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1 he nonfailing (12.8 fmol/mg) and the dilated cardiomyopathic (15.6 fmol/mg) heart tissues, but the co
2 an cardiac fibroblasts cultured from dilated cardiomyopathic and ischemic hearts.
3 njection of AEA into the hindlimb of normal, cardiomyopathic and neonatally capsaicin-treated (NNCAP)
4 -36 trimethylation (H3K36me3) enrichment for cardiomyopathic and normal human hearts.
5 n nontransgenic, tropomodulin-overexpressing cardiomyopathic, and the hybrid tropomodulin/IGF-1-overe
6                The intercross of hR120GCryAB cardiomyopathic animals with mice with reduced G6PD leve
7                      After volume loading in cardiomyopathic animals, posterior and anterior LV ERPs
8 eservation of mitochondrial integrity during cardiomyopathic challenge conditions, thereby raising th
9 velop tools that differentiate athletic from cardiomyopathic change.
10 site for determining approaches to limit the cardiomyopathic changes associated with chronic heart di
11 spring with the most severe phenotype showed cardiomyopathic changes between 2 and 4 wk after birth.
12 rine cardiac myocytes results in more severe cardiomyopathic changes in the stressed myocardium than
13 diac disorders, which may be associated with cardiomyopathic changes, are often associated with incre
14                                              Cardiomyopathic changes, such as myocyte necrosis, apopt
15 tructural protein (delta-sarcoglycan) in the cardiomyopathic (CM) hamster evaluated.
16 nd late (10 months) phases of disease in the cardiomyopathic (CM) hamster, and the combination of GH
17 , and its actions were evaluated in Bio 14.6 cardiomyopathic (CM) hamsters with heart failure.
18 hesis that these amino acids are crucial for cardiomyopathic consequences of CaMKII signaling.
19  the animal, resulting in a local picture of cardiomyopathic damage in discrete regions of the heart,
20 cell-based therapeutics intended to mitigate cardiomyopathic damage.
21 t nitrotyrosine levels in idiopathic dilated cardiomyopathic (DCM) hearts were almost double those of
22 vided into 3 groups: sham (control), dilated cardiomyopathic (DCM), and neonatal capsaicin-treated an
23  myocardial inflammation that contributes to cardiomyopathic decompensation.
24 ic value for apoptosis inhibition to prevent cardiomyopathic decompensation.
25 sed genetic analysis of GME individuals with cardiomyopathic disease identified an Iranian patient wi
26 e ability of IGF-1 to inhibit progression of cardiomyopathic disease in a defined model system and su
27 itch fiber-type specification, function, and cardiomyopathic disease.
28 smin-related cardiomyopathies and crystallin cardiomyopathic diseases.
29 conditions such as myocarditis and inherited cardiomyopathic disorders.
30  is a novel target of the antineoplastic and cardiomyopathic drug doxorubicin (Dox (adriamycin)).
31 es were identified as candidate mediators of cardiomyopathic effects in MHC-PPAR mice.
32                    mdx/WT chimeras developed cardiomyopathic features and dystrophic skeletal muscle
33  fractional shortening of 87 +/- 4%, whereas cardiomyopathic flies that contain a mutation in troponi
34 a for AM and targeted panel sequencing of 57 cardiomyopathic genes was performed.
35 ardiac growth and two functionally divergent cardiomyopathic genes.
36              The delta-sarcoglycan-deficient cardiomyopathic hamster and mice deficient in both dystr
37                                          The cardiomyopathic hamster is a naturally occurring model f
38 d stable genetic reconstitution in the adult cardiomyopathic hamster when injected directly into musc
39                                       In the cardiomyopathic hamster, the smooth muscle sarcoglycan c
40       The mutation shortened the lifespan of cardiomyopathic hamsters relative to wild types, but thi
41 fully prevented progressive heart failure in cardiomyopathic hamsters.
42 mic reticulum (SR) Ca(2+) cycling in BIO14.6 cardiomyopathic hamsters.
43 KC) activities were elevated in hypertrophic cardiomyopathic (HCM) hamster hearts and that activation
44 ion and apoptosis in the heart, leading to a cardiomyopathic heart disease phenotype in recipients.
45 n criteria included congenital, valvular, or cardiomyopathic heart disease; prior coronary artery rev
46  are decreased in human dilated/hypertrophic cardiomyopathic hearts and in murine hypertrophic hearts
47                                      Dilated cardiomyopathic hearts from mice that have undergone tra
48 lin protein expression was also increased in cardiomyopathic hearts from tropomodulin-overexpressing
49 anglia from normal, scarred, and nonischemic cardiomyopathic hearts without scar as NL (n=3), SCAR (n
50 nal size in normal, scarred, and nonischemic cardiomyopathic hearts without scar groups were 320 +/-
51 nd end-stage ischemic (ICM) or dilated (DCM) cardiomyopathic hearts.
52 tween myocytes from ischemic and nonischemic cardiomyopathic hearts.
53                               In the dilated cardiomyopathic human heart, these intrinsic enzyme acti
54 e downregulated in both ischemic and dilated cardiomyopathic human heart.
55 rom spontaneously hypertensive rat heart and cardiomyopathic human hearts.
56 d spontaneously hypertensive rat and dilated cardiomyopathic human hearts.
57  spontaneously hypertensive rats and dilated cardiomyopathic human tissue.
58 ung myocardium and is also induced following cardiomyopathic injury.
59 parameters reflect the presence of extensive cardiomyopathic involvement of the RVOT.
60           RNA sequencing and metabolomics of cardiomyopathic Mfn2 Q/Q400 hearts revealed signature ab
61 logic actions of UcnII in both wild-type and cardiomyopathic mice and support a potential beneficial
62 verload and prevented disease progression in cardiomyopathic mice with myocardial Galphaq overexpress
63                    In hearts of hypertrophic cardiomyopathic mice, CTIP2 controls P-TEFb-sensitive pa
64                  Conversely, in a transgenic cardiomyopathic mouse model that exhibits ventricular ar
65  this domain, by pathological proteolysis or cardiomyopathic mutation, may be sufficient to perturb t
66 hin filament activation and is a hotspot for cardiomyopathic mutations and variants.
67 study the functional consequences of various cardiomyopathic mutations in human cardiac alpha-tropomy
68                         We suggest that most cardiomyopathic mutations in the troponin tail alter mus
69 tudied the structural and dynamic effects of cardiomyopathic mutations on the region.
70  that is directly altered in the presence of cardiomyopathic mutations.
71 tive caspase 3 and Ki-67 proteins in dilated cardiomyopathic myocytes.
72 ation; and 3) estimate contemporary risk for cardiomyopathic patients.
73                                          The cardiomyopathic phenotype and increased hypertrophy afte
74  isolated myocytes, but failed to rescue the cardiomyopathic phenotype elicited by activation of the
75 etion) of TNF is responsible for the dilated cardiomyopathic phenotype in mice with targeted, cardiac
76  of chronic kidney disease define a specific cardiomyopathic phenotype known as uremic cardiomyopathy
77  weight ratio, coupled with a severe dilated cardiomyopathic phenotype resulting in death within 1 mo
78  MHC-PPAR genotype resulted in a more severe cardiomyopathic phenotype than either did alone.
79  cardiac RGS4 overexpression ameliorated the cardiomyopathic phenotype that occurred as a result of P
80                                          The cardiomyopathic phenotype was exacerbated in MHC-PPAR mi
81 dilator properties, can alleviate the severe cardiomyopathic phenotype, restoring normal serum levels
82  energy production frequently manifests as a cardiomyopathic phenotype, underscoring the requirement
83 organization, consistent with the pedigree's cardiomyopathic phenotype.
84 se cardiovascular outcomes and an attenuated cardiomyopathic phenotype.
85 he pathogenesis of the diabetic vascular and cardiomyopathic phenotype.
86 ion of tropomyosin can rescue a hypertrophic cardiomyopathic phenotype.
87 in the mdx background would lead to a severe cardiomyopathic phenotype.
88 e show that these mice develop a progressive cardiomyopathic phenotype.
89                 ILK mutation/deletion causes cardiomyopathic phenotypes, but the functional and elect
90 hanisms, which may culminate in the distinct cardiomyopathic phenotypes.
91  dilated cardiomyopathy and paxillin in both cardiomyopathic phenotypes.
92  signaling pathway resulting in two distinct cardiomyopathic phenotypes: a lethal dilated phenotype a
93 lending partial explanation for the array of cardiomyopathic phenotypy.
94  arrhythmogenic or a marker of an underlying cardiomyopathic process.
95 lead to retardation and even reversal of the cardiomyopathic process.
96 n to exercise, known as athlete's heart, and cardiomyopathic processes capable of causing SCD.
97 ithin these enhancer regions associates with cardiomyopathic progression over time.
98 ated histological and functional evidence of cardiomyopathic progression.
99 onsidered and the authors discuss how atrial cardiomyopathic properties might guide stroke prevention
100 n on cardiac function in native and ischemic cardiomyopathic rat hearts using a novel combination of
101 blood pressure response to AEA is blunted in cardiomyopathic rats when compared to normal rats.
102 al responses of group IV afferent neurons in cardiomyopathic rats.
103 -100 and Glu-101) was found in a restrictive cardiomyopathic (RCM) pediatric patient.
104 e controls, hearts from Tg26-hDMPK developed cardiomyopathic remodeling with myocardial hypertrophy,
105                                          The cardiomyopathic response associated with MEF2A and MEF2C
106 ct of volume loading on these indexes in the cardiomyopathic setting.
107                  After establishing a severe cardiomyopathic state, high-TG mice received doxycycline
108 r stretch-mediated arrhythmogenic process in cardiomyopathic states, additional studies will be requi
109 th and prevention of pathogenesis induced by cardiomyopathic stimuli.
110 should be used with caution, especially when cardiomyopathic symptoms are caused by mitochondrial dys
111 s examined, exhibiting an autosomal dominant cardiomyopathic trait comprising a variable spectrum of
112 e only mutation fully cosegregating with the cardiomyopathic trait in 18 additional family members (o
113 ng organic heart disease; nine had ischemic, cardiomyopathic, valvular or congenital heart disorders.
114 ctly binds to WT cTnC, and we find that this cardiomyopathic variant displays tighter binding to cTnT
115    We sought to evaluate whether deleterious cardiomyopathic variants were enriched among fatal pedia
116                  For the most part, familial cardiomyopathic, vascular, or arrhythmogenic disorders h

 
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