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1  for excitation-contraction [EC] coupling in heart muscle).
2 muscles or by 6 months post gene excision in heart muscle.
3 of the myosin filament during contraction of heart muscle.
4 ld result in a hypercontractile state in the heart muscle.
5 o reconstruct the functional architecture of heart muscle.
6 d in hepatocytes, as well as in skeletal and heart muscle.
7 c cardiomyopathy (FHC), a primary disease of heart muscle.
8 o prevent development of an abnormally large heart muscle.
9  regulates Ca2+ activation of tension in the heart muscle.
10  the fast transient outward current in mouse heart muscle.
11  have the potential to regenerate functional heart muscle.
12 genic expression inhibits autophagy in mouse heart muscle.
13    Thus, NO acts on the ganglion, but not on heart muscle.
14 This study examined the function of HSP20 in heart muscle.
15  event of excitation-contraction coupling in heart muscle.
16 ds to scarring, with minimal regeneration of heart muscle.
17 inant-negative mode that impairs function of heart muscle.
18 ending support to the "sliding" mechanism in heart muscle.
19 D signal for skeletal and a 95-kD signal for heart muscle.
20 known to exist and PDE1B is present in human heart muscle.
21 n a 3.6-kb transcript for mouse skeletal and heart muscle.
22  artery disease by imaging the metabolism of heart muscle.
23  process within intact sarcomeres from mouse heart muscle.
24  as a tracer for reference images of the dog heart muscle.
25  includes pancreas, kidney, and skeletal and heart muscle.
26  account for the Pasteur effect in ischaemic heart muscle.
27 ith lung congruent with cerebellum > liver > heart muscle.
28  variance with previous reports on mammalian heart muscle.
29 empt to target MCP-1 expression to the adult heart muscle.
30 d as a tracer for glucose uptake in ischemic heart muscle.
31 and are especially abundant in epidermis and heart muscle.
32 ision after tissue damage to regenerate lost heart muscle.
33 d for an artificial means of stimulating the heart muscle.
34 ion and stabilization of its mRNA targets in heart muscle.
35 tional, and infiltrative deficiencies of the heart muscle.
36 he regulatory state of the thick filament in heart muscle.
37 e course of contraction in both skeletal and heart muscle.
38 nisms can also operate in adipose tissue and heart muscle.
39 nitially absent from the cerebral cortex and heart muscle.
40 with both inherited and acquired diseases of heart muscle.
41 ch explains the altered contractility of the heart muscle.
42 ontaining) filaments in intact sarcomeres of heart muscle.
43 benefit from an in vitro surrogate for human heart muscle.
44 ta-adrenergic stimulation on the ventricular heart muscle.
45 hemomechanical energy transducer in striated heart muscle.
46 sfrp1 is strongly induced in differentiating heart muscle.
47 ytes after cardiac injury to regenerate lost heart muscle.
48 osphorylation and glucose uptake in isolated heart muscles.
49 tochondrial biogenesis in mouse hindlimb and heart muscles.
50 isomycin also increased glucose transport in heart muscles.
51 n, which regulates contraction of Drosophila heart muscle [22] and may regulate muscle contractions i
52 cium/calmodulin-dependent protein kinases in heart muscle, acts as an anti-apoptotic factor and is a
53 -binding protein that is expressed solely in heart, muscle, adipose, and mammary tissue, remains to b
54  electrical repolarization (recovery) of the heart muscle after each contraction.
55            By contrast, zebrafish regenerate heart muscle after trauma by inducing proliferation of s
56  calcium-dependent switch for contraction in heart muscle and a potential target for drugs in the the
57        Most prominent among these are direct heart muscle and blood vessel regeneration from transpla
58 broad spectrum of conditions that injure the heart muscle and cause both structural and functional de
59 e to recapitulating the complex structure of heart muscle and might, therefore, be amenable to indust
60  destruction of vasculature in the infarcted heart muscle and progression of cardiac fibrosis lead to
61 f MCP-1 transcripts and protein in the adult heart muscle and pulmonary vein but not in skeletal musc
62 h RCAS-crescent induces formation of beating heart muscle and represses formation of blood.
63 maintenance of the contractile structures in heart muscle and that its function is regulated by postt
64        The electron microscopic structure of heart muscle and the ultrastructural basis of cardiac co
65 ded by a cDNA that is expressed primarily in heart, muscle and adipose tissue.
66 id not show positive effects in diaphragm or heart muscle, and heart pathology was worsened.
67 in-C (MyBP-C) is a key regulatory protein in heart muscle, and mutations in the MYBPC3 gene are frequ
68                  The levels of HK II mRNA in heart, muscle, and adipose tissue are paralleled by HK I
69  lower levels also in kidney, spleen, liver, heart, muscle, and brain.
70 und in the acid-insoluble fraction (>84% for heart, muscle, and liver).
71 wn to utilize fatty acids for energy such as heart, muscle, and liver.
72 ophysical targets of Mbnl proteins in brain, heart, muscle, and myoblasts by using RNA-seq and CLIP-s
73 as BRUNOL3 is expressed predominantly in the heart, muscle, and nervous system.
74 r concentration in fetal liver, gut, kidney, heart, muscle, and skin.
75    The specialized contractile properties of heart muscle are attributable to the expression of cardi
76 events of excitation-contraction coupling in heart muscle are Ca2+ sparks, which arise from one or mo
77 urgical samples of human arteries, veins and heart muscle are proving advantageous in the identificat
78 d passive stiffness in comparison with donor heart muscle as a control.
79 ion with dysfunction of liver, skeletal- and heart muscle as well as brain.
80 of stage XI-XIV blastulas were found to form heart muscle at high frequency with a timing that corres
81 is expressed at a high level in skeletal and heart muscle, at an intermediate level in pancreas and b
82 uscle has a profound capacity to regenerate, heart muscle, at least in mammals, has poor regenerative
83 e-threatening condition that occurs when the heart muscle becomes weakened and cannot adequately circ
84 distal one for the testis, front feet, bone, heart, muscle, brain, spinal cord, and tongue, while die
85      This was confirmed in mice in which the heart-muscle-brain adenine nucleotide translocator isofo
86 ogenous BAT, white adipose tissue (WAT), and heart muscle but, surprisingly, not skeletal muscle.
87 lion is insensitive to L-NA, suggesting that heart muscle (but not the ganglion) produces endogenous
88     Only the mutant mRNA was detected in the heart muscle, but in the skeletal muscle it coexisted wi
89 netics of force development in permeabilized heart muscle, but its role in vivo is unknown.
90 of serine/threonine kinases activated within heart muscle by a variety of agonists.
91           cTnT may participate in tuning the heart muscle by decreasing the speed of XB recruitment s
92 t suppress intracellular calcium handling in heart muscle by interacting with messenger RNA encoding
93 -induced AMPK activation was also blunted in heart muscles by preincubation with either anti-sauvagin
94  and mechanisms contributing to pathological heart muscle calcification remain unknown.
95 st cell-like fate and contribute directly to heart muscle calcification.
96 th a diminution in prostacyclin in infarcted heart muscle, can lead to the development of thrombotic
97                             Abnormalities of heart muscle (cardiomyopathies) and/or electrical conduc
98 ker rat hearts, whereas, in obese Zucker rat hearts, muscle carnitine palmitoyltransferase and medium
99 iomyocytes activates PARS and contributes to heart muscle cell death by apoptosis, experiments were p
100    A further role for MAP4K4 was proposed in heart muscle cell death triggered by cardiotoxic anti-ca
101 tive therapeutic target in DOX-induced human heart muscle cell death.
102 ria and cytoplasmic protein loss in a living heart muscle cell should lead to systolic dysfunction.
103 alcium current in either type of dissociated heart muscle cell, even at concentrations much higher th
104 ion, but that loss of all Tln forms from the heart-muscle cell leads to myocyte instability and a dil
105 y of human embryonic stem cells (hESCs) into heart muscle cells (cardiomyocytes) is highly sensitive
106 s show that the enhanced force observed when heart muscle cells are maximally activated by calcium is
107 ctural changes in the myofilaments of intact heart muscle cells associated with activation of myocard
108 indicate that improving the contractility of heart muscle cells by boosting intracellular calcium han
109                                          The heart muscle cells could be divided into type I and type
110 when an atrial chamber fibrillates, and when heart muscle cells die en masse after a heart attack.
111 cardiac conduction system differentiate from heart muscle cells during embryogenesis.
112                       At the cellular level, heart muscle cells generate higher force when stretched,
113 hypoblast possessed broad capacity to induce heart muscle cells in pregastrula and mid-gastrula epibl
114 art transplant model and cytokine-stimulated heart muscle cells in tissue culture.
115 n program during terminal differentiation of heart muscle cells into Purkinje fibers.
116                Contraction and relaxation of heart muscle cells is regulated by cycling of calcium be
117                                 Personalized heart muscle cells made from stem cells in the laborator
118                                              Heart muscle cells produce peptide hormones such as natr
119 ine factor, endothelin, can induce embryonic heart muscle cells to differentiate into Purkinje fibers
120 ulated increase in ICa,L seen in the type II heart muscle cells was not mediated by a PTX-sensitive G
121         Internal dialysis of isolated type I heart muscle cells with guanosine 5'-O-(3-thiotriphospha
122 ent but not proliferation of cardiomyocytes (heart muscle cells) during postnatal development.
123 l exerts a direct cardioprotective effect on heart muscle cells, an effect mediated by selective acti
124  can modulate ICa,L, but not ICa,T, in squid heart muscle cells, and that the underlying G protein pa
125 e maturation and pathogenesis of adult human heart muscle cells, and this concept may be expanded to
126 of the L-type calcium current in the type II heart muscle cells, but had no effect on the T-type calc
127            Here, we show that differentiated heart muscle cells, cardiomyocytes, can be induced to pr
128                                          The heart muscle cells, i.e., the cardiomyocytes, possess a
129 in on the actin-containing thin filaments of heart muscle cells, initiating a change in filament stru
130 s show that during and after conversion from heart muscle cells, Purkinje fibers express a unique myo
131 occur in the terminally differentiated adult heart muscle cells, studies in endomyocardial biopsies f
132 fect mechanical and electrical properties of heart muscle cells.
133 tential propagation along a linear strand of heart muscle cells.
134 graft rejection in association with death of heart muscle cells.
135 d in Purkinje fibers as compared to ordinary heart muscle cells.
136  the key moiety disrupting the physiology of heart muscle cells.
137 h immunosuppression might enhance salvage of heart-muscle cells during acute cardiac-allograft reject
138  of viral gene transfer to convert quiescent heart-muscle cells into pacemaker cells, and the success
139 ity and restoration of dystrophin protein in heart muscle compared with skeletal muscle tissues in DM
140  a greater degree in Purkinje fibers than in heart muscle, consistent with the clinical presentation
141  tissues as diverse as buccal epithelium and heart muscle contain high proportions of clonal mutant m
142                                              Heart muscle contractility and performance are controlle
143  not alter burst duration, spikes per burst, heart muscle contractility, or amplitudes of synaptic po
144  into the sarcoplasmic reticulum, modulating heart muscle contractility.
145 e regulation of overall calcium handling and heart muscle contractility.
146 ), a single-pass membrane protein, regulates heart muscle contraction and relaxation by reversible in
147 nd key for the cooperative switching between heart muscle contraction and relaxation.
148                                              Heart muscle contraction is normally activated by a sync
149                          Forces generated by heart muscle contraction must be balanced by adhesion to
150 etween cMyBP-C, myosin, and actin during the heart muscle contraction.
151 interactions between myosin and actin during heart muscle contraction.
152 trical waves meander erratically through the heart muscle, creating disordered and ineffective contra
153 tablished protein biomarkers associated with heart muscle damage and point-of-care monitoring of both
154 arnosine and anserine in murine skeletal and heart muscle depends on circulating availability of beta
155  120 RNASeq transcriptomes from skeletal and heart muscle derived from healthy and DM1 biopsies and a
156 pression as a novel mechanism for regulating heart muscle development and function, in particular the
157 catenin signaling are capable of restricting heart muscle development at these relatively late stages
158 rfamily members in regulating early steps of heart muscle development.
159  show that sfrp1 is not only able to promote heart muscle differentiation but is also required for th
160 dogenous Wnt ligand required for controlling heart muscle differentiation via canonical Wnt/beta-cate
161 n unrecognised role in the earliest steps of heart muscle differentiation, and that partial complemen
162 dogenous Wnt signalling inhibitor for normal heart muscle differentiation.
163 -MHC gene in cardiac myocyte cultures and in heart muscle directly injected with plasmid DNA.
164 hmogenic cardiomyopathy (AC) is an inherited heart muscle disease associated with point mutations in
165          Dilated cardiomyopathy is a form of heart muscle disease characterized by impaired systolic
166 cardiomyopathy (HCM) is an important genetic heart muscle disease for which prevalence in the general
167 right ventricular cardiomyopathy (ARVC) is a heart muscle disease of unknown etiology that causes arr
168 icular cardiomyopathy (ARVC) is a hereditary heart muscle disease that causes sudden cardiac death (S
169  should be relevant to the acquired forms of heart muscle disease that HCM models.
170 ion, experts in the field of cardiomyopathy (heart muscle disease) in children address 2 issues: the
171 cataracts and skeletal myopathies, including heart muscle diseases (cardiomyopathy).
172  the healthy heart and their disturbances in heart muscle diseases are described.
173 he pharmacological treatment of skeletal and heart muscle diseases rely on direct sarcomeric modulato
174 t target for small-molecule therapeutics for heart muscle diseases, and, as we describe here, other m
175 heart tissue engineering and in the study of heart muscle diseases.
176 hmogenic right ventricular cardiomyopathy, a heart muscle disorder associated with ventricular arrhyt
177            Dilated cardiomyopathy (DCM) is a heart muscle disorder characterized by atrial and ventri
178 trictive cardiomyopathy (RCM) is an uncommon heart muscle disorder characterized by impaired filling
179 mogenic cardiomyopathy (ACM) is an inherited heart muscle disorder characterized by myocardial fibrof
180 ntricular cardiomyopathy (ARVC) is a primary heart muscle disorder resulting from desmosomal protein
181 rdiomyopathy (ARVC) is an autosomal dominant heart muscle disorder that causes arrhythmia, heart fail
182 rrhythmogenic cardiomyopathy is an inherited heart muscle disorder, predisposing to sudden cardiac de
183 cally and genetically heterogeneous group of heart muscle disorders associated with high morbidity an
184 ents afflicted with ischemic and nonischemic heart muscle disorders.
185 he vertebrate heart to form, surrounding the heart muscle during embryogenesis and providing signalin
186 cesses fail to work properly or effectively, heart muscle dysfunction can occur with or without accom
187 al benefits, and teratoma risk of engineered heart muscle (EHM) in a chronic myocardial infarction mo
188 stem cells (PSCs) and deployed as engineered heart muscle (EHM) may overcome all of these formidable
189                  However, forming Engineered Heart Muscle (EHM) typically requires >1 million cells p
190                            Tissue engineered heart muscles (EHMs) were generated by casting human emb
191  the strength and dynamics of contraction in heart muscle, enabling those structures to be targeted t
192 ohydrate ketogenic diet) to demonstrate that heart muscle engages a metabolic response that limits ke
193  in a number of embryonic tissues, including heart muscle, epidermis and neuroepithelium.
194                                 Skeletal and heart muscle excitability is based upon the pool of avai
195                                              Heart muscle excitation-contraction (E-C) coupling is go
196          We show that Xenopus anterior lymph heart muscle expresses skeletal muscle markers such as m
197 f Hh signaling and upon en1 knockdown, lymph heart muscle fails to develop, despite the normal develo
198 happens when plaque forms in an artery, when heart muscle fibers cross-link and weaken, when an atria
199 g complex, has been shown to be required for heart muscle formation in mouse.
200 d non-canonical Wnt signalling in regulating heart muscle formation.
201                             NOx is formed in heart muscle from NO; NO originates through the activity
202                                   Engineered heart muscles from TTS-iPSC-CMs showed an impaired force
203 rdiac contractility due to direct changes in heart muscle function independent of vascular disease.
204 chrome c oxidase (COX) subunits VIa and VIIa heart/muscle (H) and ubiquitous (L) isoforms.
205 sgenic mice, the contractile defect in human heart muscle has not been studied.
206        The engineering of 3-dimensional (3D) heart muscles has undergone exciting progress for the pa
207 d the three troponin subunits found in human heart muscle, how the isoform profiles of these proteins
208 tablished model of pressure overload-induced heart muscle hypertrophy caused by transverse aortic con
209 ing, as a marker of complement activation in heart muscle in a murine model of myocardial IRI.
210 echanisms of mesodermal commitment to create heart muscle in mammals are largely unknown.
211 , adult zebrafish vigorously regenerate lost heart muscle in response to injury.
212 so required for the formation of normal size heart muscle in the embryo.
213 enon that describes an intrinsic property of heart muscle in which increased cardiac filling leads to
214 hese studies is proregenerative responses in heart muscle induced by systemic chemical suppression of
215 lustrate that the cells of the lens, retina, heart muscle, inner ear, and bone are dependent on XylT2
216                       Optical control of the heart muscle is a promising strategy for cardiology beca
217                                              Heart muscle is characterized by a regular array of prot
218 e creatine kinase (MCK) gene in skeletal and heart muscle is controlled in part by a 5' tissue-specif
219            Compared with the adult, neonatal heart muscle is less sensitive to deactivation by acidic
220                                              Heart muscle is metabolically versatile, converting ener
221 layer lines in x-ray diffraction patterns of heart muscle is not due to an inherently more disordered
222                                     Although heart muscle is particularly sensitive to metabolic stre
223                     ABSTRACT: Contraction of heart muscle is triggered by a transient rise in intrace
224                               Contraction of heart muscle is triggered by calcium binding to the acti
225 .523delC, p.Q175RfsX38), which codes for the heart-muscle isoform of the adenine nucleotide transloca
226 luding the ATP synthase beta subunit and the heart-muscle isoform of the adenine nucleotide transloca
227              We have mapped the gene for the heart/muscle isoform of cytochrome c oxidase (COX) subun
228 mined the mitochondria from mice lacking the heart/muscle isoform of the adenine nucleotide transloca
229 e generated 'knockout' mice deficient in the heart/muscle isoform of the adenine nucleotide transloca
230                                 As a result, heart muscle isolated from bag3(-/-) mice exhibited myof
231  the pore channel was commonly unoccupied in heart muscle-isolated cardiac cells, yet a dense materia
232 ac growth; simultaneously, blood flow to the heart muscle itself is increased, and reserve blood flow
233 dominantly in postmitotic tissues, including heart, muscle, kidney, and brain.
234 7/BL 6 mouse tissues including brain, liver, heart, muscle, kidney, and testis.
235 pt indicated its occurrence in liver, brain, heart, muscle, kidney, lung, testis, and spleen.
236 orylation and maximal activation of BCKDC in heart, muscle, kidneys, and liver with reduction in plas
237 , which is recognized by the protein kinase, heart muscle kinase and can be specifically labeled with
238 ence, an antibody recognition epitope, and a heart muscle kinase site, was engineered and expressed i
239 d to isolate a full-length human cDNA from a heart muscle library.
240 impulse-conducting Purkinje cells within the heart muscle lineage and also may provide a basis for ti
241 C16 was only expressed in testis, and not in heart, muscle, liver, ovaries, or eggs, whereas the mRNA
242 lect adult tissues, TIMP3 mRNA is present in heart, muscle, liver, skin, intestine and ovaries.
243             Cardiomyocytes, the cells of the heart muscle, lose nearly all of their proliferative cap
244              (Does a Drug Allopurinol Reduce Heart Muscle Mass and Improve Blood Vessel Function in P
245 s targeting CRM1-dependent nuclear export in heart muscle may have salutary effects on cardiac functi
246                Thus, MCP-1 expression in the heart muscle may provide a model to investigate myocardi
247                                 Skeletal and heart muscle mitochondria of the CAP(R) mice were enlarg
248 solution which could allow the creation of a heart muscle model, enabling the growth of cardiac cells
249 nes features of EHM and cardiospheres: Micro-Heart Muscle (muHM) arrays, in which elongated muscle fi
250                               The vertebrate heart muscle (myocardium) develops from the first heart
251 iogenic mesoderm begin to differentiate into heart muscle (myocardium).
252 ials of the kidney enzyme in comparison with heart muscle Na(+),K(+)-ATPase, in agreement with experi
253 d by progressive inflammatory destruction of heart, muscles, nerves, and gastrointestinal (GI) tract
254 fter gastrulation, with major defects in the heart muscle, neuroepithelium and skin epithelium, all o
255 al ribonucleic acids have been identified in heart muscle of a subset of patients with myocarditis an
256  leg (p = 0.038), diaphragm (p = 0.042), and heart muscles (p < 0.001).
257 ys an essential role in healthy and diseased heart muscle, particularly in Ca(2+)-induced Ca(2+) rele
258 role of 111In-antimyosin in the detection of heart muscle pathology, radiation dose estimates were ma
259  with the highest level of expression in the heart, muscle, peripheral blood leukocytes, and brain.
260 unrecognized structural element close to the heart muscle plasma membrane at the intercalated disc wh
261 n is a compensatory response to decreases in heart muscle power output.
262 sophila mesoderm into visceral, somatic, and heart muscle precursors.
263 evels are in contrast preserved in the aging heart muscle, presumably due to its incessant aerobic ac
264 rp1 controls the size of the differentiating heart muscle primarily by regulating cell fate within th
265 h in the United States in large part because heart muscle regenerates poorly.
266                               The premise of heart muscle regeneration by the transdifferentiation of
267 hts into the fundamental pathways that drive heart muscle regeneration have begun to arise as well as
268  multiple novel approaches to the problem of heart muscle regeneration.
269 xide synthase (NOS) is strongly expressed in heart muscle relative to other muscles.
270  events driving deleterious calcification of heart muscle remains elusive.
271 f cardiac signaling, the function of PKD1 in heart muscle remains unclear.
272                                              Heart muscle requires a constant supply of oxygen.
273           Excitation-contraction coupling in heart muscle requires the activation of Ca(2+)-release c
274 generating zebrafish retina, caudal fin, and heart muscle revealed additional candidate genes potenti
275 ow measureable specific binding of F-Dapa in heart, muscle, salivary glands, liver, or brain.
276                        Mice deficient in the heart/muscle specific isoform of the adenine nucleotide
277                           Here, we show that heart/muscle-specific knockdown of MED13 or MED12, anoth
278 t level of expression in testis, followed by heart muscle, spleen and prostate.
279                         Contracting slow and heart muscles stretched under load could employ this enh
280                   The level of p204 in mouse heart muscle strongly increased during differentiation;
281 the adult chicken liver but not in the adult heart, muscle, testis, or brain.
282 corporated in a patient to a higher level in heart muscle than skeletal muscle, causing X-linked dila
283  anatomical and physiological changes of the heart muscle that are potentially reversible with beta-b
284 diomyopathy (HCM) is an inherited disease of heart muscle that can be caused by mutations in sarcomer
285           Myocarditis is inflammation of the heart muscle that can follow various viral infections.
286     Cardiomyopathies are disorders affecting heart muscle that usually result in inadequate pumping o
287                                  In isolated heart muscles, the AMPK activator 5-aminoimidazole-4-car
288 Compared with postmitotic cardiac cells from heart muscle, these proliferative and differentiating st
289  to develop strategies for restoring healthy heart muscle through the regeneration and repair of dama
290 rdiogenic mesoderm later differentiates into heart muscle tissue (myocardium) and non-muscular heart
291 ration, and assembly of these cells into the heart muscle tissue, the pacemaker and conduction system
292 lize with I-band titin N2A epitopes in adult heart muscle tissues.
293                             The inability of heart muscle to regenerate by replication of existing ca
294 trophin gene excision, ranging from ~ 25% in heart muscle to ~ 30-35% in skeletal muscles in vivo.
295 e for delivering oxygen to the anaemic fetal heart muscle using contrast-enhanced echocardiography.
296 ls to generate replacement cells for damaged heart muscle, valves, vessels and conduction cells holds
297 plicing activity is inhibited postnatally in heart muscle via expression of a nuclear dominant negati
298  humans is higher in skeletal muscle than in heart muscle, we propose that the hnRNP G/Tra2beta ratio
299       In contrast, histograms of contracting heart muscle were peaked and asymmetric, suggesting that
300 lower in the cerebral cortex, cerebellum and heart muscle, whereas Bcl-x was not downregulated in any

 
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