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otitis media/l tyrosin
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Exome sequencing identifies a missense mutation in Isl1 associated with low penetrance otitis media in dearisch mice.
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BACKGROUND
Inflammation of the middle ear (otitis media) is very common and can lead to serious complications if not resolved. Genetic studies suggest an inherited component, but few of the genes that contribute to this condition are known. Mouse mutants have contributed significantly to the
Expression of vascular endothelial growth factor receptors in experimental otitis media in the rat.
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OBJECTIVE
Increased vascular permeability and endothelial cell growth are important in the pathogenesis of otitis media with effusion (OME) and vascular endothelial growth factor (VEGF) is known to play an important role in the increased vascular permeability and angiogenesis associated with OME.
A single nasal dose of fms-like tyrosine kinase receptor-3 ligand, but not peritoneal application, enhances nontypeable Haemophilus influenzae-specific long-term mucosal immune responses in the nasopharynx.
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Nasal vaccination is an effective therapeutic regimen for preventing otitis media. In the development of nasal vaccine, an appropriate adjuvant is required. In the present study, we examined the efficacy of fms-like tyrosine kinase receptor-3 ligand (Flt3L) as a mucosal adjuvant. Flt3L was
Tubulin tyrosine ligase-like 1 deficiency results in chronic rhinosinusitis and abnormal development of spermatid flagella in mice.
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Tubulin tyrosine ligase-like 1 (TTLL1) protein is a member of the tubulin tyrosine ligase superfamily of proteins that are involved in the posttranslational polyglutamylation of tubulin in axonemal microtubules within cilia and flagella. To investigate the physiological role of TTLL1, the authors
A novel Bruton's tyrosine kinase gene (BTK) invariant splice site mutation in a Malaysian family with X-linked agammaglobulinemia.
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X-linked agammaglobulinemia (XLA) is a rare genetic disorder caused by mutations in the Bruton's tyrosine kinase (BTK) gene. These mutations cause defects in early B cell development. A patient with no circulating B cells and low serum immunoglobulin isotypes was studied as were his mother and
Absence of autoantibodies connected to autoimmune polyendocrine syndrome type I and II and Addison's disease in girls and women with Turner syndrome.
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BACKGROUND
A disturbance in the immune system has been described in Turner syndrome (45,X), with an association to low levels of IgG and IgM and decreased levels of T- and B-lymphocytes. Also different autoimmune diseases have been connected to Turner syndrome (45,X), thyroiditis being the most
Clinical and mutational features of Vietnamese children with X-linked agammaglobulinemia.
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BACKGROUND
X-linked agammaglobulinemia (XLA) is a primary immune deficiency characterized by recurrent bacterial infections and profoundly depressed serum immunoglobulin levels and circulating mature B cells. It is caused by mutations of the Bruton tyrosine kinase (BTK) gene and is the most common
A novel BTK gene mutation, c.82delC (p.Arg28 Alafs*5), in a Korean family with X-linked agammaglobulinemia.
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X-linked agammaglobulinemia (XLA) is a hereditary humoral immunodeficiency that results from Bruton's tyrosine kinase (BTK) gene mutations. These mutations cause defects in B-cell development, resulting in the virtual absence of these lymphocytes from the peripheral circulation. Consequently, this
Effects of cigarette smoking on mucin production in human middle ear epithelial cells.
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OBJECTIVE
Otitis media (OM) is the most common disease in preschool age children related to passive cigarette smoking as risk factor. In this study, we investigate whether the cigarette smoking can induce the inflammation in human middle ear epithelial cell, and cigarette smoke-induced inflammation
X-linked agammaglobulinemia in northern Thailand.
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X-linked agammaglobulinemia (XLA) is a primary immunodeficiency characterized by a failure to generate immunoglobulins of all isotypes due to the absence of mature B cells and plasma cells, secondary to mutations in the Bruton's tyrosine kinase (Btk) gene. We report six patients with XLA, confirmed
D-amino acids do not inhibit Pseudomonas aeruginosa biofilm formation.
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Pseudomonas aeruginosa, a known biofilm-forming organism, is an opportunistic pathogen that plays an important role in chronic otitis media, tracheitis, cholesteatoma, chronic wounds, and implant infections. Eradication of biofilm infections has been a challenge because the biofilm phenotype
[X-linked agammaglobulinemia: experience in a Portuguese hospital].
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BACKGROUND
X-Linked agammaglobulinemia (XLA) is characterized by an arrest of B cell differentiation, leading to recurrent bacterial infections. Lifelong immunoglobulin replacement therapy (IRT) is indicated to prevent infections and their complications.
METHODS
A retrospective study of patients
[Expression of PTKs CDK4 and p15 in the middle ear cholesteatomatous epithelium].
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OBJECTIVE
To explore the cells proliferation and its molecular regulating mechanisms of cholesteatomatous epithelium from the aspect of protein tyrosine kinases (PTKs) signal transduction and cell cycle control.
METHODS
The expressions of phosphated PTKs, CDK4 and p15 were investigated by
Eczema and X-linked agammaglobulinaemia.
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An 8-year-old boy presented with eczematous skin lesions, recurrent otitis media and unexplained pyrexias. X-linked agammaglobulinaemia was diagnosed and treatment commenced with intravenous immunoglobulin replacement therapy. X-linked agammaglobulinaemia (XLA) is a primary immunodeficiency syndrome
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
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