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Relevant bibliographies by topics / Histomorphometric / Books

Books on the topic 'Histomorphometric'

To see the other types of publications on this topic, follow the link: Histomorphometric.

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Kirpalani, Anish. A hemodynamic and histomorphometric analysis of the human right coronary artery. Ottawa: National Library of Canada, 1996.

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2

Freedman, Douglas Marc. The effects of cyclosporine on bone volume and bone formation rate: A dose response histomorphometric analysis in the rat model. [New Haven: s.n.], 1990.

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3

W, Axelrod Douglas, and Melsen Flemming, eds. Bone histomorphometry. New York: Raven Press, 1994.

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4

Angelopoulos, Gerassimos G. Long-term stability of temporomandibular joint remodelling following continuous mandibular advancement in the juvenile macara fascicularis : a histomorphometric, cephalometric and electromyographic investigation. [Toronto: Faculty of Dentistry, University of Toronto], 1991.

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5

Rehman, Mirza Tariq Anisu. The role of bone histomorphometry in the management of postmenopausal osteoporosis. Manchester: University of Manchester, 1994.

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6

Ross, Nancy Ann. A quantitative skeletal aging technique utilizing histomorphometry of the rib for forensic and bioarchaeological investigators. [Dallas, Tex.]: [s.n.], 1992.

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7

Kimble, Robert Benjamin. Histomorphometric analysis of tibiotarsal bone from T lymphocyte-deficient chickens. 1990.

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8

Abdominal aorta: A patient-specific hemodynamic model and histomorphometric analysis. Ottawa: National Library of Canada, 2002.

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9

Norton, Keith D. Histomorphometric analysis of cervical vertebrae from horses with cervical vertebral malformation. 1986.

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10

P, Garetto Lawrence, and United States. National Aeronautics and Space Administration., eds. Cell kinetic and histomorphometric analysis of microgravitational osteopenia: PARE.03B : final report : NAG 2-756. [Washington, DC]: National Aeronautics and Space Administration, 1998.

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11

United States. National Aeronautics and Space Administration., ed. Cell Kinetic And Histomorphometric Analysis Of Microgravitational Osteopenia: PARE.038 Final Report... NASA/CR-1998-207003... Apr. 7, 1998. [S.l: s.n., 1999.

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12

Voudouris, John C. *. Glenoid fossa and condylar remodeling following progressive mandibular protrusion in the juvenile "Macaca fascicularis": a computerized histomorphometric, cephalometric, and electromyographic investigation. 1988.

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13

Long-term stability of temporomandibular joint remodelling following continuous mandibular advancement in the juvenile macaca fascicularis: A histomorphometric, cephalometric and electromyographic investigation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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14

R, Recker Robert, ed. Bone histomorphometry: Techniques and interpretation. Boca Raton, Fla: CRC Press, 1990.

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15

Rummens, Katrien. Environmental Regulation of Fetal Mineralization: Studies in Guinea-Pigs & Mice, With an Emphasis on Bone Histomorphometry (Acta Biomedica Lovaniensia, 279). Leuven Univ Pr, 2003.

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16

Sprague, Stuart M., and Menaka Sarav. Chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0115_update_001.

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The kidneys play a critical role in maintaining normal serum calcium and phosphorus concentrations, under the regulation of three main hormones: parathyroid hormone, calcitriol, and fibroblast growth factor 23. With the progression of chronic kidney disease (CKD), most patients develop CKD–mineral and bone disorder (CKD-MBD), which is a systemic disorder involving derangement in mineral metabolism, renal osteodystrophy, and extraskeletal calcification. Disturbances in mineral metabolism develop early in CKD and include phosphate retention, hypocalcaemia, vitamin D deficiency, and hyperparathyroidism. Renal osteodystrophy involves pathologic changes of bone morphology related to progressive CKD and is quantifiable by histomorphometry, based on bone biopsy. CKD-MBD is associated with significant morbidity, including bone loss, fractures, cardiovascular disease, immune suppression, as well as increased mortality. As the disorder begins early in the course of CKD, a proactive approach with intervention is important. Therapeutic strategies could then be employed to prevent and correct these disturbances, aiming to improve cardiovascular outcomes and survival. Current practice guidelines for CKD-MBD are based on insufficient data and high-quality studies are required before specific treatment can be advocated strongly.

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17

Sprague, Stuart M., and James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.

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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.

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18

Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

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