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Sökning: WFRF:(Lissner Andreas)

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1.
  • Sundström, Johan, Professor, 1971-, et al. (författare)
  • Rationale for a Swedish cohort consortium
  • 2019
  • Ingår i: Upsala Journal of Medical Sciences. - : Taylor & Francis Group. - 0300-9734 .- 2000-1967. ; 124:1, s. 21-28
  • Tidskriftsartikel (refereegranskat)abstract
    • We herein outline the rationale for a Swedish cohort consortium, aiming to facilitate greater use of Swedish cohorts for world-class research. Coordination of all Swedish prospective population-based cohorts in a common infrastructure would enable more precise research findings and facilitate research on rare exposures and outcomes, leading to better utilization of study participants' data, better return of funders' investments, and higher benefit to patients and populations. We motivate the proposed infrastructure partly by lessons learned from a pilot study encompassing data from 21 cohorts. We envisage a standing Swedish cohort consortium that would drive development of epidemiological research methods and strengthen the Swedish as well as international epidemiological competence, community, and competitiveness.
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2.
  • Holmgren, Anton, et al. (författare)
  • Detailed analyzes of the relation between childhood BMIand gain in height during puberty, separated into different Components
  • 2016
  • Ingår i: International Journal of Obesity. - 0307-0565 .- 1476-5497.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Background: We have previously found that childhood BMI is inversely related to pubertal height gain: overweight/obese children of both genders have less specific pubertal height gain. The QEPS-model (describing total growth in height as a combination of four mathematical functions), can be used for calculation of estimates of pubertal growth. Growth in height during puberty can be described as a combination of continuous ongoing growth, Q(ES), and a specific pubertal growth function, P. Objectives: To investigate the importance of when overweight/obesity starts during childhood in relation to subsequent growth in height during puberty; and to study the relationship between childhood BMI and pubertal growth functions from the QEPS-model in greater detail than previously presented. Material/Methods: The longitudinally followed GrowUpGothenburg 1990 birth cohort, with growth data from birth until adult height was analyzed, using the QEPS-model. Individual BMI-SDS values, from 3.5–8.0 years of age (n = 1901) were calculated for linear and subgroup analyses (normal /underweight, NwUw, overweight/obese, OwOb), based on the IOTF 2012 reference2. Relationships between childhood-BMI and total pubertal height gain were considered according to P-function and Q(ES)-function. Results: We found no significant difference in pubertal height gain depending on when in childhood the BMI-SDS peaked, in either sex. In general, the total pubertal growth in girls depended more on the continuous Q(ES)-function than P-function and this balance was shifted towards less P-function with higher BMI-SDS, especially for Ob girls (figure, left). NwUw boys had pubertal gain mostly from the P-function, for the Ow boys the pattern was more mixed and for Ob boys all had less P- than Q(ES)-function (figure, right). Conclusion: The results of the present study have shown that the reduced pubertal gain in height for OwOb children is not related to when during childhood the BMI peaked. For both genders, the pubertal gain shifted to less specific pubertal growth (P) and relatively more continuous growth (Q(ES)) with higher BMI-SDS.
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3.
  • Holmgren, Anton, et al. (författare)
  • Higher childhood BMI is associated with less pubertal gain
  • 2015
  • Ingår i: Obesity Facts (The European Journal of Obesity). - : S. Karger AG. - 1662-4025 .- 1662-4033.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Objective: Our objective was to investigate the impact of body mass index (BMI) in childhood on the pattern of growth during puberty. Methods: The longitudinally followed Grow up 1990 Gothenburg birth cohort, with growth data from birth until adult height was analyzed, using the QEPS growth model (describing total height as a combination of four mathematical functions; Quadratic -Q, Exponential -E, Pubertal -P and Stop –S, Fig 1.), for calculation of estimates for pubertal growth (1). Individual BMI-SDS values, from 3.5–8 years of age (n = 1908) were calculated for linear and subgroup analyses (low/normal- nw, overweight – ow, obese– ob), based on the IOTF 2012 reference. Results: Ow/ob children already at birth were heavier and grew faster in height in the pre pubertal period compared to nw, due to an increased Q function. Ow/ob children of both genders had 3.4–4.3 months earlier puberty, reduced growth during puberty, boys and girls had 3 cm and 2 cm, respectively, less pubertal gain from the specific pubertal growth function (P) compared to their nw peers. We saw a negative dose-response effect of childhood BMI on pubertal gain, across the whole BMI spectrum (Fig 2–3.). The adult height was not related to BMI in childhood. Conclusion: For the first time, the result of the present study has shown that; the higher the BMI is in childhood, the less is the pubertal gain. Higher childhood BMI was also associated with increased pre pubertal growth due to an increased Q-function and the resulting adult height was similar for ow/ob and nw children. Reference 1.Holmgren A et al.: Horm. res. in paed. 2013;80(suppl. 1):177.
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4.
  • Holmgren, Anton, et al. (författare)
  • Pubertal height gain is inversely related to peak BMI in childhood.
  • 2017
  • Ingår i: Pediatric research. - : Springer Science and Business Media LLC. - 1530-0447 .- 0031-3998. ; 81:3, s. 448-454
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundChildhood BMI may influence subsequent growth in height as well as the timing of puberty. The aim of the present study was to investigate associations between BMI in childhood and subsequent height gain/pubertal growth.MethodsLongitudinal growth data were used (GrowUp1990 Gothenburg cohort, n=1901). The QEPS growth-model was used to characterize height gain in relation to the highest BMISDS value between 3.5 and 8 years of age. Children were defined as overweight/obese (OwOb) or normal weight/underweight (NwUw), using the 2012 International Obesity Task Force criteria.ResultsA negative association between childhood BMISDS and pubertal height gain was observed. Already at birth, OwOb children were heavier than NwUw children, and had a greater height velocity during childhood. Onset of puberty was 3.5/3.0 months earlier in OwOb girls/boys, and they had 2.3/3.1cm less pubertal height gain from the QEPS-models specific P-function than NwUw children. Adult height was not related to childhood BMI.ConclusionWe found that pubertal height gain was inversely related to peak BMI in childhood. Higher childhood BMISDS was associated with more growth before onset of puberty, earlier puberty and less pubertal height gain, resulting in similar adult heights for OwOb and NwUw children.
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5.
  • Holmgren, Anton, et al. (författare)
  • The Pubertal Gain in Height is Inversely Related to BMI in Childhood
  • 2015
  • Ingår i: Hormone Research in Paediatrics. ; 84:Supplement 1, s. 268-69
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Background: Weight in childhood may influence the pubertal timing and pattern of growth. Objective: To investigate the impact of BMI in childhood on further growth, especially the specific pubertal pattern of growth. Method: The longitudinally followed GrowUpGothenburg1990 birth cohort, was analyzed using the QEPS growth model (Nierop et al. Horm Res in Ped.2013; 80(suppl 1):152–153) (describing total height as a combination of four mathematical functions; Quadratic – Q, Exponential – E, Pubertal – P and Stop – S). Individual BMISDS values, from 3.5–8 years of age were calculated for linear and subgroup analyses (low/normal – Lw/Nw, overweight/obese – Ow/Ob), based on the IOTF 2012 reference (Cole TJ, Lobstein T. Pediatric obesity. 2012; 7(4):284–94.). Results: Across the whole BMI range a negative dose-response effect of childhood BMI on pubertal gain (Pmax) was found. Already at birth Owob children were heavier, and they grew faster in height in the prepubertal period compared to Lw/Nw, as evidenced by an increased Q function. Owob children of both genders had earlier puberty (91–117 days), P = 0.0004, reduced growth during puberty, boys/girls 3.13/2.26 cm less pubertal gain P<0.0001, from the specific pubertal growth function (Pmax). The adult height was not related to BMI in childhood. Conclusion: The higher BMI in childhood, the faster the prepubertal growth, the earlier onset of puberty, the less pubertal gain. This was evident across the whole BMI-range, making weight status an important modifier of growth. Funding information: This work was supported by the Swedish Research Council (VR no 7509 and VR 2006-7777), VR/FORMAS/FORTE/VINNOVA (259-2012-38 and 2006-1624); EpiLife-TEENS research program, Pfizer AB, the Governmental Grants for University Hospital Research (ALF), the R&D Department, County of Halland, and the Foundation Växthuset for children.
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6.
  • Holmgren, Anton, et al. (författare)
  • The Specific Pubertal Height Gain is Higher in Boys as Well as in Children with Lower BMISDS
  • 2016
  • Ingår i: Hormone Research in Paediatrics. - 1663-2818 .- 1663-2826.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Background: Growth in height during puberty can be described by the QEPS-model as a combination of continuous basal growth, QES, and a specific pubertal growth function, P. Objective and hypotheses: To study the relationship between childhood BMISDS and the prepubertal gain and pubertal gain related to growth functions from the QEPS-model. Method: The longitudinally followed GrowUpGothenburg 1990 birth cohort, was analyzed, by the QEPS-model. Individual maximal BMISDS values, from 3.5–8.0 years of age (n=1901) were calculated for linear and subgroup analyses, underweight (blue cross), normal (blue open circles), overweight (red open circles), obese (red circles). Results: For girls (Figure left), total pubertal gain (Tpubgain) depended more on QESgain during puberty. For boys, total pubertal gain depended more on specific Pgain (Figure right). With higher BMISDS this balance was shifted towards less Pgain for both girls and boys. Before puberty, children with higher BMISDS were taller, expressed as higher QESgain, with a linear correlation over the whole BMI–range (P<0.001for both girls/ boys). Conclusion: During puberty, girls grew more due to the QES than the P functions, with opposite findings in boys. For both boys and girls, there were less Pgain and more QES- gain with higher childhood BMISDS. Before puberty, children with higher BMISDS were taller.
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7.
  • Loos, Stefan, et al. (författare)
  • Electromodified NiFe Alloys as Electrocatalysts for Water Oxidation : Mechanistic Implications of Time-Resolved UV/Vis Tracking of Oxidation State Changes
  • 2019
  • Ingår i: ChemSusChem. - : Wiley-VCH Verlagsgesellschaft. - 1864-5631 .- 1864-564X. ; 12:9, s. 1966-1976
  • Tidskriftsartikel (refereegranskat)abstract
    • Facile electromodification of metallic NiFe alloys leads to a series of NiFe oxyhydroxide surface films with excellent electrocatalytic performance in alkaline water oxidation. During cyclic voltammetry and after sudden potential jumps between noncatalytic and catalytic potentials, Ni oxidation/reduction was tracked with millisecond time resolution by a UV/Vis reflectance signal. Optimal catalysis at intermediate Ni/Fe ratios is explained by two opposing trends for increasing Fe content: a)pronounced slowdown of the Ni2+/Ni3+ oxidation step and b)increased reactivity of the most oxidized catalyst state detectable at catalytic potentials. This state may involve an equilibrium between Ni4+ ions and Ni2+ ions with neighboring ligand holes, possibly in the form of bound peroxides.
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8.
  • Mehlig, Kirsten, 1964, et al. (författare)
  • Associations between alcohol and liver enzymes are modified by coffee, cigarettes, and overweight in a Swedish female population.
  • 2022
  • Ingår i: Scandinavian journal of gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 57:3, s. 319-324
  • Tidskriftsartikel (refereegranskat)abstract
    • To examine whether positive associations between alcohol and liver enzymes were modified by coffee consumption, smoking, or weight status in a female population. Regular consumption of beer, wine, and spirits was assessed in a representative cohort of 1462 Swedish women aged 38-60 in 1968, and re-assessed in 1974. In 1980, gamma-glutamyltransferase (GGT) and aspartase transaminase (AST) were measured in 1130 women. Exposures were averaged over values obtained in 1968 and 1974. Multivariable linear regression linked total ethanol intake to log-transformed enzyme values, including interactions by coffee, smoking, and overweight in mutually adjusted models.Coffee consumption significantly modified the association between ethanol intake and liver enzymes. One g/day higher ethanol intake was associated with 5.5 (3.5, 7.5)% higher values of GGT, and 1.2 (0.4, 2.1)% higher values of AST in women consuming 0-1 cups of coffee per day, while smaller or no effects were observed in women consuming ≥2 cups/day. Synergistic interactions were observed for ethanol and smoking, and for ethanol and overweight. Average alcohol-related effects on GGT in smokers and non-smokers were given by 3.8 (2.7, 4.9)% and 2.1 (0.9, 3.2)% per g ethanol/day, and by 0.9 (0.4, 1.4)% and 0.2 (-0.3, 0.7)% for AST. Similarly, in overweight women, 1g/day higher ethanol intake was associated with 4.3 (3.0, 5.6)% higher GGT compared to 1.6 (0.7, 2.5)% in non-overweight women.The results suggest that coffee consumption reduces the enzyme-raising effect of ethanol in the presence of synergistic interactions with smoking and overweight, specifically in women.
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