ライフサイエンスコーパス: obese children

1 ring childhood, especially in overweight and obese children.

2 Energy expended in activity was lower in the obese children.

3 Obese parents are more likely to have obese children.

4 hemostatic variables in a biethnic group of obese children.

5 e in regulating plasma hemostatic factors in obese children.

6 inflammation in a cohort of African American obese children.

7 appropriate weight-based dosing strategy for obese children.

8 rnatives more reinforcing than do overweight/obese children.

9 and dicarboxylated fatty acids were seen in obese children.

10 rylcarnitine, were significantly elevated in obese children.

11 creased steroid derivatives may be unique to obese children.

12 NAFLD was identified in 24% of the recruited obese children.

13 isease (NAFLD) are frequently encountered in obese children.

14 increase physical activity in overweight and obese children.

15 ficantly longer lengths of hospital stay for obese children.

16 bserved only in adults, is also occurring in obese children.

17 allele would influence the risk of NAFLD in obese children.

18 thood between MHO children and nonoverweight/obese children.

19 r the direction of evidence-based therapy in obese children.

20 ence of metabolic syndrome in overweight and obese children.

21 In total, 597 overweight or obese children (10.4%) were identified, and 219 of them

22 TC varies between 4.8% and 12.3% (higher in obese children [12.3%] and at the ages when TC naturally

23 lerance was detected in 25 percent of the 55 obese children (4 to 10 years of age) and 21 percent of

24 In obese children, 4-mo periods of physical training did no

25 Seventy-five overweight or obese children (41 girls [55%], 34 whites [45%], 20 Hisp

26 d high-sensitivity C-reactive protein in 108 obese children, 54 with (HFF >/=5%) and 54 without NAFLD

27 geal reflux scores were higher in overweight/obese children (9.6 vs 23.2; P = .003) and appear to med

28 In obese children a moderate to good correlation between CA

29 In obese children, age, vigorous activity, diet, and baseli

30 acterization of 171 AT samples from lean and obese children aged 0 to 18 years.

31 ontrolled trials conducted in overweight and obese children aged 18 years or younger, comparing dieta

32 The participants were 71 obese children aged 7-11 y (22 boys, 49 girls; 31 whites

33 me of distribution, or drug concentration in obese children (aged </=18 years).

34 nd 87 rodent obesity genes in 2,548 severely obese children and 1,117 controls.

35 < 1 x 10(-5)) in an additional 971 severely obese children and 1,990 controls identified 4 new loci

36 icroarray platform on sorted monocytes of 35 obese children and 16 lean controls.

37 We studied 455 obese children and adolescents (181 Caucasians, 139 Afri

38 s58542926 SNP in a multiethnic cohort of 957 obese children and adolescents (42% Caucasians, 28% Afri

39 do whites, although the data are limited for obese children and adolescents and for boys.

40 Severely obese children and adolescents have lower health-related

41 Instead of overweight and obese children and adolescents having higher confectione

42 pared with healthy children and adolescents, obese children and adolescents reported significantly (P

43 Obese children and adolescents show a disturbance in som

44 e risk for impaired health-related QOL among obese children and adolescents to target interventions t

45 Obese children and adolescents were more likely to have

46 In obese children and adolescents with prediabetes, intramy

47 OL total score (mean [SD], 53.8 [13.3]) than obese children and adolescents without obstructive sleep

48 ence of the metabolic syndrome is high among obese children and adolescents, and it increases with wo

49 In severely obese children and adolescents, inpatient treatment was

50 ose tolerance in a multiethnic cohort of 167 obese children and adolescents.

51 omains (mean [SD] total score, 67 [16.3] for obese children and adolescents; 83 [14.8] for healthy ch

52 Systematic screening of 431 obese children and adults for mutations in the coding se

53 Obese children and adults, particularly those with abdom

54 sociated with up to 6% frequency in morbidly obese children and adults.

55 plain the increased leukemia relapse rate in obese children and adults.

56 Obese children and African-American children were more i

57 would be useful in diagnosing overweight and obese children and in developing effective strategies fo

58 We examined these genetic variants in obese children and tested whether their effects on NAFLD

59 h and without physical training on leptin in obese children and to explore the determinants of leptin

60 ectional analysis of data from overweight or obese children and young adults 3 to 19 years of age who

61 al weight, 10.8% of overweight, and 26.9% of obese children) and age (8.9% of 9- to 11-year olds and

62 e screening and assessment of overweight and obese children, and those with an elevated WHtR should u

63 oxidative stress and inflammation evident in obese children are associated with distinct metabolomic

64 Obese children are at increased risk for developing obst

65 Prospective pharmacokinetic trials in obese children are needed to ensure therapeutic efficacy

66 besity, and altered MAIT cell frequencies in obese children are positively associated with insulin re

67 clear, reliable assessment and treatment of obese children are still wanting in many cases.

68 NASH is now a significant health issue for obese children as well, leading to cirrhosis in some.

69 Steroid derivatives were markedly higher in obese children as were markers of inflammation and oxida

70 TDEE and RMR were significantly higher in obese children, as a result of their greater fat-free ma

71 cardiovascular disease does not manifest in obese children, assessment of the subclinical markers of

72 rly understood interplay might be present in obese children, assessment of the vasculature directly,

73 Obese children (body mass index z score >1.65) and nonob

74 ences have consistently been demonstrated in obese children, but the time course and development of a

75 patic steatosis in a series of overweight or obese children by using the imperfect gold standard meth

76 escriptions of echocardiographic findings in obese children, children engaged in athletic activities,

77 The reason overweight/obese children commonly report worse asthma control rema

78 wing 13 years with normal weight status, and obese children could expect to live 9.8 years with obese

79 and a childhood cancer has been identified: obese children diagnosed with high-risk acute lymphoblas

80 Obese children displayed a distinctive monocyte gene exp

81 caregivers (PACs) as "agents of change" for obese children, evaluating the strength of evidence that

82 Obese children experience less relapse posttransplant co

83 pharmacokinetic alterations were observed in obese children for 65% (11 of 17) of the studied drugs.

84 Overweight and obese children, for example, may be more susceptible to

85 rown-like structures, was increased in AT of obese children from 6 years on and was associated with h

86 However, obese children had greater brachial diameters and restin

87 Overweight and obese children had higher heart rates (mean 72.4 +/- 11

88 Obese children had lower odds of receiving a living dono

89 A total of 23.3% of the recruited obese children had NAFLD.

90 h and without OSA at initial study; however, obese children had significantly higher insulin (106.1 +

91 Obese children had twice the risk of high DHEAS (OR: 2.1

92 Past studies of asthma in overweight/obese children have been inconsistent.

93 enditure has shown clearly that, as a group, obese children have higher energy expenditures than do t

94 esearch purporting to show that, as a group, obese children have lower energy intakes than do lean ch

95 ciation cannot rule out the possibility that obese children ingest food with higher BPA content or ha

96 NAFLD in overweight and obese children is strongly associated with multiple card

97 drug safety, pharmacokinetics, and dosing in obese children is unknown.

98 In obese children, leptin concentration decreased during 4

99 Obese children may maintain their obese state by spendin

100 etabolic flexibility in fuel use observed in obese children may occur through the activation of alter

101 Obese children may show favorable changes in their behav

102 ol (Fisher exact test; P = .003); overweight/obese children more often reported shortness of breath (

103 Plasma exosomes isolated from either obese children or nonobese children with OSA were primar

104 enerally comparable to that of nonoverweight/obese children (P > 0.05 in most cases).

105 n than in metabolically abnormal, overweight/obese children (P = 0.003).

106 the investigation and treatment of asthma in obese children, particularly in comparison with current

107 isceral adiposity in sedentary overweight or obese children, regardless of sex or race.

108 Global metabolomic profiling in nonobese and obese children replicates the increased BCAA and acylcar

109 V1 1.87 vs 0.45 mg/mL; P < .012), overweight/obese children reported more than thrice frequent rescue

110 ying the hypertrophy and hyperplasia seen in obese children, respectively.

111 es (RR = 1.08) complied more, but overweight/obese children (RR = 0.81), earlier maturing children (R

112 The obese children spent less time engaged in activity or en

113 The median number of obese children studied per drug was 10 (range, 1-112) an

114 The lower relative REE of older obese children suggests the importance of early interven

115 is linked to increased inflammation in AT in obese children, thereby providing evidence that obesity-

116 Obese children under three years of age without obese pa

117 g energy expenditure, it has been shown that obese children underreport intake significantly more tha

118 Obese children were 3-6 times more likely to have hypert

119 These alterations in AT composition in obese children were accompanied by decreased basal lipol

120 We have examined two severely obese children who are members of the same highly consan

121 nd improves obesity-related comorbidities in obese children, who are insulin-resistant.

122 Three morbidly obese children, who were congenitally deficient in lepti

123 region that includes SIM1, were reported in obese children with a Prader-Willi-like syndrome; howeve

124 he most common and is predominantly found in obese children with an early onset of walking.

125 is associated with increased morbidity among obese children with asthma and may partly explain their

126 RATIONALE: For unclear reasons, obese children with asthma have higher morbidity and red

127 compared the CD4(+) T-cell transcriptome in obese children with asthma with that in normal-weight ch

128 Among overweight/obese children with asthma, dysanapsis was associated wi

129 Overweight/obese children with early-onset asthma display poorer as

130 erefore, mediate the higher risk of death in obese children with ESRD.

131 HEAS (OR: 2.16; 95% CI: 1.51, 3.09); at 7 y, obese children with high DHEAS were fatter and more cent

132 We studied 14 obese children with impaired glucose tolerance and 14 wi

133 A significant proportion of obese children with increased WHtRs have abnormal cardio

134 Obese children with indirect lung injury pediatric acute

135 Asymptomatic obese children with NAFLD exhibit features of early LV d

136 ed for age, gender, and pubertal status, and obese children with NAFLD were matched for body mass ind

137 Obese children with newly diagnosed BP-ALL are at increa

138 growth from 0 to 7 y of age in nonobese and obese children with normal and high DHEAS (>/=75th perce

139 7 +/- 0.6 nmol/L; p = 0.005) and a trend for obese children with persisting OSA to have elevated insu

140 s with insulin resistance (pre-diabetes) and obese children with type 2 diabetes, years before overt

141 s the odds of having NAFLD as overweight and obese children without metabolic syndrome.

142 diastolic blood pressure than overweight and obese children without NAFLD.

143 o have elevated insulin levels compared with obese children without OSA (p = 0.07).