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  • 1
    Electronic Resource
    Electronic Resource
    Rapid hip bone loss in active Crohn's disease patients receiving short-term corticosteroid therapy (2004)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 20 (2004), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Uncertainty over whether corticosteroids cause bone loss in patients with Crohn's disease may reflect their short, intermittent use.Aim : We investigated whether a 2-month course of prednisolone is associated with detectable bone loss.Methods : Fifteen patients with active Crohn's disease and 19 controls with inactive Crohn's disease were recruited. Bone mineral density of the lumbar spine and hip was measured at baseline and 2 and 8 months.Results : At 2 months, significant bone loss was found in patients with active disease (femoral neck −2.7%, P 〈 0.002; Ward's triangle −3.9%, P 〈 0.01). Although bone mineral density was still lower at 8 months, these differences were no longer significant (−1.3% and −3.4%, femoral neck and Ward's triangle, respectively). No significant change in hip bone mineral density was observed in controls. Previous corticosteroid use was not significantly associated with baseline bone mineral density, although significant independent associations were observed between weight, site of disease and lumbar spine bone mineral density, and between dietary calcium deficiency and femoral neck and Ward's triangle bone mineral density.Conclusion : Significant bone loss at the hip can be detected in patients receiving corticosteroid treatment for 2 months for active Crohn's disease ; however, it remains unclear whether this is because of disease activity or its treatment. This rapid bone loss may represent a risk factor for fracture and justify bone protective therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2004.02207.x
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  • 2
    Electronic Resource
    Electronic Resource
    Neridronate Preferentially Suppresses the Urinary Excretion of Peptide-Bound Deoxypyridinoline in Postmenopausal Women (1996)
    Springer
    Calcified tissue international 59 (1996), S. 407-409 
    Details
    ISSN: 1432-0827
    Keywords: Key Words: Neridronate, Bisphosphonate, Deoxpyridinoline, Collagen Crosslink
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: SUMMARY ELISAs for measuring the urinary excretion of collagen crosslinks and related peptides appear to show marked differences in sensitivity to anti-resorptive therapy. This presumably reflects variations in specificity of the anylate being detected in these assays, and the way in which they respond to treatment. To clarify these points, we used HPLC analysis to assess the effect of four weeks treatment with the amino-bisphosponate, neridronate, on free and peptide-bound fractions of the collagen cross-links deoxypyridinoline (Dpd) and pyridinoline (Pyd). Six postmenopausal women, in whom two hour morning urine samples were obtained at baseline (x2), and one, two and four weeks after commencing treatment, were included. We found that neridronate had relatively little effect on peptide-bound or free urinary Pyd, but markedly reduced peptide-bound urinary Dpd. However, urinary excretion of free Dpd was not significantly affected. As a consequence of these differential effects on collagen cross-link excretion, neridronate led to a striking increase in the free/total Dpd ratio, and in the peptide-bound Pyd/Dpd ratio. We conclude that neridronate, and presumably other bisphosphonates, selectively suppresses peptide-bound Dpd excretion, possibly reflecting altered processing of collagen crosslinks released during bone resorption.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002239900148
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  • 3
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    Genome-wide association study of primary tooth eruption identifies pleiotropic loci associated with height and craniofacial distances (2013)
    Oxford University Press
    Details
    Publication Date: 2013-08-23
    Description: Twin and family studies indicate that the timing of primary tooth eruption is highly heritable, with estimates typically exceeding 80%. To identify variants involved in primary tooth eruption, we performed a population-based genome-wide association study of ‘age at first tooth’ and ‘number of teeth’ using 5998 and 6609 individuals, respectively, from the Avon Longitudinal Study of Parents and Children (ALSPAC) and 5403 individuals from the 1966 Northern Finland Birth Cohort (NFBC1966). We tested 2 446 724 SNPs imputed in both studies. Analyses were controlled for the effect of gestational age, sex and age of measurement. Results from the two studies were combined using fixed effects inverse variance meta-analysis. We identified a total of 15 independent loci, with 10 loci reaching genome-wide significance ( P 〈 5 x 10 –8 ) for ‘age at first tooth’ and 11 loci for ‘number of teeth’. Together, these associations explain 6.06% of the variation in ‘age of first tooth’ and 4.76% of the variation in ‘number of teeth’. The identified loci included eight previously unidentified loci, some containing genes known to play a role in tooth and other developmental pathways, including an SNP in the protein-coding region of BMP4 (rs17563, P = 9.080 x 10 –17 ). Three of these loci, containing the genes HMGA2 , AJUBA and ADK , also showed evidence of association with craniofacial distances, particularly those indexing facial width. Our results suggest that the genome-wide association approach is a powerful strategy for detecting variants involved in tooth eruption, and potentially craniofacial growth and more generally organ development.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 4
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    Using Mendelian randomization to investigate a possible causal relationship between adiposity and increased bone mineral density at different skeletal sites in children (2016)
    Oxford University Press
    Details
    Publication Date: 2016-11-09
    Description: Background: Lean mass is positively associated with bone mineral density (BMD). However, the relationship between adiposity and BMD is more controversial. In particular, it is unclear if the observational association between the two reflects a causal effect of fat mass on BMD. Previous Mendelian randomization (MR) studies using variants in the FTO and MC4R genes as genetic instruments for adiposity have suggested that fat mass does indeed causally influence BMD. However, it is possible that these genetic variants pleiotropically influence lean mass and affect BMD through pathways independent of adiposity, invalidating one of the core assumptions of MR and complicating interpretation of the analysis. Methods: To investigate whether adiposity causally affects BMD, we investigated the relationship between fat mass and BMD at the skull (SK), upper limbs (UL) and lower limbs (LL), spine (SP) and pelvis (PE), using 32 body mass index (BMI)-associated SNPs, including a variant near ADCY3 that was strongly associated with fat but not lean mass in our sample. Dual-energy X-ray absorptiometry (DXA) scans and genetic data were available for 5221 subjects (mean age 9.9 years) from the Avon Longitudinal Study of Parents and Children. We performed a series of MR analyses involving single BMI-associated SNPs and allelic scores of these SNPs. We used new extensions of the MR method including MR Egger regression and multivariable MR, which are more robust to possible confounding effects due to horizontal pleiotropy and, in the case of multivariable MR, specifically account for the effect of lean mass in the analysis. Bidirectional Mendelian randomization analysis was also performed to examine whether BMD causally affected BMI and adiposity. Results: Observationally, fat mass was strongly positively related to BMD at all sites, but more weakly at the skull. Instrumental variables (IV) analyses using an allelic score of BMI SNPs suggested that fat mass was causally related to LL-BMD, UL-BMD, SP-BMD and PE-BMD but not SK-BMD. Multivariable MR, Egger regression and IV analyses involving the ADCY3 variant suggested a positive causal effect of adiposity on all sites except the skull, and that an effect was present even after taking lean mass into account. Finally, IV analyses using BMD allelic scores showed no evidence of reverse causality between BMD and fat mass. Conclusions: Our results suggest that adiposity is causally related to increased BMD at all sites except the skull, perhaps reflecting positive effects of loading on bone formation at weighted but not unweighted sites. In contrast, we found no evidence for BMD causally affecting BMI or measures of adiposity. Our results illustrate how MR can be used profitably to investigate clinical questions relevant to osteoporosis.
    Print ISSN: 0300-5771
    Electronic ISSN: 1464-3685
    Topics: Medicine
    Published by Oxford University Press
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  • 5
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    Authors response to Hartwig and Davies (2016)
    Oxford University Press
    Details
    Publication Date: 2016-11-09
    Print ISSN: 0300-5771
    Electronic ISSN: 1464-3685
    Topics: Medicine
    Published by Oxford University Press
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  • 6
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    Genetic variants in adult bone mineral density and fracture risk genes are associated with the rate of bone mineral density acquisition in adolescence (2015)
    Oxford University Press
    Details
    Publication Date: 2015-06-23
    Description: Previous studies have identified 63 single-nucleotide polymorphisms (SNPs) associated with bone mineral density (BMD) in adults. These SNPs are thought to reflect variants that influence bone maintenance and/or loss in adults. It is unclear whether they affect the rate of bone acquisition during adolescence. Bone measurements and genetic data were available on 6397 individuals from the Avon Longitudinal Study of Parents and Children at up to five follow-up clinics. Linear mixed effects models with smoothing splines were used for longitudinal modelling of BMD and its components bone mineral content (BMC) and bone area (BA), from 9 to 17 years. Genotype data from the 63 adult BMD associated SNPs were investigated individually and as a genetic risk score in the longitudinal model. Each additional BMD lowering allele of the genetic risk score was associated with lower BMD at age 13 [per allele effect size, 0.002 g/cm 2 (SE = 0.0001, P = 1.24 x 10 –38 )] and decreased BMD acquisition from 9 to 17 years ( P = 9.17 x 10 –7 ). This association was driven by changes in BMC rather than BA. The genetic risk score explained ~2% of the variation in BMD at 9 and 17 years, a third of that explained in adults (6%). Genetic variants that putatively affect bone maintenance and/or loss in adults appear to have a small influence on the rate of bone acquisition through adolescence.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 7
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    High impact activity is related to lean but not fat mass: findings from a population-based study in adolescents (2012)
    Oxford University Press
    Details
    Publication Date: 2012-08-30
    Description: Background Objective measures of physical activity calibrated against energy expenditure may have limited utility in studying relationships with musculoskeletal phenotypes. We wished to assess an alternative approach using an accelerometer calibrated according to impact loading. Methods Of the 17-year olds from the Avon Longitudinal Study of Parents and Children (ALSPAC), 732 wore Newtest accelerometers while performing day-to-day activities for a mean of 5.8 days. Outputs were categorized as light, moderate, high and very high impact, based on the thresholds identified in 22 adolescents during graded activities. In subsequent regression analyses, activity data and fat mass were normalized by log transformation. Results The number of counts relating to high impact activity was ~2% that of light impact activity, and 33% greater in boys when compared with girls. High impact activity was more strongly related to lean mass [light: 0.033 (95% CI –0.023 to 0.089), moderate: 0.035 (95% CI –0.010 to 0.080) and high: 0.044 (95% CI 0.010 to 0.078)] (β = SD change in outcome per doubling in activity, height adjusted, boys and girls combined). In contrast, lower impact activity was more strongly related to fat mass [light: –0.069 (95% CI –0.127 to –0.011), moderate: –0.060 (95% CI –0.107 to –0.014) and high: –0.033 (95% CI –0.069 to 0.003)]. In a more fully adjusted model including other activity types and fat/lean mass, lean mass was related to only high activity (boys and girls combined), whereas fat mass was related to only moderate activity (girls only). Conclusions Using an accelerometer calibrated according to impact loading revealed that high impact activity is related to lean but not fat mass.
    Print ISSN: 0300-5771
    Electronic ISSN: 1464-3685
    Topics: Medicine
    Published by Oxford University Press
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