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1 centration-dependent increase in myofilament disarray.
2 significantly reduced anthracycline-induced disarray.
3 lar wall thickness, myocyte hypertrophy, and disarray.
4 ix pathologies are-in many cases-in striking disarray.
5 Losartan had no effect on myocyte disarray.
6 the corneas of lumican-deficient mice is in disarray.
7 hitecture intermixed with focal myofibrillar disarray.
8 societal inequities and persisting political disarray.
9 eby the loss of DLC1 results in myofibrillar disarray.
10 genic genetic variants of HCM had no myocyte disarray.
11 of myocardium and lead to significant fiber disarray.
12 healthy opportunists to exploit the temporal disarray.
13 ardial mechanics in the development of fiber disarray.
14 d calcium handling, apoptosis, and sarcomere disarray.
15 al muscle disorder associated with sarcomere disarray.
16 ntricular (LV) hypertrophy and myocyte fiber disarray.
17 ion between vascular dispersion and cellular disarray.
18 e used to evaluate sarcomere and microtubule disarray.
19 tole resulting in hypertrophy and sarcomeric disarray.
20 ESRD is a state of small-molecule disarray.
21 s altered, and the microtubule ribbon was in disarray.
22 acement collagen was in short strands and in disarray.
23 contractile proteins and profound sarcomere disarray.
24 cardiac abnormalities including myofibrillar disarray.
25 y cardiac hypertrophy, fibrosis, and myocyte disarray.
26 .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
28 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
30 nctional deficit is accompanied by myofibril disarray, altered calcium handling, and differential alt
31 mutant transgene showed substantial myocyte disarray and a 3-fold increase in interstitial collagen
32 ocyte level, we demonstrated that sarcomeric disarray and accumulation of the physical aggregates res
33 A weak negative correlation between myocyte disarray and age at surgery was identified (p = -0.22; p
34 umulation, and mitochondrial ultrastructural disarray and bioenergetic dysfunction - were mitigated b
35 clinical, and environmental services--are in disarray and decline in much of the developing world, pa
36 Electron microscopy revealed myofibrillar disarray and degeneration with hyaline-like inclusions.
37 g technique might be used to detect cellular disarray and degenerative changes in this sensitive circ
38 nounced hypertrophy of cardiomyocytes, fiber disarray and development of fibrosis and can be divided
39 an be used to detect and quantify myocardial disarray and fibrosis and determine myocardial mass in H
40 r detection and quantification of myocardial disarray and fibrosis by direct comparison with histopat
41 with published histology demonstrating that disarray and fibrosis invade circumferentially aligned m
42 sized that FA would be reduced in HCM due to disarray and fibrosis that may represent the anatomic su
43 d relaxation, delayed early filling, myocyte disarray and fibrosis, and increased chamber end-systoli
45 ant mice (20 weeks old), which develop fiber disarray and fibrosis, had diastolic and systolic kineti
46 ent of cardiac hypertrophy with myofibrillar disarray and fibrosis, in addition to activation of path
47 2 family members did not demonstrate myocyte disarray and fibrosis, indicating that this phenotype is
48 ficant cardiac hypertrophy with myofibrillar disarray and fibrosis, similar to what was observed in t
49 ndividuals with MYH11 mutations revealed SMC disarray and focal hyperplasia of SMCs in the aortic med
52 nsgenic mouse hearts demonstrate myocellular disarray and have a reduced number of cardiac myocytes t
55 trast, TnI(146Gly) mice showed cardiomyocyte disarray and interstitial fibrosis and suffered prematur
57 n T (cTnT-Q(92)) mice, which exhibit myocyte disarray and interstitial fibrosis, to treatment with lo
59 n hypertrophic cardiomyopathy (HCM), myocyte disarray and microvascular disease (MVD) have been impli
63 ltrastructural analysis showed thin-filament disarray and revealed the presence of leptomeres after t
64 only macrophage misalignment but also matrix disarray and Schwann cell disorganization, leading to mi
67 ar abnormalities in the development of fiber disarray and their subsequent impact on cardiac pumping
68 a putative role of constipation in potassium disarrays and also support (with a careful consideration
70 ervation of titin, reduction in myofibrillar disarray, and attenuation of cardiomyocyte necrosis but
71 mal GBM, glomerular epithelial cells were in disarray, and endothelial and mesangial cells were extru
78 nt of ventricular hypertrophy, cardiomyocyte disarray, and myocardial fibrosis and attenuates hypertr
80 ophy without evidence of fibrosis or myocyte disarray, and significant reduction in the left ventricu
81 n, focal areas of medial SMC hyperplasia and disarray, and stenotic arteries in the vasa vasorum due
83 ith systemic symptoms attributed to cytokine disarray, and we have previously shown that the use of t
84 The mutants' rigid paralysis and sarcomeric disarray are consistent with unregulated contraction of
88 n MYL2 phosphorylation with marked sarcomere disarray as the main mechanism of osimertinib cardiotoxi
90 ocumented disease, exercise reversed myocyte disarray (but not fibrosis) and "hypertrophic" marker in
91 ed interstitial fibrosis, attenuated myocyte disarray by 50%, and improved diastolic function in the
93 misshapen and have expanded metaphyses with disarrayed chondrocyte zones in growth plates and reduce
94 that is associated with cytoskeletal protein disarray, contractile dysfunction, and reduced energy pr
98 ty, hypocontractility, and fibrosis on fiber disarray development and examines their effect on functi
101 y but their categorization currently remains disarray due to a wide diversity, resulting in frequent
102 trial and ventricular enlargement, myofibril disarray, fibrosis and mitochondrial injury, and electro
103 in the force-pCa2+ curves with cardiomyocyte disarray, fibrosis, and altered connexin43 organization.
106 receded histopathologic changes, and myocyte disarray, hypertrophy, and fibrosis increased with age.
107 ypertrophic, displayed sarcomeric structural disarray, impaired contractility, and aberrant Ca(2+)-si
109 ondrial fission and mitochondrial structural disarray in brains of hypertensive rats with hypertensio
111 olic FA could be the first in vivo marker of disarray in HCM and a potential independent risk factor.
114 rized by ventricular hypertrophy and myocyte disarray in the absence of known hypertrophic stimuli.
118 tological examination showed cardiac myocyte disarray in the mutant mice, which amounted to 1-15% of
119 on cardiac structure and function leading to disarray, increased collagen synthesis, and diastolic dy
122 haracterized by cardiac hypertrophy, myocyte disarray, interstitial fibrosis, and left ventricular (L
123 nduced hypertrophy, myocyte and myofibrillar disarray, interstitial fibrosis, and premature death, ph
124 of the myocardium revealed myocardial fiber disarray, intramural coronary arteriosclerosis, and inte
127 e cardiac muscle, significantly higher fiber disarray is observed near the epicardium compared to the
129 An acute hepatitic pattern with lobular disarray is seen in acute infection, during acute flares
130 acterized by cardiac hypertrophy and myocyte disarray, is the most common cause of sudden cardiac dea
131 eal growth retardation with cells in mitotic disarray manifesting disorganized spindle, misaligned an
132 anisotropy (lower values expected with more disarray), mean diffusivity (reflecting myocyte packing/
133 or storage diseases and detecting myocardial disarray, microvascular dysfunction, and abnormalities i
136 e of the mutation carriers showed sarcomeric disarray, myofibrillar degeneration, and increased apopt
137 rastructural degenerative changes, including disarrayed myofibrils, dilated sarcoplasmic vesicles, nu
139 nistic basis of the progressive myofibrillar disarray observed in the Drosophila models as well as th
140 impeded in mice lacking these miRNAs, due to disarray of actin stress fibers and diminished migratory
141 ause CMD-like brain malformations, including disarray of cerebral cortical layering, fusion of cerebr
142 ndritic cells and contribute to a functional disarray of dendritic cells by inhibiting their antigen-
144 ith aberrant thickening of the aortic media, disarray of elastic fibers, and increased collagen depos
145 In addition, ultrastructure analysis reveals disarray of extracellular matrix and collagen fiber orga
146 ction, fast-to-slow myofiber conversion, and disarray of muscle triads (sites of excitation- contract
148 essive impaired cardiac function caused by a disarray of several processes including derailed autopha
149 on that decreased RyR P(o) alone can produce disarray of the Ca2+ release process and initiate altern
153 , neither the extent nor location of myocyte disarray or cardiac fibrosis correlated with ex vivo sig
154 Myocyte hypertrophy (p < 0.001), myocyte disarray (p < 0.001), and interstitial fibrosis (p < 0.0
155 significantly different from MAC: epidermal disarray; pagetoid infiltration of dendritic and/or roun
157 The macroscopic findings, percentage of disarray, percentage of fibrosis, and percentage of smal
161 ess to endothelial dysfunction, nitric oxide disarrays, renal interstitial fibrosis, sarcopenia, and
162 sis and more frequently demonstrated lobular disarray, rosette formation, and hemorrhage than those w
163 indicates that the phenotype of myofibrillar disarray seen in HCM patients which harbor either of the
165 to sarcomere protein mutations (ie, myocyte disarray, small vessel disease, myocardial scarring).
166 ivation therapy with endocrine and metabolic disarray, specifically the metabolic syndrome, resulting
167 er heart weights, less fibrosis, and greater disarray than other HCM patients (mean heart weight, 380
168 suddenly had lower heart weights and greater disarray than patients who died suddenly with unknown ge
169 ion, resulting in sarcomere loss and myocyte disarray, the life-threatening hallmarks of TNNT2 mutati
170 not associated with myocyte and myofibrillar disarray, the pathognomonic features of hypertrophic car
176 ng an active stress formulation and myofiber disarray was described using a structural tensor in the
177 phy on echocardiogram, SCD occurred, myocyte disarray was found on autopsy heart, and tissue Doppler
184 llagen volume fraction and extent of myocyte disarray were increased in the cTnT-Q(92) mice (placebo
185 nduced murf1 expression and caused myofibril disarray, whereas inhibiting Calcineurin activity attenu
186 e embryonic day 13.5 and developed sarcomere disarray, whereas Rbpms or Rbpms2 single-cardiomyocyte-s
187 ar regulated kinase 1/2, causes myofibrillar disarray, whereas the enlarged cardiomyocyte phenotype i
188 f hypertrophic cardiomyopathy (HCM) is fiber disarray, which is associated with various cardiac event
192 ars to be a poor reflection of the molecular disarray within the Barrett's epithelium, and a molecula
193 solution or an increased cellular positional disarray within the representation of the amblyopic eye.
194 and fragmented elastic fibers, and cellular disarray without calcification or cell proliferation.