ライフサイエンスコーパス: cardiomyopathic

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 Cardiomyopathic changes, such as myocyte necrosis, apopt

14 tructural protein (delta-sarcoglycan) in the cardiomyopathic (CM) hamster evaluated.

15 nd late (10 months) phases of disease in the cardiomyopathic (CM) hamster, and the combination of GH

16 , and its actions were evaluated in Bio 14.6 cardiomyopathic (CM) hamsters with heart failure.

17 hesis that these amino acids are crucial for cardiomyopathic consequences of CaMKII signaling.

18 the animal, resulting in a local picture of cardiomyopathic damage in discrete regions of the heart,

19 t nitrotyrosine levels in idiopathic dilated cardiomyopathic (DCM) hearts were almost double those of

20 vided into 3 groups: sham (control), dilated cardiomyopathic (DCM), and neonatal capsaicin-treated an

21 myocardial inflammation that contributes to cardiomyopathic decompensation.

22 ic value for apoptosis inhibition to prevent cardiomyopathic decompensation.

23 e ability of IGF-1 to inhibit progression of cardiomyopathic disease in a defined model system and su

24 itch fiber-type specification, function, and cardiomyopathic disease.

25 smin-related cardiomyopathies and crystallin cardiomyopathic diseases.

26 is a novel target of the antineoplastic and cardiomyopathic drug doxorubicin (Dox (adriamycin)).

27 es were identified as candidate mediators of cardiomyopathic effects in MHC-PPAR mice.

28 fractional shortening of 87 +/- 4%, whereas cardiomyopathic flies that contain a mutation in troponi

29 ardiac growth and two functionally divergent cardiomyopathic genes.

30 The delta-sarcoglycan-deficient cardiomyopathic hamster and mice deficient in both dystr

31 The cardiomyopathic hamster is a naturally occurring model f

32 d stable genetic reconstitution in the adult cardiomyopathic hamster when injected directly into musc

33 In the cardiomyopathic hamster, the smooth muscle sarcoglycan c

34 fully prevented progressive heart failure in cardiomyopathic hamsters.

35 mic reticulum (SR) Ca(2+) cycling in BIO14.6 cardiomyopathic hamsters.

36 KC) activities were elevated in hypertrophic cardiomyopathic (HCM) hamster hearts and that activation

37 ion and apoptosis in the heart, leading to a cardiomyopathic heart disease phenotype in recipients.

38 n criteria included congenital, valvular, or cardiomyopathic heart disease; prior coronary artery rev

39 are decreased in human dilated/hypertrophic cardiomyopathic hearts and in murine hypertrophic hearts

40 Dilated cardiomyopathic hearts from mice that have undergone tra

41 lin protein expression was also increased in cardiomyopathic hearts from tropomodulin-overexpressing

42 anglia from normal, scarred, and nonischemic cardiomyopathic hearts without scar as NL (n=3), SCAR (n

43 nal size in normal, scarred, and nonischemic cardiomyopathic hearts without scar groups were 320 +/-

44 nd end-stage ischemic (ICM) or dilated (DCM) cardiomyopathic hearts.

45 tween myocytes from ischemic and nonischemic cardiomyopathic hearts.

46 In the dilated cardiomyopathic human heart, these intrinsic enzyme acti

47 e downregulated in both ischemic and dilated cardiomyopathic human heart.

48 rom spontaneously hypertensive rat heart and cardiomyopathic human hearts.

49 d spontaneously hypertensive rat and dilated cardiomyopathic human hearts.

50 spontaneously hypertensive rats and dilated cardiomyopathic human tissue.

51 ung myocardium and is also induced following cardiomyopathic injury.

52 parameters reflect the presence of extensive cardiomyopathic involvement of the RVOT.

53 logic actions of UcnII in both wild-type and cardiomyopathic mice and support a potential beneficial

54 verload and prevented disease progression in cardiomyopathic mice with myocardial Galphaq overexpress

55 In hearts of hypertrophic cardiomyopathic mice, CTIP2 controls P-TEFb-sensitive pa

56 Conversely, in a transgenic cardiomyopathic mouse model that exhibits ventricular ar

57 this domain, by pathological proteolysis or cardiomyopathic mutation, may be sufficient to perturb t

58 study the functional consequences of various cardiomyopathic mutations in human cardiac alpha-tropomy

59 We suggest that most cardiomyopathic mutations in the troponin tail alter mus

60 tive caspase 3 and Ki-67 proteins in dilated cardiomyopathic myocytes.

61 ation; and 3) estimate contemporary risk for cardiomyopathic patients.

62 The cardiomyopathic phenotype and increased hypertrophy afte

63 isolated myocytes, but failed to rescue the cardiomyopathic phenotype elicited by activation of the

64 etion) of TNF is responsible for the dilated cardiomyopathic phenotype in mice with targeted, cardiac

65 MHC-PPAR genotype resulted in a more severe cardiomyopathic phenotype than either did alone.

66 cardiac RGS4 overexpression ameliorated the cardiomyopathic phenotype that occurred as a result of P

67 The cardiomyopathic phenotype was exacerbated in MHC-PPAR mi

68 dilator properties, can alleviate the severe cardiomyopathic phenotype, restoring normal serum levels

69 energy production frequently manifests as a cardiomyopathic phenotype, underscoring the requirement

70 ion of tropomyosin can rescue a hypertrophic cardiomyopathic phenotype.

71 in the mdx background would lead to a severe cardiomyopathic phenotype.

72 e show that these mice develop a progressive cardiomyopathic phenotype.

73 ILK mutation/deletion causes cardiomyopathic phenotypes, but the functional and elect

74 hanisms, which may culminate in the distinct cardiomyopathic phenotypes.

75 dilated cardiomyopathy and paxillin in both cardiomyopathic phenotypes.

76 signaling pathway resulting in two distinct cardiomyopathic phenotypes: a lethal dilated phenotype a

77 lending partial explanation for the array of cardiomyopathic phenotypy.

78 lead to retardation and even reversal of the cardiomyopathic process.

79 n to exercise, known as athlete's heart, and cardiomyopathic processes capable of causing SCD.

80 ated histological and functional evidence of cardiomyopathic progression.

81 onsidered and the authors discuss how atrial cardiomyopathic properties might guide stroke prevention

82 n on cardiac function in native and ischemic cardiomyopathic rat hearts using a novel combination of

83 blood pressure response to AEA is blunted in cardiomyopathic rats when compared to normal rats.

84 al responses of group IV afferent neurons in cardiomyopathic rats.

85 -100 and Glu-101) was found in a restrictive cardiomyopathic (RCM) pediatric patient.

86 e controls, hearts from Tg26-hDMPK developed cardiomyopathic remodeling with myocardial hypertrophy,

87 The cardiomyopathic response associated with MEF2A and MEF2C

88 ct of volume loading on these indexes in the cardiomyopathic setting.

89 After establishing a severe cardiomyopathic state, high-TG mice received doxycycline

90 r stretch-mediated arrhythmogenic process in cardiomyopathic states, additional studies will be requi

91 th and prevention of pathogenesis induced by cardiomyopathic stimuli.

92 s examined, exhibiting an autosomal dominant cardiomyopathic trait comprising a variable spectrum of

93 e only mutation fully cosegregating with the cardiomyopathic trait in 18 additional family members (o

94 ng organic heart disease; nine had ischemic, cardiomyopathic, valvular or congenital heart disorders.

95 For the most part, familial cardiomyopathic, vascular, or arrhythmogenic disorders h