ライフサイエンスコーパス: disarray

1 hitecture intermixed with focal myofibrillar disarray.

2 al muscle disorder associated with sarcomere disarray.

3 e used to evaluate sarcomere and microtubule disarray.

4 tole resulting in hypertrophy and sarcomeric disarray.

5 ESRD is a state of small-molecule disarray.

6 s altered, and the microtubule ribbon was in disarray.

7 acement collagen was in short strands and in disarray.

8 contractile proteins and profound sarcomere disarray.

9 cardiac abnormalities including myofibrillar disarray.

10 ntricular (LV) hypertrophy and myocyte fiber disarray.

11 y cardiac hypertrophy, fibrosis, and myocyte disarray.

12 centration-dependent increase in myofilament disarray.

13 significantly reduced anthracycline-induced disarray.

14 lar wall thickness, myocyte hypertrophy, and disarray.

15 ix pathologies are-in many cases-in striking disarray.

16 Losartan had no effect on myocyte disarray.

17 the corneas of lumican-deficient mice is in disarray.

18 .4 versus 559.6+/-204.43 g, P=0.04, and mean disarray, 40.1+/-9.4% versus 20.2+/-12.6%, P=0.002, resp

19 0.7+/-0.4% versus 2.6+/-2.8%, P=0.001; mean disarray, 46.2+/-7.2% versus 24.1+/-15.9%, P<0.0001; and

20 mutant transgene showed substantial myocyte disarray and a 3-fold increase in interstitial collagen

21 ocyte level, we demonstrated that sarcomeric disarray and accumulation of the physical aggregates res

22 umulation, and mitochondrial ultrastructural disarray and bioenergetic dysfunction - were mitigated b

23 clinical, and environmental services--are in disarray and decline in much of the developing world, pa

24 Electron microscopy revealed myofibrillar disarray and degeneration with hyaline-like inclusions.

25 g technique might be used to detect cellular disarray and degenerative changes in this sensitive circ

26 d relaxation, delayed early filling, myocyte disarray and fibrosis, and increased chamber end-systoli

27 ant mice (20 weeks old), which develop fiber disarray and fibrosis, had diastolic and systolic kineti

28 ent of cardiac hypertrophy with myofibrillar disarray and fibrosis, in addition to activation of path

29 2 family members did not demonstrate myocyte disarray and fibrosis, indicating that this phenotype is

30 ficant cardiac hypertrophy with myofibrillar disarray and fibrosis, similar to what was observed in t

31 ndividuals with MYH11 mutations revealed SMC disarray and focal hyperplasia of SMCs in the aortic med

32 tion of sarcomeric proteins, gross myofibril disarray and growth-retarded hearts.

33 nsgenic mouse hearts demonstrate myocellular disarray and have a reduced number of cardiac myocytes t

34 Neither phenotype showed myofibril disarray and hypertrophic hearts were hypercontractilein

35 trast, TnI(146Gly) mice showed cardiomyocyte disarray and interstitial fibrosis and suffered prematur

36 Myocyte disarray and interstitial fibrosis, pathological feature

37 n T (cTnT-Q(92)) mice, which exhibit myocyte disarray and interstitial fibrosis, to treatment with lo

38 odeling with myocardial hypertrophy, myocyte disarray and interstitial fibrosis.

39 by electron microscopy revealed myofibrillar disarray and mild fibrosis.

40 opathologic findings of myocyte hypertrophy, disarray and replacement fibrosis.

41 ltrastructural analysis showed thin-filament disarray and revealed the presence of leptomeres after t

42 lved with cellular detection of microtubular disarray and subsequent activation of JNK/SAPK.

43 y left ventricular hypertrophy, myofibrillar disarray and sudden cardiac death.

44 ervation of titin, reduction in myofibrillar disarray, and attenuation of cardiomyocyte necrosis but

45 mal GBM, glomerular epithelial cells were in disarray, and endothelial and mesangial cells were extru

46 mass, contractile dysfunction, myofibrillar disarray, and fibrosis.

47 ing conditions, cadiomyocyte hypertrophy and disarray, and increased myocardial fibrosis.

48 Exercise prevented fibrosis, myocyte disarray, and induction of "hypertrophic" markers includ

49 haracterized by cardiac hypertrophy, myocyte disarray, and interstitial fibrosis.

50 haracterized by cardiac hypertrophy, myocyte disarray, and interstitial fibrosis.

51 nt of ventricular hypertrophy, cardiomyocyte disarray, and myocardial fibrosis and attenuates hypertr

52 ophy without evidence of fibrosis or myocyte disarray, and significant reduction in the left ventricu

53 n, focal areas of medial SMC hyperplasia and disarray, and stenotic arteries in the vasa vasorum due

54 ular and/or septal hypertrophy, myofibrillar disarray, and sudden cardiac death.

55 ith systemic symptoms attributed to cytokine disarray, and we have previously shown that the use of t

56 The mutants' rigid paralysis and sarcomeric disarray are consistent with unregulated contraction of

57 Because myocyte dysfunction and disarray are the primary abnormalities in HCM, we reason

58 tures of HCM include myocyte hypertrophy and disarray, as well as interstitial fibrosis.

59 ocumented disease, exercise reversed myocyte disarray (but not fibrosis) and "hypertrophic" marker in

60 ed interstitial fibrosis, attenuated myocyte disarray by 50%, and improved diastolic function in the

61 hich features misplaced cortical neurons and disarrayed cerebral lamination.

62 that is associated with cytoskeletal protein disarray, contractile dysfunction, and reduced energy pr

63 t cardiac hypertrophy, more than fibrosis or disarray, correlates with arrhythmic risk.

64 With a health system in total disarray, coverage of basic health interventions remains

65 Myocyte disarray (disorganized cell-cell contact) and cardiac fi

66 trial and ventricular enlargement, myofibril disarray, fibrosis and mitochondrial injury, and electro

67 in the force-pCa2+ curves with cardiomyocyte disarray, fibrosis, and altered connexin43 organization.

68 thology of myocyte hypertrophy, myofibrillar disarray, fibrosis, and dystrophic calcification.

69 receded histopathologic changes, and myocyte disarray, hypertrophy, and fibrosis increased with age.

70 stribution of N-cadherin and reduced myocyte disarray in 2 independent randomized studies.

71 ondrial fission and mitochondrial structural disarray in brains of hypertensive rats with hypertensio

72 In vitro studies showed cytoskeleton disarray in cells transfected with mutated Cypher/ZASP.

73 embryonic development, and frequently are in disarray in pathologies such as cancer.

74 rized by ventricular hypertrophy and myocyte disarray in the absence of known hypertrophic stimuli.

75 We propose that extensive myocyte disarray in the absence of marked hypertrophy is the pat

76 esolution of foveal cells, and topographical disarray in the cellular map.

77 ebellum with that of dividing cells revealed disarray in the external germinal zone.

78 tological examination showed cardiac myocyte disarray in the mutant mice, which amounted to 1-15% of

79 on cardiac structure and function leading to disarray, increased collagen synthesis, and diastolic dy

80 haracterized by cardiac hypertrophy, myocyte disarray, interstitial fibrosis, and left ventricular (L

81 nduced hypertrophy, myocyte and myofibrillar disarray, interstitial fibrosis, and premature death, ph

82 of the myocardium revealed myocardial fiber disarray, intramural coronary arteriosclerosis, and inte

83 An acute hepatitic pattern with lobular disarray is seen in acute infection, during acute flares

84 acterized by cardiac hypertrophy and myocyte disarray, is the most common cause of sudden cardiac dea

85 eal growth retardation with cells in mitotic disarray manifesting disorganized spindle, misaligned an

86 Myocardial disarray (multifocal) and increase in cardiomyocyte diam

87 embrane in normal myocardium, was diffuse in disarrayed myocardium.

88 rastructural degenerative changes, including disarrayed myofibrils, dilated sarcoplasmic vesicles, nu

89 o be an important precursor to the costamere disarray observed in dystrophin-deficient muscle.

90 impeded in mice lacking these miRNAs, due to disarray of actin stress fibers and diminished migratory

91 ause CMD-like brain malformations, including disarray of cerebral cortical layering, fusion of cerebr

92 ndritic cells and contribute to a functional disarray of dendritic cells by inhibiting their antigen-

93 ith aberrant thickening of the aortic media, disarray of elastic fibers, and increased collagen depos

94 In addition, ultrastructure analysis reveals disarray of extracellular matrix and collagen fiber orga

95 ction, fast-to-slow myofiber conversion, and disarray of muscle triads (sites of excitation- contract

96 of HCM such as left ventricular hypertrophy, disarray of myofibers, and interstitial fibrosis.

97 essive impaired cardiac function caused by a disarray of several processes including derailed autopha

98 on that decreased RyR P(o) alone can produce disarray of the Ca2+ release process and initiate altern

99 We found substantial disarray of the functional properties of myeloid and pla

100 ype, with no significant fibrosis or myocyte disarray on histological examination.

101 , neither the extent nor location of myocyte disarray or cardiac fibrosis correlated with ex vivo sig

102 significantly different from MAC: epidermal disarray; pagetoid infiltration of dendritic and/or roun

103 The macroscopic findings, percentage of disarray, percentage of fibrosis, and percentage of smal

104 However, focal regions of disarray persist where sublaminae do not form properly.

105 cortex heterotopias and hippocampal neuronal disarray, remain to be confirmed.

106 ess to endothelial dysfunction, nitric oxide disarrays, renal interstitial fibrosis, sarcopenia, and

107 sis and more frequently demonstrated lobular disarray, rosette formation, and hemorrhage than those w

108 indicates that the phenotype of myofibrillar disarray seen in HCM patients which harbor either of the

109 This neuronal disarray should be accompanied by synaptic abnormalities

110 to sarcomere protein mutations (ie, myocyte disarray, small vessel disease, myocardial scarring).

111 ivation therapy with endocrine and metabolic disarray, specifically the metabolic syndrome, resulting

112 er heart weights, less fibrosis, and greater disarray than other HCM patients (mean heart weight, 380

113 suddenly had lower heart weights and greater disarray than patients who died suddenly with unknown ge

114 ion, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutati

115 not associated with myocyte and myofibrillar disarray, the pathognomonic features of hypertrophic car

116 embryos displayed dilated blood vessels and disarrayed vascular architecture.

117 aused a significant increase in myofibrillar disarray versus doxorubicin alone.

118 Myocyte disarray was associated with increased levels of phospho

119 Myofibrillar disarray was present in all RAS animals and was signific

120 In addition, muscle disarray was seen adjacent to channel-associated fibrosi

121 Disarray was unchanged.

122 llagen volume fraction and extent of myocyte disarray were increased in the cTnT-Q(92) mice (placebo

123 nduced murf1 expression and caused myofibril disarray, whereas inhibiting Calcineurin activity attenu

124 This field of study has long been in disarray with the genus level taxonomy of this group rem

125 Myofibrillar disarray with variable penetrance occurred in the left v

126 atients with troponin T mutations had severe disarray, with only mild hypertrophy and fibrosis.

127 ars to be a poor reflection of the molecular disarray within the Barrett's epithelium, and a molecula

128 solution or an increased cellular positional disarray within the representation of the amblyopic eye.

129 and fragmented elastic fibers, and cellular disarray without calcification or cell proliferation.