otitis media/phosphatase

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Bone resorption in chronic otitis media. A light-microscopical and histochemical investigation of acid phosphatase activity.

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As a continuation of our previous work, where we have demonstrated that in chronic otitis media the picture in the submucosa-bone marginal zone is dominated by capillary proliferation and occurrence of a mononuclear, histiocyte-like cell containing lysosome-like cytoplasmatic bodies, we now report

Curcumin Inhibits NTHi-Induced MUC5AC Mucin Overproduction in Otitis Media via Upregulation of MAPK Phosphatase MKP-1.

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Otitis media (OM), characterized by the presence of mucus overproduction and excess inflammation in the middle ear, is the most common childhood infection. Nontypeable Haemophilus influenzae (NTHi) pathogen is responsible for approximately one-third of episodes of bacteria-caused OM. Current

Vinpocetine inhibits Streptococcus pneumoniae-induced upregulation of mucin MUC5AC expression via induction of MKP-1 phosphatase in the pathogenesis of otitis media.

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Mucin overproduction is a hallmark of otitis media (OM). Streptococcus pneumoniae is one of the most common bacterial pathogens causing OM. Mucin MUC5AC plays an important role in mucociliary clearance of bacterial pathogens. However, if uncontrolled, excessive mucus contributes significantly to

Alteration of adenoid tissue alkaline and acid phosphatase in children with secretory otitis media.

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OBJECTIVE The role of pharyngeal lymphoid tissue in etiopathogenesis of secretory otitis is not yet defined. The influence of tonsillar and adenoid mass, weight, obstruction of naspharyngeal orrifitium, bacterial reservoire or some immunological events are of scientific interest. Tissue nonspecific

Comparison of free radicals and antioxidant enzymes in chronic otitis media with and without tympanosclerosis.

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OBJECTIVE The pathogenesis of tympanosclerosis is unclear. The study was performed to investigate the role of nitric oxide, free oxygen radicals, and antioxidants in development of tympanosclerosis in patients with chronic otitis media. METHODS A prospective study in patients with nasal

CYLD negatively regulates nontypeable Haemophilus influenzae-induced IL-8 expression via phosphatase MKP-1-dependent inhibition of ERK.

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Nontypeable Haemophilus influenzae (NTHi), a Gram-negative bacterium, is the primary cause of otitis media in children and the exacerbation of chronic obstructive pulmonary disease in adults. A hallmark of both diseases is an overactive inflammatory response, including the upregulation of

Phosphodiesterase 4B mediates extracellular signal-regulated kinase-dependent up-regulation of mucin MUC5AC protein by Streptococcus pneumoniae by inhibiting cAMP-protein kinase A-dependent MKP-1 phosphatase pathway.

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Otitis media (OM) is the most common childhood bacterial infection and the major cause of conductive hearing loss in children. Mucus overproduction is a hallmark of OM. Streptococcus pneumoniae is the most common gram-positive bacterial pathogen causing OM. Among many mucin genes, MUC5AC has been

Hydrolase activity in acute otitis media with effusion.

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Biochemical studies of middle ear effusions (MEE) from patients with chronic or recurrent otitis media with effusion (OME) have demonstrated the presence of significant levels of certain hydrolytic and oxidative enzymes. We have examined MEE from patients with acute OME for the content of a number

Bone resorption in chronic otitis media. The role of cholesteatoma, a must or an adjunct?

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The paper contains the results of light microscopical, electron microscopical and histochemical examinations of chronic otitis media, with and without cholesteatoma, with special focus on the problems regarding bone resorption. It is demonstrated that bone resorption takes place without the presence

Certain oxidative and hydrolytic enzymes in the middle ear effusion in serous otitis media.

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Activities of various oxidative (LDH, MDH) and hydrolytic (LAP, alkaline- and acid phosphatase, and lysozyme) enzymes in serous middle ear effusions (MEE) and serum from patients with serous otitis media were studied. The ratio of enzyme activity between MEE and serum (MEE/serum) was greater than

Bone resorption in chronic otitis media.

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Bone resorption is an important aspect of chronic otitis media contributing to many complications of this disease. It is postulated that the mechanism of this localized destructive process is chemical in origin. Collagenase, lysosomal enzymes, prostaglandins, and other cell mediators are thought to

Ultrastructural evaluation of biochemical events of bone resorption in human chronic otitis media.

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Bone resorption is a significant component of chronic inflammatory ear disease. Bone is a unique tissue requiring both demineralization and collagen degradation for breakdown. Mineral removal probably occurs prior to collagen destruction. A localized change in pH may be one of the mechanisms that

Evidence of T-helper cell 2 cytokine regulation of chronic otitis media with effusion.

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Cytokine and cellular patterns of effusions may reflect stages of middle ear inflammation. The local interplay between IL-2 and -4 is likely to play a crucial role in the switching of inflammation in the chronic stage. The T-helper cell 2 (Th2) cytokines IL-4, -5 and -13 and the Th2/Th1 cytokine

Glucocorticoids inhibit nontypeable Haemophilus influenzae-induced MUC5AC mucin expression via MAPK phosphatase-1-dependent inhibition of p38 MAPK.

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Glucocorticoids are highly effective in the control of many inflammatory and immune diseases. Despite the importance of glucocorticoids in suppressing immune and inflammatory responses, the molecular basis for the inhibitory effect of glucocorticoids on mucin overproduction, a hallmark of chronic

Transforming growth factor-beta-Smad signaling pathway negatively regulates nontypeable Haemophilus influenzae-induced MUC5AC mucin transcription via mitogen-activated protein kinase (MAPK) phosphatase-1-dependent inhibition of p38 MAPK.

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In contrast to the extensive studies on the role of transforming growth factor-beta (TGF-beta) in regulating cell proliferation, differentiation, and apoptosis over the past decade, relatively little is known about the exact role of TGF-beta signaling in regulating host response in infectious

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