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Träfflista för sökning "WFRF:(Marcus Claude) srt2:(2005-2009)"

Sökning: WFRF:(Marcus Claude) > (2005-2009)

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1.
  • Albertsson-Wikland, Kerstin, 1947, et al. (författare)
  • Dose-dependent effect of growth hormone on final height in children with short stature without growth hormone deficiency
  • 2008
  • Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 93:11, s. 4342-4350
  • Tidskriftsartikel (refereegranskat)abstract
    • CONTEXT: The effect of GH therapy in short non-GH-deficient children, especially those with idiopathic short stature (ISS), has not been clearly established owing to the lack of controlled trials continuing until final height (FH).OBJECTIVE: The aim of the study was to investigate the effect on growth to FH of two GH doses given to short children, mainly with ISS, compared with untreated controls.DESIGN AND SETTING: A randomized, controlled, long-term multicenter trial was conducted in Sweden.INTERVENTION: Two doses of GH (Genotropin) were administered, 33 or 67 microg/kg.d; control subjects were untreated.SUBJECTS: A total of 177 subjects with short stature were enrolled. Of these, 151 were included in the intent to treat (AllITT) population, and 108 in the per protocol (AllPP) population. Analysis of ISS subjects included 126 children in the ITT (ISSITT) population and 68 subjects in the PP (ISSPP) population.MAIN OUTCOME MEASURES: We measured FH sd score (SDS), difference in SDS to midparenteral height (diff MPHSDS), and gain in heightSDS.RESULTS: After 5.9+/-1.1 yr on GH therapy, the FHSDS in the AllPP population treated with GH vs. controls was -1.5+/-0.81 (33 microg/kg.d, -1.7+/-0.70; and 67 microg/kg.d, -1.4+/-0.86; P<0.032), vs. -2.4+/-0.85 (P<0.001); the diff MPHSDS was -0.2+/-1.0 vs. -1.0+/-0.74 (P<0.001); and the gain in heightSDS was 1.3+/-0.78 vs. 0.2+/-0.69 (P<0.001). GH therapy was safe and had no impact on time to onset of puberty. A dose-response relationship identified after 1 yr remained to FH for all growth outcome variables in all four populations.CONCLUSION: GH treatment significantly increased FH in ISS children in a dose-dependent manner, with a mean gain of 1.3 SDS (8 cm) and a broad range of response from no gain to 3 SDS compared to a mean gain of 0.2 SDS in the untreated controls. 
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  • Cederholm, Tommy, et al. (författare)
  • Forskaren, samhället och jäv
  • 2008
  • Ingår i: Läkartidningen. - 0023-7205. ; 105:16, s. 7-1206
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Jacobsson, Josefin A., et al. (författare)
  • Major gender difference in association of FTO gene variant among severely obese children with obesity and obesity related phenotypes.
  • 2008
  • Ingår i: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier BV. - 0006-291X .- 1090-2104. ; 368:3, s. 476-482
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent studies have shown that SNPs in the FTO gene predispose to childhood and adult obesity. In this study, we examined the association between variants in FTO and KIAA1005, a gene that maps closely to FTO, and obesity, as well as obesity related traits among 450 well characterised severely obese children and 512 normal weight controls. FTO showed significant association with several obesity related traits while SNPs in KIAA1005 did not. When stratified by gender, the FTO variant rs9939609 showed association with obesity and BMI among girls (P=0.006 and 0.004, respectively) but not among boys. Gender differences were also found in the associations of the FTO rs9939609 with obesity related traits such as insulin sensitivity and plasma glucose. This study suggests that FTO may have an important role for gender specific development of severe obesity and insulin resistance in children.
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9.
  • Jingxiong, Jiang, 1963- (författare)
  • Intervention for Childhood Obesity in Beijing, China
  • 2006
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Childhood obesity appears to be increasing throughout the world. China has joined the global epidemic. Childhood obesity is not only a chronic disease which is associated with lifestyle, but also a public health problem in children. Obesity intervention should become a public health priority in China. This thesis reports on intervention to treat and prevent childhood obesity. The field work was implemented in Beijing, China. This thesis is based on four papers: Paper I evaluated the feasibility and impact of family-based behavior treatment on obese children. Two years of intervention resulted in obese children with improvements in body mass index, total cholesterol, triglycerides, and blood pressure. Paper II assessed the effects of a school-based intervention on obesity among primary school children. After a three-year intervention, the prevalence of overweight and obesity were significantly lower in the intervention schools than in the control schools. Fewer non-obese children became obese in the intervention schools than in the control schools. Paper III explored the family related factors of overweight in 2- to 6-year-old children. Significant associations were observed between children’s overweight and parent characteristics for frequency of eating in restaurants, daily time spent viewing television, and engaging in physical activity. Child overweight was associated with parental overweight, low maternal education level and television watching >2h/d. Paper IV investigated how grandparents influence their young grandchildren’s eating behaviors in Chinese three-generation families, using qualitative method. Three domains identified through the seven themes included: (1) Grandparents as primary caretakers of children in the three-generation family, (2) Grandparents' attitudes to child nutrition and healthy eating habits, and (3) The role of food as an educational and emotional tool. The results showed that nutrition education involving grandparents is thus a potential framework for improving healthy dietary behaviors in young children.
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10.
  • Johansson, Lovisa, et al. (författare)
  • Genetic variance in the adiponutrin gene family and childhood obesity.
  • 2009
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 4:4
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: The adiponutrin gene family consists of five genes (PNPLA1-5) coding for proteins with both lipolytic and lipogenic properties. PNPLA3 has previously been associated with adult obesity. Here we investigated the possible association between genetic variants in these genes and childhood and adolescent obesity. METHODS/RESULTS: Polymorphisms in the five genes of the adiponutrin gene family were selected and genotyped using the Sequenom platform in a childhood and adolescent obesity case-control study. Six variants in PNPLA1 showed association with obesity (rs9380559, rs12212459, rs1467912, rs4713951, rs10947600, and rs12199580, p<0.05 after adjustment for age and gender). Three variants in PNPLA3 showed association with obesity before, but not after, adjustment for age and gender (rs139051, rs12483959, and rs2072907, p>0.05). When analyzing these SNPs in relation to phenotypes, two SNPs in the PNPLA3 gene showed association with insulin sensitivity (rs12483959: beta = -0.053, p = 0.016, and rs2072907: beta = -0.049, p = 0.024). No associations were seen for PNPLA2, PNPLA4, and PNPLA5. CONCLUSIONS: Genetic variation in the adiponutrin gene family does not seem to contribute strongly to obesity in children and adolescents. PNPLA1 exhibited a modest effect on obesity and PNPLA3 on insulin sensitivity. These data, however, require confirmation in other cohorts and ethnic groups.
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