43 research outputs found
Wide-area 308-nm phototherapy with nonlaser light in the treatment of psoriasis: results of a pilot study.
The 18 kDa cytosolic acid phosphatase from bovine liver has phosphotyrosine phosphatase activity on the autophosphorylated epidermal growth factor receptor
AbstractIn this paper we demonstrate that the cytosofic low-Mr acid phosphatase purified from bovine liver has phosphotyrosine protein phosphatase acitivity on 32P-autophosphorylated epidermal growth factor (EGF) receptor. This activity was significantly inhibited by orthovanadate and p-hydroxymercuribenzoate; the latter result indicates that free sulfhydryl groups are required for phosphotyrosine phosphatase activity. The enzyme was active in a broad pH range, with maximum activity between pH 5.5 and 7.5. The apparent Km for 32P-EGF receptor dephosphorylation was 4 nM. The enzyme appeared to be specific for phosphotyrosine in that it dephosphorylated the autophosphorylated EGF receptor and L-phosphotyrosine, but not 32P-Ser-casein, L-phosphoserine or L-phosphothreonine. These data suggest that the cytosolic low-Mr acid phosphatase might play a regulatory role in EGF receptor-dependent transmembrane signalling
The oligosaccharidic component of the glycoconjugates in lichen planus, granuloma annulare, seborrheic keratosis and palmoplantar keratoderma: lectin histochemical study
It is well known that cell surface glycoconjugates play an important role in cell proliferation, adhesion and differentiation. The aim of this investigation was to define the changes of the glycoconjugate saccharidic moieties in the epidermis and derma of patients affected by several skin pathologies such as seborrheic keratosis, lichen planus, granuloma annulare and palmoplantaris keratoderma.Bioptical specimens from skin lesions as well as from normal skin were fixed in Carnoy's fluid and routinely processed. The sections were treated with HRP-lectins (PNA, DBA, SBA, WGA, ConA, LTA and UEAI). Cytochemical controls were performed for specificity of lectin-sugar reaction. Some sections were pre-treated with neuraminidase prior to staining with I-IRP lectins. In comparison with normal human skin, epidermal lectin binding pattern in the considered diseases showed considerable qualitative and quantitative variations. In general, in all the considered pathologies, a lack andtor a decrease in lectin binding at the epidermal layers was observed; among the various diseases, differences in cellular localisation of the sugar residues were also noted. In such respect, an exception was represented by seborrheic keratosis, where the cells of the basal layer showed PNA reactivity, which was absent in the basal layer of the normal skin. Although seborrheic keratosis and lichen planus have been studied by others authors, our findings are not in total accordance concerning lectin binding; this is probably due to the different fixatives employed. Our findings seem to reveal significant changes in keratinocyte glycoconjugate oligosaccharides in the previously mentioned diseases, providing clues to their pathogenesis
The oligosaccharidic component of the glycoconjugates in lichen planus, granuloma annulare, seborrheic keratosis and palmoplantar keratoderma: lectin histochemical study
It is well known that cell surface glycoconjugates
play an important role in cell proliferation,
adhesion and differentiation. The aim of this
investigation was to define the changes of the glycoconjugate
saccharidic moieties in the epidermis and
derma of patients affected by several skin pathologies
such as seborrheic keratosis, lichen planus, granuloma
annulare and palmoplantaris keratoderma.
Bioptical specimens from skin lesions as well as
from normal skin were fixed in Carnoy's fluid and
routinely processed. The sections were treated with
HRP-lectins (PNA, DBA, SBA, WGA, ConA, LTA and
UEAI). Cytochemical controls were performed for
specificity of lectin-sugar reaction. Some sections were
pre-treated with neuraminidase prior to staining with
I-IRP lectins. In comparison with normal human skin,
epidermal lectin binding pattern in the considered
diseases showed considerable qualitative and quantitative
variations. In general, in all the considered
pathologies, a lack andtor a decrease in lectin binding at
the epidermal layers was observed; among the various
diseases, differences in cellular localisation of the sugar
residues were also noted. In such respect, an exception
was represented by seborrheic keratosis, where the cells
of the basal layer showed PNA reactivity, which was
absent in the basal layer of the normal skin. Although seborrheic keratosis and lichen planus have been studied
by others authors, our findings are not in total
accordance concerning lectin binding; this is probably
due to the different fixatives employed. Our findings
seem to reveal significant changes in keratinocyte glycoconjugate
oligosaccharides in the previously mentioned
diseases, providing clues to their pathogenesis