PubMed Health⌕ Search

Biomedical subjects

B Knopf

Publications and source records attributed to B Knopf.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Acrosyringial keratinocytes--no abnormal differentiation in psoriasis vulgaris].

Histochemical investigations were performed in normal and psoriatic epidermis to evaluate possible differences in the acrosyringial reactivity. Luminal (abundant in glycoconjugates, immunoreactive) and outer (almost nonreactive) epithelial cells could be distinguished. Psoriasis did not affect the staining pattern. The findings argue against a primary involvement of acrosyringial keratinocytes in the abnormal differentiation pathway of psoriatic epidermal cells. Moreover, they underline the relative independence of the acrosyringium from interfollicular epidermis.

Biopsy↗
PubMed1990

[Hyde's nodular prurigo--preference for creases of the skin].

The arrangement of papules in prurigo nodularis Hyde along the cleavage lines of the skin, but not Blaschko's lines, supports the classification of prurigo nodularis Hyde as a traumatic chronic papulosis with cutaneous neural hyperplasia of xerodermal skin.

Depression↗
PubMed1990

[The effect of monochromatic and polychromatic UV irradiation and of 8-MOP on phagocytosis of neutrophilic granulocytes].

We investigated the inhibition of granulocyte phagocytosis by 8-MOP and monochromatic or polychromatic UV light. After application of 8-MOP and UV there was an additional inactivation compared with UV alone, as expected from studies on other cell species. This additional inhibition of phagocytosis was found to be increasing with 8-MOP level. The action spectra of granulocyte inactivation by 8-MOP and UV involves the investigated UVB range (until 300 nm). A marked inactivation of granulocytes was seen after erythemogenic fluences only. Therefore we assume that inactivation of granulocytes by direct UV action does not play an essential role in UV therapy in vivo.

Cells, Cultured↗
PubMed1990

[Immunohistologic studies of the distribution of proliferative compartments in the appendages of adult human skin].

Both, calmodulin (CaM) as well as the antigen Ki67 show a close relationship to cell proliferation. By means of specific antibodies against them, it has become possible to study the spatial distribution of proliferative compartments in tissues. We performed an indirect immunofluorescence study on unfixed frozen sections of human adult skin to gain more informations about the spatial distribution of immunoreactive CaM and Ki67 in skin appendages, i.e. anagen hair follicle, sebaceous and eccrine sweat gland. Two major patterns of immunoreactivity were seen: Type (1) or epidermis-like, which was present in the interfollicular epidermis and the pilosebaceous unit. Type (2) or sweat gland type, which was seen in eccrine sweat glands. Both types disclosed significant differences in the relative number of proliferative cells in S-phase, which might be a consequence of a quiet different tissue architecture. Furthermore, myoepithelial cells of secretory coils were likely to represent mainly SQ-cells. Their immunoreactivity in human skin was quiet different from other parts of eccrine sweat glands suggesting another ontogenetic pathway.

Adult↗
PubMed1990

[Psoriatic osteopathy--results of histomorphometric studies].

In 23 patients with psoriatic arthritis and 9 patients with psoriasis without joint involvement, we took bone biopsies from the iliac crest. Histomorphometrical investigations showed that the volume density of the bone was not decreased in either group of patients, but we found a high rate of turnover remodelling. An elevated rate of bone turnover is regarded as the characteristic principle of "psoriatic osteopathy", which--more exactly--should be called "latent osteopathy". Deficiency of vitamin D is discussed as a possible etiological factor.

Adult↗
PubMed1990

[Hydroxyproline excretion in psoriasis and psoriatic arthritis].

In the morning urine of 24 patients with psoriasis and that of 24 patients with psoriatic arthritis, we determined the excretion of hydroxyproline (mg HP/mumol crea), after preceding diet low in collagen. Surprisingly, psoriatic patients without articular involvement showed a significantly higher excretion of HP than those with psoriatic arthritis. Further differentiation revealed that there were no clear-cut correlations between the amount of HP excretion and the activity of the articular process; we proved, however, that the amount of HP excretion was definitely related to the activity of the skin eruptions in both groups of patients. We discuss whether an osteopathy pathogenetically associated with the skin disease (irrespective of synovitis in psoriatic arthritis) may possibly be responsible for these results.

Adult↗
PubMed1989

[The Ro/SSA antigen-antibody system. Studies of the effect of UVA-/PUVA irradiation and fibroblast activity on immune reaction with autoantibodies].

The Ro/SSA antigen-antibody system is of great importance with regard to the cutaneous manifestations and the photosensitivity of patients suffering from lupus erythematosus (LE). On account of in vitro investigations on cultured fibroblasts taken from psoriatic skin, we evaluated both the effect of UVA/PUVA irradiation and that of the metabolic activity of cells on this antigen-antibody system. We found that UVA irradiation is able to demask Ro/SSA. Thus it becomes accessible so subsequent antibody binding, which can be seen as nuclear fluorescence positive for IgM. Incubation of vital cells with these autoantibodies and subsequent irradiation resulted in a high degree of cytoplasmic fluorescence (IgG, IgM) in part of the fibroblasts exposed to UVA. Regarding the clinical application of light protective agents in LE patients with antibodies to Ro/SSA, UVA light--aside from UVB--should be taken into consideration.

Antibodies, Antinuclear↗
PubMed1989

[Psoriasis vulgaris--unchanged endothelial reactivity with histochemical markers].

Frozen sections from psoriatic lesions were investigated regarding their reactivity with endothelial markers (UEA I, EEA I, LTA, Con A, factor VIII-related antigen). We compared the findings obtained with those of both uninvolved psoriatic skin and normal skin. Although all lectins showed altered epidermal binding in comparison to the controls, the endothelial lectin binding as well as the expression of factor VIII-related antigen were the same in both psoriatric lesions and controls. Our findings argue for (1) intact dimorphic genetic control of ABH expression in both epidermal and endothelial cells, (2) altered epidermal differentiation of lesional psoriatric skin, and (3) secondary vascular alterations.

Biomarkers↗
PubMed1989

[Histochemical studies of transepidermal elimination of nevus cells in nevus cell nevi of the corium].

Dermal nevocytic nevi (NN) were histochemically studied with the help of FITC-conjugated lectins as well as antisera against keratin and plasminogen activators of the urokinase type. 3 out of 18 NN showed interpenetrating nevus cells in atrophic parts of the epidermis. These cells revealed strong lectin reactivity both with Con A (cytoplasmatic binding) and WGA/RCA II (membraneous binding). In addition we found membraneous reaction with anti-urokinase, whereas there was no anti-keratin staining. Our findings suggest active transepidermal elimination of nevus cells in dermal nevocytic nevi.

Fluorescent Antibody Technique↗
PubMed1989

[Lectin histochemical studies of nevus cell nevi of the corium].

Using 11 different kinds of lectins, we histochemically studied 18 dermal nevocytic nevi (NCN). The investigation included both unfixed frozen sections and pretreated sections fixed with acetone (pretreatment: chloroform/methanol, Triton X-100, neuraminidase). In this way, we hoped to get some information both on the expression of surface glycoconjugates and the chemical nature of the sites of lectin binding. Our results argue for an abundance of glucosyl, mannosyl, galactosyl, and N-acetyl galactosamine residues on the surface of nevus cells. In comparison to keratinocytes, we found a greater sensitivity to chloroform/methanol, which suggests a relative increase of glycolipids. Dermal NCN showed heterogenic lectin binding: The highest intensity was seen in the marginal nevus cells, the lowest in the central cells of epidermal nests. Dermal cells showed a moderate binding intensity. Epidermal cells lying above the NCN disclosed some modifications of their lectin binding pattern. In contrast to normal epidermis, basal keratinocytes failed to bind LCA; suprabasal cells showed cytoplasmic staining. In some NCN, we observed an intensive perinuclear staining of the upper keratinocytes with granular ConA. Our results suggest (1) a modified lectin binding pattern of nevus cells depending on their microenvironment, as well as (2) a distinctly altered lectin binding of keratinocytes in the adjacent epidermis.

Adolescent↗
PubMed1989

Distribution of glycoconjugates in human skin appendages.

The purpose of this paper is to describe the occurrence and distribution of glycoconjugates in normal human epidermis and skin appendages (pilosebaceous unit, eccrine sweat gland) by means of FITC-labelled lectins (ConA, WGA, UEA I). Both the outer hair root and the follicular ostium-epithel disclosed a glycoconjugate expression with close homology to interfollicular epidermis. The acinar epithelium of sebaceous glands and the inner layers of hair follicles showed a more or less distinct staining pattern. Lectin binding of eccrine sweat glands revealed marked differences between ducts and secretory coils. The epithelial distribution of glycoconjugates indicates a relatively independent differentiation pathway of eccrine sweat glands compared with other specialized epithelia of the human skin.

Acetylglucosamine↗
PubMed1989

FITC-insulin binding to normal and psoriatic epidermis.

FITC-insulin was prepared and applied to frozen human skin sections. In normal and nonlesional psoriatic epidermis, the binding was cytoplasmic in suprabasal cells. In psoriatic lesions, fairly stained or even unstained cells were littered in suprabasal epidermis indicating the expansion of selected basal cell qualities into the stratum spinosum.

Biopsy↗
PubMed1989

Calmodulin inhibition by anthralin? Investigations in vitro and in vivo.

Increased epidermal calmodulin (CaM) levels have been reported in psoriatic lesions. It has been suggested that CaM inhibition might be of relevance in the treatment of psoriasis vulgaris. Therefore we investigated the possible CaM inhibition by the antipsoriatic drug anthralin in vitro and in vivo. For in vitro studies, anthralin (0.44 mM) effects on the CaM-dependent Ca++-ATPase of CaM-depleted erythrocyte ghosts were assessed. At 100 microM Ca++, no enzyme inhibition was measured either in the presence or absence of CaM. At 2 microM Ca++ anthralin inhibited the CaM stimulation of membrane-bound ATPase for 50% in presence of CaM. For in vivo studies, skin biopsies were taken from anthralin-treated psoriatic lesions without scaling but still palpable infiltration during the first 3 weeks of therapy. Lesions with anthralin-induced irritation were excluded. The epidermal CaM level was determined by measuring the ability of soluble epidermal protein to activate the Ca++-ATPase in CaM-depleted erythrocyte ghosts. Epidermal CaM was 7.07 +/- 4.57 (mean +/- SD) microgram CaM/mg soluble epidermal protein. This is a 6-fold increase compared to normal human epidermis and a 3-fold increase compared to nontreated lesional psoriatic epidermis (p less than 0.01 and 0.02, respectively). The results argue against CaM inhibition of psoriatic epidermal keratinocytes as the primary event in the antipsoriatic action of anthralin.

Anthralin↗
PubMed1989

[Direct immunofluorescence study of active psoriasis lesions].

Active psoriatic lesions have been investigated by direct immunofluorescence technique with polyclonal antisera to immunoglobulins and C3. We observed a cytoplasmic fluorescence of suprapapillary, suprabasally keratinocytes with tight topographical relationship to the parakeratotic horny layer. The intracellular deposits were IgA (in 60% of cases), IgG (53%), IgM (47%), C3 (30%). IgE und IgD have not been detected. The relationship of cytoplasmic protein deposition in vivo to parakeratosis is discussed briefly.

Autoantibodies↗