osteopetrosis/phosphatase

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Alkaline phosphatase activity in serum of guinea fowl bearing bone tumours induced by osteopetrosis virus strain PTS-56.

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Alkaline phosphatase (AP) activities of sera from guinea fowl infected with osteopetrosis virus strain PTS-56 were investigated. Enzyme activities in birds of infected and control groups varied. AP activities in control guinea fowls, 10 to 15 weeks of age, were twice as high as those of 1-year-old

Measurement of tartrate-resistant acid phosphatase and the brain isoenzyme of creatine kinase accurately diagnoses type II autosomal dominant osteopetrosis but does not identify gene carriers.

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Autosomal dominant osteopetrosis type II (ADO2) is typically diagnosed from radiographs, which demonstrate the pathognomonic findings of osteosclerosis and endobone formation. Individuals with ADO2 also have elevated serum levels of tartrate-resistant acid phosphatase (TRAP) and the BB isoenzyme of

Osteoclast-derived serum tartrate-resistant acid phosphatase 5b in Albers-Schonberg disease (type II autosomal dominant osteopetrosis).

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BACKGROUND Albers-Schönberg disease, or autosomal dominant osteopetrosis type II (ADO2), is caused by ineffective osteoclastic bone resorption resulting from mutations in the chloride channel 7 (ClCN7) gene. Individuals with ADO2 have increased numbers of large ineffective osteoclasts in addition to

Mice lacking tartrate-resistant acid phosphatase (Acp 5) have disrupted endochondral ossification and mild osteopetrosis.

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Mature osteoclasts specifically express the purple, band 5 isozyme (Acp 5) of tartrate-resistant acid phosphatase, a binuclear metalloenzyme that can generate reactive oxygen species. The function of Acp 5 was investigated by targeted disruption of the gene in mice. Animals homozygous for the null

Serum phosphatase in osteopetrosis.

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Biochemical evidence of disturbed bone metabolism and calcium homeostasis in two types of autosomal dominant osteopetrosis.

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Biochemical markers of bone resorption and bone formation were measured in 14 patients with autosomal dominant osteopetrosis, and compared with age- and sex-matched controls. There were eight patients with the radiological type I characterized by diffuse, symmetrical osteosclerosis with pronounced

Osteopetrosis. A genetic and epidemiological study.

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By a systemic search of osteopetrosis in the county of Funen, Denmark, the prevalence was 5.5/100,000 inhabitants. The study disclosed 33 patients of whom 32 had the mild, autosomal dominant form of osteopetrosis. Two obligate carriers, who had the genotype but were not phenotypically affected, were

A new heterozygous mutation (R714C) of the osteopetrosis gene, pleckstrin homolog domain containing family M (with run domain) member 1 (PLEKHM1), impairs vesicular acidification and increases TRACP secretion in osteoclasts.

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We studied phenotypic and cellular aspects in a patient with a heterozygous mutation of the PLEKHM1 gene and obtained some indications regarding the role of the protein in bone cell function. Plekhm1 is involved in osteoclast endosomal vesicle acidification and TRACP exocytosis, contributing to

Bone mineral density and laboratory evaluation of a type II autosomal dominant osteopetrosis carrier.

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Type II autosomal dominant osteopetrosis (ADO2) is an inherited disorder characterized by increased skeletal mass and characteristic abnormalities evident on radiography. Although previous investigators have described nonpenetrant individuals (carriers), it is not known whether carriers manifest

Replication of an osteopetrosis-inducing avian leukosis virus in fibroblasts, osteoblasts, and osteopetrotic bone.

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Avian leukosis virus (ALV)-induced osteopetrosis is caused by the abnormal growth and differentiation of osteoblasts. To evaluate the role of infection in osteopetrosis induction, the replication of an osteopetrosis-inducing virus (Br21) has been compared in osteopetrotic bone, calvarial-derived

Osteopetrosis, hypophosphatemia, and phosphaturia in a young man: a case presentation and differential diagnosis.

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We report the case of a 30-year-old African-American male with osteopetrosis and hypophosphatemia, presenting with diffuse myalgias. Laboratory evaluation performed revealed a low serum phosphorus level with urinary phosphate wasting, low calcium, and 25-hydroxyvitamin D concentrations, as well as

Bone morphogenetic protein-induced heterotopic bone in osteopetrosis.

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The objectives of the present research on the osteopetrotic mouse are to investigate the factors influencing heterotopic bone development. The osteopetrotic mutant was deficient in macrophage colony stimulating factor and failed to activate functioning monocytes, macrophages, and osteoclasts.

Osteoclast abnormalities in idiopathic osteopetrosis. Reference to the ultrastructural histochemistry study.

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In order to investigate skeletal abnormalities in a case of idiopathic osteopetrosis, a bone biopsy was taken from the anterior iliac crest and prepared for ultrastructural and histochemical study. There was a drastic reduction in osteoclastic bone resorption. The ruffle border and sealing zone,

Osteopetrosis with micro-lacunar resorption because of defective integrin organization.

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In vitro differentiated monocytes were used to characterize the cellular defect in a type of osteopetrosis with minimally functional osteoclasts, in which defects associated with common causes of osteopetrosis were excluded by gene sequencing. Monocytes from the blood of a 28-year-old patient were

A case of cavernous sinus thrombophlebitis and meningitis as a complication in osteopetrosis.

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Osteopetrosis is a rare genetic bone disease characterized by increased bone density but prone to breakage due to defective osteoclastic function. Among two primary types of autosomal dominant osteopetrosis (ADO), osteopetrosis type II is characterized by sclerosis of bones, predominantly involving

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