1 d here allows totally noninvasive imaging of
muscular activity (heart, somatic musculature).
2 ions, which is similar to what was found for
muscular activity patterns.
3 chanism of DVT pathogenesis in which loss of
muscular activity results in loss of oscillatory shear-d
4 perivalvular sites in human veins following
muscular activity, but not in the immobile state or afte
5 adaptations requiring significant changes in
muscular activity.
6 can induce substantial unconscious motor and
muscular adjustments is not known.
7 86.98 more per quarter, P=0.035; subjective
muscular AE: 417.95, P<0.0001; nervous system AE: 273.60
8 m AE: 273.60, P<0.0001), but fewer objective
muscular AEs (-125.23 per quarter, P<0.0001).
9 reports showed signals for higher objective
muscular AEs relative to all other statins (reporting od
10 ve AEs were defined as hepatic and objective
muscular AEs.
11 enhanced running performance and upregulated
muscular and adipose Pgc-1alpha transcript levels, where
12 rcury - bound proteins present in samples of
muscular and hepatic tissue from fish collected in the r
13 disease domains (seizure, cognitive failure,
muscular and motor control and brain-malformation) to co
14 oscopy, we describe the organization of both
muscular and nervous systems in the sea gooseberry, Pleu
15 ine predators, with integrated neurosensory,
muscular and organ systems.
16 e the major source of elastin for the IEL in
muscular and resistance arteries.
17 ted in numerous disorders that often display
muscular and/or neurological symptoms due to the high-en
18 Subjective AEs included fatigue, subjective
muscular,
and nervous system AEs.
19 es developed specific innovations in neural,
muscular,
and receptor systems.
20 However,
muscular arteries have a well-defined internal elastic l
21 the IEL was absent or severely disrupted in
muscular arteries.
22 ic arteries but synthesize little elastin in
muscular arteries.
23 formation in the ascending aorta but not in
muscular arteries.
24 atients with genetically confirmed 5q spinal
muscular atrophy (age 16-65 years) with a homozygous del
25 Spinal and bulbar
muscular atrophy (SBMA) is a hereditary neuromuscular di
26 ar atrophy (SMA), X-linked spinal and bulbar
muscular atrophy (SBMA), and amyotrophic lateral scleros
27 Spinal
muscular atrophy (SMA) is a devastating infantile geneti
28 Spinal
Muscular Atrophy (SMA) is a monogenic neurodegenerative
29 Spinal
muscular atrophy (SMA) is a motor neuron disease.
30 Spinal
muscular atrophy (SMA) is a neurodegenerative disease ca
31 otor phenotype.SIGNIFICANCE STATEMENT Spinal
muscular atrophy (SMA) is a neurodegenerative disease, c
32 Spinal
muscular atrophy (SMA) is a neuromuscular disease caused
33 Spinal
muscular atrophy (SMA) is a neuromuscular disease caused
34 Spinal
muscular atrophy (SMA) is a neuromuscular disease causin
35 Spinal
muscular atrophy (SMA) is a neuromuscular disease charac
36 Spinal
muscular atrophy (SMA) is a neuromuscular disorder cause
37 Spinal
muscular atrophy (SMA) is an autosomal recessive motor n
38 BACKGROUNDSpinal
muscular atrophy (SMA) is caused by deficient expression
39 Spinal
muscular atrophy (SMA) is caused by loss-of-function mut
40 Spinal
muscular atrophy (SMA) is caused by mutation or deletion
41 A pathological hallmark of spinal
muscular atrophy (SMA) is severe motor neuron (MN) loss,
42 Spinal
muscular atrophy (SMA) occurs as a result of cell-ubiqui
43 activation of SMN2 exon 7 splicing in spinal
muscular atrophy (SMA) patient fibroblasts, suggesting a
44 asuring SMN1 and SMN2 copy numbers in spinal
muscular atrophy (SMA) samples has not been reported.
45 Spinal
muscular atrophy (SMA) type 0 is the most severe form of
46 n a large cohort of 199 patients with spinal
muscular atrophy (SMA) type III assessed using the Hamme
47 een amyotrophic lateral sclerosis and spinal
muscular atrophy (SMA), and 3 mutations of the ASC-1 gen
48 f cell-cell interaction at the NMJ in spinal
muscular atrophy (SMA), X-linked spinal and bulbar muscu
49 hich causes the neuromuscular disease spinal
muscular atrophy (SMA)-binds to ribosomes and that this
50 nfantile-onset motor neuron disorder, spinal
muscular atrophy (SMA).
51 to neurodegenerative diseases such as spinal
muscular atrophy (SMA).
52 en two motor neuron diseases, ALS and spinal
muscular atrophy (SMA).
53 ogical disorder characterized by progressive
muscular atrophy and respiratory failure.
54 ogressing and fatal disease characterized by
muscular atrophy due to loss of upper and lower motor ne
55 erference selectively in muscle cells caused
muscular atrophy in larval stages and pupal lethality.
56 issue oedema, presence of synovial effusion,
muscular atrophy in the affected extremity, osteopaenia,
57 5q-Associated spinal
muscular atrophy is a hereditary neuromuscular disease l
58 ication of virus-mediated GT to treat spinal
muscular atrophy is a significant milestone, serving to
59 Spinal
muscular atrophy is caused by reduced levels of SMN resu
60 novo variants in BICD2 cause SMALED2 (spinal
muscular atrophy lower extremity dominant 2), and a subs
61 n is approved for the treatment of 5q spinal
muscular atrophy of all types and stages in patients of
62 h nusinersen in a cohort of 85 type I spinal
muscular atrophy patients of ages ranging from 2 months
63 In addition to the benefit to spinal
muscular atrophy patients, there are discoveries from nu
64 n resting energy expenditure (REE) in spinal
muscular atrophy type I (SMAI) is still limited.
65 A pronounced
muscular atrophy was detected in the esophagus and colon
66 In 6% of them
muscular atrophy was severe, and they had posture-gait d
67 sickle cell disease, cystic fibrosis, spinal
muscular atrophy, alpha-thalassemia, and beta-thalassemi
68 treatment of inherited blindness and spinal
muscular atrophy, and long-term therapeutic effects have
69 arcot-Marie-Tooth disease type 2Z and spinal
muscular atrophy, and the onset of symptoms ranges from
70 els of neuromuscular disease, such as spinal
muscular atrophy, NMJ disorder and muscular dystrophy.
71 , for Duchenne muscular dystrophy and spinal
muscular atrophy, offers hope not only for additional ne
72 Secondary radiological findings, such as
muscular atrophy, synovitis, posture-gait deterioration,
73 en in the treatment of adults with 5q spinal
muscular atrophy, with clinically meaningful improvement
74 of the neuromuscular disorder spinal bulbar
muscular atrophy.
75 by recent successful interventions of spinal
muscular atrophy.
76 as been approved for the treatment of spinal
muscular atrophy.
77 n lower extremities or pelvic bones, 73% had
muscular atrophy.
78 icacy of nusinersen in adults with 5q spinal
muscular atrophy.
79 nsional, live observations inside the large,
muscular avian oviduct.
80 urther studies are needed to investigate how
muscular changes after stroke may impede variable gearin
81 y along the course of the involved nerve and
muscular changes secondary to denervation.
82 Gastrointestinal and
muscular complications of cystinosis were studied in a g
83 d with cardiac resonance for the presence of
muscular connection (PMCs) away from the PM base.
84 ion (NMJ) is designed to faithfully elicit a
muscular contraction in response to neural input.
85 of resistance training, there are neural and
muscular contributions to the gain in strength.
86 e previously shown that the presence of dual
muscular coronary sinus (CS) to left atrial (LA) connect
87 The OcrlY/- mice show
muscular defects with dysfunctional locomotricity and pr
88 ntiated pleomorphic sarcomas with incomplete
muscular differentiation.
89 At myectomy, a long
muscular discontinuity displaced the anterior mitral lea
90 Muscular discontinuity was present in each of 6 patients
91 VA-DOT) applied to AE data from 70 Mendelian
muscular disease patients showed accuracy in detecting g
92 However, systemic use of ASOs for this
muscular disease remains challenging due to poor drug di
93 d monitoring of newly developed therapies in
muscular diseases.
94 ed, for instance, diabetes, cardiac disease,
muscular disorders, cancer, and glycogen storage disease
95 pe VI collagen is well known for its role in
muscular disorders, however its function in bone is stil
96 sociated with pathologies such as cancer and
muscular disorders.
97 l muscle samples from control mice and three
muscular dystrophic mouse models at different ages and p
98 subtypes of autosomal recessive limb-girdle
muscular dystrophies (LGMDR3, LGMDR4, LGMDR5 and LGMDR6)
99 Dystrophin proteomic regulation in
muscular dystrophies (MDs) remains unclear.
100 esent an attractive cell source for treating
muscular dystrophies (MDs) since they easily allow for t
101 iated with mitochondrial damage in different
muscular dystrophies (MDs; Duchenne muscular dystrophy,
102 in components of the DGC are responsible for
muscular dystrophies and congenital myopathies.
103 Muscular dystrophies are a heterogeneous group of geneti
104 Muscular dystrophies are debilitating disorders that res
105 Muscular dystrophies are primary diseases of muscle due
106 hnology could offer a one-time treatment for
muscular dystrophies by correcting the culprit genomic m
107 potential for, and challenges of, correcting
muscular dystrophies by editing disease-causing mutation
108 Cell-based therapies in
muscular dystrophies have been pursued experimentally fo
109 In
muscular dystrophies, it has been hypothesized that fibr
110 enerative response is often provoked in many
muscular dystrophies, little is known about whether a re
111 In
muscular dystrophies, muscle membrane fragility results
112 own for its role in a spectrum of congenital
muscular dystrophies, which are often accompanied by res
113 ing to the class of laminopathies, including
muscular dystrophies.
114 ding cancer, neurodegenerative diseases, and
muscular dystrophies.
115 ne muscular dystrophy (DMD) or milder Becker
muscular dystrophy (BMD).
116 Duchenne
muscular dystrophy (DMD) affects 1 in 3500 live male bir
117 y has been evaluated in humans with Duchenne
Muscular Dystrophy (DMD) and in mouse models including t
118 ement of upper extremity muscles in Duchenne
muscular dystrophy (DMD) and showed the feasibility of M
119 Duchenne
muscular dystrophy (DMD) causes severe disability and de
120 onsidered to be outcome measures in Duchenne
muscular dystrophy (DMD) clinical trials.
121 Patients affected by Duchenne
muscular dystrophy (DMD) develop a progressive dilated c
122 The essential product of the Duchenne
muscular dystrophy (DMD) gene is dystrophin(1), a rod-li
123 Duchenne
muscular dystrophy (DMD) is a devastating neuromuscular
124 Duchenne
muscular dystrophy (DMD) is a devastating X-linked disea
125 Duchenne
muscular dystrophy (DMD) is a fatal genetic disorder cau
126 Duchenne
muscular dystrophy (DMD) is a fatal muscle disorder char
127 Duchenne
muscular dystrophy (DMD) is a fatal muscle-wasting disea
128 Duchenne
muscular dystrophy (DMD) is a fatal neuromuscular diseas
129 Duchenne
muscular dystrophy (DMD) is a fatal X-linked disorder ca
130 Duchenne
muscular dystrophy (DMD) is a genetic disorder caused by
131 Duchenne
Muscular Dystrophy (DMD) is a lethal muscle disorder, ca
132 Duchenne
muscular dystrophy (DMD) is a lethal neuromuscular disor
133 Duchenne
muscular dystrophy (DMD) is a lethal, X-linked disease c
134 Duchenne
muscular dystrophy (DMD) is a progressive muscle disease
135 Duchenne
muscular dystrophy (DMD) is a rare genetic disease affec
136 Duchenne
muscular dystrophy (DMD) is a severe X-linked neuromuscu
137 Duchenne
muscular dystrophy (DMD) is a uniformly fatal condition
138 The cardiomyopathy of Duchenne
muscular dystrophy (DMD) is an important cause of morbid
139 Duchenne
muscular dystrophy (DMD) is an X-linked genetic disease
140 Duchenne
muscular dystrophy (DMD) is an X-linked, lethal muscle d
141 Duchenne
muscular dystrophy (DMD) is caused by loss of dystrophin
142 Duchenne
muscular dystrophy (DMD) is caused by mutations in the D
143 Duchenne
muscular dystrophy (DMD) is characterized by progressive
144 Duchenne
muscular dystrophy (DMD) is the most common and severe f
145 Patients with Duchenne
muscular dystrophy (DMD) lack the protein dystrophin, wh
146 w preclinical efficacy for heart in Duchenne
muscular dystrophy (DMD) models but also improve skeleta
147 whether they presented with severe Duchenne
muscular dystrophy (DMD) or milder Becker muscular dystr
148 corticosteroids is recommended for Duchenne
muscular dystrophy (DMD) patients to slow the progressio
149 from most independent FSHD, DM2 or Duchenne
muscular dystrophy (DMD) studies compared to control bio
150 rged as a leading cause of death in Duchenne
muscular dystrophy (DMD), limited studies and therapies
151 promising therapeutic strategy for Duchenne
muscular dystrophy (DMD), which should be applicable to
152 promising therapeutic approach for Duchenne
muscular dystrophy (DMD).
153 clinical study for the treatment of Duchenne
muscular dystrophy (DMD).
154 s contributes to the progression of Duchenne
muscular dystrophy (DMD).
155 c disease in the mdx mouse model of Duchenne
muscular dystrophy (DMD); however, a mechanistic underst
156 Using a murine model of Emery-Dreifuss
muscular dystrophy (EDMD), we show here that lamin A los
157 Facioscapulohumeral
muscular dystrophy (FSHD) is a common, dominantly inheri
158 Facioscapulohumeral
muscular dystrophy (FSHD) is a myopathy with prevalence
159 Facioscapulohumeral
muscular dystrophy (FSHD) is a prevalent, incurable skel
160 Facioscapulohumeral
muscular dystrophy (FSHD) is a prevalent, inherited skel
161 Facioscapulohumeral
muscular dystrophy (FSHD) is an autosomal-dominant myopa
162 Facioscapulohumeral
muscular dystrophy (FSHD) is an incurable disorder linke
163 Facioscapulohumeral
muscular dystrophy (FSHD) is caused by loss of repressio
164 Facioscapulohumeral
muscular dystrophy (FSHD) is caused by the expression of
165 Facioscapulohumeral
muscular dystrophy (FSHD) is characterized by sporadic d
166 Facioscapulohumeral
muscular dystrophy (FSHD) is one of the most common type
167 cles plays a key role in facioscapulohumeral
muscular dystrophy (FSHD) pathogenesis, although the mol
168 Facioscapulohumeral
muscular dystrophy (FSHD) results from expression of the
169 of diseases including facio-scapulo-humeral
muscular dystrophy (FSHD), acute lymphoblastic leukemia,
170 is applied here to study facioscapulohumeral
muscular dystrophy (FSHD), simultaneously recording the
171 n skeletal muscle causes facioscapulohumeral
muscular dystrophy (FSHD).
172 ver, is toxic and causes facioscapulohumeral
muscular dystrophy (FSHD).
173 disease progression in the golden retriever
muscular dystrophy (GRMD) dog model of DMD.
174 Laminin-alpha2 related congenital
muscular dystrophy (LAMA2-CMD) is a fatal muscle disease
175 Muscular dystrophy (MD) is a group of genetic disorders
176 Muscular dystrophy (MD) is a group of progressive geneti
177 ardiomyopathy is a common complication among
muscular dystrophy (MD) patients and often results in ad
178 rom blood serum of a mouse model of Duchenne
muscular dystrophy (mdx) and control mice.
179 Oculopharyngeal
muscular dystrophy (OPMD) is a genetic disorder caused b
180 Oculopharyngeal
muscular dystrophy (OPMD) is a late-onset, primarily aut
181 Oculopharyngeal
muscular dystrophy (OPMD) is a rare autosomal dominant l
182 Oculopharyngeal
muscular dystrophy (OPMD) is a rare late onset genetic d
183 enic muscle loss is a feature of limb girdle
muscular dystrophy 2B (LGMD2B) - a disease caused by mut
184 PMD) is a rare autosomal dominant late-onset
muscular dystrophy affecting approximately 1:100 000 ind
185 (DMD) is the most common and severe form of
muscular dystrophy and affects boys in infancy or early
186 ted in a diverse range of diseases including
muscular dystrophy and cancer metastasis.
187 with the clinical severity of milder Becker
muscular dystrophy and DMD patients.
188 It is considered a late-onset form of
muscular dystrophy and leads to asymmetric muscle weakne
189 This success, for Duchenne
muscular dystrophy and spinal muscular atrophy, offers h
190 e chromosome 10 associated with body mass in
muscular dystrophy as skeletal muscle contributes signif
191 We describe a new
muscular dystrophy associated with this gene.
192 ystroglycan complex (DGC) result in not only
muscular dystrophy but also cognitive impairments.
193 ilencing and indicate that lamin A-dependent
muscular dystrophy can be ascribed to intrinsic epigenet
194 o from iPSC, opening interesting avenues for
muscular dystrophy cell therapy.
195 s are responsible for Cystinosis and Duchene
Muscular Dystrophy diseases, respectively.
196 Like other single-gene disorders,
muscular dystrophy displays a range of phenotypic hetero
197 The degree to which exercise alters
muscular dystrophy has been evaluated in humans with Duc
198 GALGT2 overexpression in muscle can inhibit
muscular dystrophy in mouse models of the disease by ind
199 us histological and physiological aspects of
muscular dystrophy in small and large animal models.
200 Duchenne
muscular dystrophy is a deadly muscle-wasting disorder c
201 Duchenne
muscular dystrophy is a genetic disorder that shows chro
202 Additionally,
muscular dystrophy is linked to mutations in genes that
203 modifiers capable of altering the course of
muscular dystrophy is one approach to deciphering gene-g
204 the haploinsufficiency of Dock3 in Duchenne
muscular dystrophy mice improved dystrophic muscle patho
205 gitudinal studies in a large-animal Duchenne
muscular dystrophy model in pigs, and then applied this
206 animal as well as in the C. elegans Duchenne
muscular dystrophy model.
207 an effective treatment for a select group of
muscular dystrophy patients with end-stage heart failure
208 te that the restoration of TIPE2 ameliorates
muscular dystrophy phenotype through a reduction in infl
209 mimicked Galgt2-dependent neuromuscular and
muscular dystrophy phenotypes.
210 Limb-girdle
muscular dystrophy R1 (LGMD R1) is caused by mutations i
211 tion of recombinant annexin A6 in a model of
muscular dystrophy reduced serum creatinine kinase, a bi
212 the same pathway vary greatly, ranging from
muscular dystrophy to spastic paraplegia to a childhood
213 se-modifying gene associated with congenital
muscular dystrophy type 1A (MDC1A) using the CRISPR acti
214 ved cell lines for two diseases: limb-girdle
muscular dystrophy type 2G (LGMD2G)(1) and Hermansky-Pud
215 parate diseases, one of which is Limb-girdle
muscular dystrophy type 2H (LGMD2H).
216 late-onset muscle disease termed limb-girdle
muscular dystrophy type D1 (LGMDD1), which is characteri
217 case control study of patients with Duchenne
muscular dystrophy who underwent serial cardiac magnetic
218 s the most common autosomal dominant form of
muscular dystrophy with a prevalence of ~1 in 8000 indiv
219 Patients with Duchenne
muscular dystrophy with an LV ejection fraction >=55% on
220 Congenital
muscular dystrophy with megaconial myopathy (MDCMC) is a
221 The
muscular dystrophy X-linked mouse (mdx) is the most comm
222 In the most common form, Duchenne
muscular dystrophy, a few personalised therapies have re
223 hy (FSHD) is one of the most common types of
muscular dystrophy, affecting roughly one in 8000 indivi
224 nital muscular dystrophy, Ullrich congenital
muscular dystrophy, and alpha-dystroglycanopathy).
225 cated in the pathology of diseases including
muscular dystrophy, and neurodegenerative diseases, such
226 n conditions such as cerebral palsy, stroke,
muscular dystrophy, Charcot-Marie-Tooth disease, and sar
227 cross neurodevelopmental, neurodegenerative,
muscular dystrophy, epilepsy, chronic pain and neoplasti
228 ival, and in the mdx mouse model of Duchenne
muscular dystrophy, exosomes secreted by the engineered
229 ystrophy type 1 (DM1), the most common adult
muscular dystrophy, is an autosomal dominant disorder ca
230 rophin-deficient mdx mouse model of Duchenne
muscular dystrophy, limb muscles are especially fragile.
231 ifferent muscular dystrophies (MDs; Duchenne
muscular dystrophy, megaconial congenital muscular dystr
232 ne muscular dystrophy, megaconial congenital
muscular dystrophy, Ullrich congenital muscular dystroph
233 the potential beneficial effect of TIPE2 in
muscular dystrophy, we performed intramuscular injection
234 For example, Duchenne
muscular dystrophy, which is caused by mutations in the
235 sfunction before the onset of overt Duchenne
muscular dystrophy-associated cardiomyopathy (DMDAC) may
236 Muscular dystrophy-dystroglycanopathies comprise a heter
237 ions in SMCHD1 can cause facioscapulohumeral
muscular dystrophy.
238 as spinal muscular atrophy, NMJ disorder and
muscular dystrophy.
239 may be effective in treating this inherited
muscular dystrophy.
240 verity, including limb-girdle and congenital
muscular dystrophy.
241 and following DUX4 expression that leads to
muscular dystrophy.
242 diseases, including haemophilia and Duchenne
muscular dystrophy.
243 em myopathy to the severe Ullrich congenital
muscular dystrophy.
244 commonly used preclinical model for Duchenne
muscular dystrophy.
245 ercross strategy in mice to map modifiers of
muscular dystrophy.
246 he clamp method in the mdx model of Duchenne
muscular dystrophy.
247 celerates muscle loss and causes limb girdle
muscular dystrophy.
248 ommonly deleted in individuals with Duchenne
muscular dystrophy.
249 lacking for muscle diseases such as Duchenne
muscular dystrophy.
250 activity in the setting of muscle growth and
muscular dystrophy.
251 or developing intervention aimed at treating
muscular dystrophy.
252 m) mouse is a murine model of human Duchenne
muscular dystrophy.
253 (DM1), the most common form of adult on-set
muscular dystrophy.
254 ng the efficacy of therapeutics for Duchenne
muscular dystrophy.
255 Higher preflight upper body
muscular endurance was associated with a 39% reduced ris
256 Standardized tests of maximal strength,
muscular endurance, flexibility, and cardiorespiratory f
257 ement and therefore relatively little active
muscular energy, and may be used by a wide range of fish
258 aerobic threshold, peak expiratory flow, and
muscular exercise capacity.
259 change of cortical thickness associated with
muscular expression along a phenotypic trajectory that d
260 lobe where children with greater upper-body
muscular fitness showed higher FA (P(FWE-corrected) = 0.
261 s predictive of cognition and interacts with
muscular fitness to predict cognition.
262 se findings indicate that the association of
muscular fitness with white matter microstructure might
263 aptic NMJ function, and maintaining skeletal
muscular function and structure.
264 .SIGNIFICANCE STATEMENT Neurons that control
muscular function progressively degenerate in patients w
265 s pulls the tongue base posteriorly, and the
muscular hydrostat or intrinsic tongue muscle hypothesis
266 der, seizures, variable brain malformations,
muscular hypotonia, and scoliosis.
267 with profound neurodevelopmental disability,
muscular hypotonia, feeding abnormalities, recurrent fev
268 gitudinal strain), autonomic, pulmonary, and
muscular impairments increased risk.
269 eATP blockade dampened the
muscular inflammatory response and enhanced the recruitm
270 ebrovascular disease with ocular, renal, and
muscular involvement.
271 These findings suggest that a long
muscular mitral-aortic discontinuity could predispose to
272 In 2016 we identified, at myectomy,
muscular mitral-aortic discontinuity in 5 young patients
273 We report, for the first time,
muscular mitral-aortic discontinuity in HCM.
274 minary findings and assess the prevalence of
muscular mitral-aortic discontinuity in obstructive HCM.
275 Muscular mitral-aortic discontinuity was identified in 2
276 We demonstrate that independent
muscular,
neural, and vascular insults contribute to neu
277 other components of physical fitness (i.e.,
muscular or motor fitness) are associated with white mat
278 The tongue is a highly specialised
muscular organ with a complex anatomy required for norma
279 and vascular mural cells across four murine
muscular organs: heart, skeletal muscle, intestine and b
280 quires viral replication in affected muscle,
muscular pathology is mediated by host immunological fac
281 notypes but all affected individuals display
muscular pathology.
282 accretion, skeletal muscle hypertrophy, and
muscular performance improvements can be achieved with d
283 ailable to the human foot, which can enhance
muscular performance in a specific locomotion task.
284 ve (electrical activity of the diaphragm and
muscular pressure over time) and P0.1ref.
285 EMG showed that learning augments the
muscular response evoked by motoneuron output and that t
286 aracteristic echinoderm-like plated theca, a
muscular stalk reminiscent of the hemichordates and a pa
287 asic with sedation because there was minimal
muscular stimulation.
288 an heart are covered by a complex network of
muscular strands that is thought to be a remnant of embr
289 Fitness was operationalized as
muscular strength (push-ups) and aerobic endurance (PACE
290 In HSA(LR) mice, the drug restored
muscular strength and histopathology signs and reduced t
291 nt injury and modulation of such by altering
muscular strength.
292 by the extensive development of ciliated and
muscular structures including the presence of giant musc
293 systematically characterize both neural and
muscular systems in Aglantha, summarizing and expanding
294 lack of microanatomical data about the neuro-
muscular systems in this group of animals.
295 and we demonstrated their ability to improve
muscular systolic function, with no impact on diastolic
296 and tetanus stresses, as measured using the
Muscular Thin Film (MTF) assay.
297 d phospholipases A(2) (sPLA(2)s) block neuro-
muscular transmission by poisoning nerve terminals.
298 Data herein details the
muscular weakness and wasting exhibited by D2.mdx skelet
299 short-living hSOD1/rag2 mice is preceded by
muscular weakness as early as one month before death.
300 ressive spasticity, exaggerated reflexes and
muscular weakness.