limit post-ischemic contractile dysfunction.
56 nt attenuation of both diaphragm atrophy and contractile dysfunction.
57 lease across the myocyte and contributing to contractile dysfunction.
58 egy protecting the heart from arrhythmia and contractile dysfunction.
59 a significant factor contributing to cardiac contractile dysfunction.
60 cularity, does not prevent mitochondrial and contractile dysfunction.
61 preserve mitochondrial function and prevent contractile dysfunction.
62 ilure suggests a novel mechanism of cellular contractile dysfunction.
63 target for the treatment of arrhythmias and contractile dysfunction.
64 ne cell infiltration, myocardial injury, and contractile dysfunction.
65 plicing defects, enlarged hearts, and severe contractile dysfunction.
66 c maladaptation precedes the onset of severe contractile dysfunction.
67 entilation promote diaphragmatic atrophy and contractile dysfunction.
68 dimer formation and attenuated H2O2-induced contractile dysfunction.
69 ventilator-induced diaphragmatic atrophy and contractile dysfunction.
70 entilation-induced diaphragmatic atrophy and contractile dysfunction.
71 usion with occasional resultant postischemic contractile dysfunction, a state associated with signifi
78 on and reduced myocardial injury and cardiac contractile dysfunction after regional ischemia/reperfus
79 ggravated cardiac hypertrophy, fibrosis, and contractile dysfunction after transverse aortic constric
80 t may in addition to contributing to myocyte contractile dysfunction also contribute to the induction
82 mine whether chronic CGP treatment mitigates contractile dysfunction and arrhythmias in an animal mod
83 r Ca(2)(+) homeostasis is a central cause of contractile dysfunction and arrhythmias in failing myoca
87 ryanodine receptor (RyR2) may contribute to contractile dysfunction and arrhythmogenesis in heart fa
95 1 activity in the adult heart may ameliorate contractile dysfunction and cellular injury in the face
96 n the hearts of ZDF rats was associated with contractile dysfunction and changes in gene expression s
97 rylation in the failing heart contributes to contractile dysfunction and decreased adrenergic reserve
98 F mice with CIMP significantly abrogated the contractile dysfunction and decreased the oxidative stre
99 iographic findings suggestive of subclinical contractile dysfunction and diastolic filling abnormalit
100 -myosin heavy chain promoter) did not induce contractile dysfunction and did not affect mitochondrial
101 r myocytes that, when disrupted, can lead to contractile dysfunction and dilated cardiomyopathy.
102 e had unaltered NDPK-C expression but showed contractile dysfunction and exacerbated cardiac remodeli
103 tic potential of beta subunits to ameliorate contractile dysfunction and excitability in heart failur
106 Ischemic heart disease is characterized by contractile dysfunction and increased cardiomyocyte deat
108 se pathway in interleukin 6-mediated cardiac contractile dysfunction and inotrope insensitivity.
109 ion in hypertrophied hearts protects against contractile dysfunction and LV dilation after chronic pr
111 n of MEK-ERK signaling prevented TAC-induced contractile dysfunction and pathological remodeling.
113 fibrillation (AF) is associated with severe contractile dysfunction and structural and electrophysio
114 S contributes importantly to post-infarction contractile dysfunction and subsequent LV remodeling, su
115 suggests that rod formation is secondary to contractile dysfunction and that load-dependent processe
116 ibrillar energetics may contribute to atrial contractile dysfunction and that protein nitration may b
117 ay explain the observed disparity between LV contractile dysfunction and the extent of myocardial inj
119 rdiac gp130 signaling in the pathogenesis of contractile dysfunction and ventricular arrhythmias.
120 a(2+) ATPase pump (SERCA2a) may improve both contractile dysfunction and ventricular arrhythmias.
121 mice die as juveniles with hearts displaying contractile dysfunction and ventricular chamber enlargem
122 cytes by AdPLB-dn gene transfer reversed the contractile dysfunction (and restored positive FFR) by i
123 ice develop spontaneous cardiac hypertrophy, contractile dysfunction, and "fetal" gene induction.
125 e heart predisposes the heart to arrhythmia, contractile dysfunction, and clinical heart failure.
126 in association with myocardial inflammation, contractile dysfunction, and death of cardiomyocytes by
127 tabolism (protein loss, insulin resistance), contractile dysfunction, and disruption of myogenesis.
128 viduals developed left ventricular dilation, contractile dysfunction, and episodic ventricular arrhyt
130 itions but caused left ventricle dilatation, contractile dysfunction, and heart failure with intersti
131 te phase led to decreased capillary density, contractile dysfunction, and impaired cardiac growth.
133 microinfarcts with an inflammatory response, contractile dysfunction, and reduced coronary reserve.
134 sociated with cytoskeletal protein disarray, contractile dysfunction, and reduced energy production.
135 ith the development of diaphragm atrophy and contractile dysfunction, and respiratory muscle weakness
136 reduction in total myocyte number per heart, contractile dysfunction, and ventricular dilatation in z
138 ired mitochondrial function and dynamics and contractile dysfunction are observed in diabetic patient
140 at total loss of Ryr2 leads to cardiomyocyte contractile dysfunction, arrhythmia, and reduced heart r
141 mic insult has been shown to protect against contractile dysfunction, arrhythmias, and infarction.
142 nuclear leukocytes (PMNs) results in cardiac contractile dysfunction as well as cardiomyocyte injury.
143 KO mice developed cardiac hypertrophy and contractile dysfunction as well as sarcomere disruption
148 ights significantly improve understanding of contractile dysfunction at a level of noninvasive interr
150 ed mechanical ventilation worsened diaphragm contractile dysfunction, augmented diaphragm interleukin
153 ver, knockdown of SERCA2a resulted in severe contractile dysfunction both in vitro and in vivo, which
154 d protect against endotoxin-mediated cardiac contractile dysfunction by attenuating NO production and
155 tethering, suggesting the hypothesis that PM contractile dysfunction can actually diminish MR due to
156 ed chronic MI, the TEI approaches 50% before contractile dysfunction can be systematically identified
157 e, a reduction in Ca transient amplitude and contractile dysfunction can by caused by Ca leak through
159 onded to chronic catecholamine toxicity with contractile dysfunction, cardiomyocyte hypertrophy, card
160 important to both cellular and to myocardial contractile dysfunction caused by chronic, severe pressu
161 I reduced myocardial infarction and improved contractile dysfunction caused by ischemia/reperfusion i
165 ES volume index following MV repair indicate contractile dysfunction, despite pre-surgical LVEF >60%.
167 fused mouse hearts and diminished injury and contractile dysfunction during ischemia/reperfusion.
169 demonstrate that chronic hypoxia can induce contractile dysfunction even before substantial ventricu
170 artment into RAG2KO mice before TAC enhanced contractile dysfunction, fibrosis, collagen accumulation
172 ompensated, is associated with cardiomyocyte contractile dysfunction from depressed sarcoplasmic reti
175 ether viable myocardial regions with chronic contractile dysfunction have true reduction in rest myoc
176 aracterized by exercise intolerance, cardiac contractile dysfunction, hepatopulmonary congestion and
177 but Nox4-null animals developed exaggerated contractile dysfunction, hypertrophy, and cardiac dilata
179 ablished betaAR abnormalities and ameliorate contractile dysfunction in a large animal model of heart
180 n the endothelium would reduce the extent of contractile dysfunction in a murine model of infarct-ind
182 emission protects against fibre atrophy and contractile dysfunction in both cardiac and skeletal mus
184 tion of recombinant rat C5a induced dramatic contractile dysfunction in both sham and CLP cardiomyocy
186 d ASK1 activation, cTnT phosphorylation, and contractile dysfunction in cardiomyocytes showed similar
188 the development of cardiac mitochondrial and contractile dysfunction in endotoxin-induced sepsis.
191 hin might provide a final common pathway for contractile dysfunction in heart failure and these chang
192 nscriptional mechanism may contribute to the contractile dysfunction in heart failure patients with d
193 tes cardiac contractility and contributes to contractile dysfunction in heart failure, although the p
194 onship between reduced ATP-CK metabolism and contractile dysfunction in HF has never been demonstrate
198 (2+) release associated with arrhythmias and contractile dysfunction in inherited and acquired cardia
199 ns in the heart and induces acute myocardial contractile dysfunction in ischemia-reperfusion injury.
200 d no evidence of structural abnormalities or contractile dysfunction in Kv4.2W362FxKv1.4(-/-) mouse h
202 that the isoform-specific, acidic pH-induced contractile dysfunction in myocytes appears to lie in th
203 e, reperfused MI, revealing the existence of contractile dysfunction in noninfarcted regions of the h
205 of microtubule depolymerization on cellular contractile dysfunction in pressure overload cardiac hyp
206 DG precedes and triggers the onset of severe contractile dysfunction in pressure-overload left ventri
207 tenuate or prevent ventricular expansion and contractile dysfunction in response to hypertension, inf
208 reased microtubule density causes cardiocyte contractile dysfunction in right ventricular (RV) pressu
211 chronic hibernating myocardium with regional contractile dysfunction in the absence of heart failure.
214 ated circulating levels of TNF-alpha provoke contractile dysfunction in the diaphragm through an endo
217 epsis produces significant mitochondrial and contractile dysfunction in the heart, but the role of su
218 contributes to cell death and electrical and contractile dysfunction in the post-ischemic heart.
219 tors may be more important in the genesis of contractile dysfunction in the remodeled rat heart up to
220 contribute to reduced cardiac efficiency and contractile dysfunction in the type 1 diabetic Akita mou
221 y of PLN ablation to correct hypertrophy and contractile dysfunction in two well-characterized and hi
223 how haploinsufficiency of MLCK may result in contractile dysfunction in vivo, leading to dissections
224 mic episode is associated with metabolic and contractile dysfunction, including reduced tension devel
228 In Galphaq-induced cardiomyopathy, myocyte contractile dysfunction is mediated, at least in part, b
229 levels and activity are decreased and severe contractile dysfunction is present, overexpression of SE
232 phragmatic weakness, due to both atrophy and contractile dysfunction, is a well-documented response f
233 overloading (gradient, 152+/-16 mm Hg) with contractile dysfunction, LV function was measured at bas
235 otection against endotoxemia-induced cardiac contractile dysfunction, most probably by preserving myo
236 motional stress can produce left ventricular contractile dysfunction, myocardial ischemia, or disturb
237 showed increased left ventricular (LV) mass, contractile dysfunction, myofibrillar disarray, and fibr
238 Isolated perfused Mif-/- hearts had greater contractile dysfunction, necrosis, and JNK activation th
242 the reduction of its phosphorylation and the contractile dysfunction observed in human heart failure.
243 tion of MV-induced diaphragmatic atrophy and contractile dysfunction occurred in conjunction with a r
245 24) with ischemic heart disease that chronic contractile dysfunction occurs in myocardial regions wit
247 ply does not match myocardial demand cardiac contractile dysfunction occurs, and prolongation of this
249 arction rat heart failure model and reversed contractile dysfunction of failing myocardium in vivo an
251 ellular Ca2+ is likely to play a role in the contractile dysfunction of HF because the amplitude and
252 tion of the sarcomere's thin filament to the contractile dysfunction of human cardiomyopathy is not w
253 scous loading of active myofilaments, causes contractile dysfunction of hypertrophied and failing pre
254 um, which represents "prolonged postischemic contractile dysfunction of myocardium salvaged by reperf
255 2.5 versus 55.3+/-2.2, P:<0.01) and regional contractile dysfunction of noninfarcted myocardium (% sy
257 of S100A1 protein critically contributes to contractile dysfunction of the diseased heart, which is
258 abolic maladaptation plays a pivotal role in contractile dysfunction of the heart, the understanding
262 CA2a can protect diabetic hearts from severe contractile dysfunction, presumably by improving the cal
263 they relate to the excessive hypertrophy and contractile dysfunction regularly observed in patients w
266 Although the mechanism of rapid rate-related contractile dysfunction remains unknown, ischemia, pH ch
267 resence of antibody to erbB2 may explain the contractile dysfunction seen in patients receiving concu
268 ng physiologic mechanisms underlying chronic contractile dysfunction should consider the role played
269 d protein kinase (AMPK), partially prevented contractile dysfunction, suggesting that cardiac deleter
270 by reperfusion is associated with transient contractile dysfunction, termed "stunning." It is not cl
271 Ddtfl/fl mice exhibited more necrosis and LV contractile dysfunction than control hearts after corona
274 sensitizer EMD57033 produced an even greater contractile dysfunction than the I79N mutation at fast p
275 s an important mechanism for the ventricular contractile dysfunction that develops in large mammals w
276 tioxidants are known to mitigate the cardiac contractile dysfunction that follows brief periods of is
277 tomyosin cross-bridges may contribute to the contractile dysfunction that is apparent after low-flow
278 scous loading of active myofilaments, causes contractile dysfunction that is normalized by microtubul
279 etal abnormality is important in the in vivo contractile dysfunction that occurs in experimental aort
280 ents the development of cardiac dilation and contractile dysfunction, the hallmarks of heart failure.
281 ls and subsequently results in cardiomyocyte contractile dysfunction through dysregulation of calcium
282 ress-induced fructose metabolism, growth and contractile dysfunction, thus defining signalling compon
283 ffective against myocardial inflammation and contractile dysfunction, thus representing a promising c
286 pressure overload or doxorubicin treatment, contractile dysfunction was attenuated in both cases.
288 l histone doses (30 mg/kg), left ventricular contractile dysfunction was the prominent abnormality wi
290 interleukin-1 in myocardial inflammation and contractile dysfunction, we treated a patient with fulmi
291 ecrosis, apoptosis, interstitial fibrosis or contractile dysfunction, were not observed in either of
292 nd insulin resistance (IR), as well as major contractile dysfunction, which was associated with alter
293 s with respect to ET-1 signaling and myocyte contractile dysfunction with cardioplegic arrest and rep
294 provide a framework to study development of contractile dysfunction with disease and evaluate the ma
296 obesity was associated with less pronounced contractile dysfunction without any significant perturba
299 led mechanical ventilation-induced diaphragm contractile dysfunction without preventing atrophy.
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