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1 cently identified as a positive regulator of muscle mass).
2 n-6 and MCP-1 levels, and decreased skeletal muscle mass.
3 Myostatin is a negative regulator of muscle mass.
4 this ligand as a negative regulator of adult muscle mass.
5 .007] were independent predictors of reduced muscle mass.
6 emale gravidity and increased male hind limb muscle mass.
7 n excretion, reflecting the loss of skeletal muscle mass.
8 body weight, total body protein and fat, and muscle mass.
9 nhibit protein synthesis, leading to loss of muscle mass.
10 mor-induced inflammation and loss of fat and muscle mass.
11 e primary outcome was change in appendicular muscle mass.
12 o be the best performer in the estimation of muscle mass.
13 ted with fat-free mass, which is a marker of muscle mass.
14 synthesis is essential to preserve skeletal muscle mass.
15 to underestimate SM among those with larger muscle mass.
16 h which mechanical stimuli regulate skeletal muscle mass.
17 ) protein BRD4 as an epigenetic regulator of muscle mass.
18 t the BMP pathway is a positive regulator of muscle mass.
19 as significantly reduced after adjusting for muscle mass.
20 ating inquiries into molecular regulation of muscle mass.
21 terized by impaired regeneration and loss of muscle mass.
22 essive mitochondrial dysfunction and loss of muscle mass.
23 , and this leads to only a small increase in muscle mass.
24 splice variant PGC1alpha4 increase skeletal muscle mass.
25 1 are potent negative regulators of skeletal muscle mass.
26 protein could also be important enhancers of muscle mass.
27 y member, and negative regulator of skeletal muscle mass.
28 resistance exercise, promote an increase in muscle mass.
29 cephalopathy through an increase in skeletal muscle mass.
30 ed with increased body weight, bone size and muscle mass.
31 hat SNARK may function in the maintenance of muscle mass.
32 b bud where they form the dorsal and ventral muscle masses.
33 in vitro Unexpectedly, a marked decrease in muscle mass (10%) was found after Alk4 AON treatment in
34 achectic patients had reduced (appendicular) muscle mass (-10%), muscle fiber atrophy (-27%), and dec
35 ght TA muscles exhibited 20 +/- 3% decreased muscle mass, 2-fold decreased phosphorylated (P)-Akt, an
36 antially less muscle atrophy, an increase in muscle mass after denervation, and reorganization of mot
37 P signaling is essential for conservation of muscle mass after disruption of the neuromuscular juncti
38 deletion of Pak1 and Pak2 results in reduced muscle mass and a higher proportion of myofibers with a
39 ental ablation of these cells causes loss of muscle mass and a reduction of B-lymphopoiesis and eryth
40 th ACVR2B/Fc showed significant increases in muscle mass and amelioration of fibrotic changes normall
43 ass, improved grip strength, higher skeletal muscle mass and diameter, and an increase in type 2 fibe
44 was significantly associated with decreased muscle mass and exercise tolerance; untreated LH/FSHD wa
45 ircumference, can be used as an indicator of muscle mass and fat tissue, which are distributed differ
47 Sod1(-/-) mice leads to accelerated loss of muscle mass and force during aging, but the losses do no
48 ve mechanical loading attenuates the loss of muscle mass and force-generation capacity associated wit
51 tegies that can slow the age-related loss of muscle mass and function are needed to help older adults
52 lated oxidative damage or rescue the loss of muscle mass and function associated with aging of skelet
53 ave been used in clinical trials to increase muscle mass and function but most showed limited efficac
54 essential for our ability to restore loss of muscle mass and function in cases where the natural abil
55 n-3 PUFA therapy slows the normal decline in muscle mass and function in older adults and should be c
63 icial effects of metallothionein blockade on muscle mass and function was also observed in the settin
64 ng, yet despite the necessity of maintaining muscle mass and function with age, the effect of obesity
65 estigated the effects on age-related loss of muscle mass and function, changes in redox homeostasis,
78 aralysis, or bed rest leads to rapid loss of muscle mass and function; however, the molecular mechani
81 in airway remodeling, with increased smooth muscle mass and increased fibrosis in the absence of air
82 in is a major negative regulator of skeletal muscle mass and initiates multiple metabolic changes, in
86 k of bed rest substantially reduces skeletal muscle mass and lowers whole-body insulin sensitivity, w
87 In contrast, reductions in both skeletal muscle mass and Mito(VD) have been reported following mo
89 nown if there are age-related differences in muscle mass and muscle anabolic and catabolic responses
96 RDA or twice the RDA (2RDA) affects skeletal muscle mass and physical function in elderly men.In this
97 ctive of how sarcopenia is defined, both low muscle mass and poor muscle strength are clearly highly
98 tor 2B signaling, has been shown to preserve muscle mass and prolong survival in tumor hosts, and to
100 er, D2O heralds promise for coupling MPS and muscle mass and providing insight into the control of hy
101 raining was very effective in restoring both muscle mass and qualitative muscle changes, indicating t
102 animals had proportionally less contractile muscle mass and smaller gills and foot compared with you
103 hways are essential for maintaining skeletal muscle mass and strength and for protection against canc
104 s in mice showed that hyperammonemia reduced muscle mass and strength and increased myostatin express
107 rical muscle stimulation appears to preserve muscle mass and strength in long-stay participants and i
111 to ageing, could also accelerate decrease of muscle mass and strength, and this effect could be a mai
116 to overestimate SM among women with smaller muscle mass and to underestimate SM among those with lar
117 (Delta/Delta) ) would exhibit an increase in muscle mass and total force production, a reduction in s
120 e) is common in humans and reduces strength, muscle mass, and fast-twitch fiber diameter, but increas
121 maximum tetanic tension, decreased tibialis muscle mass, and fiber diameter due to inflammation alon
122 ta = -0.75; P = 0.03), appendicular skeletal muscle mass, and grip strength than did controls, but th
123 ith high muscle mass, low adiposity with low muscle mass, and HA-LM-and a subclassification of the ph
124 nicotinic acetylcholine receptor expression, muscle mass, and histologic changes (structural paramete
125 s another family member negatively regulates muscle mass, and its blockade enhances muscle growth see
126 for mechanically induced changes in skeletal muscle mass, and previous studies have suggested that me
127 activin A as a second negative regulator of muscle mass, and suggest that inhibition of both ligands
128 Inhibition of myostatin signaling increases muscle mass, and therapeutic approaches based on this ar
131 yostatin induced a more profound increase in muscle mass ( approximately 45%), demonstrating a more p
132 extracellular matrix (ECM) and larger smooth muscle mass are correlated with increased airway respons
134 ed to prevent age-dependent loss of skeletal muscle mass associated with myofiber atrophy or alter a
137 stronger effect in preventing aging-related muscle mass attenuation and leg strength loss in older p
138 de decreased body and facial hair, decreased muscle mass, breast growth, and redistribution of fat.
139 dipose tissue expansion and reduced skeletal muscle mass, but not the systemic inflammation or increa
140 a mechanically induced increase in skeletal muscle mass, but the mechanism(s) through which mechanic
141 ls play a critical role in the regulation of muscle mass, but the molecules that sense mechanical sig
142 etary protein was positively associated with muscle mass, but the relation of this distribution to ph
145 uggest a novel role for SIRT6 in maintaining muscle mass by controlling expression of atrophic factor
146 hic (CT) metrics of bone mineral density and muscle mass can improve the prediction of noncancer deat
147 hypertrophy that was sufficient to preserve muscle mass comparable to that of untreated sham-operate
152 -knockout (Mstn(-/-)) mice exhibit increased muscle mass due to both hypertrophy and hyperplasia, and
153 even though gene expression of regulators of muscle mass (e.g., MAFbx, MURF1, and myostatin) had peak
154 The sarcopenia index is a fair measure for muscle mass estimation among ICU patients and can modest
155 rovement in TA muscle morphology and gain in muscle mass evident in the WT mice was not noticeable in
157 tant across O2 delivery conditions for large muscle mass exercise, but this consistency is equivocal
160 atures of airway remodeling including smooth muscle mass, extracellular matrix deposition and pro-fib
161 rcise capacity (6-min-walk distance [6MWD]), muscle mass (fat-free mass [FFM]), and systemic inflamma
162 and immobilization, the decrease in tibialis muscle mass, fiber diameter, and maximum tetanic tension
163 Many factors contribute to the erosion of muscle mass following burn trauma and we propose that an
164 Many factors contribute to the erosion of muscle mass following burn trauma, and we have previousl
165 resumed habitual physical activity, restored muscle mass from a reduction of 51% after 14 d TTX to a
166 er survival, GTx-026 treatment increased the muscle mass, function and survival, indicating that andr
170 ombination of the 2 [high adiposity with low muscle mass (HA-LM)] are relevant phenotypes, but data o
171 mposition phenotypes-low adiposity with high muscle mass, high adiposity with high muscle mass, low a
173 been associated with reduced adult skeletal muscle mass; however, the mechanisms responsible for thi
175 increased body fat, (ii) decreased relative muscle mass, (iii) redistributed muscle mass to lower li
176 sty, a new technique to reduce airway smooth muscle mass, improves symptoms and reduces exacerbations
178 se training (RET) is widely used to increase muscle mass in athletes and also aged/cachectic populati
181 been shown to underlie the loss of skeletal muscle mass in many acquired and genetic muscle disorder
183 ER stress and UPR in regulation of skeletal muscle mass in naive conditions and during cancer cachex
184 th isocaloric control preserves appendicular muscle mass in obese older adults during a hypocaloric d
185 re modifiable factors associated with higher muscle mass in older adults but not with losses over 2 y
187 arch directives designed to protect skeletal muscle mass in physically active, normal-weight adults.
188 anistically, the better recovery of skeletal muscle mass in PINTA745-MCAO mice involved an increased
190 causes muscle wasting, PGC-1alpha preserves muscle mass in several conditions, including functional
195 tivated transcriptional profiles to increase muscle mass in wild type and R6/2 mice but did little to
196 statin deficiency (Mstn(tm1Sjl/+)) increases muscle mass in wild-type offspring, suggesting an intrau
197 hat road salt runoff can result in increased muscle mass (in males) and neural investment (in females
198 connective tissue locations adjacent to the muscle masses, including cells in the vasculature wall.
199 gs had apparent DM phenotype, and individual muscle mass increased by 100% over their wild-type contr
201 graphy data available, unilateral pectoralis muscle mass indexed to body surface area and attenuation
202 vation prevented the severe loss of skeletal muscle mass induced in mice engrafted with Lewis lung ca
203 known or potential circulating modulators of muscle mass--insulin-like growth factor-1, myostatin, an
208 use attenuating the extent to which skeletal muscle mass is lost during energy deficit could prevent
209 On the basis of study results showing that muscle mass is only moderately related to functional out
212 ion of skeletal muscle protein synthesis and muscle mass, it does not appear to be a prerequisite for
214 ompositions such as high adiposity (HA), low muscle mass (LM), or a combination of the 2 [high adipos
219 h high muscle mass, high adiposity with high muscle mass, low adiposity with low muscle mass, and HA-
222 est impact of myostatin in the regulation of muscle mass may not be to induce atrophy directly, but r
223 scle depletion is characterized by a reduced muscle mass (myopenia) and increased infiltration by int
226 mon peroneal nerve-resulted in reductions in muscle mass of 7, 29, and 51% with corresponding reducti
227 Correlation of the gene expression versus muscle mass or age changes, and functional annotation an
228 eatinine independent of GFR (eg, extremes of muscle mass or diet), or interference with the assay, cy
229 ng creatinine excretion, such as extremes of muscle mass or diet, the albumin excretion rate should b
230 0% that of control mice, but no reduction in muscle mass or isometric force was observed in SynTgSod1
231 than control littermates, no differences in muscle mass or strength were observed between genotypes
232 pplementation did not affect the increase in muscle mass or the acute change in protein synthesis, bu
234 fore, PGC1beta activation negatively affects muscle mass over time, particularly fast-twitch muscles,
235 (1.7-kg gain, P < 0.001), relative skeletal muscle mass (P = 0.009), android distribution of fat (P
236 ed muscles, and SIRT1 levels correlated with muscle mass, paired box protein 7 (Pax7), proliferating
237 ty, and only following exercise with a large muscle mass (PEI following leg cycling) is there a contr
238 at PGC1beta progressively decreases skeletal muscle mass predominantly associated with loss of type 2
239 ucine-, and vitamin D-enriched supplement on muscle mass preservation during intentional weight loss
240 produced significant increases in body mass, muscle mass, quadriceps myofiber size, and survival, but
241 isons between number of muscle deficits (low muscle mass, quadriceps strength and physical performanc
242 ring muscles account for <3% of total flight muscle mass, raising the question of how they can modula
249 are surrogates for bone mineral density and muscle mass, respectively, were independent predictors o
253 discrimination of patients with low skeletal muscle mass (sarcopenic patients) using computed tomogra
254 as having at least two of the following: low muscle mass, self-reported exhaustion, low energy expend
255 d >/= three of the following conditions: low muscle mass, self-reported exhaustion, low energy expend
256 regional fat distribution and the amount of muscle mass should be introduced into regular clinical p
257 ng LLC-induced cachexia, skm-gp130 regulates muscle mass signaling through STAT3 and p38 for the acti
259 aging results in a gradual loss of skeletal muscle mass, skeletal muscle function and regenerative c
261 ms were to characterize deficits in skeletal muscle mass, strength and physical performance, and exam
265 MIGIRKO mice displayed a marked reduction in muscle mass that was linked to increases in proteasomal
267 ough endurance-based exercise) and increased muscle mass (through resistance-based exercise), typical
268 f cellular senescence, and imaging to assess muscle mass to detect sarcopenia, may provide insight in
270 ed relative muscle mass, (iii) redistributed muscle mass to lower limbs, and (iv) decreased relative
271 of an adaptive mechanism aimed at preserving muscle mass under conditions in which insulin action is
273 vely evaluated for skeletal muscle deficits: muscle mass using bioelectrical impedance, quadriceps, r
275 values of fat mass and appendicular skeletal muscle mass utilizing the LMS statistical procedure.
276 Mechanistically, we show that YAP regulates muscle mass via interaction with TEAD transcription fact
277 -beta proteins to the negative regulation of muscle mass via their activation of the Smad2/3 signalin
278 correlation (r) between sarcopenia index and muscle mass was 0.62 and coefficient of determination (r
281 mong obese patients, cachexia, as defined by muscle mass, was common, with 56% of those with BMI abov
282 tin, a master negative regulator of skeletal muscle mass, was strongly increased in skeletal muscle i
283 that determine the recuperative capacity of muscle mass, we studied offspring of FVB mouse dams fed
284 otein requirements, particularly to maintain muscle mass.We investigated whether controlled protein c
286 Participants' LBM and appendicular skeletal muscle mass were measured using dual energy x-ray absorp
288 Muscle loading is important for maintaining muscle mass; when load is removed, atrophy is inevitable
290 d by a continuous loss of locomotor skeletal muscle mass, which causes profound muscle weakness.
291 activins are negative regulators of skeletal muscle mass, which have been reported to primarily signa
292 dominantly results from the loss of skeletal muscle mass, which is in part associated with apoptosis.
293 restriction (IUGR) suffer from reductions in muscle mass, which may contribute to insulin resistance
294 uscle ablation resulted in a 40% increase in muscle mass, which was associated with a significant inc
295 -specific overexpression of Tp53inp2 reduced muscle mass, while deletion of Tp53inp2 resulted in musc
297 s developed and grew normally, had increased muscle mass with decreased fat accumulation compared wit
298 reases muscle protein synthesis acutely, and muscle mass with training, but the role of translational
300 en, -2.12; P=0.011), lower right ventricular muscle mass (women, 1.58; men 2.45; P=0.001), poorer pea
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