ライフサイエンスコーパス: severe obesity

1 markedly enhanced food intake, resulting in severe obesity.

2 y to prevent cardiovascular complications in severe obesity.

3 y, except for those with at least moderately severe obesity.

4 nical trials have evaluated the treatment of severe obesity.

5 ntly associated with incident obesity and/or severe obesity.

6 Similar results were found for severe obesity.

7 had mild developmental delay in addition to severe obesity.

8 ree patients the deletion co-segregated with severe obesity.

9 s needed on the prognostic influence of more severe obesity.

10 ricular function in patients with clinically severe obesity.

11 is mediated some of the protective effect of severe obesity.

12 tly increase the risk of obesity, especially severe obesity.

13 in obese individuals, especially those with severe obesity.

14 ed with depression mainly among persons with severe obesity.

15 omized 7B2 nulls also developed unexpectedly severe obesity.

16 function mutations has been associated with severe obesity.

17 fibrillation among persons being treated for severe obesity.

18 number of genes that when mutated result in severe obesity.

19 as its absence in rodents and humans causes severe obesity.

20 eptin, were used to study the role of p55 in severe obesity.

21 r the treatment of obesity, in patients with severe obesity.

22 racial differences in obesity, specifically severe obesity.

23 n or resistance to the protein leptin causes severe obesity.

24 ent of anticoagulant dosing in patients with severe obesity.

25 is (LF) in European cohorts of patients with severe obesity.

26 ement and reduce mortality for patients with severe obesity.

27 these important outcomes in adolescents with severe obesity.

28 rove insulin sensitivity in individuals with severe obesity.

29 s currently the most effective treatment for severe obesity.

30 from mice or humans leads to hyperphagia and severe obesity.

31 fter surgical and conventional treatments of severe obesity.

32 ient to achieve weight loss in patients with severe obesity.

33 adipose tissues of patients with T2D and/or severe obesity.

34 eased risk, particularly for long-lasting or severe obesity.

35 r acute ischemic stroke, less is known about severe obesity.

36 (95% UI, 2.43 to 3.65) for 19-year-olds with severe obesity.

37 s in leptin and the LepR have low BP despite severe obesity.

38 es in bone and mineral metabolism related to severe obesity.

39 tant from insulin-sensitive individuals with severe obesity.

40 skeletal muscle insulin sensitivity, despite severe obesity.

41 variants influencing BMI also contribute to severe obesity, a condition at the extreme of the phenot

42 Among patients with severe obesity, a lifestyle intervention involving diet

43 OB mothers developed severe obesity accompanied by higher maternal and fetal

44 Severe obesity affects 4% to 6% of US youth and is incre

45 Severe obesity afflicts between 4% and 6% of all youth i

46 an independent sample of 1,062 patients with severe obesity alone, the smaller 16p11.2 deletion was f

47 subjects were characterized by hyperphagia, severe obesity, alterations in immune function, and dela

48 udy suggested that the greater prevalence of severe obesity among African-American women explained al

49 The higher prevalence of severe obesity among black women may play an important r

50 The prevalence of severe obesity among children and young adults has incre

51 se methods were applied to a large data set, severe obesity and BIV prevalence ranged from 7.2% to 8.

52 Ms J is a 52-year-old woman with severe obesity and depression, anxiety, and osteoarthrit

53 exact role of surgery in patients with less severe obesity and diabetes are considered a priority.

54 in or its receptor have been associated with severe obesity and diabetes, such mutations do not appea

55 sessed metabolic alterations associated with severe obesity and distinct bariatric procedures.

56 Further validation in cohorts with severe obesity and engineering the variants in model org

57 ing performed on adolescents with clinically severe obesity and experience suggests that it is effect

58 because disruption of the POMC gene leads to severe obesity and hyperphagia.

59 on in POMC in a child of Turkish origin with severe obesity and hypoadrenalism.

60 E1m-/+ mice had more severe obesity and insulin resistance and lower metaboli

61 leus (Arc)POMC-deficient mice, which develop severe obesity and insulin resistance, unexpectedly exhi

62 tion, a macrophage phenotype associated with severe obesity and insulin resistance.

63 2 diabetes in cells and in a mouse model of severe obesity and insulin resistance.

64 othalamus and paraventricular nucleus showed severe obesity and insulin resistance.

65 is occurring in conjunction with the rise of severe obesity and is probably mediated in part by metab

66 ective and increasingly common treatment for severe obesity and its many comorbidities.

67 ither leptin or its receptor (LepR) leads to severe obesity and metabolic disorders.

68 c bypass (RYGB) is an effective treatment of severe obesity and one of the fastest growing surgical p

69 he management of adolescents with clinically severe obesity and should be performed by specialists de

70 ency or resistance, respectively, results in severe obesity and the development of a syndrome resembl

71 atory cases, including those associated with severe obesity and vocal cord dysfunction (VCD).

72 ader-Willi-like syndrome features (including severe obesity) and 4 other rare variants (p.T46R, p.E62

73 rweight, mild obesity, moderate obesity, and severe obesity) and fibrosis stage (F0-F3).

74 MC) results in a syndrome of hypoadrenalism, severe obesity, and altered skin and hair pigmentation.

75 acious and enduring treatment for clinically severe obesity, and as a result, the number of bariatric

76 general population, obesity and, especially, severe obesity are consistently and strongly related wit

77 Advice 2: EBTs can be used in patients with severe obesity as a bridge to traditional bariatric surg

78 ht children and adolescents progress towards severe obesity as adults.

79 chromosomal loci existed that were linked to severe obesity, as well as to utilize the increased heri

80 nding--62+/-52 months ago for the control of severe obesity associated with PTC.

81 firm link between SIM1 loss of function and severe obesity associated with, or independent of, Prade

82 went Roux-en-Y gastric bypass for clinically severe obesity at a paediatric academic medical centre i

83 ted deletion of Mrap2, both of which develop severe obesity at a young age.

84 a staged approach for surgical treatment of severe obesity between January 2002 and February 2004.

85 kg/m2) increased markedly, and prevalence of severe obesity (BMI > or = 40.0 kg/m2) doubled in all ra

86 sk prediction overall, even among those with severe obesity (BMI >/=35 kg/m(2); improvement in C stat

87 cular disease, cerebrovascular accident, and severe obesity (body mass index > or = 35 kg/m2).

88 esity (body mass index > or =30 kg/m(2)) and severe obesity (body mass index > or =35 kg/m(2)) was ev

89 Severe obesity (body mass index >/=35 [calculated as wei

90 ditions, except that EA had a higher rate of severe obesity (body mass index >35).

91 Severe obesity (body mass index [BMI] >/=35) is associat

92 dren and adolescents aged 8 to 18 years with severe obesity (body mass index [BMI] z score, >/=3.0 or

93 Severe obesity (body mass index of >or=35: RR = 1.29, 95

94 Class 3 (severe) obesity (body mass index > or =40) was associate

95 idered for the treatment of adolescents with severe obesity, but few prospective adolescent-specific

96 urgery improves survival among patients with severe obesity, but research among veterans has shown no

97 GBS is increasingly used to treat severe obesity, but there are limited outcome data.

98 c mouse model of early-onset hyperphagia and severe obesity by selectively blocking the expression of

99 Severe obesity can result in proteinuria and progressive

100 A total of 1156 patients with severe obesity comprised three groups: 418 patients who

101 he impact of mild (D-BMI, 30-35 kg/m) versus severe obesity (D-BMI, >/=35 kg/m) on pancreas allograft

102 long-term outcomes are few, many youth with severe obesity do not qualify for surgery, and access is

103 d Koletsky (fa(k)/fa(k)) rats, which develop severe obesity due to the genetic absence of leptin rece

104 -) and heterozygotic (neil1+/-) mice develop severe obesity, dyslipidemia, and fatty liver disease an

105 ctomy as a definitive therapeutic option for severe obesity, even in high-risk, high-BMI patients.

106 mutations in MC4R are a significant cause of severe obesity, extending this finding to North American

107 The severe obesity found in these congenitally leptin-defici

108 in 262 Caucasian subjects with a history of severe obesity from childhood.

109 y and other risk factors, male patients with severe obesity-grade 3 obesity [adjusted odds ratio (AOR

110 Patients with severe obesity (> or =35) did not have increased total m

111 y (30.0-34.9 kg/m(2)), and class II and III (severe) obesity (>/=35.0 kg/m(2)).

112 Male and female patients with severe obesity had a 2.5- to 4-fold higher risk of devel

113 Although severe obesity has received much attention in the clinic

114 -based treatment interventions in youth with severe obesity have demonstrated modest improvement in b

115 Adolescents with severe obesity have musculoskeletal pain that limits the

116 ptin deficiency, which includes hyperphagia, severe obesity, hypogonadism, and impaired immunity, has

117 ost-effective treatment for adolescents with severe obesity if assessed over a time horizon of 5 year

118 Adjustment for severe obesity in a logistic regression model reduced th

119 therapy use predict incident obesity and/or severe obesity in a multiracial cohort of women transiti

120 of the orexin neurons develop hypophagia and severe obesity in addition to the narcolepsy phenotype.

121 Severe obesity in adolescence is associated with reduced

122 eceptor agonist therapy for the treatment of severe obesity in adolescents.

123 ED displayed a markedly higher prevalence of severe obesity in adulthood (body mass index >/=40) than

124 over time to determine whether they develop severe obesity in adulthood, thus limiting effective int

125 y associated with increased risk of incident severe obesity in adulthood, with variations by sex and

126 of-function mutations in either gene causing severe obesity in both mice and humans.

127 Severe obesity in childhood is a major health problem wi

128 associated with adult obesity and a few with severe obesity in childhood; however, less progress has

129 r and recommend a standardized definition of severe obesity in children and adolescents; (2) raise aw

130 Severe obesity in children and young adults was associat

131 genetic variation in TBC1D1 confers risk for severe obesity in females.

132 percentage of the genetic predisposition to severe obesity in females.

133 ignaling to energy balance dysregulation and severe obesity in humans and rodents.

134 C1D1 R125W missense variant confers risk for severe obesity in humans.

135 of the MC4R promoter may also be a cause of severe obesity in humans.

136 MC4R promoter is not a significant cause of severe obesity in humans.

137 Its disruption causes severe obesity in mice and humans.

138 unction of MC4R or MC3R were associated with severe obesity in North American adults.

139 te hormone leptin and the demonstration that severe obesity in ob/ob and db/db mice results from muta

140 in 4 receptor in the PVN, is responsible for severe obesity in our subject.

141 determine whether MC4R has a role in causing severe obesity in Pima Indians, we sequenced the coding

142 e of its natural variants, Ob-Ra, results in severe obesity in rodents.

143 or of energy homeostasis and its loss causes severe obesity in rodents.

144 diagnosis in any child with hyperphagia and severe obesity in the absence of developmental delay or

145 that MC3R mutations are not associated with severe obesity in this population.

146 confirmed in an independent linkage study of severe obesity in Utah pedigrees.

147 ts were significantly more likely to develop severe obesity in young adulthood than normal-weight or

148 s limiting effective interventions to reduce severe obesity incidence and its potentially life-threat

149 -age growth chart or BMI >/=30.0) on risk of severe obesity incidence in adulthood (aged >/=20 years;

150 Of the 206 adolescents with severe obesity included in the study, 156 were female (7

151 The odds of incident severe obesity increased with surgical menopause (odds r

152 revalent among children and adolescents with severe obesity, irrespective of ethnic group.

153 ishing weight loss is the determination that severe obesity is a disease associated with multiple adv

154 Severe obesity is associated with a risk of lower extrem

155 Severe obesity is associated with increased poststroke m

156 Severe obesity is associated with mobility limitations a

157 Severe obesity is associated with multiple comorbidities

158 e that bariatric surgery in adolescents with severe obesity is associated with significant improvemen

159 urgery for the treatment of adolescents with severe obesity is becoming more common, but data on cost

160 Severe obesity is common before and after liver transpla

161 Treatment of severe obesity is difficult; in the past, lifestyle meas

162 Severe obesity is frequently associated with significant

163 The prevalence of severe obesity is increasing markedly, as is prevalence

164 Severe obesity is increasingly common in the adolescent

165 The prevalence of severe obesity is rising in the United States.

166 anial hypertension), a known complication of severe obesity, is associated with severe headaches, pul

167 ntrols identified 4 new loci associated with severe obesity (LEPR, PRKCH, PACS1 and RMST).

168 ery is the most cost-effective treatment for severe obesity, less than 1% of severely obese patients

169 On average, individuals with severe obesity lived 10 fewer years without glucose impa

170 a, with low level lead intoxication, or with severe obesity/metabolic syndrome.

171 port a 19-year-old male with hyperphagia and severe obesity, mild learning difficulties and hypogonad

172 re well known to cause leptin deficiency and severe obesity, no common loci regulating circulating le

173 However, despite severe obesity, ob/ob-aP2-mal1(-/-) mice remained euglyc

174 gain a better understanding of the impact of severe obesity on trauma outcomes.

175 dds ratio [OR], 2.47; 95% CI, 1.36 to 4.51), severe obesity (OR, 4.04; 95% CI, 1.46 to 11.19), and ed

176 associated with the risk of type 2 diabetes, severe obesity, or marked hyperinsulinemia, but that the

177 EGR1 locus was significantly associated with severe obesity (P = 6.6 x 10(-7)).

178 of the DOCK5 VNTRs with childhood and adult severe obesity (P(empirical)= 8.9 x 10(-8) and P= 3.1 x

179 In this series, adolescents with severe obesity presented with abundant comorbid conditio

180 surgery is the most effective treatment for severe obesity, producing marked sustained weight loss w

181 years, cumulative incidences of obesity and severe obesity reached 21.8% and 12.3%, respectively.

182 20%; adjustment for both waist:hip ratio and severe obesity reduced the odds ratio by 27%.

183 ot associated with an increased YLL and only severe obesity resulted in YLL.

184 These data suggest that GBP surgery for severe obesity should be provided earlier to patients to

185 d be considered for patients with clinically severe obesity, since currently it appears to offer the

186 alterations in each of these axes result in severe obesity, such cases remain rare.

187 ic surgery is the most effective therapy for severe obesity that can reduce body weight and obesity-a

188 ostatic control system is highlighted by the severe obesity that results from dysfunction of any of s

189 For children with severe obesity, the chance they will no longer be obese

190 Among participants with severe obesity, there was substantial weight loss 3 year

191 Adults with severe obesity undergoing bariatric surgery were recruit

192 Among a cohort of participants with severe obesity undergoing bariatric surgery, a large per

193 study of adolescents (aged 13-18 years) with severe obesity undergoing Roux-en-Y gastric bypass at th

194 INTERPRETATION: Adolescents with severe obesity undergoing Roux-en-Y gastric bypass had s

195 eight, class 1 obesity, class 2 obesity, and severe obesity) using Kaplan-Meier methods.

196 Severe obesity was associated with an approximately twof

197 Severe obesity was associated with both race and stage a

198 Severe obesity was defined as a body-mass index (BMI, th

199 le with a complex developmental syndrome and severe obesity was heterozygous for a de novo missense m

200 verely obese (26% vs. 7%, respectively), and severe obesity was significantly associated with diagnos

201 To investigate the genetic architecture of severe obesity, we performed a genome-wide association s

202 n all F0-F3 patients with mild, moderate, or severe obesity were $48,836/QALY, $24,949/QALY, and $19,

203 ntributed to the metabolomic fingerprints of severe obesity were aromatic and branched-chain amino ac

204 Obesity and severe obesity were associated with stillbirth resulting

205 New cases of adult-onset severe obesity were calculated by sex, race/ethnicity, a

206 ensitive and insulin-resistant patients with severe obesity were compared indicate that the insulin-r

207 nalling increases food intake and results in severe obesity, whereas enhanced cholinergic signalling

208 Patients with severe obesity who are unable to reduce successfully wit

209 ty in this region in women with a history of severe obesity who have successfully lost weight (ie, fo