ライフサイエンスコーパス: cachexia

1 interventions, such as exercise, for cancer cachexia.

2 sity, metabolic syndrome, lipodystrophy, and cachexia.

3 scles in these patients who often experience cachexia.

4 ly promote the muscle atrophy program during cachexia.

5 uscle atrophy which occurs in sarcopenia and cachexia.

6 acids in TB14 rats during the development of cachexia.

7 and bone density, typical characteristics of cachexia.

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

9 tolerance to chemotherapy induced by cancer cachexia.

10 f immunometabolic response in AT from cancer cachexia.

11 erapeutic target in the management of cancer cachexia.

12 a systemic acceleration of autophagy during cachexia.

13 ry response during the development of cancer cachexia.

14 aracterised by low LM such as sarcopenia and cachexia.

15 -6 trans-signaling may be targeted in cancer cachexia.

16 d thereby induce muscle wasting described as cachexia.

17 ion for mitigating pancreatic cancer-induced cachexia.

18 atients who had gastrointestinal cancer with cachexia.

19 causes skeletal muscle wasting during cancer cachexia.

20 d lead to neurodegeneration, depression, and cachexia.

21 option for patients with cancer anorexia and cachexia.

22 patients die due to complexities related to cachexia.

23 e mass in naive conditions and during cancer cachexia.

24 ia rather than clear diagnostic criteria for cachexia.

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

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

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

28 d strength and for protection against cancer cachexia.

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

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

31 which may provide informative biomarkers of cachexia.

32 muscle wasting, in particular sarcopenia and cachexia.

33 and safety in patients with cancer anorexia-cachexia.

34 peutic agents due to their ability to induce cachexia.

35 the role of miRNAs in cancer development and cachexia.

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

37 ge number of biological processes, including cachexia.

38 in patients with advanced HF complicated by cachexia.

39 contributes to the broader aspects of cancer cachexia.

40 cle atrophy meets the clinical definition of cachexia.

41 was correlated with the presence of cardiac cachexia.

42 g the causes and treatment options of cancer cachexia.

43 diates the pathophysiology of CKD-associated cachexia.

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

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

46 n established model of colorectal cancer and cachexia.

47 enesis, tumour invasiveness, metastases, and cachexia.

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

49 o gastrointestinal (GI) symptoms and cardiac cachexia.

50 easurement of drug potency and tumor-related cachexia.

51 nockout are increased lactate production and cachexia.

52 appetite improvement in patients with cancer cachexia.

53 n the pathogenesis of endotoxemic and cancer cachexia.

54 One patient also suffered with marked cachexia.

55 gical approach to prevent muscle wasting and cachexia.

56 nutritional intervention to stop or reverse cachexia.

57 and caspase) in muscle wasting during cancer cachexia.

58 ons specifically for the treatment of cancer cachexia.

59 7 is a promising drug candidate for treating cachexia.

60 etabolism in a mouse model of CKD-associated cachexia.

61 regulated in multiple mouse models of cancer cachexia.

62 to anorexia, metabolic changes, and eventual cachexia.

63 lamic inflammatory gene expression in cancer cachexia.

64 caregivers with advice for the management of cachexia.

65 y locus of neuromuscular pathology in cancer cachexia.

66 al muscle of patients with cancer exhibiting cachexia.

67 rapeutic targets by which to mitigate cancer cachexia.

68 a Lewis lung carcinoma (LLC) model of cancer cachexia.

69 ssembly receptor (MasR), for treating cancer cachexia.

70 ve conditions and in a mouse model of cancer cachexia.

71 lic alterations and muscle atrophy in cancer cachexia.

72 DK4 and the changes in muscle size in cancer cachexia.

73 sis may cause thromboinflammation and cancer cachexia.

74 may be useful in PDAC and cancer-associated cachexia.

75 daptive immunity, neutrophil activation, and cachexia.

76 survival in C26 oxfu mice in late stages of cachexia.

77 t chronic illness and are presumably free of cachexia?

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

79 sue and skeletal muscle, hallmarks of cancer cachexia(2-4).

80 to 0 months before PDAC diagnosis (phase 3, cachexia), a significant proportion of patients had hype

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

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

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

84 Cachexia, a devastating wasting syndrome characterized b

85 Cachexia, a progressive weight loss in cancer patients t

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

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

88 e ability of IL-1R(-/-) mice to recover from cachexia, an immune-metabolic disease of muscle wasting

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

90 insight into the pathophysiology of chronic cachexia and a tool to test therapeutics for disease rev

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

92 ntributes to the paraneoplastic syndromes of cachexia and anemia.

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

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

95 impaired muscle protein synthesis in cancer cachexia and could point to novel therapeutic targets by

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

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

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

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

100 cted Il18-transgenic (Il18tg) mice developed cachexia and hyperinflammation comparable to Prf1-/- mic

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

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

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

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

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

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

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

108 s as a diagnostic tool for cancer-associated cachexia and is detrimental to serum 25-hydroxyvitamin D

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

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

111 and preserved fat mass and lean mass during cachexia and LPS-induced anorexia.

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

113 rentiation factor 15 (GDF15) correlates with cachexia and reduced survival in patients with cancer(5-

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 However, the mechanisms of cachexia and the potential therapeutic interventions rem

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

118 Cancer patients included those with cachexia and weight-stable disease.

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

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

121 the NLR associates with greater weight loss, cachexia, and lower serum 25-hydroxyvitamin D (25(OH)D)

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

123 NLR associates with greater weight loss and cachexia, and potentially, a lower serum 25(OH)D concent

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

125 Muscle atrophy and cachexia are common comorbidities among patients sufferi

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

127 a regulator of host homeostasis and point to cachexia as a cost of long-term reliance on IL-1-mediate

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

129 Development of cachexia, as well as liver and skeletal muscle fibrosis,

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

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

132 chronic IL-1R signaling could be leading to cachexia-associated fibrosis.

133 the timing of interventions that may improve cachexia-associated outcomes.

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

135 d substantial clinical challenges related to cachexia, atherosclerosis, and poor clinical outcomes.

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

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

138 scular junction (NMJ) may play a key role in cachexia, but this has yet to be investigated in human p

139 ing, a cardinal feature of cancer-associated cachexia (CAC), is a major clinical problem with few the

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

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

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

143 Cancer-associated cachexia, characterized by muscle wasting, is a lethal m

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

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

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

147 ial and early intervention to prevent cancer cachexia could take advantage of exercise, improving pat

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

149 actors either directly or indirectly promote cachexia development and examine how signals from the me

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

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

152 Cytokines linked to cancer-associated cachexia did not contribute to IAC.

153 to be a promising treatment for human cancer cachexia due to its selective inhibition of p38beta MAPK

154 ltrating myeloid cells as well as attenuated cachexia during PDAC.

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

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

157 on in tumor-bearing mice and prevents cancer cachexia, even under calorie-restricted conditions.

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

159 Currently, the cachexia field lacks animal models that recapitulate the

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

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

162 Understanding of the mechanisms that drive cachexia has remained limited, especially for infection-

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

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

167 limited, especially for infection-associated cachexia (IAC).

168 n lead to extreme weight loss in animals and cachexia in cancer patients.

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

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

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

172 represent a viable therapeutic strategy for cachexia in CKD.

173 the first time, the impact of tumor-related cachexia in different cell lines.

174 sent paper we describe a model of reversible cachexia in mice with chronic viral infection and identi

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

176 ade of Nox4 activity abrogated tumor-induced cachexia in mice.

177 induces anti-tumor responses and attenuates cachexia in murine models of pancreatic ductal adenocarc

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 sing therapeutic opportunities for targeting cachexia in the context of metastatic cancers.

182 s Perspective, we discuss the development of cachexia in the context of metastatic progression.

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

184 notypes identified in mouse models of cancer cachexia, including muscle fiber atrophy, sarcolemmal fr

185 in tumor-induced systemic wasting and cancer cachexia, including muscle wasting and lipid loss.

186 ype of muHuR-KO mice protects against cancer cachexia-induced muscle loss.

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

190 may be a marker for the early initiation of cachexia interventions.

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

192 Cachexia is a debilitating condition characterized by ex

193 Cancer cachexia is a devastating metabolic syndrome characteriz

194 Cachexia is a devastating syndrome that causes morbidity

195 over the past few decades demonstrates that cachexia is a disease with specific, targetable mechanis

196 Cachexia is a hallmark of pulmonary tuberculosis and is

197 Cancer cachexia is a highly prevalent condition associated with

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

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

200 Cachexia is a life-threatening wasting syndrome lacking

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

202 Cancer cachexia is a major cause of patient morbidity and morta

203 Cancer cachexia is a multifactorial syndrome characterized by a

204 Cancer cachexia is a multifactorial syndrome characterized by a

205 Cancer cachexia is a multifactorial syndrome characterized by b

206 Cachexia is a muscle-wasting syndrome that contributes s

207 Cachexia is a progressive muscle wasting disease that co

208 Cachexia is a serious complication of many chronic disea

209 Cachexia is a wasting condition defined by skeletal musc

210 Cachexia is a wasting disorder of adipose and skeletal m

211 Cachexia is a wasting syndrome associated with cancer, A

212 Cachexia is an exacerbating event in many types of cance

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

214 Cachexia is associated with poor prognosis and high mort

215 Cancer cachexia is characterized by a continuous loss of locomo

216 Cancer cachexia is characterized by reductions in peripheral le

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

218 Cachexia is frequently accompanied by severe metabolic d

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

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

223 -induced muscle wasting, a syndrome known as cachexia, is lethal.

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

225 We used 3 rat models of anorexia and cachexia (LPS, methylcholanthrene sarcoma, and 5/6 subto

226 ted improvements in behavioral and molecular cachexia manifestations, resulting in a near-doubling of

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

228 e longevity of the T. gondii-induced chronic cachexia model revealed that cachectic mice develop peri

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

230 In cancer cachexia models, maintaining skeletal muscle expression

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

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

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

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

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

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

237 fiber atrophy (P < 0.0001) in patients with cachexia, NMJ morphology was fully conserved.

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

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

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

241 cardio and cerebrovascular disease, obesity, cachexia or hypercholesterolemia.

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

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

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

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

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

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

248 6 months before PDAC diagnosis (phase 2, pre-cachexia), patients had significant increases in hypergl

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

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

251 However, the molecular mechanisms driving cachexia remain poorly defined, and there are currently

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

253 elated sarcopenia, the mechanisms underlying cachexia remain poorly understood.

254 Cancer cachexia remains a largely intractable, deadly condition

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

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

257 ase inhibitor, nilotinib, ameliorates cancer cachexia, representing a potential therapeutic strategy

258 Cachexia represents a leading cause of morbidity and mor

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

260 Cachexia robs patients of their strength and capacity to

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

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

263 Despite cachexia sharing pathophysiological features with a numb

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

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

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

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

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

269 ntact in rectus abdominis in both cancer and cachexia, suggesting that denervation of skeletal muscle

270 r, largely failed to preserve muscle mass in cachexia, suggesting that other mechanisms might be invo

271 The cachexia syndrome is a debilitating state of cancer that

272 The cachexia syndrome is a debilitating state of cancer that

273 Cancer anorexia-cachexia syndrome is associated with increased morbidity

274 much as 10-100-fold, leading to an anorexia-cachexia syndrome, which is often fatal.

275 induces immunometabolic modulation in cancer cachexia syndrome.

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

277 nalcoholic fatty liver disease, and anorexia-cachexia syndrome.

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

279 al muscle wasting in murine models of cancer cachexia that is disrupted in skeletal muscle of patient

280 ssion but also address comorbidities such as cachexia that limit quality and quantity of life.

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

282 bilitating muscle-wasting syndrome, known as cachexia, that is associated with decreased tolerance to

283 In mice with cancer cachexia, the MasR agonist AVE 0991 slowed tumor develop

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

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

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

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

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

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

290 These signatures of muscle atrophy and cachexia were not influenced by Zip14 ablation, however.

291 Weight loss and cachexia were significantly (both p < 0.05) greater and

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

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

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

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

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

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

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