exostoses/phosphatase

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Periosteal hyperostosis (exostosis) in DBA/1 male mice.

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Periosteal hyperostosis (exostosis) was identified in 5.9% (11/188) of DBA/1 male mice 10-14 weeks old used for collagen-induced arthritis (CIA) efficacy testing of immunomodulatory biologics. Mice with and without CIA in the affected limb, and also control and treated groups, were involved, with

A novel EXT1 splice site mutation in a kindred with hereditary multiple exostosis and osteoporosis.

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BACKGROUND Hereditary multiple exostosis (HME) is an autosomal dominant disorder characterized by the development of benign cartilage-capped tumors at the juxta-epiphyseal regions of long bones. HME is usually caused by mutations of EXT1 or EXT2. OBJECTIVE The objective of this study was to

The effect of aminoacetonitrile on calcium metabolism and bone in the rat.

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1. The effect of the osteolathyrogen aminoacetonitrile (AAN) on plasma calcium, phosphate and alkaline phosphatase, on bone, on growth rates, on absorption of calcium and phosphate in the gut and on their urinary excretion, has been examined in rats. 2. AAN caused a general deterioration in the

Pseudomonas-associated discospondylitis in a two-month-old llama.

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A 2-month-old female llama with a history of tetraparesis was presented for necropsy. This cria was apparently normal until it became ataxic during its second week of life. It had diminished flexor reflexes of the left forelimb and both hind limbs. Hematology and serum biochemistry revealed

Correlation of Pain and Fluoride Concentration in Allogeneic Hematopoietic Stem Cell Transplant Recipients on Voriconazole.

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Supportive care guidelines recommend antimold prophylaxis in hematopoietic stem cell transplant (HSCT) recipients deemed to have high risk for invasive fungal infection, leading to long-term use of voriconazole after allogeneic HSCT in patients who remain immunocompromised. Voriconazole has been

Intraosseous atypical chondroid tumor or chondrosarcoma grade 1 in patients with multiple osteochondromas.

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BACKGROUND The autosomal dominant condition multiple osteochondromas, formerly called multiple hereditary exostoses, is associated with a risk of malignant progression of osteochondroma into secondary peripheral chondrosarcoma. Most patients with multiple osteochondromas have exostosin-1 or

Asymmetric bone remodeling in mandibular and maxillary tori.

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OBJECTIVE Tori are frequent paucisymptomatic bony outgrowths of the oral cavity in three locations: torus palatinus (TP), mandibularis (TM), and maxillaris (TMax). Their usually described histological characteristics are unspecific: normal cortical bone with more or less trabecular bone. The aim of

Two outbreaks of fluorosis in cattle and sheep.

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Two outbreaks of fluorosis in cattle and sheep were investigated in the Northern Transvaal. The animals exhibited severe dental lesions, lameness and exostoses. Plasma fluoride concentrations were high and there was an inversion of the albumin/globulin ratio. Alkaline phosphatase activity was

Targeted disruption of Shp2 in chondrocytes leads to metachondromatosis with multiple cartilaginous protrusions.

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Metachondromatosis is a benign bone disease predominantly observed in the hands and feet of children or young adults demonstrating two different manifestations: a cartilage-capped bony outgrowth on the surface of the bone called exostosis and ectopic cartilaginous nodules inside the bone called

Fluoride excess and periostitis in transplant patients receiving long-term voriconazole therapy.

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BACKGROUND We describe a heart transplant patient with painful periostitis and exostoses who was receiving long-term therapy with voriconazole, which is a fluoride-containing medication. Elevated plasma and bone fluoride levels were identified. Discontinuation of voriconazole therapy led to

SHP2 Regulates the Osteogenic Fate of Growth Plate Hypertrophic Chondrocytes.

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Transdifferentiation of hypertrophic chondrocytes into bone-forming osteoblasts has been reported, yet the underlying molecular mechanism remains incompletely understood. SHP2 is an ubiquitously expressed cytoplasmic protein tyrosine phosphatase. SHP2 loss-of-function mutations in chondroid cells

Ptpn11 deletion in a novel progenitor causes metachondromatosis by inducing hedgehog signalling.

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The tyrosine phosphatase SHP2, encoded by PTPN11, is required for the survival, proliferation and differentiation of various cell types. Germline activating mutations in PTPN11 cause Noonan syndrome, whereas somatic PTPN11 mutations cause childhood myeloproliferative disease and contribute to some

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