ライフサイエンスコーパス: cachexia

1 sity, metabolic syndrome, lipodystrophy, and cachexia.

2 scles in these patients who often experience cachexia.

3 c approach for at least some types of cancer cachexia.

4 ge number of biological processes, including cachexia.

5 in patients with advanced HF complicated by cachexia.

6 contributes to the broader aspects of cancer cachexia.

7 was correlated with the presence of cardiac cachexia.

8 g the causes and treatment options of cancer cachexia.

9 diates the pathophysiology of CKD-associated cachexia.

10 eading to tissue wasting and, ultimately, to cachexia.

11 increased angiotensin II (Ang II) levels and cachexia.

12 n established model of colorectal cancer and cachexia.

13 enesis, tumour invasiveness, metastases, and cachexia.

14 s fasting, denervation, diabetes, and cancer cachexia.

15 o gastrointestinal (GI) symptoms and cardiac cachexia.

16 nockout are increased lactate production and cachexia.

17 appetite improvement in patients with cancer cachexia.

18 n the pathogenesis of endotoxemic and cancer cachexia.

19 One patient also suffered with marked cachexia.

20 and bone density, typical characteristics of cachexia.

21 gical approach to prevent muscle wasting and cachexia.

22 nutritional intervention to stop or reverse cachexia.

23 ls, to be responsible for tumor induction of cachexia.

24 and caspase) in muscle wasting during cancer cachexia.

25 c resistance to the muscle wasting of cancer cachexia.

26 he physiologic perturbations associated with cachexia.

27 rogression of muscle atrophy associated with cachexia.

28 sponse to anorexia during the development of cachexia.

29 f a temporal stimulation of thermogenesis in cachexia.

30 hway are increased in skeletal muscle during cachexia.

31 h is a surgically curable tumor that induces cachexia.

32 tolerance to chemotherapy induced by cancer cachexia.

33 the definition and classification of cancer cachexia.

34 f immunometabolic response in AT from cancer cachexia.

35 nt of the pathogenesis of LLC tumour-induced cachexia.

36 tages--precachexia to cachexia to refractory cachexia.

37 erapeutic target in the management of cancer cachexia.

38 ctRIIB pathway and the development of cancer cachexia.

39 ausing ascites, bowel obstruction, and tumor cachexia.

40 ed for the prevention or treatment of cancer cachexia.

41 l settings, including denervation and cancer cachexia.

42 a systemic acceleration of autophagy during cachexia.

43 take and may have a role in the treatment of cachexia.

44 ation may contribute to the effect of cancer cachexia.

45 ssible contributory mechanism for rheumatoid cachexia.

46 DNA loss, even when given after the onset of cachexia.

47 y an active role in protecting the host from cachexia.

48 tially be useful for the treatment of cancer cachexia.

49 ly promote the muscle atrophy program during cachexia.

50 ry response during the development of cancer cachexia.

51 aracterised by low LM such as sarcopenia and cachexia.

52 -6 trans-signaling may be targeted in cancer cachexia.

53 d thereby induce muscle wasting described as cachexia.

54 atients who had gastrointestinal cancer with cachexia.

55 uscle atrophy which occurs in sarcopenia and cachexia.

56 causes skeletal muscle wasting during cancer cachexia.

57 d lead to neurodegeneration, depression, and cachexia.

58 option for patients with cancer anorexia and cachexia.

59 e mass in naive conditions and during cancer cachexia.

60 ia rather than clear diagnostic criteria for cachexia.

61 (LLC) and Apc(Min/+) mouse models of cancer cachexia.

62 increased angiotensin II (Ang II) levels and cachexia.

63 with advanced non-small-cell lung cancer and cachexia.

64 d strength and for protection against cancer cachexia.

65 onse is key in the aetiology of burn-induced cachexia.

66 umor-induced weight loss, an early marker of cachexia.

67 which may provide informative biomarkers of cachexia.

68 muscle wasting, in particular sarcopenia and cachexia.

69 acids in TB14 rats during the development of cachexia.

70 and safety in patients with cancer anorexia-cachexia.

71 peutic agents due to their ability to induce cachexia.

72 the role of miRNAs in cancer development and cachexia.

73 t chronic illness and are presumably free of cachexia?

74 mass index, and were more likely to display cachexia (19%).

75 and 56.4% increase in lung weight, P<0.001), cachexia (37.8% decrease in body weight, P<0.001), and e

76 ith a 2.3 times increased risk of developing cachexia (95% CI: 1.2, 4.3; P = 0.014).

77 the definition and classification of cancer cachexia a panel of experts participated in a formal con

78 Cachexia, a condition that kills about one-fifth of canc

79 ere weight loss is characteristic for cancer cachexia, a condition that significantly impairs functio

80 Chemotherapy promotes the development of cachexia, a debilitating condition characterized by musc

81 Cachexia, a progressive weight loss in cancer patients t

82 ely one-third of cancer deaths are caused by cachexia, a severe form of skeletal muscle and adipose t

83 In fact, excessive proteolysis causes cachexia, accelerates disease progression, and worsens l

84 key cachexins causing muscle wasting in mice.Cachexia affects many cancer patients causing weight los

85 of the host can influence the development of cachexia among patients with gastroesophageal malignancy

86 l need for safe and effective treatments for cachexia, anamorelin might be a treatment option for pat

87 d spontaneous mouse models of cancer-induced cachexia and anemia.

88 ntributes to the paraneoplastic syndromes of cachexia and anemia.

89 increased angiotensin II (Ang II) levels and cachexia and Ang II causes skeletal muscle wasting in ro

90 n progressive stages of clinical lung cancer cachexia and assessed whether circulating factors can in

91 Levels of interleukin (IL)-6 correlate with cachexia and death due to an increase in tumour burden.

92 eletion of Hrpt2 in adult mice led to severe cachexia and death within 20 days.

93 espread use of mice to examine mechanisms of cachexia and diaphragm abnormalities in PH.

94 function in skeletal muscle against cardiac cachexia and exercise intolerance in CHF.

95 dant enzyme(s) in protection against cardiac cachexia and exercise intolerance in CHF.

96 muscle protein loss, which may contribute to cachexia and general protein loss during severe illness.

97 underlying metabolic abnormalities of cancer cachexia and have limited long-term impact on patient qu

98 f noninvasive biomarkers for the presence of cachexia and identification of new therapeutic targets.

99 tal parasitic disease associated with fever, cachexia and impaired protective T-cell responses agains

100 P might hold promise for ameliorating cancer cachexia and improving patient survival.

101 n muscle in three different models of cancer cachexia and in glucocorticoid-treated mice.

102 tabolic responses observed in cancer-induced cachexia and in wasting induced by chronic obstructive p

103 evelopment to involvement in the etiology of cachexia and indicate that Fn14 antibodies may be a prom

104 members are increased during cancer-related cachexia and induce intracellular signaling through glyc

105 stemic and local inflammation was evident in cachexia and intermediate in precachexia, but the plasma

106 IL-12/IL-23p40 neutralization abrogates both cachexia and intestinal inflammation and reduces the num

107 th clinical and biological markers of cancer cachexia and is associated with a shorter survival in me

108 ed antitumor effects and induced significant cachexia and lethal bone toxicities in two mouse strains

109 for myostatin in the pathogenesis of cancer cachexia and link this condition to tumor growth, with i

110 t an important role of LIF-JAK2-STAT3 in C26 cachexia and point to a therapeutic approach for at leas

111 with IL-13Ralpha2-positive cancer displayed cachexia and poor prognosis.

112 or normal muscle fiber atrophy during cancer cachexia and sepsis, and further suggest that basal leve

113 inhibited muscle fiber atrophy during cancer cachexia and sepsis.

114 mprove the prognosis of patients with cancer cachexia and systemic inflammation (i.e., those with a m

115 that Fn14, when expressed in tumors, causes cachexia and that antibodies against Fn14 dramatically e

116 The prevalence of cachexia and the impact of this disorder on the patient

117 Infections and inflammation can lead to cachexia and wasting of skeletal muscle and fat tissue b

118 on the orexigenic peptide ghrelin, in human cachexia and wasting.

119 IDS, were presented at a symposium entitled "Cachexia and Wasting: Recent Breakthroughs in Understand

120 to study the mechanism of radiation-induced cachexia and will aid in efficacy studies of mitigators

121 n, with enlarged, necrotic liver granulomas, cachexia, and >80% mortality by 8 wk postinfection, desp

122 disease characterized by neurodegeneration, cachexia, and accelerated aging.

123 tion, increased metabolic demand, infection, cachexia, and eventually death.

124 for an immune cell subset in protection from cachexia, and further suggest that the mechanism of prot

125 ove management of problems such as dyspnoea, cachexia, and haemoptysis for patients across care setti

126 ders, Alzheimer's disease, social disorders, cachexia, and obesity.

127 ntaneous T cell and myeloid cell activation, cachexia, and premature lethality seen in A20-deficient

128 balance, clinical and biological markers of cachexia, and survival.REE was measured with the use of

129 Cancer cachexia/anorexia is a complex syndrome that involves pr

130 The underlying causes of cachexia are incompletely understood, and currently no t

131 nally found that, even among obese patients, cachexia, as defined by muscle mass, was common, with 56

132 Whereas, the abundance of cancer cachexia associated bacteria, such as Dysgonomonas spp.

133 eficial bacteria, and down-regulating cancer-cachexia associated bacteria.

134 The role of platelet activation in cachexia-associated mortality warrants additional studie

135 ded and develop cataracts, lordokyphosis and cachexia at a young age.

136 Unlike skeletal muscle cachexia, atrophic hearts do not upregulate the ubiquiti

137 than host, is responsible for inducing this cachexia because tumors in Fn14- and TWEAK-deficient hos

138 wasting is considered the central feature of cachexia, but the potential for skeletal muscle anabolis

139 one may not prevent muscle loss secondary to cachexia, but, in combination with the use of an anaboli

140 as an endocrine organ in promoting systemic cachexia by secreting peptide factors such as myostatin.

141 Using an established mouse model of cancer cachexia (C26 adenocarcinoma), we determined how these d

142 to determine whether colon-26 (C-26) cancer cachexia causes diaphragm muscle fiber atrophy and weakn

143 These data demonstrate that C-26 cancer cachexia causes profound respiratory muscle atrophy and

144 Cancer-induced cachexia, characterized by muscle wasting, is a lethal m

145 Cachexia, characterized by muscle wasting, is a major co

146 In models of muscular dystrophy and cancer cachexia, combined inhibition of activins and myostatin

147 mmune inflammatory syndrome characterized by cachexia, conjunctivitis, and dermatitis.

148 adaptation of increased protein degradation (cachexia), decreased rate of muscle protein synthesis (i

149 age III or IV non-small-cell lung cancer and cachexia (defined as >/=5% weight loss within 6 months o

150 c-lysosomal proteolytic system during cancer cachexia development in humans.

151 s a tactic to evaluate hypothesized roles in cachexia development.

152 for infection, 0.63 (95% CI, 0.41-0.95) for cachexia/dialysis withdrawal, 1.06 (95% CI, 0.81-1.37) f

153 in a variety of clinical settings, including cachexia, disuse, and denervation.

154 both young and old animals, suggestive of a cachexia effect.

155 from patients and an animal model of cancer cachexia enabled us to identify early disruption in Adl

156 y-onset, severe inflammatory phenotype, with cachexia, erosive arthritis, left-sided cardiac valvulit

157 ted with pancreatitis, male infertility, and cachexia, features characteristic of cystic fibrosis and

158 as a key molecule playing multiple roles in cachexia, from fat "browning" factor to potential therap

159 as a key molecule playing multiple roles in cachexia, from fat 'browning' factor to potential therap

160 With no effective treatment of cancer cachexia, future therapies directed at preserving muscle

161 Although cachexia has a major effect on both the morbidity and mo

162 Experimental models of cancer cachexia have indicated that systemic inflammation induc

163 Muscle wasting and cachexia have long been postulated to be key determinant

164 Previous studies investigating HF-related cachexia have not examined the impact of RV function on

165 confidence interval (CI): 2.18 to 4.45]) and cachexia (hazard ratio: 2.90 [95% CI: 2.00 to 4.12]) in

166 es have been shown to be mediators of cancer cachexia; however, the role of cytokines in denervation-

167 x and muscle wasting are hallmarks of cancer cachexia; however, the underlying mechanism is undefined

168 se has associated factors including obesity, cachexia, hypertension, diabetes, proteinuria, uremic so

169 ing of events associated with cancer-induced cachexia (i.e., weight loss).

170 Moreover, depletion of TRAF6 prevents cancer cachexia in an experimental mouse model.

171 muscle regeneration, likely contributing to cachexia in CHF and chronic kidney disease.

172 g, likely contributing to the development of cachexia in CHF and CKD.

173 y an important role in mechanisms leading to cachexia in chronic disease states such as CHF and CKD.

174 It is not clear why cardiac or renal cachexia in chronic diseases is associated with poor car

175 represent a viable therapeutic strategy for cachexia in CKD.

176 leptin receptor antagonist (PLA) attenuates cachexia in mice with CKD.

177 of metabolic changes induced by the onset of cachexia in normal tissues.

178 orelin, a novel ghrelin-receptor agonist, on cachexia in patients with advanced non-small-cell lung c

179 tamucosal bacterial growth, GI symptoms, and cachexia in patients with HF.

180 s include negative effects related to cancer cachexia in patients with low BMI, increased drug delive

181 transcription factors that are required for cachexia in the mouse C26 colon carcinoma model of cance

182 age metastatic progression and tumor-induced cachexia in tumor-bearing mice.

183 Muscle atrophy (cachexia) in cancer patients is a life-threatening condi

184 l consequences of bedrest may mimic those of cachexia, including rapid loss of muscle, insulin resist

185 ts attenuated infection-induced anorexia and cachexia, indicating that the SCN mediate the effects of

186 complex are cardioprotective against cancer cachexia-induced cardiac atrophy and systolic dysfunctio

187 is involved in mediating the pathogenesis of cachexia-induced muscle wasting in tumor-bearing mice.

188 Chronic inflammation is associated with cachexia-induced skeletal muscle mass loss in cancer.

189 In this study, we investigated the impact of cachexia-inducing colorectal tumor on BAT in mice.

190 In vivo, cachexia-inducing murine adenocarcinoma (MAC)16 tumors w

191 th extracellular vesicles (EVs) from diverse cachexia-inducing tumor cells, resulting in elevated ser

192 Cancer-induced cachexia is a complex and poorly understood life-threate

193 Cancer cachexia is a complex metabolic condition characterized

194 Cachexia is a consequence of tumor burden caused by ill-

195 Muscle protein wasting in cancer cachexia is a critical problem.

196 Cachexia is a debilitating condition characterized by ex

197 Cancer cachexia is a devastating metabolic syndrome characteriz

198 Cachexia is a devastating syndrome that causes morbidity

199 Cachexia is a hallmark of pulmonary tuberculosis and is

200 Skeletal muscle wasting with accompanying cachexia is a life threatening complication in congestiv

201 Cancer cachexia is a life-threatening syndrome that affects mos

202 Cachexia is a life-threatening wasting syndrome lacking

203 Cachexia is a major cause of death in cancer patients.

204 Cancer cachexia is a multifactorial syndrome characterized by b

205 Cachexia is a muscle-wasting syndrome that contributes s

206 Cachexia is a serious complication of many chronic disea

207 Cancer cachexia is a severe wasting syndrome characterized by t

208 Cachexia is a wasting condition defined by skeletal musc

209 Cachexia is a wasting disorder of adipose and skeletal m

210 Cachexia is a wasting syndrome associated with cancer, A

211 Cachexia is an exacerbating event in many types of cance

212 Cancer cachexia is an unmet medical need and our data suggest t

213 Cancer cachexia is characterized by a continuous loss of locomo

214 Cardiac cachexia is characterized by an exaggerated loss of skel

215 Cachexia is characterized by inexorable muscle wasting t

216 Cachexia is defined as loss of muscle, with or without f

217 We propose that cancer-induced cachexia is driven at least in part by the expansion of

218 One key characteristic of cachexia is higher resting energy expenditure levels tha

219 noninvasively image the presence or onset of cachexia is important to better treat this condition, to

220 Distal upper limb myopathy/cachexia is not previously described with dominant POLG

221 In lung cancer patients, were cachexia is prevalent, there was a significant correlati

222 Cachexia is the dramatic weight loss and muscle atrophy

223 Muscle wasting, also known as cachexia, is associated with many chronic diseases, whic

224 been exposed to high dose radiation manifest cachexia-like symptoms in a time- and dose-dependent man

225 Targeted inhibition of myostatin in cardiac cachexia might be a therapeutic option in the future.

226 a non-human primate (NHP) radiation-induced cachexia model based on clinical and molecular pathology

227 evels approximating those observed in cancer cachexia models induced a more rapid and profound body w

228 Here, we show that in several cancer cachexia models, pharmacological blockade of ActRIIB pat

229 observed that in an in vivo model of cancer cachexia, Mstn expression coupled with downregulation of

230 s has been implicated in the pathogenesis of cachexia (muscle wasting) and the hallmark symptom, exer

231 In cancer cachexia, muscle depletion is related to morbidity and m

232 op an inflammatory syndrome characterized by cachexia, myeloid hyperplasia, dermatitis, and erosive a

233 ts with lung cancer precachexia (n = 10) and cachexia (n = 16) were cross-sectionally compared with 2

234 mited to a few indications, notably HIV/AIDS cachexia, nausea/vomiting related to chemotherapy, neuro

235 lternatively activated macrophages, prevents cachexia, neutrophilia, and endotoxemia during acute sch

236 The lethal bone toxicity and cachexia observed after cell-based immunotherapy targeti

237 RV dysfunction and cardiac cachexia often coexist, have additive adverse impact, an

238 study presents a useful model to deconstruct cachexia, opening a pathway to determining which tumorki

239 n that indicate targets for the treatment of cachexia or other eating disorders.

240 ationship is explained by confounding due to cachexia or other factors associated with low body mass

241 Research on the effects of these agents in cachexia or wasting conditions, characterized by progres

242 s occurs during aging (sarcopenia), disease (cachexia), or inactivity (atrophy).

243 Cachexia, or muscle wasting, is a serious health threat

244 any primary conditions including sarcopenia, cachexia, osteoporosis, HIV/AIDS, and chronic kidney dis

245 r vomiting were most severe in patients with cachexia (p < 0.05).

246 r, and GH insensitivity has been reported in cachexia patients.

247 hthalmoplegia; gastrointestinal dysmotility; cachexia; peripheral neuropathy; and leucoencephalopathy

248 disease conditions, including cancer-related cachexia, preterm labor with delivery, and osteoporosis.

249 ficient in CD8 T cells presented with severe cachexia, pulmonary inflammation, viral dissemination, a

250 ons to identify patients at highest risk for cachexia rather than clear diagnostic criteria for cache

251 TTP(-/-) mice when CCL3 was absent, although cachexia, reflecting systemic inflammation, was notably

252 However, the mechanisms of cancer cachexia remain poorly understood.

253 The role of hypermetabolism in cancer cachexia remains unclear.We studied the relation between

254 rious biological functions, including cancer cachexia, renal and heart failure, atherosclerosis and m

255 However, a similar cachexia response is not seen with equivalent growth of

256 Cachexia, sarcopenia, and atrophy due to inactivity are

257 s in a plethora of diseases including cancer cachexia, sarcopenia, and muscular dystrophy.

258 e tumor, phenotypes that resemble the cancer cachexia seen in human patients.

259 We concluded that, during LLC-induced cachexia, skm-gp130 regulates muscle mass signaling thro

260 In addition, we found cachexia stage results similar to those of animals in Me

261 ollected on d 0, 4, 7 (early stage), and 14 (cachexia stage) after tumor cell injection.

262 Akita/Nfc1 mice showed progressive cachexia starting at early age and increased mortality b

263 rtial-body irradiation developed symptoms of cachexia such as body weight loss in a time- and dose-de

264 Anorexia-cachexia syndrome (ACS) is a major determinant of cancer

265 may be related to malnutrition-inflammation cachexia syndrome (MICS).

266 An agreement was made that the cachexia syndrome can develop progressively through vari

267 The cachexia syndrome is a debilitating state of cancer that

268 The cachexia syndrome is a debilitating state of cancer that

269 Cancer anorexia-cachexia syndrome is associated with increased morbidity

270 induces immunometabolic modulation in cancer cachexia syndrome.

271 nse profile in patients with cancer anorexia-cachexia syndrome.

272 burns result in significant skeletal muscle cachexia that impedes recovery.

273 in Fn14- and TWEAK-deficient hosts developed cachexia that was comparable to that of wild-type mice.

274 t al. now identify a new target for treating cachexia, the activin type-2 receptor (ActRIIB).

275 In several mouse models of cachexia, the authors reversed wasting of skeletal and c

276 ife by the Functional Assessment of Anorexia/Cachexia Therapy (FAACT) questionnaire.

277 ibodies may be a promising approach to treat cachexia, thereby extending lifespan and improving quali

278 In a model of cancer cachexia, they significantly reduce muscle atrophy, and

279 ively through various stages--precachexia to cachexia to refractory cachexia.

280 d behavioral responses (anorexia, anhedonia, cachexia) to simulated gram-negative bacterial infection

281 The dire effects of cancer-induced cachexia undermine treatment and contribute to decreased

282 The pronounced cachexia (unexplained wasting) seen in Huntington's dise

283 tients with pancreatic cancer, we found that cachexia was associated with a type of muscle damage res

284 Cachexia was confirmed by weight loss as well as analyse

285 Cancer cachexia was defined as a multifactorial syndrome define

286 The agreed diagnostic criterion for cachexia was weight loss greater than 5%, or weight loss

287 d as weight loss progressed, thus preventing cachexia, we developed a molecular autoregulatory system

288 using a Lewis lung carcinoma model of cancer cachexia, we show that tumour-derived parathyroid-hormon

289 Using this model, and a model of cancer cachexia, we test the hypothesis that CD4(+)CD44(v.low)

290 es in circulating leukocytes and LPS-induced cachexia were eliminated by OBx.

291 linically important in ageing, bed-rest, and cachexia, where muscle weakening leads to disability, pr

292 increased muscle proteolysis in lung cancer cachexia, whereas the absence of downstream changes in p

293 ibed mechanism for the development of cancer cachexia, whereby progressive MDSC expansion contributes

294 ed cancer frequently experience anorexia and cachexia, which are associated with reduced food intake,

295 bout half of all cancer patients suffer from cachexia, which impairs quality of life, limits cancer t

296 ing >/=4) and nutritional status (absence of cachexia) who arrived at the emergency department of one

297 a promising new approach for treating cancer cachexia, whose inhibition per se prolongs survival.

298 ight regulatory disorder, such as obesity or cachexia, will require evaluation in man.

299 ansgenic mice had significant attenuation of cachexia with preserved whole body muscle strength and e

300 may be able to provide a risk assessment of cachexia, with possible implications for therapeutic dev