GLORIA

GEOMAR Library Ocean Research Information Access

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Bone diseases in children. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (795 pages)
    Edition: 1st ed.
    ISBN: 9780080538556
    DDC: 611.7/1
    Language: English
    Note: Front Cover -- Pediatric Bone: Biology and Diseases -- Copyright Page -- Table of Contents -- Contributors -- Foreword -- Preface -- Chapter 1. Structure of Growth Plate and Bone Matrix -- Introduction -- Type I Collagen -- Type V Collagen -- Type II Collagen -- Type IX Collagen -- Type XI Collagen -- Type X Collagen -- Aggrecan -- Cartilage Link Protein 1 -- Small, Leucine-Rich, Interstitial Proteoglycans -- Perlecan -- Matrilins -- Thrombospondins -- Osteonectin -- Osteocalcin -- Matrix Gla Protein -- Bone Sialoprotein -- Bone Acidic Glycoprotein-75 -- Dentin Matrix Acidic Phosphoprotein-1 -- Osteopontin -- References -- Chapter 2. Bone Cell Biology: Osteoblasts, Osteocytes, and Osteoclasts -- Introduction -- Ontogeny of Osteoblasts and Control of Osteoblast Development -- Osteoprogenitor Cells and Regulation of Osteoblast Differentiation and Activity -- Regulation of Osteoblast Differentiation and Activity -- Osteocytes -- Morphological Features of Osteoclasts -- Mechanisms of Osteoclastic Bone Resorption -- Origin of Osteoclasts -- Regulation of Ostoclast Activity and Differentiation -- Osteoclast Size: Multinucleation and Function -- Stem Cell, Osteoblast, and Osteoclast Changes in Disease -- Tissue Engineering and Stem Cell Therapy for Skeletal Diseases -- References -- Chapter 3. Prenatal Bone Development: Ontogeny and Regulation -- Introduction -- Skeletogenesis -- Skeletal Organization and Embryonic Origin of Bones -- Molecular Regulation of Bone Formation -- References -- Chapter 4. Postnatal Bone Growth: Growth Plate Biology, Modeling, and Remodeling -- Endochondral and Intramembranous Bone Formation -- Growth Hormone and Insulin-Like Growth Factor- 1 -- Fibroblast Growth Factors -- Thyroid Hormone -- Estrogen and Androgen -- Osteoblasts and Bone Growth -- Endocrine Regulation of Bone Formation -- References. , Chapter 5. Parathyroid Hormone and Calcium Homeostasis -- Cellular and Extracellular Calcium Homeostasis -- Parathyroids and Secretion and Metabolism of Parathyroid Hormone -- Assay of PTH -- Parathyroid Hormone Action -- References -- Chapter 6. Phosphate Homeostasis Regulatory Mechanisms -- Introduction -- Physiological Aspects -- Cellular and Molecular Aspects -- Pathophysiological Aspects -- References -- Chapter 7. Vitamin D Biology -- Metabolic Activation of Vitamin D -- Mechanism of Action -- Role of Vitamin D in Calcium Homeostasis -- Summary and Perspectives -- References -- Chapter 8. Other Factors Controlling Bone Growth and Development: Calcitonin, CGRP, Osteostatin, Amylin, and Adrenomedullin -- Introduction -- Calcitonin -- Calcitonin Gene-Related Peptide -- Parathyroid Hormone-Related Protein -- Amylin -- Adrenomedullin -- References -- Chapter 9. Peak Bone Mass and Its Regulation -- Definition and Importance of Peak Bone Mass -- Characteristics of Peak Bone Mass Acquisition -- Calcium-Phosphate Metabolism During Growth -- Determinants of Bone Mass Gain -- Conclusions -- References -- Chapter 10. Pregnancy and Lactation -- Introduction -- Mineral Fluxes from Mother to Offspring -- Pregnancy -- Lactation -- Summary -- References -- Chapter 11. Fetal Mineral Homeostasis -- Fetal Adaptive Goals -- Placental Calcium Transport -- Placental Transport of Magnesium and Phosphate -- Fetal Parathyroids -- Calcium-Sensing Receptor -- Thymus -- Fetal Kidneys and Amniotic Fluid -- Fetal Skeleton -- Maternal Skeleton -- Fetal Response to Maternal Hypoparathyroidism -- Fetal Response to Maternal Hypoparathyroidism -- Integrated Fetal Calcium Homeostasis -- References -- Chapter 12. Noninvasive Techniques for Bone Mass Measurement -- Indications for Bone Mass Measurements. , Challenges to Interpreting Bone Mass Measurements in Childhood and Adolescence -- Noninvasive Measurement Techniques -- Data Interpretation -- References -- Chapter 13. Assessment of Maturation: Bone Age and Pubertal Assessment -- Background -- Initial Considerations -- Methods of Assessment -- Reliability -- Comparability of the Atlas and Bone-Specific Methods -- Secondary Sexual Development -- References -- Chapter 14. Biochemical Markers o f Bone Metabolism -- Introduction -- Markers of Bone Formation -- Markers of Bone Resorption -- Bone Markers During Normal Development -- Puberty -- Bone and Collagen Markers in Metabolic Bone Diseases -- Clinical and Research Value of Biochemical Markers of Bone Metabolism -- References -- Chapter 15. Bone Histomorphometry -- Introduction -- Methodology -- Pediatric Bone Histomorphometry in Health and Disease -- Indications for Bone Biopsy and Histomorphometry in Pediatric Bone Diseases -- References -- Chapter 16. A Diagnostic Approach to Skeletal Dysplasias -- Introduction -- Background -- History and Physical Examination -- Diagnostic Imaging -- Biochemical Investigations -- Cartilage Histology -- Molecular Basis -- Prenatal Detection of Suspected Skeletal Dysplasia -- Conclusion -- References -- Chapter 17. The Spectrum of Pediatric Osteoporosis -- Abstract -- Introduction -- Definition and Diagnosis of Osteopenia/Osteoporosis in Pediatric Patients -- The Role of the Mechanostat in the Pathogenesis of Pediatric Osteoporosis -- The Scope of the Problem -- Approach to Prevention and Intervention -- Differentiating Child Abuse from Bone Fragility Conditions -- Summary and Future Directions -- References -- Chapter 18. Osteogenesis Imperfecta -- Introduction -- Classification -- Types of OI -- Differential Diagnosis -- General Clinical Findings -- Pathophysiology -- Therapy -- References. , Chapter 19. Sclerosing Bony Dysplasia -- Introduction -- Defects in Osteoclastic Bone Resorption -- Skeletal Abnormalities Related to Overproduction of Bone: Involvement of Transforming Growth Factors -- Summary -- References -- Chapter 20. Parathyroid Disorders -- Introduction -- PTH Gene Structure and Function -- Hypocalcemic Disorders -- Hypercalcemic Diseases -- Conclusion -- References -- Chapter 21. Fibrous Dysplasia -- Introduction -- Clinical Features -- Molecular Genetics -- Determinants of Phenotypic Variability -- Pathology -- Pathogenesis -- Management and Treatment -- References -- Chapter 22. Nutritional Rickets -- Introduction -- Definition of Rickets -- Classification of Rickets -- Nutritional Rickets -- References -- Chapter 23. Metabolic Bone Disease of Prematurity -- Introduction -- In Utero Mineral Accretion and Bone Growth -- Physiological Changes in Mineral Homeostasis at Birth -- Metabolic Bone Disease -- Skeletal Health in Preterm Infants -- Suggested Guidelines for the Prevention of Metabolic Bone Disease in Preterm Infants -- Conclusions -- References -- Chapter 24. Rickets Due to Hereditary Abnormalities of Vitamin D Synthesis or Action -- Introduction -- Biosynthesis of Vitamin D -- Vitamin D Biosynthetic Enzymes -- Vitamin D 25-Hydroxylase and 24-Hydroxylase -- Vitamin D laL-Hydroxylase -- Rickets Due to Abnormalities of Vitamin D Metabolism -- Rickets Due to Abnormalities of Vitamin D Action -- References -- Chapter 25. Familial Hypophosphatemia and Related Disorders -- Introduction -- Clinical Description of Disease Entities -- Treatment -- Family/Genetic Studies -- Molecules, Pathophysiology, and Lessons from Animal Models -- Current Problems and Unresolved Questions -- References -- Chapter 26. Rickets Due to Renal Tubular Abnormalities -- Introduction -- Fanconi Syndrome -- Renal Magnesium Wasting -- Hypercalciuria. , Renal Tubular Acidosis -- Conclusion -- References -- Chapter 27 . Hypophosphatasia -- Biology of Alkaline Phosphatase -- Clinical Hypophosphatasia -- References -- Chapter 28. Renal Osteodystrophy: Pathogenesis , Diagnosis, and Treatment -- Introduction -- The Spectrum of Renal Osteodystrophy -- Pathogenesis of Renal Osteodystrophy -- Clinical Manifestations -- Biochemical Determinations -- Histologic Manifestations -- Radiographic Features of Renal Osteodystrophy -- Long-Term Consequences -- Treatment -- References -- Chapter 29. Bone Tumors in Children -- Introduction -- General Principles of Treatement -- Diagnosis -- Classification and Nomenclature -- Back Pain and Spinal Neoplasms in Children -- Fibrous Tumors of Bone -- Cartilage-Forming Tumors -- Bone-Forming Tumors -- Hematopoietic -- Vascular -- Neurogenic -- Adipose -- Mixed -- Notochord -- Tumor-Like -- Conclusion -- References -- Index -- Color Plate Section.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Vitamin D. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (1970 pages)
    Edition: 2nd ed.
    ISBN: 9780080543642
    DDC: 612.399
    Language: English
    Note: 9780122526879v1 -- Front Cover -- Vitamin D -- Copyright Page -- Contents -- List of Contributors -- Preface to the 2nd Edition -- Preface to the 1st Edition -- Abbreviations -- Introduction -- Chapter 1. Historical Perspective -- Section I: CHEMISTRY, METABOLISM, AND CIRCULATION -- Chapter 2. Vitamin D Metabolism -- Chapter 3. Photobiology of Vitamin D -- Chapter 4. The Vitamin D 25-Hydroxylase -- Chapter 5. The 25-Hydroxyvitamin D 1- -Hydroxylase -- Chapter 6. The 25-Hydroxyvitamin D 24-Hydroxylase -- Chapter 7. Mutant Mouse Models of Vitamin D Metabolic Enzymes -- Chapter 8. Vitamin D Binding Protein -- Chapter 9. New Aspects of DBP -- Chapter 10. Endocytic Pathways for 25-(OH) Vitamin D3 -- Section II: MECHANISM OF ACTION -- Chapter 11. The Vitamin D Receptor -- Chapter 12. Vitamin D Receptor Promoter and Regulation of Receptor Expression -- Chapter 13. Nuclear Vitamin D Receptor: Structure-Function, Molecular Control of Gene Transcription, and Novel Bioactions -- Chapter 14. Vitamin D Receptor Cofactors: Function, Regulation, and Selectivity -- Chapter 15. VDR LBD Crystal Structures -- Chapter 16. Comodulators of VDR-Mediated Gene Expression -- Chapter 17. Promoter Targeting of VDR Through A Chromatin Remodeling Complex -- Chapter 18. Molecular Basis of the Diversity of Vitamin D Target Genes -- Chapter 19. Intranuclear Organization of the Regulatory Machinery for Vitamin D-Mediated Control of Skeletal Gene Expression -- Chapter 20. Mouse Models of Vitamin D Receptor Ablation -- Chapter 21. Intranuclear Vitamin D Response Element Binding Proteins -- Chapter 22. VDR and RXR Subcellular Trafficking -- Chapter 23. 1 ,25(OH)2-Vitamin D3 Mediated Rapid and Genomic Responses are Dependent upon Critical Structure-Function Relationships for Both the Ligand and Receptor(s) -- Section III: MINERAL HOMEOSTASIS. , Chapter 24. Vitamin D and the Intestinal Absorption of Calcium: A View and Overview -- Chapter 25. Intestinal Calcium Absorption: Lessons from Knockout Mice and Men -- Chapter 26. Phosphate Homeostasis -- Chapter 27. Mineralization -- Chapter 28. Modeling and Remodeling: How Bone Cells Work Together -- Chapter 29. Vitamin D and the Kidney -- Chapter 30. Vitamin D and the Parathyroids -- Chapter 31. Calcium-Sensing Receptor -- Section IV: TARGET ORGANS AND TISSUES -- Chapter 32. Bone -- Chapter 33. Cartilage and Vitamin D: Genomic and Nongenomic Regulation by 1,25(OH)2D3 and 24,25(OH)2D3 -- Chapter 34. Dento-alveolar Bone Complex and Vitamin D -- Chapter 35. Vitamin D: Role in Skin and Hair -- Chapter 36. Regulation of Immune Responses by Vitamin D Receptor Ligands -- Chapter 37. Vitamin D and Osteoblasts -- Chapter 38. Vitamin D and Osteoclastogenesis -- Chapter 39. Vitamin D Control of the Calcitonin Gene in Thyroid C Cells -- Chapter 40. Vitamin D Regulation of Type I Collagen Expression in Bone -- Chapter 41. Target Genes: Bone Proteins -- Chapter 42. The Calbindins: Calbindin-D9K and Calbindin-D28K -- Chapter 43. Target Genes: PTHrP -- Chapter 44. Effects of 1,25-Dihydroxyvitamin D3 on Voltage-Sensitive Calcium Channels in the Vitamin D Endocrine System -- Chapter 45. Vitamin D and the Cellular Response to Oxidative Stress -- Section V: HUMAN PHYSIOLOGY -- Chapter 46. Vitamin D: Role in the Calcium Economy -- Chapter 47. Effects of Race, Geography, Body Habitus, Diet, and Exercise on Vitamin D Metabolism -- Chapter 48. Perinatal Vitamin D Actions -- Chapter 49. Vitamin D Deficiency and Calcium Absorption During Infancy and Childhood -- Chapter 50. Vitamin D Metabolism and Aging -- Chapter 51. Vitamin D Metabolism in Pregnancy and Lactation -- Chapter 52. Vitamin D and Reproductive Organs. , Chapter 53. Vitamin D Receptor as a Sensor for Toxic Bile Acids -- Chapter 54. Vitamin D and the Renin-Angiotensin System -- Chapter 55. Vitamin D and Muscle -- Chapter 56. Vitamin D and Cardiovascular Medicine -- 9780122526879v2 -- Front Cover -- Vitamin D -- Copyright Page -- Contents -- List of Contributors -- Preface to the 2nd Edition -- Preface to the 1st Edition -- Abbreviations -- Section VI: DIAGNOSIS AND MANAGEMENT -- Chapter 57. Approach to the Patient with Metabolic Bone Disease -- Chapter 58. Detection of Vitamin D and Its Major Metabolites -- Chapter 59. Bone Histomorphometry -- Chapter 60. Radiology of Rickets and Osteomalacia -- Chapter 61. The Pharmacology of Vitamin D, Including Fortification Strategies -- Section VII: DISORDERS OF THE VITAMIN D ENDOCRINE SYSTEM -- Chapter 62. How to Define Normal Values for Serum Concentrations of 25-Hydroxyvitamin D? An Overview -- Chapter 63. Vitamin D and the Pathogenesis of Rickets and Osteomalacia -- Chapter 64. The Hypocalcemic Disorders: Differential Diagnosis and Therapeutic Use of Vitamin D -- Chapter 65. Vitamin D Deficiency and Nutritional Rickets in Children -- Chapter 66. Vitamin D Insufficiency in Adults and the Elderly -- Chapter 67. Vitamin D and Osteoporosis -- Chapter 68. Genetic Vitamin D Receptor Polymorphisms and Risk of Disease -- Chapter 69. Clinical Disorders of Phosphate Homeostasis -- Chapter 70. Disorders of Phosphate Metabolism: Autosomal Dominant Hypophosphatemic Rickets, Tumor Induced Osteomalacia, Fibrous Dysplasia, and the Pathophysiological Relevance of FGF23 -- Chapter 71. Vitamin D Pseudodeficiency -- Chapter 72. Hereditary 1,25-Dihydroxyvitamin D Resistant Rickets -- Chapter 73. Glucocorticoids and Vitamin D -- Chapter 74. Drug and Hormone Effects on Vitamin D Metabolism -- Chapter 75. Bone Disorders Associated with Gastrointestinal &. , Hepatobiliary Disease -- Chapter 76. Vitamin D and Renal Failure -- Chapter 77. Idiopathic Hypercalciuria and Nephrolithiasis -- Chapter 78. Hypercalcemia Due to Vitamin D Toxicity -- Chapter 79. Extra-renal 1 -hydroxylase Activity and Human Disease -- Section VIII: NEW VITAMIN D ANALOGS -- Overview -- Chapter 80. Overview: Rational Design of 1 ,25-Dihydroxyvitamin D3 Analogs (Deltanoids) -- Chapter 81. Analog Metabolism -- Chapter 82. Mechanisms for the Selective Actions of Vitamin D Analogs -- Chapter 83. Molecular Basis for Differential Action of Vitamin D Analogs -- Chapter 84. Development of New Vitamin D Analogs -- Chapter 85. Gemini: The 1,25-dihydroxy Vitamin D Analogs with Two Side-Chains -- Chapter 86. Development of OCT and ED-71 -- Chapter 87. 2-Carbon-Modified Analogs of 19-Nor-1 , 25-Dihydroxyvitamin D3 -- Chapter 88. Non-steroidal Analogs -- Section IX: VITAMIN D AND CANCER -- Chapter 89. Vitamin D: Cancer and Differentiation -- Chapter 90. Vitamin D, Sunlight, and the Natural History of Prostate Cancer -- Chapter 91. Epidemiology of Cancer Risk: Vitamin D and Calcium -- Chapter 92. Differentiation and the Cell Cycle -- Chapter 93. Vitamin D and Breast Cancer -- Chapter 94. Vitamin D and Prostate Cancer -- Chapter 95. Vitamin D and Colon Cancer -- Chapter 96. Vitamin D and Hematological Malignancy -- Chapter 97. Clinical Development of Calcitriol and Calcitriol Analogs in Oncology: Progress and Considerations for Future Development -- Section X: EMERGING USES -- Chapter 98. Vitamin D3: Autoimmunity and Immunosuppression -- Chapter 99. Vitamin D and Diabetes -- Chapter 100. Vitamin D, A Neuroactive Hormone: From Brain Development to Neurodegenerative Disorders -- Chapter 101. Psoriasis and Other Skin Diseases -- Chapter 102. Muscles and Falls -- Chapter 103. Renal Failure and Secondary Hyperparathyroidism. , Chapter 104. Inhibition of Benign Prostatic Hyperplasia by Vitamin D Receptor Ligands -- Index.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Bone diseases in children. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (885 pages)
    Edition: 2nd ed.
    ISBN: 9780123820419
    DDC: 611.7/1
    Language: English
    Note: Front Cover -- Pediatric Bone : Biology & -- Diseases -- Copyright -- Contents -- Preface to the Second Edition -- List of Contributors -- Chapter 1 - Bone Cell Biology: Osteoclasts, Osteoblasts, Osteocytes -- Introduction to Bone -- Osteoclasts -- The osteoblast Cell Lineage -- The Osteocyte -- Conclusion -- References -- Chapter 2 - Bone Matrix and Mineralization -- Structural Hierarchy in Bone -- Organic Matrix of Bone -- Mineralization of Bone -- References -- Chapter 3 - Prenatal Bone Development -- Modes of Bone Formation -- Timing and Sequence of Bone Formation in Humans -- Molecular Regulation of Skeletal Development -- References -- Chapter 4 - Postnatal Bone Growth: Growth Plate Biology, Bone Formation, and Remodeling -- Endochondral and Intramembranous Bone Formation -- Cellular and Molecular Control of Skeletal Growth -- Endocrine Control of Postnatal Bone Growth -- Concluding remarks -- References -- Chapter 5 - Dental Development and Maturation, from the Dental Crypt to the Final Occlusion -- The tooth bud -- Mechanism of single tooth eruption -- Development of the dental occlusion -- Maturation of the Periodontal Ligament -- Dento-alveolar growth and displacement of bone structures -- Dental defects and syndromes -- Conclusion -- References -- Chapter 6 - Parathyroid Hormone and Calcium Homeostasis -- Introduction -- Physiological Role of PTH -- PTH-Dependent Regulation of Calcium Homeostasis -- Parathyroid Hormone-Related Peptide -- Receptors for PTH and PTHrP -- Summary -- References -- Chapter 7 - Phosphate Homeostasis Regulatory Mechanisms -- Introduction -- Physiological Aspects -- Endocrine Regulation of Phosphate Homeostasis -- References -- Chapter 8 - Vitamin D Biology -- Metabolic Activation of Vitamin D -- Mechanism of Action -- Role of Vitamin D in Calcium Homeostasis -- Summary and Perspectives -- References. , Chapter 9 - Peak Bone Mass and Its Regulation -- Definition and Importance of Peak Bone Mass -- Characteristics of Bone Mass and Strength Acquisition -- Determinants of Peak Bone Mass and Strength -- Conclusions -- References -- Chapter 10 - Pregnancy and Lactation -- Introduction -- Mineral Fluxes from Mother to Offspring -- Pregnancy -- Lactation -- Summary -- References -- Chapter 11 - Fetal Mineral Homeostasis -- Fetal Adaptive Goals -- Minerals -- Calciotropic Hormones -- Fetal Parathyroids and Thymus -- Calcium Sensing Receptor -- Placental Calcium Transport -- Placental Transport of Magnesium and Phosphorus -- Fetal Kidneys and Amniotic Fluid -- Fetal Skeleton -- Fetal Response to Maternal Hyperparathyroidism -- Fetal Response to Maternal Hypoparathyroidism -- Integrated Fetal Calcium Homeostasis -- References -- Appendix -- Chapter 12 - Radiology -- Imaging Techniques, Interpretation, and Strategies -- Imaging Strategies -- Genetic Disorders -- Rickets and Metabolic Bone Disorders -- A Radiological Approach to Non-Accidental Injury -- References -- Chapter 13 - Non-invasive Techniques for Bone Mass Measurement -- Introduction -- Indications for Bone Mass Measurements -- Assessment of Bone Quality in Children -- Classification of Bone Health in Children -- Radiation Dose in Bone Densitometry -- Non-Invasive Measurement Techniques -- Summary -- References -- Chapter 14 - Assessment of Maturation: Bone Age and Pubertal Assessment -- Background -- The Methods of Assessment -- Reliability -- Comparability of the Atlas, Bone-Specific and Automatic Methods -- Secondary Sexual Development -- References -- Chapter 15 - Biochemical Markers of Bone Metabolism -- Introduction -- What is bone metabolism in children? -- Biochemical considerations -- Markers of bone formation -- Markers of bone resorption -- Pediatric reference data. , Bone markers during normal development -- Bone and collagen markers in metabolic bone diseases -- Clinical areas of interest -- Clinical and research value of biochemical markers of bone metabolism -- References -- Chapter 16 - Pediatric Bone Histomorphometry -- Introduction -- Basic concepts -- Methodology -- Histomorphometric measures -- Pediatric bone histomorphometry in health and disease -- Indications for bone biopsy and histomorphometry in pediatric bone disorders -- References -- Chapter 17 - A Diagnostic Approach to Skeletal Dysplasias -- Introduction -- Background -- History and physical examination -- Diagnostic imaging -- Biochemical investigations -- Cartilage histology -- Molecular basis -- Prenatal detection of suspected skeletal dysplasia -- Conclusion -- References -- Chapter 18 - The Spectrum of Pediatric Osteoporosis -- Introduction -- Definition and diagnosis of osteoporosis in pediatric patients -- The mechanostat model: muscle-bone interaction in bone growth and development -- The spectrum of pediatric osteoporosis -- General aspects of prevention and treatment -- Summary and future directions -- Appendix: differentiating child abuse from bone fragility conditions -- References -- Chapter 19 - Osteogenesis Imperfecta -- Introduction -- Classification -- The Widening Spectrum of OI Types -- Differential Diagnosis -- General Clinical Findings -- Pathophysiology -- Therapy -- References -- Chapter 20 - Sclerosing Bone Dysplasias -- Introduction -- Neonatal Osteosclerotic Dysplasias -- Diseases without Major Changes in Bone Shape -- Increased Bone Density Group with Metaphyseal and/or Diaphyseal Involvement -- Conclusions -- References -- Chapter 21 - Parathyroid Disorders -- Introduction -- PTH Gene Structure and Function -- Hypocalcemic Disorders -- Hypercalcemic Diseases -- Concluding Remarks -- References. , Chapter 22 - Fibrous Dysplasia -- Introduction -- Clinical Features -- Molecular Genetics -- Determinants of Phenotypic Variability -- Pathology -- Pathogenesis -- Management and Treatment -- References -- Chapter 23 - Nutritional Rickets -- An Overview of Rickets -- Nutritional Rickets -- References -- Chapter 24 - Metabolic Bone Disease in the Neonatal Period and its Later Sequelae -- Early Life Influences on Skeletal Health and Development -- Skeletal Development and Mineral Accretion in Utero -- Physiological Changes in Mineral Homeostasis at Birth -- Preterm Delivery and Bone Metabolism -- Skeletal Health and Metabolic Bone Disease in Preterm Infants -- Recommendations -- Neonatal Hypocalcemia -- Term Infants: Early Growth and Later Bone Development -- Specific Environmental Exposures in Utero -- Potential Mechanisms: Developmental Plasticity, Gene-Environment Interactions and Epigenetics -- Summary -- References -- Chapter 25 - Rickets Due to Hereditary Abnormalities of Vitamin D Synthesis or Action -- Introduction -- Biosynthesis of Vitamin D -- Vitamin D Biosynthetic Enzymes -- Rickets Due to Abnormalities of Vitamin D Metabolism -- Rickets Due to Abnormalities of Vitamin D Action -- References -- Chapter 26 - Familial Hypophosphatemia and Related Disorders -- Introduction -- Regulation of phosphate homeostasis -- Clinical disorders of phosphate homeostasis -- Molecules, pathophysiology, and lessons from animal models -- Current problems and unresolved questions -- References -- Chapter 27 - Hereditary Tubular Disorders of Mineral Handling -- Introduction -- Phosphate -- Calcium and Magnesium -- Acid-base -- Conclusion -- References -- Chapter 28 - Hypophosphatasia -- Introduction -- Biochemistry and molecular biology of alkaline phosphatase -- Physiology of skeletal formation and alkaline phosphatase function -- Hypophosphatasia. , Physiological role of tissue-non-specific alkaline phosphatase explored in hypophosphatasia -- References -- Chapter 29 - Chronic Kidney Disease Mineral and Bone Disorder -- Introduction -- Pathogenesis of CKD-MBD -- Renal Osteodystrophy -- Treatment of CKD-MBD -- Bone Disease after Successful Kidney Transplantation -- References -- Chapter 30 - Extraskeletal Bone Formation -- Introduction -- Non-hereditary forms of pediatric heterotopic ossification -- Fibrodysplasia ossificans progressiva (FOP) -- Progressive osseous heteroplasia (POH) -- Conclusions -- References -- Index -- Color Plates.
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Hypophosphatemia is a genetically heterogeneous disease. Here, we mapped an autosomal recessive form (designated ARHP) to chromosome 4q21 and identified homozygous mutations in DMP1 (dentin matrix protein 1), which encodes a non-collagenous bone matrix protein expressed in osteoblasts and ...
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 33 (1981), S. 173-175 
    ISSN: 1432-0827
    Keywords: Vitamin D-resistant rickets ; hypophosphatemia ; 1,25-dihydroxyvitamin D ; 1,25-(OH)2D ; calcitriol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Fasting serum 1α,25-dihydroxyvitamin D (1,25-(OH)2D) levels were measured in 3 groups of hypophosphatemic vitamin D-resistant rickets (VDRR) patients: those untreated; those treated with vitamin D and phosphate; and those treated with 1,25-(OH)2D3 and phosphate. In the untreated patients, the mean 1,25-(OH)2D level was higher than in our age-matched control group. Except for one at 66 pg/ml, individual values were however within normal limits. Long term vitamin D2 therapy was accompanied by a slight but significant decrease in 1,25-(OH)2D concentrations; nonetheless the levels remained within the normal range. In the third group of patients, the concentration of 1,25-(OH)2D rose to supranormal levels when sampling was done 1–3 hours after administration of the hormone, decreasing rapidly to levels below that of normal subjects when the specimens were collected 12–24 hours later. Our data show that an alteration of the vitamin D activation pathway is unlikely to be part of the pathogenic mechanism underlying the VDRR condition. Calcitriol (1α,25-(OH)2D3) as RocaltrolR in capsules of 0.25 and 0.50 µg was kindly supplied by Dr. Patrick Le Morvan (Hoffmann-La Roche Ltd, Vaudreuil, Que., Canada).
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 35 (1983), S. 383-391 
    ISSN: 1432-0827
    Keywords: Phosphate ; 1,25(OH)2D3 ; Bone collagen synthesis ; Hyp mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Calvarial bones from hypophosphatemic (Hyp) mice and normal littermates were cultured in a chemically defined medium to determine: (a) the effect of medium phosphate (Pi) concentration (1, 2, and 3 mM) on collagen synthesis; (b) the effect of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] (10−12M–10−7M) on collagen synthesis; and (c) whether bone responsiveness to 1,25(OH)2D3 was affected by changes in medium Pi concentration. Bone collagen synthesis was evaluated by measuring [3H]hydroxyproline formation. The distribution of labeled hydroxyproline between bone explant and culture medium (total and dialyzable fraction) was studied. These experiments confirm that 1,25(OH)2D3 inhibits specifically bone collagen synthesis in vitro. We did not detect any effect of medium Pi concentration on basal collagen synthesis but were able to demonstrate that lowering medium Pi concentration increased the 1,25(OH)2D3-induced inhibition of collagen synthesis. Bones from both genotypes responded to 1,25(OH)2D3, but modulation of this response by changes in Pi concentration was altered in Hyp bone as, in contrast to normal bone, its response to 1,25(OH)2D3 was unaffected when medium Pi concentration was decreased from 3 to 2 mM. These findings support the hypothesis of an altered response of bone to 1,25(OH)2D3 in the Hyp mouse.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 35 (1983), S. 443-448 
    ISSN: 1432-0827
    Keywords: Periosteocytic lesions ; Bone mineralization ; Vitamin D-resistant rickets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary Hypomineralized periosteocytic lesions (HPL) are peculiar bone features associated with osteomalacia in vitamin D-resistant rickets (VDRR). To determine whether HPL result from defective bone mineralization, tetracycline double-labeled cortical bone specimens from VDRR children were analyzed before (n=13) and after treatment with phosphate supplements combined with vitamin D2 (Pi+D, n=20) or 1,25-dihydroxyvitamin D3 (Pi+1,25) (n=22). On microradiographs of undecalcified sections, the percentage of osteocytes with HPL was determined separately in the old interstitial bone, the well calcified resting osteons, and in the less mineralized growing osteons. Using histomorphometric methods, dynamic parameters of cortical bone mineralization were assessed on the same samples. In untreated patients, HPL were more prominent in the less calcified bone areas, in accordance with the reported decrease with bone aging. In contrast to therapy with Pi+D, Pi+1,25 reduced HPL frequency in all cortical areas in correlation with improvement of dynamic parameters of bone mineralization. In addition, HPL frequency progressively decreased with the duration of treatment, further demonstrating that the lesion resulted in part from the defective cortical bone mineralization. However, HPL frequency was unrelated to the severity of osteomalacia in untreated children and the lesion persisted in more than 20% of young osteocytes despite complete correction of bone mineralization parameters. The data support the hypothesis that an abnormal osteocytic function, which may be part of the VDRR phenotype, is involved along with overall impaired bone mineralization in the etiology of the periosteocytic lesion.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 34 (1982), S. 158-164 
    ISSN: 1432-0827
    Keywords: Hypophosphatemia ; Vitamin D metabolites ; Bone mineralization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary The hypophosphatemic male mouse (Hyp/y), the proposed model for human vitamin D-resistant rickets (VDRR), is characterized by chronic hypophosphatemia, dwarfism, and rachitic and osteomalacic bone lesions. We have reported that treatment of Hyp/y mice with phosphate salts (Pi) heals rickets but does not correct the defective endosteal bone mineralization. In an attempt to cure osteomalacia, mutant male animals were treated with Pi combined with 25-hydroxyvitamin D3 (25OHD3, 1 µg/kg/day), 24,25-dihydroxyvitamin D3 [24,25(OH)2D3, 0.5 µg/kg/day], or 1,25-dihydroxyvitamin D3 [1,25(OH)2D3, 0.05–0.25 µg/kg/day] infused constantly for 3 weeks. The biochemical and skeletal effects of treatment were assessed by analytical methods and bone histomorphometry. The results show that only 1,25(OH)2D3 produced a dose-dependent elevation of serum calcium and phosphorus, and greatly improved bone mineralization at doses high enough to increase serum calcium and phosphorus concentrations within or above the normal range. Better improvement of bone mineralization was obtained when Pi was combined to 1,25(OH)2D3. In conjunction with the correction of hypocalcemia, Pi+1,25(OH)2D3 suppressed the stimulation of bone turnover induced by Pi supplementation. The results show that, as in VDRR children, 1,25(OH)2D3 produces beneficial effects on bone lesions in Hyp/y mice, mainly through enhancement of mineral availability. However, the persistence of osteomalacia despite correction of serum mineral concentrations suggests that there is a specific bone cell resistance to mineral and/or hormonal influences in Hyp/y mice.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Calcified tissue international 33 (1981), S. 77-79 
    ISSN: 1432-0827
    Keywords: Collagen crosslinking ; Hypophosphatemia ; Vitamin D-resistant rickets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary In order to evaluate the influence of bone mineralization on collagen metabolism, the bone collagen crosslinks were determined in femur diaphyses of mice with X-linked hypophosphatemia and of control littermates. No quantititative difference could be elicited between the two groups. It was also noted that in the mouse, cortical bone maturation is accompanied by a slight increase in the number of reducible crosslinks.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...