ライフサイエンスコーパス: wasting

1 of adaptation to more overt undernutrition (wasting).

2 p-Mef2c, which causes Hspb7-dependent muscle wasting.

3 rential MEK activation in tumor-induced host wasting.

4 cancer-induced alterations, worsening muscle wasting.

5 etal muscles to combat cancer-induced muscle wasting.

6 nomously activate host Pvr/MEK signaling and wasting.

7 d with aridity, hypoxia, acid rain, and mass wasting.

8 heir fate in response to promoters of muscle wasting.

9 y mediator of cancer-induced skeletal muscle wasting.

10 acterized by progressive muscle weakness and wasting.

11 t were resistant to LLC tumor-induced muscle wasting.

12 s muscle health and causes subsequent muscle wasting.

13 ncreased glucagon, without preventing muscle wasting.

14 dy weight loss and muscle and adipose tissue wasting.

15 ect of selected miRNAs on age-related muscle wasting.

16 severe wasting and <115-125 mm for moderate wasting.

17 ino acid catabolism without affecting muscle wasting.

18 inhibitor, benzamil, reversed excessive K(+) wasting.

19 sary and sufficient for tumor-induced muscle wasting.

20 xhibited severe hypokalemia and urinary K(+) wasting.

21 salt wasting, low BP, and profound potassium wasting.

22 abnormal substrate utilization and lean mass wasting.

23 mation and massive muscle and adipose tissue wasting.

24 reverted airway fibrosis and systemic muscle wasting.

25 mo and at 1 y-for reducing the risk of child wasting.

26 eting TLR4 alone effectively abrogate muscle wasting.

27 for the development of therapies for muscle wasting.

28 ren younger than 5 years with anthropometric wasting.

29 nsible for tumor's capacity to induce muscle wasting.

30 therapeutic target of cancer-induced muscle wasting.

31 e DOX-induced cardiac atrophy and whole-body wasting.

32 ed by elevated urinary calcium and phosphate wasting.

33 the fiber area by 20%, protecting them from wasting.

34 ation and cleavage of ENaC, despite the salt wasting.

35 ) cotransporter (NCC) manifest profound salt wasting.

36 pproximately 7.5% of children suffering from wasting.

37 toplasmic CELF1 functions in skeletal muscle wasting.

38 wly progressive skeletal muscle weakness and wasting.

39 therapeutic target of cancer-induced muscle wasting.

40 is necessary and sufficient to cause muscle wasting.

41 wn as the driver of cancer-associated muscle wasting.

42 ile mice lacking Myoc showed enhanced muscle wasting.

43 on in disease states characterized by muscle wasting.

44 c and degradative pathways preventing muscle wasting.

45 lators, as protective factors against muscle wasting.

46 ng sarcopenia, frailty, and secondary muscle wasting.

47 6, spared LLC tumor-bearing mice from muscle wasting.

48 Underweight (13%), wasting (4%), and stunting (33%) were common.

49 rystal suspension into the path of the XFEL, wasting a vast amount of sample due to the pulsed nature

50 Muscle wasting, a cardinal feature of cancer-associated cachexi

51 ein intake is associated with protein-energy wasting, a risk factor that affects outcome.

52 Debilitating cancer-induced muscle wasting, a syndrome known as cachexia, is lethal.

53 at column capacity is usually underutilized, wasting adsorbent and reducing productivity.

54 Muscle wasting, also known as cachexia, is associated with many

55 diagnostic performance of MUAC for detecting wasting among infants aged 1-6 mo.

56 <=112 mm performed well in detecting severe wasting among infants aged 1-6 mo.

57 ence (MUAC) with a cutoff <115 mm for severe wasting and <115-125 mm for moderate wasting.

58 Muscle wasting and atrophy are regulated by multiple molecular

59 toskeletal proteins and contribute to muscle wasting and atrophy.

60 Presentations vary from neonatal salt wasting and atypical genitalia, to adult presentation of

61 ay essential roles in tumor-induced systemic wasting and cancer cachexia, including muscle wasting an

62 cular disease that causes progressive muscle wasting and cardiomyopathy.

63 imilar phenotype to Bartter syndrome of salt wasting and dehydration due to reduced Na-K-2Cl-cotransp

64 LE: Critical illness is hallmarked by muscle wasting and disturbances in glucose, lipid, and amino ac

65 significantly deterred cancer-induced muscle wasting and dysfunction in a preclinical model of pancre

66 beyond these research fields, including food wasting and food sharing, mental energy conservation, di

67 duced natriuresis as well as renal potassium wasting and hypokalemia.

68 tor 23 (FGF23), which causes renal phosphate wasting and hypophosphataemia, rickets, skeletal deformi

69 y fed contribute to bone and skeletal muscle wasting and impose risk of adrenocortical atrophy.

70 fr1393 knockout mice exhibit urinary glucose wasting and improved glucose tolerance, despite euglycem

71 the most common cause of inherited phosphate wasting and is associated with severe complications such

72 gait and motor problems, in contrast to the wasting and lethal disease that occur during acute infec

73 d that host MEK activation results in muscle wasting and lipid loss, while tumor MEK activation is re

74 asting and cancer cachexia, including muscle wasting and lipid loss.

75 As loss-of-function mutations lead to salt wasting and low blood pressure, it has been surmised tha

76 nd arl15b knockdown resulted in renal Mg(2+) wasting and metabolic disturbances.

77 e exhibited a phenotype that included muscle wasting and metabolic endotoxemia.

78 oves cancer plus chemotherapy-induced muscle wasting and mitochondrial alterations.

79 Both wasting and obesity are associated with inflammation, bu

80 in called laminin-alpha1, ameliorates muscle wasting and paralysis in mouse models of MDC1A, demonstr

81 hondrial dysfunction is implicated in muscle wasting and perturbed lipid metabolism, speculating that

82 ed; the other two had transient massive salt-wasting and polyuria reminiscent of antenatal Bartter's

83 Exogenous miR-26a suppresses muscle wasting and renal fibrosis in obstructive kidney disease

84 nderstanding of conditions of adipose tissue wasting and review microenvironmental determinants of ad

85 d the maternal mortality ratios and reducing wasting and stunting for children.

86 s to describe the interrelationships between wasting and stunting in children aged <2 y.

87 The etiologic relationship between wasting and stunting is poorly understood, largely becau

88 Levels of wasting and stunting were high in this population, peaki

89 which is characterised by progressive muscle wasting and the discovery of reliable blood-based biomar

90 ed in the quadriceps of patients with muscle wasting and to determine the molecular pathways by which

91 dministration to C26 mice exacerbated muscle wasting and triggered autophagy or mitophagy, decreased

92 LMN) syndromes typically present with muscle wasting and weakness and may arise from pathology affect

93 disease characterized by progressive muscle wasting and weakness and premature death.

94 n a variety of clinical conditions with both wasting and weakness associated with an impairment of ph

95 is known on pathological age-related muscle wasting and weakness termed sarcopenia, which directly i

96 ion, has demonstrated the substantial muscle wasting and weakness, along with disruption of muscle's

97 plays a role in ameliorating skeletal muscle wasting and weakness.

98 hypoaminoacidemia, without affecting muscle wasting and without a sustained impact on blood glucose.

99 habitat showed low adult mass and condition (wasting), and low immature mass and length (stunting).

100 eus; (3) denervation is likely to drive this wasting, and (4) the neuromuscular synapse is a primary

101 atures of ataxia, paralysis, skeletal muscle wasting, and degeneration.

102 nases would lead to polyuria and severe salt-wasting, and generated SPAK/OSR1 double knockout mice to

103 ial syndrome characterized by anorexia, body wasting, and muscle and adipose tissue loss, impairing p

104 ith motor neuron degeneration, severe muscle wasting, and premature death by 6 mo of age.

105 n mice, miR-542 overexpression caused muscle wasting, and reduced mitochondrial function, 12S rRNA ex

106 We considered 3 outcomes (underweight, wasting, and stunting) and measured precipitation using

107 factors contribute to cancer-induced muscle wasting, and therefore therapy requires combinational st

108 , iron and vitamin A deficiencies, stunting, wasting, and underweight.

109 on in childhood is associated with stunting, wasting, and underweight.

110 nd with purified enzymes differed among salt-wasting- and nonclassical-associated variants, but these

111 TNF signaling promoted systemic wasting, anemia, and neutrophilia in the FMF-KI mice.

112 ting: aOR 0.83, 95% CI 0.77-0.88, p < 0.001; wasting: aOR 0.90, 95% CI 0.83-0.99, p = 0.03; underweig

113 ever, the pathogenic molecular mechanisms of wasting are still poorly understood.

114 pathway in muscle suppresses the deleterious wasting associated with cancer.

115 ty may have relevance to disorders of muscle wasting associated with sustained proinflammatory signal

116 ary outcomes were stunting, underweight, and wasting at a 12 month follow-up.

117 aluate the performance of MUAC for detecting wasting at community level and for predicting mortality

118 se, prevents oxidative stress-induced muscle wasting, at least partially, by improving the antioxidan

119 t of two ubiquitin ligases induced in muscle wasting, atrogin-1 and MuRF1, suggesting a possible clin

120 ope" hypothesis explains differences in food-wasting behaviors among humans.

121 umor-bearing mice not only alleviated muscle wasting, but also prolonged survival.

122 and lipid metabolism, did not affect muscle wasting, but drastically suppressed markers of hepatic a

123 ger cash transfer had the greatest effect on wasting, but only at 6 mo.

124 ould see a 37% increase in the prevalence of wasting by 2100, and central and eastern Africa 25%.

125 und that p300 mediates cancer-induced muscle wasting by activating C/EBPbeta, which then upregulates

126 ptor 4 (TLR4) mediates cancer-induced muscle wasting by directly activating muscle catabolism as well

127 both kinases causes severe polyuria and salt-wasting by generating SPAK/OSR1 double knockout (DKO) mi

128 ngth for age (HAZ or LAZ); and 39% exhibited wasting by weight/height or (length) for age (W/HZ or W/

129 d to prevent neuronal dysfunction and muscle wasting caused by protein misfolding in HD.

130 Skeletal muscle wasting causes both morbidity and mortality of cancer pa

131 ical features with a number of neuromuscular wasting conditions, including age-related sarcopenia, th

132 therapy for cancer and other serious muscle wasting conditions.

133 nd its genetic deficiency exacerbates muscle wasting; conversely, sestrin overexpression suffices to

134 ce also had inflammatory symptoms, including wasting, dermatitis, colitis, hypereosinophilia, and hig

135 on skeletal muscle and thereby induce muscle wasting described as cachexia.

136 Childhood wasting did not differ between groups (OR 0.92, 95% CI 0

137 g born to muntjac dams infected with chronic wasting disease (CWD) (1).

138 is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmi

139 Chronic wasting disease (CWD) in cervids and bovine spongiform e

140 Chronic wasting disease (CWD) is a fatal, progressive disease th

141 Chronic wasting disease (CWD) is a naturally occurring, fatal ne

142 Chronic wasting disease (CWD) is a prionopathy affecting wild an

143 Chronic wasting disease (CWD) is a rapidly spreading prion disea

144 Chronic wasting disease (CWD) is a rapidly spreading prion disor

145 Chronic wasting disease (CWD) is a relentless epidemic disorder

146 to precede neuroinvasion.IMPORTANCE Chronic wasting disease (CWD) is a universally fatal transmissib

147 Chronic wasting disease (CWD) is an emerging infectious prion di

148 Chronic wasting disease (CWD) is caused by an unknown spectrum o

149 Chronic wasting disease (CWD) is the only prion disease naturall

150 In nature, cervids are infected with chronic wasting disease (CWD) prions by oral and nasal mucosal e

151 ative errors to test deer saliva for chronic wasting disease (CWD) prions.

152 nterpart, contagious transmission of chronic wasting disease (CWD) results from shedding of prions pr

153 lations that have been infected with chronic wasting disease (CWD), a contagious, fatal prion disease

154 e, we removed the lipid content from chronic wasting disease (CWD)-infected white-tailed deer brain h

155 The first signs of sea star wasting disease (SSWD) epidemic occurred in just few mon

156 e challenged domestic swine with the chronic wasting disease agent by inoculation directly into the b

157 and with prions causing deer and elk chronic wasting disease and transmissible mink encephalopathy un

158 e muscular dystrophy (DMD) is a fatal muscle-wasting disease arising from mutations in the dystrophin

159 trophy (DMD) is an incurable X-linked muscle-wasting disease caused by mutations in the dystrophin ge

160 phy (DMD) is a severe and progressive muscle-wasting disease caused by mutations in the dystrophin ge

161 ographic spread in the prevalence of chronic wasting disease in white-tailed deer (Odocoileus virgini

162 Chronic wasting disease is a fatal, neurological disease caused

163 lar dystrophy is a rare, progressive, muscle-wasting disease leading to severe disability and prematu

164 prions in human nasal brushings and chronic wasting disease prions in deer-ear homogenates.

165 Cachexia is a progressive muscle wasting disease that contributes to death in a wide rang

166 PORTANCE The facile dissemination of chronic wasting disease within captive and free-range cervid pop

167 re consistent with observed data on sea star wasting disease, which suggests that environmental stres

168 ovine spongiform encephalopathy; and chronic wasting disease.

169 arrhea in an infant with presumed renal salt-wasting disease.

170 Triple(lo)CD4(+) T cells induced colitis and wasting disease.

171 Its dysregulation is implicated in muscle wasting diseases.

172 chenne muscular dystrophy is a deadly muscle-wasting disorder caused by loss of dystrophin protein.

173 nd its dysfunction is associated with a salt-wasting disorder known as Bartter syndrome.

174 is a severe and progressive striated muscle wasting disorder that leads to premature death from resp

175 further cohorts with these and other muscle-wasting disorders would suggest that MRI biomarkers migh

176 ion improves the phenotype in several muscle wasting disorders.

177 elevated in the serum of progressive muscle wasting DM1 patients compared to disease-stable DM1 pati

178 aring TLR4(-/-) mice were spared from muscle wasting due to a blockade in muscle catabolic pathways.

179 ein response pathways causes skeletal muscle wasting during cancer cachexia.

180 id, and amino acid homeostasis and in muscle wasting during critical illness.

181 that it may, in fact, exert a relative salt-wasting effect.

182 ated to efficiently produce proteins without wasting energy or substrate.

183 ata herein details the muscular weakness and wasting exhibited by D2.mdx skeletal muscle, as well as

184 ation of recent and present-day martian mass wasting features, as much less water may be required to

185 rovement in sCr-eGFR is likely due to muscle wasting following LVAD surgery.

186 In these mice, muscle wasting has been ameliorated as evidenced by increased m

187 rome across vertebrate species that includes wasting, hepatosteatosis, and thymus atrophy.

188 ied mice, we have shown that renal phosphate wasting hypophosphatemic states arising from high levels

189 l show similar morphometric "warning signs" (wasting in adults, stunting in immatures); selected morp

190 We determined the cutoffs for MUAC to detect wasting in Bangladeshi children aged 6-60 mo.A secondary

191 t AVE 0991 holds promise for reducing muscle wasting in cancer.

192 In clinical settings, wasting in childhood has primarily been assessed with th

193 as an independent diagnostic tool to detect wasting in children aged 6-59 mo.

194 ategy for adipose tissue browning and muscle wasting in CKD patients.

195 agents reverted cancer cell-induced myotube wasting in culture conditions and mouse models.

196 brogates tumor-induced muscle catabolism and wasting in cultured myotubes and in mice.

197 arkers for monitoring the progress of muscle wasting in DM1 patients.

198 re associated with the progression of muscle wasting in DM1 patients.

199 egeneration are major contributors to muscle wasting in Duchenne muscular dystrophy (DMD).

200 eresting opportunity to prevent increases in wasting in humanitarian aid settings.

201 stic performance of MUAC in detecting severe wasting in infants aged 1-6 mo.

202 e targeted deletion of PERK increases muscle wasting in Lewis lung carcinoma tumor-bearing mice.

203 IRE1alpha arm of the UPR, ameliorates muscle wasting in LLC tumor-bearing mice.

204 ed activation of XBP1 causes skeletal muscle wasting in LLC tumor-bearing mice.

205 70 and Hsp90 as key cachexins causing muscle wasting in mice.Cachexia affects many cancer patients ca

206 onal mechanism that mediates skeletal muscle wasting in murine models of cancer cachexia that is disr

207 fined, it is unknown if persistent phosphate wasting in nephropathic cystinosis is associated with a

208 6 could suppresses renal fibrosis and muscle wasting in obstructive kidney disease.

209 receptors (Ifnar1 or Ifngr1) does not rescue wasting in Pdgfrb(+/D849V) mice, indicating that interfe

210 the incidences of underweight, stunting, or wasting in Tanzanian infants.

211 n with hypophosphataemia and renal phosphate wasting in the absence of vitamin D or calcium deficienc

212 has been focus on rising rates of childhood wasting in the short term, maternal and child undernutri

213 lower limb has been shown to reverse muscle wasting in these patients but its effect on cardiometabo

214 enario (coverage reductions of 9.8-18.5% and wasting increase of 10%) over 6 months would result in 2

215 nario (coverage reductions of 39.3-51.9% and wasting increase of 50%) over 6 months would result in 1

216 Skeletal muscle wasting is a devastating consequence of cancer that cont

217 Skeletal muscle wasting is also common in COPD, but less is known about

218 Muscle wasting is associated with increased mortality and morbi

219 s reduced by 9.8-51.9% and the prevalence of wasting is increased by 10-50%.

220 The association for wasting is not robust.

221 Skeletal muscle wasting is prevalent in many chronic diseases, necessita

222 er-induced cachexia, characterized by muscle wasting, is a lethal metabolic syndrome with undefined e

223 associated cachexia, characterized by muscle wasting, is a lethal metabolic syndrome without defined

224 Cachexia, characterized by muscle wasting, is a major contributor to cancer-related mortal

225 Cachexia, or muscle wasting, is a serious health threat to victims of radiol

226 -for-age), underweight (low weight-for-age), wasting (low weight-for-height), and low birth weight in

227 ney-specific MR-knockout mice exhibited salt wasting, low BP, and hyperkalemia.

228 of Kir4.1 in these mice led to moderate salt wasting, low BP, and profound potassium wasting.

229 ht-for-age, weight-for-length, stunting, and wasting <=18 y of age.

230 Cirrhosis is characterized by muscle wasting, malnutrition, and functional decline that confe

231 -mm increase = 0.94, 95% CI: 0.92, 0.97) and wasting (marginal RR per 50-mm increase = 0.93, 95% CI:

232 tabolism, such as insulin resistance, muscle wasting, mitochondrial dysfunction and hyperlactatemia.

233 ted that glycine preserves muscle in various wasting models.

234 ch correlated with the progression of muscle wasting observed in DM1 patients.

235 ntially at synapses on slow fibers, precedes wasting of mutant soleus; (3) denervation is likely to d

236 ystrophies are characterized by weakness and wasting of skeletal muscle tissues.

237 signaling pathway is downregulated in muscle wasting or atrophying diseases, with a decrease of myost

238 50 21A2 variants associated with either salt-wasting or nonclassical forms of CAH were expressed, pur

239 t elevated PDGFRbeta signaling causes tissue wasting or overgrowth reminiscent of human genetic syndr

240 Muscle wasting, or muscle atrophy, can occur with age, injury,

241 thermore, there was no evidence of potassium wasting (P=0.20) or renal dysfunction (P>0.11 for all bi

242 ed by motor neuron loss, resulting in muscle wasting, paralysis and eventual death.

243 Muscle wasting pathway proteins were upregulated while those th

244 diseases characterized by connective tissue wasting (Penttinen syndrome) or overgrowth (Kosaki overg

245 predisposes hepsin-deficient mice to a salt-wasting phenotype, with a decreased salt sensitivity.

246 ppression alone is sufficient to abolish the wasting phenotypes without affecting tumor growth.

247 e capacity due to aging, frailty, and muscle wasting poses major unmet clinical needs.

248 ation in bodyweight, tachycardia, and muscle wasting, predisposing affected individuals to substantia

249 The increase in wasting prevalence would account for 18-23% of additiona

250 Impact, eolian, and mass wasting processes have dominantly modified the surface.

251 ing that metal ligation inhibits this energy wasting reaction is of direct relevance to solar energy

252 Muscle wasting reduces functional capacity and increases cardio

253 How sarcopenia and muscle wasting relate to such poor outcomes requires looking be

254 cachexins that mediate cancer-induced muscle wasting remain elusive.

255 4 expression leads to the generalized muscle wasting remains unclear.

256 However, off-target electrolyte wasting, renal dysfunction, and neurohormonal activation

257 Here, we report cancer-induced muscle wasting requires the transcriptional cofactor p300, whic

258 hat some recipients may not use the product, wasting resources (overinclusion).

259 chologically, and can harm health systems by wasting resources and deflecting investments in both pub

260 myostatin increased mass or prevented muscle wasting, respectively, highlighting the potential therap

261 uniformly fatal condition of striated muscle wasting resulting in premature death from respiratory an

262 ermatitis, multiple allergies, and metabolic wasting (SAM) syndrome, caused by biallelic desmoglein 1

263 ve overgrowth, a distinct phenotype from the wasting seen in Stat1(+/-)Pdgfrb(+/D849V) mice.

264 The pronounced cachexia (unexplained wasting) seen in Huntington's disease (HD) patients sugg

265 the impact of SGLT2 to prevent renal glucose wasting, SGLT2 inhibitors have been developed to treat d

266 furcating systems in nature prevented energy-wasting short-circuiting reactions that have large drivi

267 e are failing to recognize the importance of wasting simply because it tends to be more acute and tre

268 hysiology of FGF23-dependent renal phosphate wasting states and implicate pharmacologic CYP24 inhibit

269 ally manifested by postweaning multisystemic wasting syndrome (PMWS), respiratory and enteric disease

270 A viral etiology of sea star wasting syndrome (SSWS) was originally explored with vir

271 DV, has been their association with sea star wasting syndrome (SSWS), a disease that has decimated se

272 a, IL-6, and CCL2 mRNAs), and attenuated the wasting syndrome and severity of colitis ( approximately

273 Cachexia, a devastating wasting syndrome characterized by severe weight loss wit

274 sporadic cases of postweaning multisystemic wasting syndrome in Canada in the early 1990s, an epidem

275 viremia contribute to immunosuppression and wasting syndrome in HIV/AIDS.

276 Cachexia is a life-threatening wasting syndrome lacking effective treatment, which aris

277 astatic cancer develop a debilitating muscle-wasting syndrome, known as cachexia, that is associated

278 , a debilitating age-related skeletal muscle wasting syndrome.

279 hexia, an immune-metabolic disease of muscle wasting that impairs fitness of wild-type mice.

280 novel mechanism of cancer-associated muscle wasting that is similarly disrupted in muscle of patient

281 space with high-quality solutions and avoid wasting time in non-promising areas.

282 succinate mitigates infection-induced lipid wasting to extend survival of V. cholerae-infected flies

283 The final samples for wasting, underweight and stunting include 668.463, 693.3

284 ute respiratory infections (ARIs), stunting, wasting, underweight, or anaemia in children aged 0-5 ye

285 per understanding of these pathways, we risk wasting valuable resources on mitigating behavioural eff

286 ion mobility, animal domestication, and food-wasting visibility.

287 C curve accuracy level in identifying severe wasting was 0.86 (95% CI: 0.82, 0.89).

288 of stunting was 14%, underweight was 8%, and wasting was 1% and did not differ by group.

289 Severe wasting was defined as having a weight for length z scor

290 The prevalence of severe and moderate wasting was n = 101 (21.6%) and n = 61 (13.0%), respecti

291 In low-income countries, childhood wasting was the leading cause of DALYs in Afghanistan, S

292 To study their role in diabetic muscle wasting, we created mice with muscle-specific triple kno

293 Using a fly model of tumor-induced organ wasting, we observed aberrant MEK activation in both tum

294 ng [height-for-age z score (HAZ) < -2SD] and wasting [weight-for-height z score (WHZ) < -2SD] prevale

295 The prevalence of stunting and wasting were 20% and 13%, respectively; no children had

296 s a key mediator of LLC tumor-induced muscle wasting whose acetyltransferase activity may be targeted

297 ous form of undernutrition, characterized by wasting with or without edema.

298 rate coordinate induction of systemic muscle wasting with tumour-autonomous Yorkie-mediated SLC36-fam

299 ed locomotor activity, and attenuated muscle wasting, with the majority of these effects dependent on

300 k of severe (WHZ <-3) and moderate (WHZ <-2) wasting would be <120 and <125 mm for ages 6-24 mo, <125