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Biomedical subjects

H Schaarschmidt

Publications and source records attributed to H Schaarschmidt.

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

[A combination of psoriasis vulgaris and nevus cell nevus--clinical, histopathologic and histochemical findings].

In a study on 76 patients suffering from psoriasis, we found melanocytic nevi (MCN) within psoriatic lesions in 7%, and in perilesional areas of about 2 cm in 13% of the patients. Under magnification (operating microscope), we failed to detect any signs of psoriasis in both the epidermis covering the MCN and the adjacent epidermis. Histopathologically, 6 out of 7 MCN examined did not show any psoriatic alterations of the epidermis, and in all the 7 cases, the adjacent epidermis was free of psoriasis. Using unfixed frozen sections in histochemistry, we studied the lectin binding of FITC-labeled ConA and UEA I in 5 MCN. The epidermal reaction was comparable to that of psoriatic lesions. In contrast to psoriatic lesions, there was no staining of the spinous layer with a polyclonal antiserum against calmodulin, but only the staining of basal cells as in non-lesional psoriasis. We discuss possible 'protective' factors against psoriasis.

Cell Division↗
PubMed1990

[Detection of IgA in diseased skin and serum of patients with psoriasis vulgaris].

Origin and function of IgA in the psoriatic skin are unknown. Including a monoclonal antibody against the secretory component (SC) of the secretory IgA (SIga), we have tried to characterize the IgA in psoriasis. With help of a polyclonal antiserum we found depots of IgA in the skin in 69% of all investigated patients. There was a correlation between the degree of akanthosis and the amount of intraepidermal IgA. In the serum of the psoriasis total IgA was significant increased, but never we found SC-bound SIgA in the skin or elevated levels in serum of patients.

Adult↗
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↗
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

[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↗
PubMed1988

[Lectin histochemical study of epidermal nevi].

3 epidermal nevi were investigated by means of FITC-labeled lectins (LCA, RCA II, ConA, WGA). In comparison with normal skin, we observed selective modifications of the lectin-binding patterns. These findings suggest an increased presence of GlcNAc residues.

Adult↗
PubMed1988

[UV-A exposure of the human epidermis enhances the binding of antibodies to SSA/Ro in vitro].

Normal and psoriatic skin specimens (n = 15) were processed to give 4-micron-thick frozen sections and exposed to a single UV irradiation in vitro. We used monochromatic UV-B (313 nm) and UV-A (365 nm). The doses were as follows: 10(3)/10(4) J/m2 (UV-B) or 4.10(3)/8.10(4) J/m2 (UV-A). We investigated the effect on epidermal binding of antibodies to SSA/Ro using the indirect immunofluorescence technique. Untreated and UV-B-treated human skin failed to bind anti-SSA/Ro. UV-A exposure disclosed reticular or granular staining of epidermal nuclei and a perinuclear halo. The effect was nearly the same throughout the dosage range. The combination of UV-A and methoxsalen increased the intensity of staining. Normal and psoriatic skin behaved in the same way.

Autoantibodies↗
PubMed1987

[PUVA irradiation decreases the binding of membrane and basement membrane markers to human epidermis in vitro].

PUVA effects on frozen sections of human epidermis were investigated (20 micrograms 8-methoxypsoralen/ml; UVA wavelength 365 +/- 5 nm; radiation dose between 2 X 10(2) and 2 X 10(2) J/m2). The quality of the glycocalyx was characterized by lectins labeled with FITC (HPA, PHA, LCA, PNA, SBA, RCA, GCA I, UEA I). Serum antibodies of bullous pemphigoid (BP) served as membrane markers for the basement membrane. Fixed BP antibodies were detected by FITC-antihuman IgG. The fluorescence intensity was markedly decreased at a dose of 2 X 10(5) J/m2; 2 X 10(4) J/m2 were less effective. At 2 X 10(3) J/m2, there was nearly no alteration of the fluorescence intensity observed. Changes were seen in the case of BP antibodies and lectins, except UEA I. The relatively high intensity (radiation dose) and the effects immediately observable suggest direct membrane alterations by PUVA in vitro.

Antibodies↗
PubMed1987

[Effect of dithranol therapy on membrane, basement membrane and nuclear markers in psoriasis lesions].

We investigated the effects of anti-psoriatic therapy with dithranol (1/20-1%) in salicylic acid (0.5%) in white petrolatum on lesional skin. FITC-labeled lectins and pemphigus vulgaris antibodies (PV) served as analytical means to study the glycocalyx. Antibodies of bullous pemphigoid (BP) were used as basal membrane markers. Nuclear antigens were recorded according to the binding of speckled, anti-nuclear antibodies (ANA) as well as antibodies to dsDNA. With some lectins, dithranol therapy resulted in pronounced fluorescence of the lower parts of the basal cells. ConA was fixed by the basal cell layer. To a lesser degree, ANA were fixed by nuclei of keratinocytes. PV antibodies were not fixed at all.

Adult↗