ライフサイエンスコーパス: muscle protein

1 of lipid stores, and severe loss of skeletal muscle protein.

2 cts the intense oxidative degradation of the muscle proteins.

3 y demonstrations linking FHC to mutations in muscle proteins.

4 ns, which form an important class of ABDs in muscle proteins.

5 known structures of similar ABDs from other muscle proteins.

6 IA reduced (p < 0.05) the GFA of Jumbo squid muscle proteins.

7 tial for the accelerated degradation of most muscle proteins.

8 fiber-type switching, and the degradation of muscle proteins.

9 oteasome, which increases the degradation of muscle proteins.

10 nergistically to increase the degradation of muscle proteins.

11 in is one of the least well understood major muscle proteins.

12 velopments involving (2) H(2) O labelling of muscle proteins.

13 he effects of disease-producing mutations in muscle proteins.

14 ells induced SM actin, calponin1, and smooth muscle protein 22-alpha (SM22alpha) in a dose- and time-

15 nx2, increased expression of vascular smooth muscle protein 22-alpha, and restored aortic expression

16 nd vascular smooth muscle cells using smooth muscle protein 22-driven Cre recombinase (SMGRKO mice) a

17 e recombinase allele regulated by the smooth muscle protein-22 (SM22) promoter (Tsc1c/cSM22cre+/-) to

18 smooth muscle actin), and SM22-alpha (smooth muscle protein 22alpha) and an increase in synthetic mar

19 Mice with smooth muscle protein-22alpha promotor-driven deficiency of the

20 glycogen stores seems to potentiate skeletal muscle protein abundance and gene expression.

21 t of resistance-type exercise stimulates net muscle protein accretion during acute postexercise recov

22 Hindlimb weight, linear growth rate, muscle protein accretion rate and fractional synthetic r

23 ncy that develop to slow hindlimb growth and muscle protein accretion.

24 importance of the degradation of individual muscle proteins after exercise in human skeletal muscle.

25 increasing physical activity can enhance the muscle protein anabolic effect of essential amino acid (

26 ability during hyperinsulinemia improves the muscle protein anabolic effect of insulin in older adult

27 le in stimulating translation initiation and muscle protein anabolism and is the focus of ongoing res

28 Our objective was to measure muscle protein anabolism in response to Leu and its meta

29 Nutrient stimulation of muscle protein anabolism is blunted with aging and may c

30 ccompanied by lower synthesis rates of mixed muscle protein and the myofibrillar and sarcoplasmic mus

31 sotopically label newly synthesized skeletal muscle proteins and DNA.

32 There were correlations between log K(pw) of muscle proteins and log K(ow) (R(2) = 0.83-0.86, SD: 0.3

33 and simultaneous identification of skeletal muscle proteins and peptides as well as other components

34 etic ablation of TWEAK decreases the loss of muscle proteins and spared fiber cross-sectional area, m

35 Loss of muscle proteins and the consequent weakness has importan

36 neration, including strong downregulation of muscle proteins and upregulation of oncogenes, developme

37 membrane integrity and repair, expression of muscle proteins, and regulation of signaling pathways.

38 Major muscle proteins are extensively hydrolysed firstly by en

39 cell phenotype, as levels of critical smooth muscle proteins are gradually reduced in mutant mice.

40 actions are triggered by the calcium-binding muscle protein beta-parvalbumin, which was shown to have

41 trogin1/MAFbx, increased LC3-II, and loss of muscle proteins both in myotubes and mouse muscle.

42 on to assess muscle protein synthesis (MPS), muscle protein breakdown (MPB), and muscle mass by using

43 hanges in muscle protein synthesis (MPS) and muscle protein breakdown (MPB).

44 HMB consumption also attenuated muscle protein breakdown (MPB; -57%) in an insulin-indep

45 that Ang II, via its type 1 receptor, causes muscle protein breakdown and apoptosis and inhibits sate

46 Identified mediators of muscle protein breakdown include inflammation, metabolic

47 -1 and muscle ring finger 1 (MuRF1), mediate muscle protein breakdown through the ubiquitin proteasom

48 known to regulate proteasomal and lysosomal muscle protein breakdown was also evident.

49 From the perspective of muscle protein breakdown, muscle-specific E3-ligases (MA

50 Because IL-6 stimulates muscle protein breakdown, we conclude that CKD increases

51 ription can lead to enhanced proteolysis and muscle protein breakdown.

52 in synthesis with no apparent stimulation of muscle protein breakdown; furthermore, muscle of immobil

53 indicated that systemic inflammation induces muscle-protein breakdown and wasting via muscular nuclea

54 fic analysis and differentiation of skeletal muscle proteins by direct surface desorption.

55 ting suggests that the reversible binding to muscle proteins can be considered to be nonspecific bind

56 clude membrane and storage lipids, serum and muscle proteins, carbohydrates, algae, mussels, polydime

57 During the cleavage of muscle proteins, caspase-3 leaves behind a characteristi

58 on of dietary uptake, de novo synthesis, and muscle protein catabolism.

59 strategies that counter CKD-induced abnormal muscle protein catabolism.

60 TLR4 muscle protein content correlated with the severity of i

61 terations more than loss of myosin and other muscle protein content.

62 malities in insulin/IGF-I signaling activate muscle protein degradation in the UPS and caspase-3, a p

63 lly in skeletal muscle (mXIAP) and evaluated muscle protein degradation induced by CKD.

64 Under these conditions, activation of muscle protein degradation requires endogenous glucocort

65 en to mice with muscle-specific IR deletion, muscle protein degradation was accelerated.

66 n, at the level of PDC, and up-regulation of muscle protein degradation, in LPS-induced endotoxaemia.

67 uence of the GR contributes to activation of muscle protein degradation.

68 ubiquitination pathway in the physiology of muscle protein degradation.

69 function, and decreased muscle fibrosis and muscle protein degradation.

70 There was a 29% reduction in the muscle protein: DNA ratio, a 56% reduction in pyruvate d

71 evented the LPS-induced 40% reduction in the muscle protein:DNA ratio and decrease in Akt phosphoryla

72 The muscle protein Dok-7 is essential for activation of the

73 y affected due to oxidative modifications of muscle proteins during its processing.

74 Deficiency of the vital muscle protein dystrophin triggers Duchenne/Becker muscu

75 gene leading to the absence of the essential muscle protein dystrophin.

76 permits evaluation of turnover of plasma and muscle proteins (e.g. dynamic proteomics) in addition to

77 ly, chronic binge alcohol increased skeletal muscle protein expression of protein-tyrosine phosphatas

78 was increased in the presence of denervated muscle protein extracts.

79 body protein synthesis per fat-free mass and muscle protein fractional synthesis rate (FSR) were lowe

80 to quantify whole-body protein breakdown and muscle protein fractional synthesis rate using liquid ch

81 To quantify skeletal muscle protein fractional synthesis rates, a flooding do

82 ay in the training period by measurements of muscle protein fractional synthetic rate and phosphoryla

83 Protein synthesis measured by the muscle protein fractional synthetic rate was depressed i

84 Muscle protein from sardine (Sardina pilchardus) and hor

85 Muscle proteins from sardine (Sardina pilchardus) and sm

86 eutral organic chemicals were measured using muscle proteins (from chicken, fish, and pig), collagen

87 Muscle protein functionality plays an important role in

88 teins, K(pw) values were often in the order: muscle proteins > collagen >/= gelatin.

89 eversible event in SMA and also suggest that muscle proteins have the potential to act as novel bioma

90 oding Muscle RING Finger 1 (MuRF1) maintains muscle protein homeostasis by tagging the sarcomere prot

91 Ethanol causes dysregulated muscle protein homeostasis while simultaneously causing

92 Spent hen muscle protein hydrolysate prepared by thermoase (SPH-T)

93 ges in protein unfolding in vivo in skeletal muscle proteins in ALS mice.

94 HCM is caused by missense mutations in muscle proteins including myosin, but how these mutation

95 in DM were deficient in a number of skeletal muscle proteins including titin.

96 eceptor recycling and mislocalization of key muscle proteins, including caveolin-3 and Fer1L5, a rela

97 esulting in elevated oxidization of skeletal muscle proteins, including the ryanodine receptor and ca

98 by inducing the overexpression of surrogate muscle proteins, including utrophin, agrin, laminins, an

99 ce model we detected alterations in skeletal muscle proteins involved in BCAA metabolism but not in o

100 ence supporting a role for specific skeletal muscle proteins involved in intramyocellular lipids, mit

101 thesized that the expression of key skeletal muscle proteins involved in lipid droplet hydrolysis, DA

102 We found that the partitioning to muscle protein is typically weaker than that to lipids,

103 In cardiac myocytes, the muscle protein kinase A-anchoring protein beta (mAKAPbet

104 Muscle protein kinetic rates were measured using isotopi

105 dy in this muscle injury model decreased the muscle protein levels of lymphotoxin alpha and Il17a by

106 els of the long isoform of TBC1D4, and lower muscle protein levels of the glucose transporter GLUT4,

107 ux through a number of different substrates (muscle proteins, lipids, glucose, DNA (satellite cells))

108 ificantly reduce muscle atrophy, and inhibit muscle protein loss and DNA loss, even when given after

109 hout acute hospital stay and had significant muscle protein loss as demonstrated by a negative muscle

110 SB202190, and abrogated cancer cell-induced muscle protein loss in C2C12 myotubes without suppressin

111 TNF-alpha directly increased net muscle protein loss, which may contribute to cachexia an

112 ation blocks atrogin1/MAFbx upregulation and muscle protein loss.

113 metabolism, and accelerating body water and muscle protein loss.

114 on of metabolic acidosis, which can suppress muscle protein losses in patients with CKD who are or ar

115 neuronally derived ligand, and the following muscle proteins: LRP4, the receptor for Agrin; MuSK, a r

116 LP and E-UN offspring, but in L-UN offspring muscle protein mass remained significantly smaller even

117 umans.We aimed to compare the whole-body and muscle protein metabolic responses after the consumption

118 To assess muscle protein metabolic responses to varied protein int

119 Skeletal muscle protein metabolism is resistant to the anabolic a

120 okines, defects in IGF-1 signaling, abnormal muscle protein metabolism, and progressive muscle atroph

121 highly conserved than myosin and most other muscle proteins, most such efforts have not targeted act

122 ent study, we tested the hypothesis that the muscle protein myostatin is involved in mediating the pa

123 e protein loss as demonstrated by a negative muscle protein net balance (-0.05% +/- 0.007 nmol/100 mL

124 Females had a significant attenuated loss in muscle protein net balance (females: -0.028+/-0.001% vs.

125 This decrease is reflected in improved muscle protein net balance and preservation of lean body

126 ting in a significant increase (P < 0.05) in muscle protein net balance.

127 ic burn patients at 6 months postinjury, leg muscle protein net deposition is unresponsive to amino a

128 Caenorhabditis elegans homolog of the giant muscle protein obscurin, UNC-89, is required for normal

129 lored for the first time to analyze skeletal muscle proteins obtained from a mixture of standard prot

130 In skeletal muscle, proteins of the calcium release complex responsi

131 These data indicate that Fstl1 is a secreted muscle protein or myokine that can function to promote e

132 ive processes, and a concomitant increase in muscle protein oxidation.

133 CKD induces loss of muscle proteins partly by suppressing muscle protein syn

134 ent through extensive qualitative changes in muscle protein pattern following ULLS, and these were re

135 markers and appearance of expression of non-muscle proteins ("proliferative phenotype").

136 d biomarker, autoantibodies against a 43-kDa muscle protein reported in 2011, has now been identified

137 Loss of skeletal muscle protein results from an imbalance between the rat

138 compared to those of squid (Dosidicus gigas) muscle proteins (SM).

139 rinsulinemia-induced increase in the rate of muscle protein synthesis (from 0.009 +/- 0.005%/h above

140 in degradation (cachexia), decreased rate of muscle protein synthesis (inactivity), or an alteration

141 mentation had no effect on the basal rate of muscle protein synthesis (mean +/- SEM: 0.051 +/- 0.005%

142 he potential role of supplemental leucine on muscle protein synthesis (MPS) and associated molecular

143 get of rapamycin on ribosome biogenesis, and muscle protein synthesis (MPS) and degradation.

144 estigated the relationship between long-term muscle protein synthesis (MPS) and hypertrophic response

145 old) participated in a study that determined muscle protein synthesis (MPS) and leg protein breakdown

146 However, muscle protein synthesis (MPS) and mitochondrial biogene

147 mass is determined by coordinated changes in muscle protein synthesis (MPS) and muscle protein breakd

148 Muscle protein synthesis (MPS) fluctuates widely over th

149 We previously showed that human muscle protein synthesis (MPS) increased during infusion

150 Muscle protein synthesis (MPS) is the driving force behi

151 ppears to attenuate the response of skeletal muscle protein synthesis (MPS) to anabolic stimuli such

152 akes, stimulates a greater acute response of muscle protein synthesis (MPS) to protein ingestion in r

153 sies were taken at 3 and 6 weeks to quantify muscle protein synthesis (MPS) via gas chromatography-py

154 Muscle protein synthesis (MPS) was measured using [1, 2-

155 to determine mitochondrial and myofibrillar muscle protein synthesis (MPS) when carbohydrate (CHO) o

156 lator of translation initiation and skeletal muscle protein synthesis (MPS), can protect skeletal mus

157 and ~6 wk after surgical resection to assess muscle protein synthesis (MPS), muscle protein breakdown

158 cle and, similarly to 3.42 g Leu, stimulated muscle protein synthesis (MPS; HMB +70% vs. Leu +110%).

159 Resistance exercise increases muscle protein synthesis acutely, and muscle mass with t

160 , which leads to the stimulation of skeletal muscle protein synthesis after ingestion of a meal that

161 synthesis rates and the ability to increase muscle protein synthesis after protein ingestion.

162 ry recruitment would improve the response of muscle protein synthesis and anabolism to insulin.

163 cirrhosis that results in impaired skeletal muscle protein synthesis and breakdown (proteostasis).

164 involved the use of stable isotopes to probe muscle protein synthesis and breakdown with two basic ex

165 se training (RET) has a beneficial effect on muscle protein synthesis and can be augmented by protein

166 debate concerning the relative importance of muscle protein synthesis and degradation to muscle mass

167 esults from an imbalance between the rate of muscle protein synthesis and degradation.

168 the habitual intake is associated with lower muscle protein synthesis and higher proteolysis rates, w

169 he habitual intake is associated with higher muscle protein synthesis and lower proteolysis rates.

170 Muscle protein synthesis and mTORC1 signalling are concu

171 otential site for the regulation of skeletal muscle protein synthesis and muscle mass, it does not ap

172 Muscle protein synthesis and net balance (nmol . min(-1)

173 controversy over the effects of older age on muscle protein synthesis and proteolysis rates.

174 The rate of muscle protein synthesis and the phosphorylation of key

175 he TOR pathway plays a key role in promoting muscle protein synthesis by inhibition of eIF4EBPs (euka

176 al muscle anabolic resistance (i.e., reduced muscle protein synthesis during anabolic conditions such

177 s of dietary protein on body composition and muscle protein synthesis during energy deficit (ED).

178 on, phenylalanine delivery, net balance, and muscle protein synthesis during the consumption of EAA+s

179 activity are both required to promote higher muscle protein synthesis during the day compared to nigh

180 chondrial changes may contribute to impaired muscle protein synthesis in cancer cachexia and could po

181 TORC1 signalling is essential for regulating muscle protein synthesis in humans, we treated subjects

182 ating the contraction-induced stimulation of muscle protein synthesis in humans, while dual activatio

183 Omega-3 fatty acids stimulate muscle protein synthesis in older adults and may be usef

184 -3 fatty acid supplementation on the rate of muscle protein synthesis in older adults.

185 ake distribution across meals increased 24-h muscle protein synthesis in young adults compared with a

186 ent studies show that during energy deficit, muscle protein synthesis is down-regulated with concomit

187 Muscle protein synthesis is increased after exercise, bu

188 The suppression of muscle protein synthesis is the primary driver of muscle

189 processes was observed, with no effect upon muscle protein synthesis or anabolic signalling.

190 otein kinetics does not significantly reduce muscle protein synthesis or increase proteolysis.

191 orn oil supplementation had no effect on the muscle protein synthesis rate and the extent of anabolic

192 During amino acid infusion, leg muscle protein synthesis rate significantly increased (P

193 ein synthesis rates or increase postprandial muscle protein synthesis rates after ingestion of 25 g p

194 ein synthesis rates or increase postprandial muscle protein synthesis rates after ingestion of 25 g p

195 ared with HIGH PRO on basal and postprandial muscle protein synthesis rates after the ingestion of 25

196 ared with HIGH PRO on basal and postprandial muscle protein synthesis rates after the ingestion of 25

197 ss maintenance is largely regulated by basal muscle protein synthesis rates and the ability to increa

198 s and blood samples were collected to assess muscle protein synthesis rates as well as dietary protei

199 Skeletal muscle protein synthesis rates did not differ between tr

200 Protein ingestion increases skeletal muscle protein synthesis rates during recovery from endu

201 Excess body fat diminishes muscle protein synthesis rates in response to hyperinsul

202 validated a strategy for monitoring skeletal muscle protein synthesis rates in rodents and humans ove

203 Muscle protein synthesis rates increased from 0.031% +/-

204 Muscle protein synthesis rates increased from 0.031% +/-

205 Slower hindlimb linear growth and muscle protein synthesis rates match reduced hindlimb bl

206 in the circulation and does not lower basal muscle protein synthesis rates or increase postprandial

207 in the circulation and does not lower basal muscle protein synthesis rates or increase postprandial

208 emonstrate slower hindlimb linear growth and muscle protein synthesis rates that match the reduced hi

209 tors other than protein intake explain lower muscle protein synthesis rates with advanced age.

210 oprotein stimulates resting and postexercise muscle protein synthesis rates, and to a greater extent

211 r resistance exercise increases postexercise muscle protein synthesis rates.

212 protein-dense foods to augment postexercise muscle protein synthesis rates.

213 this does not result in greater postprandial muscle protein synthesis rates.

214 l as whole-body protein balance and skeletal muscle protein synthesis rates.

215 ids by the fetal hindlimb and lower skeletal muscle protein synthesis rates.

216 ein after exercise did not increase skeletal muscle protein synthesis rates.

217 Protein ingestion increases muscle protein synthesis rates.

218 in ketoacid (BCKA) ingestion on postprandial muscle protein synthesis rates.

219 Insulin and IGF-1 enhance muscle protein synthesis through their receptors, but th

220 e of immobilized legs is unable to stimulate muscle protein synthesis to the same extent as that of n

221 that a sex difference exists in the rate of muscle protein synthesis under postabsorptive conditions

222 CKD suppresses muscle protein synthesis via epigenetic mechanisms that

223 s of other amino acids and as a modulator of muscle protein synthesis via the insulin-signaling pathw

224 Muscle protein synthesis was determined by stable isotop

225 efore refeeding, and 2, 7 and 21 days later, muscle protein synthesis was measured in vivo.

226 position and postabsorptive and postprandial muscle protein synthesis were assessed during WM (d 9-10

227 by their capacity to upregulate postprandial muscle protein synthesis when refed (P < 0.001), a diffe

228 Immobility per se causes a decrease in muscle protein synthesis with no apparent stimulation of

229 kt/mTORC1 signaling by Western blotting; and muscle protein synthesis, amino acid, and glucose kineti

230 tenuates intracellular proteolysis, restores muscle protein synthesis, and mitigates skeletal muscle

231 In addition, muscle protein synthesis, breakdown rates, and respectiv

232 In contrast, muscle protein synthesis, DNA, and phospholipid synthesi

233 on profile, organ function, hypermetabolism, muscle protein synthesis, incidence of wound infection s

234 DNA transcription has been proposed to limit muscle protein synthesis, making ribosome biogenesis cen

235 nsitive mTOR in the RE-induced activation of muscle protein synthesis, ribosome biogenesis, PGC-1alph

236 enhances nitrogen retention and up-regulates muscle protein synthesis, which in turn may promote posi

237 t only partially inhibited the activation of muscle protein synthesis.

238 of acutely increasing lipid availability on muscle protein synthesis.

239 acid involved in the regulation of skeletal muscle protein synthesis.

240 d conjugated linoleic acids (CLAs) stimulate muscle protein synthesis.

241 reduced (by approximately 40%) efficiency of muscle protein synthesis.

242 uired for full stimulation of human skeletal muscle protein synthesis.

243 duced increase ( approximately 40%) in human muscle protein synthesis.

244 vents in humans, particularly in relation to muscle protein synthesis.

245 ludes blunting of post-prandial increases in muscle protein synthesis.

246 moderately high-protein meals improves 24-h muscle protein synthesis.

247 oss of muscle proteins partly by suppressing muscle protein synthesis.

248 underpinned by chronic deficits in long-term muscle protein synthesis.

249 P)-containing meals may overcome the blunted muscle protein synthetic response to food intake in the

250 We assessed the mixed skeletal muscle protein synthetic response to the ingestion of a

251 rotein intake (HIGH PRO) on the postprandial muscle protein synthetic response.

252 However, muscle protein synthetic responses after the ingestion o

253 so known as connectin) is an intrasarcomeric muscle protein that functions as a molecular spring and

254 question, we biochemically isolated skeletal muscle proteins that associate with Gadd45a as it induce

255 pothesis, we biochemically isolated skeletal muscle proteins that associate with the dimerization- an

256 could be used to induce aggregation of fish muscle proteins, thereby improving gelling property of f

257 This review uses the giant muscle protein titin as an example to showcase the capab

258 The giant muscle protein titin is a major contributor to passive f

259 , and lysine-rich (PEVK) domain of the giant muscle protein titin is thought to be an intrinsically u

260 s those encoding olfactory receptors and the muscle protein titin), suggesting extensive false-positi

261 For the mechanostable muscle protein titin, a highly ductile model reconciles

262 and A168-A169, from the A-band of the giant muscle protein titin, reveal that they form tightly asso

263 Inspired by skeletal muscle protein titin, we have synthesized a biomimetic m

264 hought to involve modifications to the giant muscle protein titin, which in turn can determine the pr

265 ce of extensive myopathy or a decline in the muscle protein to DNA ratio.

266 ion, metabolic pathways, or the breakdown of muscle proteins to amino acids used in gluconeogenesis o

267 tease that disrupts the complex structure of muscle proteins to provide substrates for the UPS.

268 s protein mass by appropriate stimulation of muscle protein turnover and inhibition of protein breakd

269 s associated with major and rapid changes in muscle protein turnover and mass, and dampened insulin-s

270 t that has been shown to favorably influence muscle protein turnover and thus potentially plays a rol

271 balance on the regulation of human skeletal muscle protein turnover are not well described.

272 function with age, the effect of obesity on muscle protein turnover in older adults remains unknown.

273 the effect of tumor burden and resection on muscle protein turnover in patients with nonmetastatic c

274 Accurate measurement of muscle protein turnover is critical for understanding th

275 muscle microvascular blood volume (MBV) and muscle protein turnover under post-absorptive and fed st

276 p between energy status, protein intake, and muscle protein turnover, and explores future research di

277 ct of critical illness on muscle morphology, muscle protein turnover, and the associated muscle-signa

278 R signaling is critical to the regulation of muscle protein turnover, and this regulation depends on

279 action and stretch have different effects on muscle protein turnover, but little is known about the m

280 cer-induced alterations in the regulation of muscle protein turnover.

281 used by ill-defined catabolic alterations in muscle protein turnover.

282 s ubiquitin E3 ligases in ubiquitin-mediated muscle protein turnover.

283 or its close homolog, PGC-1beta, influences muscle protein turnover.

284 anscription factors is essential to initiate muscle protein ubiquitination and degradation during atr

285 Muscle protein ubiquitylation was also 45% lower (P<0.05

286 ontaining protein 2 gene, SORBS2, a skeletal muscle protein using a modification of the chromosome co

287 Muscle protein was subjected to mass spectrometry-based

288 Muscle protein wasting in cancer cachexia is a critical

289 cts that can suppress appetite and stimulate muscle protein wasting.

290 r distribution coefficients (log DBSAw), and muscle protein-water distribution coefficients (log Dmpw

291 stable peptide markers unique to species and muscle protein were identified following data-dependent

292 Parameters for glycation of muscle protein were optimised using the bidimensional hi

293 on of deuterium oxide into newly synthesized muscle proteins were determined by mass spectrometry.

294 In this study, we found that muscle proteins were highly modified by S-nitrosylation,

295 The most abundant skeletal muscle proteins were identified and correctly classified

296 nces in K(pw) between chicken, fish, and pig muscle proteins were small.

297 that some chemicals may sorb irreversibly to muscle proteins, which needs further research.

298 regates in addition to high molecular weight muscle proteins, while the second peak (peak 2) still co

299 Mutations in nebulin, a giant muscle protein with 185 actin-binding nebulin repeats, a

300 Nebulin is a large skeletal muscle protein wound around the thin filaments, with its