Middle ear mucosa is a modified respiratory epithelium and five genes for secreted mucins (MUCs 2, 3, 4, 5AC, 5B and 8) are expressed in the airways. In this study we have compared the composition predicted by the gene sequences of these mucins with that of mucins isolated from middle ear effusions. Three groups of mucins, (1) thick and (2) thin from anatomically normal children and (3) effusions from children with a cleft palate were studied. Amino acid analysis was performed on glycopeptide fragments corresponding to the characteristic tandem repeat domains of cloned mucin genes. There were marked differences both between the three mucin pools and from the tandem repeat sequences of the five cloned genes expressed in the airways. Serine, threonine and proline contributed 44%, 29% and 36% from groups (1) (2) and (3)respectively, in the ratios (2.4 : 2.9 : 1) (5 : 1 : 1) and (3.5 : 1 : 1.5).The serine to threonine ratio in thick effusions is similar to that found in MUC 4; however, the high proportion of serine in mucin from groups (2) and (3) is novel. Therefore, more than one mucin gene product is secreted by the human middle ear mucosa and further mucin genes expressed by the middle ear are yet to be cloned.
Posturography is extensively used in assessing instability following immersion in virtual reality (VR) environments such as flight simulators and tests including Romberg and tandem Romberg have been used. Unsteadiness following VR tends to be milder than rotational stimuli. It is important to determine the duration of any measurable instability following vestibular insult and in order to do this we used sway magnetometry (SM) which is a more sensitive test than force platforms. Movement is sampled at 40 Hz and a 486 computer displays the resultant pattern; the optimal method of re cording has already been established.1 In the following tests subjects were assessed with their eyes open and closed standing on both a firm base and foam. First,10 normal subjects underwent SM on three separate occasions.All the data was analysed using an ANOVA test (P < 0.05) and no significant difference was found between each occasion hence the reproducibility of the method was established. Second, 34 subjects with differing ages (range 18–65 years) underwent SM. These results give normative data within each decade of age and establish comparison for ‘dizzy’ patients (20–30 years: 456; 40–50 years: 360; values in mm/min). The results demonstrate the change in vestibular function with age highlighting the sensitivity of the methodology. Third, and importantly, subjects who underwent a rotatory insult to their vestibular system had SM conducted with eyes closed and on a foam base in order to establish the speed of recovery of the vestibular apparatus. Results demonstrate the mean speed of recovery was 12 s. These results bring into question experimental designs used in published trials to assess body sway following insults.
A function of nasal turbinates is the removal of particles bythe action of the cilia moving a mucous blanket. The rheologicalproperties of the mucous secretion are critical to this functionand dependent on several factors, in particular the integrity and type of mucin present. Recent work has shown that MUC5AC is a major secreted mucin in the respiratory tract and MUC2 is expressed at a much lower level.1,2 Alteration in the levels of expression of mucin genes could potentially alter the transport and lubricating properties of mucous. mRNA was isolated from inferior nasal turbinates and electrophoresis showed a polydisperse mRNA population. Northern blots were probed with 48bp digoxigenin labelled antisense oligonucleotides to the tandem repeat sequences of MUC2 and MUC5AC. The MUC2 probe gave an intense signal with the positive control (human ileum), in contrast the negative control (rat kidney) showed no binding. Turbinate mRNA also gave a strong signal although not as intense as ileum. The MUC5AC probe bound to turbinate mRNA and ileum although to a lesser extent than MUC2. The results show that both MUC2 and MUC5AC are expressed in human nasal turbinates and interestingly the level ofMUC2 was higher than that of MUC5AC (using these probes). This reversal in mucin secretory pattern, presumablya function of hyperplasia could lead to altered mucous properties. This tissue may provide a good model to study diseases in tissues of the same embryological origin and similar histology where cell proliferative changes occur, i.e. diseases of middle ear mucosa. We thank the Hearing Research Trust for their support.
Hypothesis: Hearing tests performed in General Practice at the 3½‐year developmental assessment do not correlate with objective measures of otitis media with effusion (OME: ‘glue ear’). Subjects: One hundred and thirty‐nine consecutive children attending the 3½‐year developmental assessment of four General Practitioners in a single inner‐city practice. Outcome measures: The main outcome measure was the presence or absence of effusion as determined by the ‘gold standard’ of type B and C2 tympanograms bilaterally. Independent variables were standard toy test performed by the four GPs, parental assessment of hearing on the test day, the occurrence of two or more documented episodes of otitis media, presence of a smoking parent in the dwelling place and otoscopic findings (glue/no glue) determined by the GP performing the test. Results: The incidence of bilateral OME, as determined by tympanometry, in this population of 3½‐year olds was 28%. Forward stepwise linear regression analysis indicated that the only statistically significant independent variable to correlate with tympanometric findings of OME was the GP’s hearing test (P = 0.003). Conclusion: Carefully performed GP hearing tests appear to be good predictors of OME in 3½‐year olds, and should continue.
Mucins have a polypeptide backbone, oligosaccharide side‐chains and peripheral structures that include sialic acids. Several pathogens have specific receptors for sialic acids, including human strains of influenza A virus which preferentially recognise and bind α2‐6 linked rather than α2‐3 linked sialic acids.1 The aim of this study was to identify possible disease‐related changes in the expression of sialic acids in nasal mucins. Nasal mucosal samples were placed in organ culture. Metabolically‐labelled mucins were purified by gel filtration, blotted on to nitrocellulose membranes and probed with the sialic acid‐binding lectins Sambucus nigra and Maackia amurensis. Ninety‐five mucosal samples were collected (49 turbinates, 31 nasal polyps, 15 samples from FESS). Lectin binding, expressed as optical density, showed significantly increased binding of S. nigra to cellular (P = 0.02; Kruskal–Wallis) and secreted (P = 0.045) mucin from allergic mucosa compared to non‐allergic mucosa. No significant differences were found in the binding patterns of M. amurensis. This study has demonstrated increased expression of α2‐6 linked sialic acids in the mucins synthesised and secreted by allergic compared to non‐allergic nasal mucosa. This may cause a change in the way mucins and pathogens interact in allergic rhinitis, leading to altered susceptibility to upper respiratory tract infection.
Mucins are responsible for the high viscosity of middle ear effusions preventing clearance from the middle ear. Nine mucin genes (MUC genes) have been identified. We have shown at least two biochemically distinct mucins are present in OME and ELISA studies showed no reactivity with MUC1 or MUC2, suggesting low levels of MUC5AC and higher levels of MUC5B. Here we have investigated further immuno histochemically to determine the cellular localization of these gene products. Rabbit polyclonal antisera (TEPA2) were raised to highly purified mucin from thick effusions. The monoclonal antibody NCL‐HGM‐45M1 was used to probe for MUC5AC. Surgical tissue specimens were fixed in 10% formal saline overnight, wax embedded and sectioned (5 μm). Microwave retrieval was followed with primary antibody then by biotinylated secondary antibody followed by AB complexing and haematoxylin counterstaining (see Table 1). There was no staining of non‐mucus secreting cells in test or control tissues. The pattern of staining with TEPA2 in salivary glands, trachea, stomach, and ileum matched that previously reported for MUC5B.1 MUC5AC (NCL‐HGM‐45M1) was not present in middle ear mucosa but was present in goblet cells of nasal turbinates and probably reflects a low expression of MUC5AC as seen from low levels present in the effusion (5–15% by weight of mucin). TEPA2 stained the mucous glands of middle ear mucosa but not the goblet cells. Based on TEPA2 staining MUC5B is therefore a strong candidate for the mucin produced by middle ear mucosal glands, studies continue to confirm this and to determine the gene product of the goblet cells.
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