osteomyelitis/tyrosine

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Role of fluoroethyl tyrosine positron emission tomography-computed tomography scan in differentiating ewing's sarcoma from osteomyelitis.

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Ewing's sarcoma is a kind of undifferentiated reticulocytic sarcoma, which was first reported in 1921 by James Ewing. It is difficult to differentiate Ewing's sarcoma from osteomyelitis on computed tomography (CT) and X-ray and hence cytological confirmation is needed. Fluorodeoxy glucose being a

The nonreceptor tyrosine kinase SYK induces autoinflammatory osteomyelitis in a mouse model of chronic recurrent multifocal osteomyelitis.

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Chronic recurrent multifocal osteomyelitis (CRMO) in humans can be modeled in Pstpip2^cmo mice, which carry a missense mutation in the proline-serine-threonine phosphatase-interacting protein 2 (Pstpip2) gene. As cmo disease in mice, the experimental model analogous to

Heterozygosity for the Y701C STAT1 mutation in a multiplex kindred with multifocal osteomyelitis.

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Heterozygosity for dominant-negative STAT1 mutations underlies autosomal dominant Mendelian susceptibility to mycobacterial diseases. Mutations conferring Mendelian susceptibility to mycobacterial diseases have been identified in the regions of the STAT1 gene encoding the tail segment, DNA-binding

Staphylococcus aureus causing osteomyelitis binds to a nonapeptide sequence in bone sialoprotein.

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Bone sialoprotein is a glycoprotein of the bone and dentine extracellular matrix. This protein consists of 320 amino acids, of which 25% are glutamic and aspartic acid residues. Sialic acid, containing oligosaccharides and tyrosine sulphate residues, supplies additional polyanionic properties.

A novel mutation in the JH4 domain of JAK3 causing severe combined immunodeficiency complicated by vertebral osteomyelitis.

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JAK3 is a tyrosine kinase essential for signaling downstream of the common gamma chain subunit shared by multiple cytokine receptors. JAK3 deficiency results in T-B+NK- severe combined immune deficiency (SCID). We report a patient with SCID due to a novel mutation in the JAK3 JH4 domain. The

A potential new target for autoinflammatory bone disease.

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Chronic recurrent multifocal osteomyelitis (CRMO) is an autoinflammatory bone disease mediated by the inflammatory cytokine, IL-1β. Although IL-1β is known as the key driver of bone lesions in CRMO, the signaling events leading to pathogenic levels of the cytokine are not fully understood. Using a

[Clinical features of X-linked agammaglobulinemia: analysis of 8 cases].

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OBJECTIVE X-linked agammaglobulinemia (XLA), caused by mutations in Bruton's tyrosine kinase (BTK), is a common form of inherited antibody deficiency. There were very few case reports of this disease that were diagnosed only based on clinical findings in China. The purpose of this study was to

Severe complications in wound healing and fracture treatment in two brothers with congenital insensitivity to pain with anhidrosis.

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Congenital insensitivity to pain with anhidrosis is an autosomal recessive disorder caused by mutations in the neurotrophic tyrosine receptor kinase 1 (NTRK1) gene, which encodes the receptor for nerve growth factor. We report the clinical and radiological pitfalls in the diagnosis and treatment of

Gain-of-function mutations in a member of the Src family kinases cause autoinflammatory bone disease in mice and humans.

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Autoinflammatory syndromes are characterized by dysregulation of the innate immune response with subsequent episodes of acute spontaneous inflammation. Chronic recurrent multifocal osteomyelitis (CRMO) is an autoinflammatory bone disorder that presents with bone pain and localized swelling.

Analysis of clinical presentations of Bruton disease: a review of 20 years of accumulated data from pediatric patients at Severance Hospital.

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OBJECTIVE X-linked agammaglobulinemia (XLA) is a humoral immunodeficiency disease caused by a mutation in the Bruton tyrosine kinase (BTK) gene resulting in defective B cell differentiation. Because it is a relatively rare disorder, it is difficult for clinicians to have a comprehensive

X-linked agammaglobulinemia: report on a United States registry of 201 patients.

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X-linked agammaglobulinemia (XLA) is a primary immunodeficiency caused by mutations in the gene for Bruton tyrosine kinase (BTK) that result in the deficient development of B lymphocytes and hypogammaglobulinemia. Because the disorder is uncommon, no single institution has had sufficient numbers of

PSTPIP2, a Protein Associated with Autoinflammatory Disease, Interacts with Inhibitory Enzymes SHIP1 and Csk.

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Mutations in the adaptor protein PSTPIP2 are the cause of the autoinflammatory disease chronic multifocal osteomyelitis in mice. This disease closely resembles the human disorder chronic recurrent multifocal osteomyelitis, characterized by sterile inflammation of the bones and often associated with

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