ライフサイエンスコーパス: anorexia

1 or indirectly subvert this 'illness-mediated anorexia'.

2 d intake when infected (i.e. illness-induced anorexia).

3 tive (such as in clinical settings involving anorexia).

4 a, hyperbilirubinemia, hypophosphatemia, and anorexia.

5 heir inhibition after symptom onset reverses anorexia.

6 aracterized QT adaptation during exercise in anorexia.

7 nditure, but did not affect estrogen-induced anorexia.

8 directly engage CGRP(PBN) neurons to promote anorexia.

9 pnea, abdominal swelling, bipedal edema, and anorexia.

10 uction, suggesting a role in disease-related anorexia.

11 cell recruitment to the brain and attenuated anorexia.

12 8 T cell responses and/or CD8 T cell-induced anorexia.

13 nd lean mass during cachexia and LPS-induced anorexia.

14 (0.48-0.65 AUC), autism (0.52-0.81 AUC) and anorexia (0.62-0.69 AUC).

15 eported adverse events in the QnC group were anorexia (12 [12%] of 98 patients), abnormal behaviour (

16 Anorexia (13 [6%] of 233 patients) was the most frequent

17 reported in the re-treatment ACT group were anorexia (31 [13%] of 240 patients), asthenia (20 [8%]),

18 y (27 [23%] vs 60 [51%]), but more grade 1-4 anorexia (33 [28%] vs 10 [8%]), constipation (29 [25%] v

19 rated, with fatigue (81%), nausea (48%), and anorexia (33%) being the most frequent adverse events.

20 ablation or silencing of AgRP neurons causes anorexia [4, 5], whereas selective stimulation in fed mi

21 ents (AEs) were nausea (75%), fatigue (70%), anorexia (64%), vomiting (43%), weight loss (32%), and d

22 events included fatigue (70%), nausea (70%), anorexia (66%), and vomiting (49%), which were generally

23 ed a mean of 8.2 AEs; the most frequent were anorexia (79.2%), nausea (75.5%), headache (60.4%), amne

24 Utilizing the activity-based anorexia (ABA) model and touchscreen operant learning pa

25 BL/6N mice were tested in the activity-based anorexia (ABA) model, with an extended period of food re

26 rogression of AN behaviors in activity-based anorexia (ABA) models, while SIRT1 activation accelerate

27 Activity-based anorexia (ABA), which refers to the weight loss, hypopha

28 models of schizophrenia, bipolar, autism or anorexia across 13 studies.

29 eural mechanisms mediating cisplatin-induced anorexia, advancing opportunities to develop better-tole

30 ivity, an estimate of fibers connections, in anorexia after recovery in tracts that connect taste-rew

31 nse physical effort, and was associated with anorexia and asthenia.

32 Results show that the anorexia and body weight changes induced by administrati

33 ceptor blockade attenuates cisplatin-induced anorexia and body weight loss in addition to pica, demon

34 and melanocortin receptors 3/4 reversed the anorexia and body weight loss induced by TLR2 activation

35 N-->CeA neurons attenuated cisplatin-induced anorexia and body weight loss significantly.

36 -->lPBN neurons attenuated cisplatin-induced anorexia and body weight loss significantly.

37 ral amygdala) PACAP dose-dependently induced anorexia and body weight loss without affecting locomoto

38 eceptor signaling mediates cisplatin-induced anorexia and body weight loss.

39 ns and are resistant to chemotherapy-induced anorexia and body weight loss.

40 were divided into two groups: patients with anorexia and bulimia nervosa (ABN; n = 30) and control p

41 Older women appear less likely to exhibit anorexia and bulimia nervosa and more likely to exhibit

42 Anorexia and bulimia nervosa are associated with poor pe

43 Anorexia and bulimia nervosa can have significant effect

44 ion at candidate genes (n = 13), focusing on anorexia and bulimia nervosa in very small samples with

45 ed quality of life (OHRQoL) in patients with anorexia and bulimia nervosa.

46 We used 3 rat models of anorexia and cachexia (LPS, methylcholanthrene sarcoma,

47 s with advanced cancer frequently experience anorexia and cachexia, which are associated with reduced

48 a treatment option for patients with cancer anorexia and cachexia.

49 endocrine, immune and nervous systems drive anorexia and catabolic changes in adipose tissue and ske

50 otherapies and adjuvant therapies to prevent anorexia and concurrent nutritional deficiencies during

51 as statistically significant class effect on anorexia and diarrhea AEs.

52 Anorexia and early satiety are common, but putative caus

53 ased energy intake and expenditure, although anorexia and higher weight loss have been reported in el

54 Melancholic patients experience anorexia and insomnia, whereas atypical patients experie

55 ) neurons before tumor implantation prevents anorexia and loss of lean mass, and their inhibition aft

56 randial aversive symptoms, which can lead to anorexia and malnutrition.

57 iting neutrophils to the brain, which drives anorexia and muscle catabolism.

58 nocortin pathway is central for P-NT-induced anorexia and necessary for the full synergistic effect o

59 between anorexia nervosa and schizophrenia, anorexia and obesity, and educational attainment and sev

60 targets for feeding-related diseases such as anorexia and obesity.

61 e of the activation of stress systems can be anorexia and subsequent weight loss, and both the activa

62 reas through which the PACAP system promotes anorexia and that PACAP preferentially lessens the maint

63 ease (ESKD) are considered at risk of uremic anorexia and underweight they are also exposed to the gl

64 in vivo studies demonstrated that 4c induces anorexia and weight loss in obese, but not in lean mice.

65 neuroanatomical circuit driving pathological anorexia and weight loss that accompanies chemotherapy t

66 y used to treat cancers despite accompanying anorexia and weight loss that may limit treatment adhere

67 ion in posterior BNST subregions can produce anorexia and weight loss, and corroborate growing data i

68 ting GFRAL as the receptor for GDF15-induced anorexia and weight loss, we identify a mechanistic basi

69 n neurons are required for cisplatin-induced anorexia and weight loss, we inhibited these neurons che

70 -forebrain projections for cisplatin-induced anorexia and weight loss.

71 fective treatments for, chemotherapy-induced anorexia and weight loss.

72 ull expression of cisplatin-induced malaise, anorexia, and body weight loss.

73 during hospitalization were fever, weakness, anorexia, and diarrhea, although 21% of patients were in

74 Mucositis, anorexia, and dizziness were more prevalent in the rotat

75 -HT2C, receptor is critical for weight loss, anorexia, and fat mass reduction induced by central GLP-

76 events (grade 1 or 2) were nausea, vomiting, anorexia, and fatigue, which were well managed with supp

77 adaptive sickness behaviors (e.g., fatigue, anorexia, and fever) and neuroinflammatory pathways are

78 3.2% v. 33.3%, respectively), rash, fatigue, anorexia, and hypokalemia, but not more late toxicity.

79 Patients with CKD suffer from food aversion, anorexia, and malnutrition.

80 s balanced between groups, including nausea, anorexia, and musculoskeletal pain, most of mild severit

81 iated with sickness responses such as fever, anorexia, and stress hormone release.

82 They typically have a history of lethargy, anorexia, and weight loss in the months preceding the il

83 episode (MDE), such as low mood, anhedonia, anorexia, and weight loss.

84 pathogen; significance of infection-induced anorexia; and redefinition of the role of iron during in

85 Weight loss and anorexia are common symptoms in cancer patients that occ

86 identify CD8 T cell responses and downstream anorexia as driver mechanisms of microbial dysbiosis aft

87 Temporary anorexia associated with an infection is often beneficia

88 ogical conditions such as in the fatigue and anorexia associated with autoimmune diseases, with major

89 Loss of appetite or anorexia associated with inflammation impairs quality of

90 less likely than nonpregnant women to report anorexia, asthenia, diarrhea, fever, myalgias/arthralgia

91 in two of three symptoms (pain, fatigue, or anorexia) at week 8 compared with baseline measurements.

92 s a multifactorial syndrome characterized by anorexia, body wasting, and muscle and adipose tissue lo

93 Mothers in many species enter a period of anorexia but must preserve sufficient reserves to fuel h

94 was not an indirect consequence of fever or anorexia but that it constituted an independent inflamma

95 l pathogen, Salmonella Typhimurium, inhibits anorexia by manipulating the gut-brain axis.

96 Cancer anorexia-cachexia syndrome is associated with increased

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

98 cal response profile in patients with cancer anorexia-cachexia syndrome.

99 betes, nonalcoholic fatty liver disease, and anorexia-cachexia syndrome.

100 markers, and safety in patients with cancer anorexia-cachexia.

101 lity of life by the Functional Assessment of Anorexia/Cachexia Therapy (FAACT) questionnaire.

102 Typhimurium effector, SlrP, prevented anorexia caused by IL-1beta-mediated signaling to the hy

103 Silencing of these neurons attenuates the anorexia caused by these inflammatory signals.

104 for work-up because of generalized fatigue, anorexia, chronic diarrhea, and weight loss.

105 Anorexia could be exploited to improve disease managemen

106 peripheral neuropathy, nausea, constipation, anorexia, diarrhea, and vomiting.

107 , Wang et al. identify that sickness-induced anorexia differentially shapes the metabolic requirement

108 severity for nausea, vomiting, constipation, anorexia, dysgeusia, diarrhea, fatigue, pain, paresthesi

109 e present a case of a 84-year-old woman with anorexia, dysphagia and unintentional weight loss initia

110 to illustrate how shifts in the magnitude of anorexia (e.g., via drugs) affect disease dynamics and v

111 ated with being a MVD case included hiccups, anorexia, fatigue, vomiting, sore throat, and difficulty

112 s of infection have included fever, malaise, anorexia, gastrointestinal complaints, thrombocytopenia,

113 haracterized by abdominal pain, weight loss, anorexia, generalized weakness, and fatigue.

114 eloped sickness behavior symptoms, including anorexia, hypoactivity, and hyperthermia.

115 thalamus (DMH) of rats with exercise-induced anorexia, implying that central TTR may also play a func

116 k cycle escalates into bulimia for many, and anorexia in a few.

117 nutrient self-medication and illness-induced anorexia in caterpillars of the African armyworm (Spodop

118 s clarify the complex and contextual role of anorexia in host-pathogen interactions and suggest that

119 wn of regulation associated with obesity and anorexia in humans?

120 Here, we investigated the role of anorexia in models of bacterial and viral infections.

121 st defenses, pathogen-mediated inhibition of anorexia increased host survival.

122 Anorexia is a common manifestation of chronic diseases,

123 Sickness-induced anorexia is a conserved behavior induced during infectio

124 Although induction of anorexia is a well-documented effect of PACAP, the centr

125 hanism that mediates inflammation-associated anorexia is still poorly understood.

126 itioned taste and place aversions, while the anorexia it causes can be blocked by a monoclonal antibo

127 response in adipose tissue independently of anorexia, leading to reduced adipose and muscle mass and

128 This anorexia leads to inadequate protein and energy intake,

129 stereotypic behavioral responses, including anorexia, lethargy, and social withdrawal.

130 re we investigate the contribution to cancer anorexia made by calcitonin gene-related peptide (CGRP)

131 ease melanocortin signaling tone, leading to anorexia, metabolic changes, and eventual cachexia.

132 ferase (n = 2), diarrhea (n = 1), and nausea/anorexia (n = 1).

133 (n=1), diarrhoea (n=1), hypokalaemia (n=1), anorexia (n=1), and dehydration (n=1), and no grade 4 ad

134 nced a dose-limiting toxicity, most commonly anorexia, nausea, or fatigue.

135 y patients and physicians of six toxicities (anorexia, nausea, vomiting, constipation, diarrhea, and

136 tate of the science, with a primary focus on anorexia nervosa (AN) and binge-eating behavior, and enc

137 Patients with anorexia nervosa (AN) and obesity (OB) were investigated

138 Both anorexia nervosa (AN) and obesity are complicated by aff

139 Anorexia nervosa (AN) and obsessive-compulsive disorder

140 Diagnoses for anorexia nervosa (AN) and other eating disorders (OED: b

141 tion between ADHD and various EDs, including anorexia nervosa (AN) and other EDs such as bulimia nerv

142 Anorexia nervosa (AN) and related eating disorders are c

143 sensitivity to reward, yet individuals with anorexia nervosa (AN) are not motivated to eat when star

144 ntless pursuit of thinness, individuals with anorexia nervosa (AN) engage in maladaptive behaviors (r

145 al body weight is disrupted in patients with anorexia nervosa (AN) for prolonged periods of time.

146 Anorexia nervosa (AN) is a complex and heritable eating

147 Anorexia nervosa (AN) is a complex neuropsychiatric diso

148 Anorexia nervosa (AN) is a devastating psychiatric illne

149 Anorexia nervosa (AN) is a serious disorder with high ra

150 Anorexia nervosa (AN) is a serious eating disorder chara

151 Anorexia nervosa (AN) is a serious eating disorder chara

152 Anorexia nervosa (AN) is an eating disorder observed pre

153 Anorexia nervosa (AN) is characterized by a persistent r

154 Anorexia Nervosa (AN) is characterized by Diagnostic and

155 Anorexia nervosa (AN) is characterized by extremely low

156 Individuals with anorexia nervosa (AN) override the drive to eat, forgoin

157 Individuals with anorexia nervosa (AN) restrict eating and become emaciat

158 ed a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently defined phenot

159 e heightened tolerance to self-starvation in anorexia nervosa (AN), a hypothalamic dysregulation of e

160 prospectively correlate with future onset of anorexia nervosa (AN), bulimia nervosa (BN), binge eatin

161 isms was suggested in the pathophysiology of anorexia nervosa (AN), but the role of the endogenous me

162 distribution has previously been studied in anorexia nervosa (AN), its influence in women with AN on

163 n multiple psychiatric conditions, including anorexia nervosa (AN).

164 sed physical activity is a common feature of anorexia nervosa (AN).

165 The study included 30 women with anorexia nervosa (mean age +/- standard deviation, 26 ye

166 articles and conference abstracts addressing anorexia nervosa (n = 13), bulimia nervosa (n = 6), and

167 o-controlled trial of adult outpatients with anorexia nervosa (N=152, 96% of whom were women; the sam

168 METHOD: Female adolescents with anorexia nervosa (N=21; mean age, 16.4 years [SD=1.9]) u

169 were aged 20-60 years and had a diagnosis of anorexia nervosa (restricting or binge-purging subtype)

170 Research in Anorexia Nervosa (RIAN) is a 2-group (FBT and SyFT) rand

171 Similar results were found for anorexia nervosa (suicide attempts: crude, 4.42 [4.12-4.

172 ed meal, 26 women who were in remission from anorexia nervosa (to avoid the confounding effects of ma

173 Anorexia nervosa affects 1-4% of women in United States

174 d circuit white matter fiber organization in anorexia nervosa after recovery could indicate a biologi

175 Anorexia nervosa also has large and significant genetic

176 The lifetime prevalence of DSM-5 anorexia nervosa among women might be up to 4%, and of b

177 ility, and genetic correlations (rg) between anorexia nervosa and 159 other phenotypes.

178 Sixty-one adolescent female patients with anorexia nervosa and 45 age- and sex-matched healthy vol

179 me-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight

180 examine DNA methylation across the genome of anorexia nervosa and binge-eating disorder patients.

181 e genetic correlations were observed between anorexia nervosa and body mass index, insulin, glucose,

182 agnosis EDNOS, by lowering the threshold for anorexia nervosa and bulimia nervosa, and adding BED as

183 w is reflected by the diagnostic criteria of anorexia nervosa and bulimia nervosa, which emphasize in

184 Similar patterns were found for anorexia nervosa and bulimia nervosa.

185 conducted a genome-wide association study of anorexia nervosa and calculated genetic correlations wit

186 literature on the development and course of anorexia nervosa and interpreted critical features in li

187 nalysis of the lumbar spine in patients with anorexia nervosa and normal-weight control subjects and

188 Women with anorexia nervosa and normal-weight control subjects were

189 tly are no significantly associated SNPs for anorexia nervosa and only three for educational attainme

190 disorders: stabilization of the incidence of anorexia nervosa and possibly lower incidence rates of b

191 results include genetic correlations between anorexia nervosa and schizophrenia, anorexia and obesity

192 e genetic correlations were observed between anorexia nervosa and schizophrenia, neuroticism, educati

193 processes are engaged in the development of anorexia nervosa and that stimulus-response learning (th

194 s further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder.

195 We also found an enrichment of anorexia nervosa associated genes in the adult and fetal

196 ases to promote eating, yet individuals with anorexia nervosa avoid food despite emaciation.

197 ves our understanding of the neurobiology of anorexia nervosa by suggesting disturbances in subcortic

198 in 12 case-control cohorts comprising 3,495 anorexia nervosa cases and 10,982 controls, the authors

199 hat genes from an induced stem cell study of anorexia nervosa cases are expressed at higher levels in

200 sted how brain reward learning in adolescent anorexia nervosa changes with weight restoration.

201 Patients with anorexia nervosa exhibit abnormal myocardial repolarizat

202 lled female patients (aged 11-18 years) with anorexia nervosa from six centres in Germany.

203 Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI)(8,9) and the

204 amen functional connectivity in the remitted anorexia nervosa group compared with the control group.

205 Compared with the control group, the anorexia nervosa group exhibited greater brain response

206 sponse in the control group and the remitted anorexia nervosa group, with an increase and a decrease,

207 avoidance among participants in the remitted anorexia nervosa group.

208 Results Women with anorexia nervosa had higher skewness and kurtosis, lower

209 Conclusion Patients with anorexia nervosa had increased skewness and kurtosis and

210 Anorexia nervosa has the highest mortality rate of any p

211 y, several large population-based studies of anorexia nervosa have been conducted in twins; it is pos

212 ubset of patients suffering from restrictive anorexia nervosa have enhanced habit formation compared

213 nervosa subtype predicted fatal outcome for anorexia nervosa in males.

214 at birth had an independent association with anorexia nervosa in males.

215 cterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness(1), af

216 Anorexia nervosa is a complex eating disorder with genet

217 Anorexia nervosa is a complex heritable phenotype for wh

218 Anorexia nervosa is a life-threatening illness.

219 Anorexia nervosa is a psychiatric disorder of unknown et

220 Anorexia nervosa is a severe psychiatric disorder associ

221 Anorexia nervosa is an important cause of physical and p

222 A core feature of anorexia nervosa is an over-estimation of body size.

223 Anorexia nervosa is prevalent in adolescents and young a

224 The genetic architecture of anorexia nervosa mirrors its clinical presentation, show

225 care in adolescent patients with non-chronic anorexia nervosa seems no less effective than IP for wei

226 Anorexia nervosa shows a stronger genetic correlation wi

227 and lower BMI at admission, and restrictive anorexia nervosa subtype predicted fatal outcome for ano

228 Brain circuits believed to drive anorexia nervosa symptoms can be accessed with surgical

229 ions may represent a phenotype of adolescent anorexia nervosa that does not respond well to treatment

230 contribute information about bone health in anorexia nervosa that is independent of that provided wi

231 usal genes from the largest genetic study of anorexia nervosa to date were enriched for expression in

232 This model helps explain the resistance of anorexia nervosa to interventions that have established

233 Adults with anorexia nervosa too have a realistic chance of achievin

234 The h(2)SNP of anorexia nervosa was 0.20 (SE=0.02), suggesting that a s

235 Anorexia nervosa was independently predicted by multiple

236 16 patients with treatment-refractory anorexia nervosa were enrolled between September, 2011,

237 tem responsiveness is elevated in adolescent anorexia nervosa when underweight and after weight resto

238 emor) = 39; n(treatment-resistant depression/anorexia nervosa) = 76) to identify the neuroanatomical

239 ttention-deficit/hyperactivity disorder, and anorexia nervosa) and 17 nonpsychiatric traits in more t

240 80 females (0.70%) and 453 males (0.04%) had anorexia nervosa, and 3349 females (0.30%), and 61 males

241 aptured by 3 variables (any eating disorder, anorexia nervosa, and bulimia nervosa) identified by any

242 lian randomization identifies schizophrenia, anorexia nervosa, and higher education as causal for dec

243 rption syndrome, inflammatory bowel disease, anorexia nervosa, and intestinal pseudo-obstruction.

244 uals born in 1975-1998 and followed them for anorexia nervosa, bulimia nervosa, and eating disorder n

245 rs are now recognised in diagnostic systems: anorexia nervosa, bulimia nervosa, binge eating disorder

246 moderately-to-severely ill adolescents with anorexia nervosa, but it is costly, and the risks of rel

247 placebo on weight in adult outpatients with anorexia nervosa, but no significant benefit for psychol

248 n patients with chronic treatment-refractory anorexia nervosa, DBS is well tolerated and is associate

249 isorder, depression, suicide, schizophrenia, anorexia nervosa, migraine, dementia, and PD.

250 ixteen deaths (6.5%) were recorded (lifetime anorexia nervosa, N=14; bulimia nervosa with no history

251 sa, N=14; bulimia nervosa with no history of anorexia nervosa, N=2).

252 For adults with anorexia nervosa, no one specialist treatment has been s

253 enetic correlation between the Eyes Test and anorexia nervosa, openness (NEO-Five Factor Inventory),

254 t, particularly for adolescent patients with anorexia nervosa, point to the benefits of specialised f

255 learning-based interventions for addiction, anorexia nervosa, schizophrenia, and depression.

256 Two patterns emerge: (1) anorexia nervosa, schizophrenia, obsessive-compulsive di

257 aking to eat is crucial for survival, but in anorexia nervosa, the brain persistently supports reduce

258 The authors found that individuals with anorexia nervosa, who make maladaptive food choices to t

259 Given the progress of genomic discovery in anorexia nervosa, with the identification of the first g

260 hanges in cerebral glucose metabolism in key anorexia nervosa-related structures at both 6 months and

261 I), mood, anxiety, affective regulation, and anorexia nervosa-specific behaviours at 12 months after

262 ggesting a combination of re-nourishment and anorexia nervosa-specific psychotherapy is most effectiv

263 ifetime weight and duration of amenorrhea in anorexia nervosa.

264 of obesity, dieting-induced weight gain, and anorexia nervosa.

265 degenerative diseases, obesity, bulimia, and anorexia nervosa.

266 insensitivity to these effects of hunger in anorexia nervosa.

267 or the treatment of eating disorders such as anorexia nervosa.

268 dynamics as a risk factor for arrhythmias in anorexia nervosa.

269 rtium Stage 1 and the Genetic Consortium for Anorexia Nervosa.

270 iety, depression, and the psychopathology of anorexia nervosa.

271 proach in patients with, or recovering from, anorexia nervosa.

272 it was their first admission to hospital for anorexia nervosa.

273 riods of extremely restricted food intake in anorexia nervosa.

274 ared with placebo for adult outpatients with anorexia nervosa.

275 mbocytopenia (13 [33%]), anaemia (11 [28%]), anorexia (nine [23%]), and oral mucositis (four [10%]).

276 Provision of glucose during anorexia of infection rescued effector T cells, suggesti

277 tial therapeutic target for the treatment of anorexia or other appetite disorders.

278 ocial phobia, obsessive-compulsive disorder, anorexia, or substance abuse), along with their mates.

279 s was associated with malaise (P = .007) and anorexia (P = .02), with previous giardiasis (P = .03),

280 ter infection, 6.7 days), fever, depression, anorexia, petechial rash, and lymphopenia.

281 SlrP-mediated inhibition of anorexia prevented invasion and systemic infection by wi

282 and pharmacological mechanisms mediating the anorexia produced by PACAP in the central nucleus of the

283 Women recovered from restricting-type anorexia (Recovered AN, n = 24, age = 30.3 +/- 8.1 years

284 en 3D scans of 15 women who have symptoms of anorexia (referred to henceforth as anorexia spectrum di

285 ized by cough, asthenia, sensory neuropathy, anorexia, serum sickness, and hypertensive encephalopath

286 ptoms of anorexia (referred to henceforth as anorexia spectrum disorders, ANSD) and 15 healthy contro

287 e side effects such as nausea, vomiting, and anorexia that compromise quality of life and limit treat

288 most adverse effects, ranging from 0.10 for anorexia to 0.54 for vomiting (Cohen kappa statistic).

289 We explore how hosts use anorexia to defend against infection and how parasites m

290 ainst infection and how parasites manipulate anorexia to enhance transmission.

291 verse events were fatigue, nausea, diarrhea, anorexia, vomiting, peripheral sensory neuropathy, and k

292 Intra-CeA PACAP-induced anorexia was blocked by coinfusion of either the melanoc

293 We found that anorexia was protective while nutritional supplementatio

294 Anorexia was significantly more important among colorect

295 ate quality of life (e.g., nausea, vomiting, anorexia, weight loss).

296 lead to elevated GDF15 serum levels, causing anorexia, weight loss, and alterations to metabolism, la

297 n of high-dose drug, which elicits lethargy, anorexia, weight loss, and peritoneal fibrosis, all of w

298 Vomiting, nausea, asthenia/fatigue, and anorexia were common but not severe.

299 gene slc24a4 or Nckx4), display a remarkable anorexia with severe hypophagia and weight loss.

300 ry of left inguinocrural and lumbar pain and anorexia with weight loss.