Behavior problems in otitis media.
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Biomedical subjects
Publications and source records attributed to J A Birkin.
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Protein and N-linked glycoprotein biosynthesis was studied in histologically verified normal epidermis, actinic keratoses, keratoacanthoma, intra-epidermal carcinoma and squamous-cell carcinoma using polyacrylamide gel electrophoresis (PAGE). The PAGE profiles of 3[H]-leucine-labelled proteins and 3[H]-mannose-labelled glycoprotein from all disease states studied differed from each other and from normal epidermis. A large 3[H]-mannose-labelled glycoprotein region (band A) with a peak at 97-92 kDa appeared to indicate the presence of a relatively large proportion of basaloid cells in the tissue. An associated peak in the region of 78-74 kDa also appeared in normal epidermis and what appeared to be non-invasive lesions. The main region of change in all lesions corresponded to the 66-34-kDa region (bands B and C). The absence of a group of glycoproteins and proteins in the 62-58-kDa region appeared to be specific for invasive squamous-cell carcinoma. All tumours showed a peak at 38-34 kDa which was not present in normal epidermis. Actinic keratosis had a pattern similar to normal epidermis except that the peaks of band B tended towards the higher-molecular-weight end of the band than those in normal epidermis and peaks at 28-22 kDa were seen. The latter seemed to correspond to the presence of a high proportion of spinous cells in the tissue sample.
Protein and N-linked glycoprotein biosynthesis was studied in the uninvolved epidermis of patients with psoriasis by the incorporation of radiolabelled leucine and mannose prior to and during PUVA treatment. Analysis of the polyacrylamide gel electrophoresis (PAGE) patterns of the 3[H]-labelled proteins and glycoproteins showed that the major changes in untreated uninvolved psoriatic epidermis compared to normal epidermis were: (a) a shift towards the synthesis of low-molecular-weight glycoproteins; (b) the absence of a 48-kDa peak labelled with mannose; (c) the appearance of 3[H]-mannose-labelled peaks at 40-36 kDa. PUVA treatment gradually changed the PAGE profile back more towards that expected for normal epidermis, with the reintroduction of a 52-48-kDa glycoprotein and reduction of the peaks in the 40-34-kDa region. This effect was dependent on uninterrupted treatment. The PUVA-treated PAGE profiles were compared to those expected in skin tumours (i.e. increased 3[H]-mannose-labelled peaks at 95 and 40-34 kDa with an absence of 62-kDa peaks). It appeared that these criteria were not seen generally as a result of PUVA treatment. However, the results indicate that tumour development may be possible if a patient responds to PUVA treatment by showing an increased peak at 95 and 40-34 kDa in association with a loss of an 3[H]-mannose-labelled peak at 62 kDa.
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