Impaired pyridinoline cross-link formation in patients with osteogenesis imperfecta
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[1] M. Barbagallo,et al. Collagen overglycosylation: a biochemical feature that may contribute to bone quality. , 2005, Biochemical and biophysical research communications.
[2] R. Bank,et al. Phenotypic and molecular characterization of Bruck syndrome (osteogenesis imperfecta with contractures of the large joints) caused by a recessive mutation in PLOD2 , 2004, American journal of medical genetics. Part A.
[3] S. Adami,et al. Bone turnover markers in patients with osteogenesis imperfecta. , 2004, Bone.
[4] R. Engelbert,et al. The Interaction Between Sillence Type and BMD in Osteogenesis Imperfecta , 2003, Calcified Tissue International.
[5] F. Glorieux,et al. Osteogenesis imperfecta type VII: an autosomal recessive form of brittle bone disease. , 2002, Bone.
[6] F. Glorieux,et al. Osteogenesis Imperfecta Type VI: A Form of Brittle Bone Disease with a Mineralization Defect , 2002, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[7] F. Glorieux,et al. Thirty‐three novel COL1A1 and COL1A2 mutations in patients with osteogenesis imperfecta types I‐IV , 2001, Human mutation.
[8] F. Glorieux,et al. Type V Osteogenesis Imperfecta: A New Form of Brittle Bone Disease , 2000, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[9] R. Bank,et al. Pyridinium Cross‐Links in Bone of Patients with Osteogenesis Imperfecta: Evidence of a Normal Intrafibrillar Collagen Packing , 2000, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[10] P. Delmas,et al. Racemization and isomerization of type I collagen C-telopeptides in human bone and soft tissues: assessment of tissue turnover. , 2000, The Biochemical journal.
[11] C. Fledelius,et al. Collagen fragments in urine derived from bone resorption are highly racemized and isomerized: a biological clock of protein aging with clinical potential. , 2000, The Biochemical journal.
[12] A. Juul,et al. Collagen‐derived markers of bone metabolism in osteogenesis imperfecta , 1998, Acta paediatrica.
[13] S. Mora,et al. Urinary Markers of Bone Turnover in Healthy Children and Adolescents: Age-Related Changes and Effect of Puberty , 1998, Calcified Tissue International.
[14] H. Minaguchi,et al. Differences in Bone Resorption after Menopause in Japanese Women with Normal or Low Bone Mineral Density: Quantitation of Urinary Cross-Linked N-Telopeptides , 1998, Calcified Tissue International.
[15] P. Qvist,et al. Characterization of Urinary Degradation Products Derived from Type I Collagen , 1997, The Journal of Biological Chemistry.
[16] H. Tanaka,et al. Urinary pyridinoline and deoxypyridinoline in healthy children and in children with growth hormone deficiency. , 1995, The Journal of clinical endocrinology and metabolism.
[17] C. Christiansen,et al. Immunoassay for quantifying type I collagen degradation products in urine evaluated. , 1994, Clinical chemistry.
[18] P. Delmas,et al. Assessment of bone resorption with a new marker of collagen degradation in patients with metabolic bone disease. , 1994, The Journal of clinical endocrinology and metabolism.
[19] J. Ittner,et al. Serum concentrations of procollagen I C‐terminal propeptide, osteocalcin and insulin‐like growth factor‐I in patients with non‐lethal osteogenesis irnperfecta , 1993, Acta paediatrica.
[20] D. Eyre,et al. A specific immunoassay for monitoring human bone resorption: Quantitation of type I collagen cross‐linked N‐telopeptides in urine , 1992, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[21] C. Mathew,et al. Consistent linkage of dominantly inherited osteogenesis imperfecta to the type I collagen loci: COL1A1 and COL1A2. , 1990, American journal of human genetics.
[22] P. Byers,et al. Osteogenesis imperfecta. The position of substitution for glycine by cysteine in the triple helical domain of the pro alpha 1(I) chains of type I collagen determines the clinical phenotype. , 1989, The Journal of clinical investigation.
[23] D. Sillence,et al. Genetic heterogeneity in osteogenesis imperfecta. , 1979, Journal of medical genetics.
[24] A. Williams,et al. Urinary Total Hydroxyproline: Creatinine Ratio , 1972, Archives of disease in childhood.
[25] Masao Fukunaga,et al. Guidelines for the use of biochemical markers of bone turnover in osteoporosis (2004) , 2004, Journal of Bone and Mineral Metabolism.
[26] L. Ala‐Kokko,et al. Analysis of the COL1A1 and COL1A2 genes by PCR amplification and scanning by conformation-sensitive gel electrophoresis identifies only COL1A1 mutations in 15 patients with osteogenesis imperfecta type I: identification of common sequences of null-allele mutations. , 1998, American journal of human genetics.
[27] D. Eyre,et al. Bone resorption rates in children monitored by the urinary assay of collagen type I cross-linked peptides. , 1994, Bone.
[28] P. Esposito,et al. Osteogenesis Imperfecta. , 1928, Proceedings of the Royal Society of Medicine.