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1  in overload-induced hypertrophy of skeletal muscle.
2 NSCLC lesions as well as for normal lung and muscle.
3 on protein phosphorylation in mouse skeletal muscle.
4 s angiogenesis and perfusion recovery in PAD muscle.
5  cell lines and to generating other forms of muscle.
6 amma-aminobutyric acid (GABA) secretion from muscle.
7 increasing metabolic power in human skeletal muscle.
8 elated defects that occur in rodent skeletal muscle.
9 e reconstructed microcirculation in skeletal muscle.
10 sis of stem cells and reduce fibrosis in dKO muscle.
11 a burn injury and likely hinders regrowth of muscle.
12 sed in laminin-alpha2 dyW null gastrocnemius muscle.
13 positional information is a major feature of muscle.
14 liver, adipose tissue, pancreas and skeletal muscle.
15  limb muscles when compared with respiratory muscle.
16  synthesis in both rodent and human skeletal muscle.
17 on to regulate chemorepulsion exerted by the muscle.
18 alization to actin-rich I-bands in body wall muscle.
19 ion, leading to RV formation in sIBM patient muscle.
20 cking and excitation-contraction coupling in muscle.
21 mic agility with only a small number of wing muscles.
22 a dramatic increase in pSTAT3 relative to WT muscles.
23 t ankle dorsiflexor and right wrist extensor muscles.
24 ntributions in the development of artificial muscles.
25 ostal and levator auris muscles but not limb muscles.
26 ry fatigue through remote activation of prey muscles [4].
27                                       Smooth-muscle actin expression by stellate cells and CD34 expre
28 contained reduced myosin heavy chain, smooth muscle actin, and desmin, and increased markers of dedif
29 eptor-alpha-positive cells, and alpha-smooth muscle actin-positive blood vessels were assayed at post
30     Motor function scores (MFS) and compound muscle action potential (CMAP) decreased rapidly in SMA
31 t also seems to control the dynamics of both muscle activation and relaxation.
32 ned subject-specific masseter and temporalis muscle activities per 20-N bite-force (T20 N, microV), w
33 those of postural control and gluteus medius muscle activities, respectively, in response to perturba
34                                Knee extensor muscle activity decreased slightly during exoskeleton-as
35 pontaneous recovery of ipsilateral diaphragm muscle activity is associated with increased phrenic mot
36  electrodes, whilst simultaneously recording muscle activity of the affected limbs.
37 ing of individual proteins in human skeletal muscle after a high-fat diet and resistance exercise.
38                                              Muscle alpha-tocopherol concentration was over 3.5-fold
39 n's metabolic actions in the liver, skeletal muscle and adipose tissue.
40 indicated that BmAce1 is highly expressed in muscle and BmAce2 is more ubiquitously expressed among t
41  is based on research on yeast and mammalian muscle and brain that demonstrates that the glycogen shu
42 ]FDG) was studied in EMT6 cells, tumors, and muscle and correlated to GLUT1 and GLUT5 expression leve
43 e we identify the functional organization of muscle and cutaneous afferent synapses onto immature rat
44  obese populations, but rarely with skeletal muscle and elite athlete phenotypes.
45 synthesized and tested as inhibitors against muscle and liver isoforms of glycogen phosphorylase (GP)
46 report that fully reduced HMGB1 orchestrates muscle and liver regeneration via CXCR4, whereas disulfi
47  for a number of diseases affecting striated muscle and may also be a schizophrenia risk gene.
48 ated with reduced glucose utilization in the muscle and poor exercise performance.
49 onent and a 6(th) or 7(th) rib with adjacent muscle and skin to restore bone defects, internal lining
50 the presence of ACSL6 mRNA in human skeletal muscle and the role that ACSL6 plays in lipid synthesis
51  higher, whereas sensitivity of the skeletal muscle and white adipose tissue was lower in HFHS than c
52 ect to spinal motor neurons controlling hand muscles and extensively sprout into gray matter structur
53 tive metabolic alterations occurring in SBMA muscles and induced hypertrophy of both glycolytic and o
54 put in the generation of the neural drive to muscles and provide the basis for designing physiologica
55 ocusing on communications among motoneurons, muscles and SCs, and underlying mechanisms.
56 tor commands that our brain sends to our arm muscles and the resulting motion of our hand.
57 sequent differentiation into coronary smooth muscle, and restores Wt1 activity upon MI.
58 es, opisthosomal appendages with book gills, muscles, and fine setae permits comparison with extant h
59 hils, lung Il13 levels, collagen, and smooth muscle, as well as a significant depletion of goblet cel
60 us hypersecretion and abnormal airway smooth muscle (ASM) contraction.
61 -induced protein degradation and rescued the muscle atrophy and dysfunction in a Duchenne muscular dy
62                    In mice, during the rapid muscle atrophy induced by fasting, the desmin cytoskelet
63 Endurance exercise is effective to attenuate muscle atrophy, but the underlying mechanism has not bee
64 use these steroids are also known to trigger muscle atrophy.
65                                              Muscle autophagy deficiency did not affect glucose clear
66 ay be linked to the diverse lipid storage in muscle between trained and sedentary individuals.
67                                              Muscle biopsies were taken from eight Trained, Lean sede
68  High levels of moesin were also observed in muscle biopsy specimens from DMD, Ullrich CMD, and meros
69                 It covers multiple levels of muscle biosensor assessment, e.g. membrane voltage or co
70 ostasis, the structure of tissues, including muscles, blood vessels, and connective tissues, adapts t
71 ydroavermectin B1a in fat, kidney, liver and muscle bovine tissues using UHPLC-MS/MS.
72 deamidation is not influenced by the type of muscle but is probably favored by characteristic process
73 the diaphragm, intercostal and levator auris muscles but not limb muscles.
74 ness in the liver and insulin sensitivity in muscle by eliminating glucotoxicity, which reinstates me
75 even after regeneration and reinnervation of muscle by motor and sensory afferents is completed in th
76 berrant misinnervation of the lateral rectus muscle by the oculomotor nerve.
77 age-gated sodium channels (NaV) of nerve and muscle, causing paralysis.
78 rt failure, a condition with reduced cardiac muscle cBIN1, both of which support cBIN1 release in MPs
79 ell (BmxCreER(T2)-driven)-specific or smooth muscle cell (SMC, SmmhcCreER(T2)- or TaglnCre-driven)-sp
80                              Vascular smooth muscle cell (VSMC) apoptosis precipitates AAA formation,
81 hophysiologic stimulation of vascular smooth muscle cell (VSMC) migration and proliferation.
82  rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315).
83 ut that loss of all Tln forms from the heart-muscle cell leads to myocyte instability and a dilated c
84 idence of higher biological activity (smooth muscle cell loss and fibrin deposition) in the FP-PES co
85  auxiliary beta1 subunits in arterial smooth muscle cells (myocytes).
86                     MSTN-edited fry had more muscle cells (p < 0.001) than controls, and the mean bod
87 ole of HIF-1alpha in pulmonary artery smooth muscle cells (PASMCs) remains controversial.
88 ADAM10 and ADAM17 in pulmonary artery smooth muscle cells (PASMCs).
89  differentiation into fibroblasts and smooth muscle cells (SMCs) is also described.
90 roRNAs are key regulators of vascular smooth muscle cells (VSMCs) phenotypic switch, one of the main
91                           In vascular smooth muscle cells (VSMCs), stimulation of SOCs composed of ca
92 to this ACTA2 mutation in both aortic smooth muscle cells and adventitial fibroblasts may contribute
93 nsulin-stimulated glucose uptake in skeletal muscle cells by implicating p41ARC as a new component of
94 ime imaging was performed in vascular smooth muscle cells expressing a FRET-biosensor comprising the
95                                       Smooth-muscle cells from mouse tracheas were assayed in vitro f
96 udy was to determine whether vascular smooth muscle cells in cultured microvascular networks maintain
97               The vast majority of Hofstenia muscle cells in regions tested express PCGs, suggesting
98 clonal antibodies (DMAbs) can be produced by muscle cells in vivo, potentially allowing prevention or
99 harmacological inhibition in vascular smooth muscle cells reveal that cytochrome b5 reductase 3 expre
100 promotes EZH2 degradation in differentiating muscle cells through phosphorylation of threonine 372.
101              DRP1 inhibition in human smooth muscle cells undergoing osteogenic differentiation atten
102 ent stem cell-derived cardiomyocytes, smooth muscle cells, and endothelial cells (in a 2:1:1 ratio) t
103 eduction of proliferation in vascular smooth muscle cells, but given low proliferative capacity, a si
104  causes damage to motor neurons and skeletal muscle cells.
105 o inosine (A to I) RNA editing of Ctn RNA in muscle cells.
106 gy, and the regenerative capacity of primary muscle cells.
107  vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of enhanced flow.
108 ring leg swing, and increased antagonist leg muscle coactivation during limb loading in early stance,
109 ircadian enzyme activities in mouse skeletal muscle confirmed that such timing separation occurs in v
110 gia can regain volitional, graded control of muscle contraction in his paralyzed limb.
111 tal disorder characterized by loss of smooth muscle contraction in the bladder and intestine.
112  TMEM16A control neuronal signalling, smooth muscle contraction, airway and exocrine gland secretion,
113 several methods to measure cardiomyocyte and muscle contraction, but these require customized hardwar
114 s that reflect the intensity and duration of muscle contraction.
115 eded by long-duration waves of airway smooth muscle contraction.
116 rmal sensory feedback to control coordinated muscle contractions and body posture.
117 rd injury (SCI) are debilitating involuntary muscle contractions that have been associated with incre
118                                              Muscle cramps and hypophosphatemia were more common in t
119 e nociceptive intersegmental cutaneus trunci muscle (CTM) reflex.
120  muscle force/endurance as well as increased muscle damage when compared to regular mdx mice.
121                   LTx candidates with 2 or 3 muscle deficits (42%) compared with those without any de
122  synaptic refinement and the response to the muscle-derived chemorepellant Sema2a.
123 elationship between Notch1 and miRNAs during muscle development has not been established.
124                                     Skeletal muscle development requires fusion of mononuclear progen
125 to categories related to the nervous system, muscle development, and especially to metabolic diseases
126                                              Muscle differentiation is a complex process in which mus
127  could help inform research efforts to treat muscle diseases or improve muscle function.
128 mogenic cardiomyopathy is an inherited heart muscle disorder, predisposing to sudden cardiac death, p
129 y of the gluteus medius and postural control muscles during leg swing, and increased antagonist leg m
130 trate that the vestibular influence on ankle muscles during locomotion can be adapted independently t
131 or effectors of ventilator-induced diaphragm muscle dysfunction (VIDD), but the upstream initiator(s)
132 e of 21 and 31days, respectively, pectoralis muscle dystrophy was associated with a significantly low
133           These results demonstrate that the muscle ECM is more highly organized than previously repo
134  first extracellular recordings of body-wall muscle electrophysiology inside an intact roundworm, Cae
135 ) ions across cellular membranes to regulate muscle excitability, electrolyte movement across epithel
136                                          The muscle fascicles of the right crus of diaphragm which fo
137 en with acute severe asthma with respiratory muscle fatigue and failure of medical treatment.
138    Sepsis triggers more severe and sustained muscle fiber atrophy in limb muscles when compared with
139                   Defects in this BM lead to muscle fiber damage from the force of contraction.
140 P5K orthologs in zebrafish embryos disrupted muscle fiber morphology and resulted in abnormal eye dev
141 ich is involved in the cellular structure of muscle fibers and, along with DMD, forms part of the dys
142 esis that muscles rich in type I vs. type II muscle fibers would exhibit similar changes in intramyoc
143 trate multiple degenerating and regenerating muscle fibers, increased central nuclei, elevated creati
144 al muscle fibres, the contribution of single muscle fibre adaptations to ageing-induced atrophy and f
145 te cells impaired post-burn recovery of both muscle fibre cross-sectional area and volume (P < 0.05).
146 saged limb exhibited a comparable 17% higher muscle fibre size compared to reloading alone, and myofi
147  ensures increased oxygen delivery to active muscle fibres by reducing upstream resistance via comple
148 ng, structural and functional alterations of muscle fibres occur.
149  tendon force were significantly lower; (ii) muscle fibres went through significant atrophy and impai
150 actin ratio and myosin content in individual muscle fibres were not altered; (iv) the muscle proteome
151 tudies on the impact of ageing on individual muscle fibres, the contribution of single muscle fibre a
152            mdx-knockout mice exhibited lower muscle force/endurance as well as increased muscle damag
153 ed to simulate MU firing rates and isometric muscle forces and, to that model, we added fatigue-relat
154 vivo preparation of the levator auris longus muscle from male and female late-stage R6/2 mice and age
155 ression of the JAK-STAT target gene Pim1 and muscles from 2-day and 3-week old dyW-/- mice demonstrat
156 acy of steroid dosing on sarcolemmal repair, muscle function, histopathology, and the regenerative ca
157  efforts to treat muscle diseases or improve muscle function.
158 ion co-factor CRP2 was a regulator of smooth muscle gene expression.
159     CSRP2BP synergistically activated smooth muscle gene promoters in an SRF-dependent manner.
160                             Overload-induced muscle glucose uptake and hypertrophic growth were not i
161 An X-ray crystallography study of the rabbit muscle GPb inhibitor complexes revealed structural featu
162 tra of basic behavioral activities, impaired muscle grip strength, and defects in motor coordination.
163 tly regulated to ensure appropriate skeletal muscle growth and repair.
164 rix, which enhanced subsequent airway smooth muscle growth by 1.5-fold (P < 0.05), which was dependen
165                                              Muscle growth is negatively regulated by myostatin (MSTN
166 tly increasing MMP activation, airway smooth muscle growth, and airway responsiveness.
167 n in R6/2 muscle may help compensate for the muscle hyperexcitability and contribute to motor impersi
168 aracterized by increased reflexes leading to muscle hypertonia.
169 ndactyly of 2(nd) and 3(rd) toes, and severe muscle hypotonia resulting in incapacity to stand withou
170     Gene expression analysis of dyW-/- E17.5 muscles identified a significant increase in the express
171 paired EMG recordings from tibialis anterior muscle in the 20-40 Hz frequency band was also significa
172          Due to the central role of skeletal muscle in whole-body metabolism, we aimed at studying mu
173 ion of fast-twitch extensor digitorum longus muscles in dystrophic mdx mice, a murine model of Duchen
174 ivity of a complete ensemble of wing control muscles in intact, flying flies.
175  of IMCL and EMCL content in individual calf muscles in obese vs. normal healthy human subjects.
176 the homeostasis and regenerative capacity of muscles in these patients who often experience cachexia.
177             Each unit increase in pectoralis muscle index was associated with a 27% reduction in the
178 lter the DNA methylation profile of skeletal muscle, indicating that DNA methylation constitutes a ra
179 d the activity of NF-kappaB, a key player in muscle inflammation and myogenesis.
180 trates the regenerative response to skeletal muscle injury.
181 glycosphingolipids play an important role in muscle innervation, which degenerates in amyotrophic lat
182 for insulin-stimulated glucose disposal, and muscle insulin resistance confers many negative health o
183                                              Muscle-invasive bladder cancer (MIBC) is an aggressive d
184 ancers, no such advance has been achieved in muscle-invasive bladder cancer (MIBC).
185                                              Muscle is emerging as a key mediator of this homeostatic
186                                     Skeletal muscle is the major site for insulin-stimulated glucose
187               ABSTRACT: Contraction of heart muscle is triggered by a transient rise in intracellular
188                              Pyruvate kinase muscle isozyme 2 (PKM2) is a key regulator of aerobic gl
189  fusimotor drive explicitly as a function of muscle length has important implications.
190 capsulates cells and growth factors within a muscle-like unidirectionally ordered environment of nano
191  whole-body metabolism, we aimed at studying muscle lipid profiles in a temporal manner.
192                                     Skeletal muscle, liver, and plasma samples were analyzed by gas c
193                  TRIM37 gene mutations cause muscle-liver-brain-eye (mulibrey) nanism.
194 t and obese older people face a high risk of muscle loss and impaired physical function, which may co
195 previous studies on ammonia-induced skeletal muscle loss and lay the foundation for prolonged ammonia
196 biomarkers and evaluate its association with muscle mass and patient outcomes.
197 uggest a novel role for SIRT6 in maintaining muscle mass by controlling expression of atrophic factor
198 induced a synergistic response, resulting in muscle mass increasing by as much as 150%.
199 -beta proteins to the negative regulation of muscle mass via their activation of the Smad2/3 signalin
200 , and this leads to only a small increase in muscle mass.
201      Our findings suggest that airway smooth muscle/mast cell interactions contribute to asthma sever
202 depressed neuromuscular transmission in R6/2 muscle may help compensate for the muscle hyperexcitabil
203  cerebellar-to-cerebral pathways for a given muscle may reflect aspects of cerebellum-dependent motor
204 or 1000microg.kg(-1) in fishery products and muscle meat of fish.
205 ial to establish sex-specific differences in muscle metabolism and body weight development.
206 mputer simulations of species-specific whole-muscle models indicate that maximum dynamic force and po
207     OxyHb promoted lipid oxidation in washed muscle more effectively compared to oxyMb (P<0.05).
208  that the interaction between CBFbeta-smooth muscle myosin heavy chain (SMMHC; encoded by CBFB-MYH11)
209    Here we have investigated the role of non-muscle myosin II (nmy-2) in these asymmetric divisions.
210 ncreasing shear stress and inhibition of non-muscle myosin II motors, respectively.
211 rotein kinase C, a negative regulator of non-muscle myosin IIB.
212                       The increased skeletal muscle myostatin expression, reduced mammalian target of
213                                   Increasing muscle NotchR signaling also reduced muscle size.
214 s higher in a chimpanzee muscle than a human muscle of similar size.
215 ed retrograde tracers into the medial rectus muscle of the cat, a highly visual nonprimate with front
216 n in fully activated fibers of fast skeletal muscle of the rabbit occurs during transition from isome
217 n oxidation and anti-oxidation status in the muscle of young rats.
218  antagonists into the tibialis anterior (TA) muscles of C57BL/6 mice.
219 nificantly reduced in the liver and skeletal muscles of Cry-deficient mice.
220 nitine transporter protein expression across muscles of different contractile and metabolic phenotype
221 orescently tagged calsequestrin expressed in muscles of mice.
222 d electromyogram (EMG) activity in hind limb muscles of SOD1G93A mice.
223 iagnosis and should be done on straining the muscles of the affected limb.
224 or EB (TFEB) gene was effective in improving muscle pathology in PD mice injected intramuscularly wit
225  we have investigated whether DM1-associated muscle pathology is related to deregulation of central m
226                         Clenbuterol improved muscle pathology, attenuated the glycolytic-to-oxidative
227 ests that alpha-actinin-3 deficiency reduces muscle performance at baseline, but ameliorates the prog
228 g therapy results in improvement in skeletal muscle phenotype and function and molecular perturbation
229 ergy availability is mediated by coordinated muscle-placenta metabolic adjustments linked to internal
230 ment that began to express markers of smooth muscle precursors and adventitial fibrocytes, respective
231 ifferentiation is a complex process in which muscle progenitor cells undergo determination and eventu
232 s) to investigate the effect of estrogens on muscle properties.
233 se training (RET) has a beneficial effect on muscle protein synthesis and can be augmented by protein
234 rotein intake (HIGH PRO) on the postprandial muscle protein synthetic response.
235 ux through a number of different substrates (muscle proteins, lipids, glucose, DNA (satellite cells))
236 ins and antioxidant defence systems; (v) the muscle proteome went through qualitative adaptations, na
237 ual muscle fibres were not altered; (iv) the muscle proteome went through quantitative adaptations, n
238 chanism in satellite cell homeostasis during muscle regeneration could help inform research efforts t
239  Cobra Venom Factor (CVF) result in impaired muscle regeneration following cardiotoxin-induced injury
240 e, statin use was associated with lower limb muscle-related outcomes, and some were only apparent in
241 on and the consequent MLCP activation during muscle relaxation.
242 owever, the role of calpain in airway smooth muscle remodelling remains unknown.
243       Novel strategies are needed to enhance muscle repair and function and to slow this pathological
244 hematopoietic system, whereas TL in skeletal muscle represents a minimally replicative tissue.
245 t or restoring BMAL1 exclusively in skeletal muscle, respectively.
246 s specifically deleted in heart and striated muscle, respectively.
247 nd 282 sequences showing deamidation in both muscles, respectively.
248                                              Muscle-restricted Cas9 expression enables direct editing
249 -coding RNA with MyoD-regulated and skeletal muscle-restricted expression that promotes the activatio
250                  To test the hypothesis that muscles rich in type I vs. type II muscle fibers would e
251 a-cardiac myosin S1 and rabbit fast skeletal muscle S1.
252  model of replicative senescence, decline in muscle satellite cell-mediated regeneration coincides wi
253                                              Muscle satellite cells are myogenic stem cells whose qui
254 tained in Biceps femoris and Semimembranosus muscles showed that 52% and 48% of the identified peptid
255 reasing muscle NotchR signaling also reduced muscle size.
256 xercise weight-loss intervention on skeletal muscle (SM) mass and selected organs over 2 y using MRI
257                              We employ multi-muscle spatial sampling and deconvolution of high-densit
258 Here, we developed transgenic dy2J mice with muscle-specific expression of alphaLNNd, a laminin/nidog
259    Our results demonstrate that AAV-mediated muscle-specific gene editing has significant potential f
260 pecific genes while repressing white fat and muscle-specific genes in adipocytes.
261 and hypertrophic growth were not impaired in muscle-specific GLUT4 knockout mice, demonstrating that
262 nsity lipoprotein receptor-related protein 4-muscle-specific kinase (LRP4-MuSK) pathway.
263 lonal multicolor lineage tracing of skeletal muscle stem cells (MuSCs) to address these questions.
264        Activity of satellite cells, skeletal muscle stem cells, is altered following a burn injury an
265 nal associations between functional decline, muscle strength and survival with plasma creatinine were
266 ockout mouse model, which also shows reduced muscle strength, but is protected from stretch-induced e
267 overy of alpha-DG glycosylation and improved muscle strength, suggesting a systemic supply of FKRP pr
268  of spontaneous activity (SA) in SCI bladder muscle strips.
269 mples of the same liver but differed between muscle subsamples and between tissues of the same animal
270 et the channel catfish, Ictalurus punctatus, muscle suppressor gene MSTN.
271 tration, highlighting its potential as a new muscle-targeting vector.
272  output is 1.35 times higher in a chimpanzee muscle than a human muscle of similar size.
273  provide an approach for generating skeletal muscle that is potentially applicable to other pluripote
274  this study was to determine in rat skeletal muscle the influence of a brief (two weeks) HFD on gluco
275 sed with high levels in cerebellum, skeletal muscle, thymus and kidney.
276 ad higher percentage of EPA and DHA in their muscle tissue (filets) compared to that of triploids and
277 O-ribose-methylation, is increased in murine muscle tissue during postischemic neovascularization.
278        A gastropod, Trochus erithreus, and a muscle tissue of fish, Otolithes ruber, were analyzed as
279  cells, including epithelia, vascular smooth muscle tissue, electrically excitable cells, and some tu
280  was expressed at extremely low level in the muscle tissue.
281 y exosomes determined its restoration within muscle tissues, an overall recovery of alpha-DG glycosyl
282 ages nutrient signaling pathways in skeletal muscle to maintain systemic glucose homeostasis remains
283 ay activating the iris sphincter and ciliary muscle to mediate pupillary constriction and lens accomm
284 hin protein expression in dystrophic cardiac muscles to a level approaching 40%.
285          Of note, rAAVrh.10 showed excellent muscle transduction following IP administration, highlig
286                                Airway smooth muscle treated with activated mast cell supernatants pro
287 etabolomics signature in mice overexpressing muscle uncoupling protein 3.
288 tein results in excessive damage from normal muscle use due to the compromised structural integrity o
289 HSALR mice), activation of AMPK signaling in muscle was impaired under starved conditions, while mTOR
290 oximodistal gradient of involvement of vasti muscles was a consistent finding in these patients, incl
291 rophy, which is characterised by progressive muscle wasting and the discovery of reliable blood-based
292 ed by increased glucagon, without preventing muscle wasting.
293          As sAnk1 is coexpressed with SLN in muscle, we sought to determine whether these two protein
294 tic neuromuscular disease in which crippling muscle weakness is evident from birth.
295  higher ICU and hospital mortality, and limb muscle weakness was associated with longer duration of M
296 e-onset multisystem disease with progressive muscle weakness.
297 ammation, mucus, fibrosis, and airway smooth muscle were no different in Ormdl3(Delta2-3/Delta2-3)/CC
298 e and sustained muscle fiber atrophy in limb muscles when compared with respiratory muscle.
299 hannels are broadly expressed in neurons and muscle where they modulate cellular activity.
300 itine pool is primarily confined to skeletal muscle, where it regulates carbohydrate (CHO) and fat us

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