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Biomedical subjects

A Skiendzielewska

Publications and source records attributed to A Skiendzielewska.

12 recordsLinked to original sources
PubMed1992

Adhesion of peripheral blood mononuclear cells to vascular endothelium in patients with systemic sclerosis (scleroderma).

OBJECTIVE: Perivascular infiltrates in skin, subcutaneous tissue, and internal organs are a characteristic feature of early systemic sclerosis (SSc). We studied the first step of migration of peripheral blood mononuclear cells (PBMC) through the vessel wall to the extravascular space, i.e., adhesion of PBMC to endothelial cells (EC), in patients with various forms of SSc (limited scleroderma, diffuse scleroderma, and the transitional form). METHODS: Radioisotope-labeled patient PBMC were coincubated with umbilical cord EC in vitro, and the percentage adhesion was measured. RESULTS: Adhesion of PBMC to EC was markedly decreased, while adhesion of isolated active rosette-forming cells (ARFC) was significantly increased, in SSc patients compared with healthy controls. Decreased adhesion of PBMC to EC was found to correlate with a diminished percentage of ARFC in the peripheral blood. Preincubation of PBMC from healthy donors with interleukin-2 (IL-2) enhanced their adhesion to EC, while preincubation of PBMC from SSc patients with this cytokine resulted in a decrease in adhesion in 10 of 14 individuals. IL-1, interferon-gamma, and transforming growth factor beta had no significant effect on adhesion of SSc patient PBMC to EC. Differences in adhesion of PBMC to EC among the SSc subgroups were not significant. CONCLUSION: Our findings suggest that in SSc, activation of subpopulations of PBMC leads to their enhanced adhesion to vascular endothelium in vivo and to migration of these cells to the extravascular space, resulting in the elimination from the peripheral blood of those PBMC with high ability to adhere to EC.

Adult↗
PubMed1991

Acitretin decreases tumor cell-induced angiogenesis.

The effects of acitretin and etretinate on angiogenesis induced in Balb/c mice by intradermal injection of keratinocyte tumor cell lines were evaluated. It was shown that both retinoids are capable of inhibiting angiogenesis evoked by a human epidermoid carcinoma cell line (A431). Acitretin, but not etretinate, inhibited also angiogenesis induced by the spontaneously transformed murine keratinocyte cell line Pam 212 and by the established tumorigenic SKv cell line harboring the HPV16 genome. We suggest that inhibition of blood vessel formation may be one of the mechanisms responsible for the anticancerogenic effect of retinoids.

Acitretin↗
PubMed1991

Beta-carotene in prevention of cutaneous carcinogenesis.

Beta-carotene, administered orally to mice, caused a decrease in angiogenesis evoked by HPV-transformed tumorigenic cell lines (SKv-t, HeLa). It did not affect angiogenesis induced by the non-tumorigenic SKv (not-t) cell line, and increased lymphocyte-induced immune angiogenesis. We suggest that the anti-cancerogenic effect of beta-carotene may be due, at least in part, to its inhibitory effect on formation of new blood vessels within the tumour mass.

Animals↗
PubMed1990

Cytotoxic effects of sera from patients with systemic scleroderma: comparison of three different in vitro methods.

Sera from 93 patients with systemic scleroderma including incipient or prodromal acroscleroderma and from 43 healthy individuals were studied for cytotoxic effects on endothelial cells by means of three different in vitro methods. Inhibition of 3H-thymidine incorporation by endothelium was caused by about 33% of sera, almost exclusively from patients with diffuse scleroderma and the transitional form: acroscleroderma--diffuse scleroderma. An antibody-dependent cellular cytotoxicity assay revealed cytotoxicity of about 37% of sera from patients with diffuse scleroderma and the transitional form but also of a proportion of sera from patients with CREST syndrome with pronounced vascular changes. Serum cytotoxic activity, revealed by both methods, was related with more frequent involvement of muscle and kidney in the patients. A direct 51Cr release assay showed the cytotoxicity only in 4 of 68 cases in diffuse scleroderma with pronounced internal organ involvement. Thus, depending on the method used, various types of cytotoxicity could be detected in sera from patients with systemic scleroderma.

Adult↗
PubMed1979

Biogenic amines derived from tryptophan in systemic and cutaneous scleroderma.

Blood levels of serotonin (5-HT) and urinary excretion of 5-hydroxyindole-acetic acid (5-HIAA), tryptamine (T), and indole-acetic acid (IAA) were determined in 39 cases of systemic scleroderma and in 7 cases of very severe cutaneous scleroderma. The T/IAA ratio was normal and serotonin elevated in mild and rather severe acrosclerosis alike, i.e. in systemic scleroderma with pronounced vascular involvement. The T/IAA ratio was increased and serotonin normal in severe acroscleroderma, representing an intermediate form or transition to diffuse scleroderma, in severe diffuse scleroderma, and in severe cutaneous scleroderma. The T/IAA ratio and serotonin level were both elevated in a few cases of systemic scleroderma and in severe generalized morphea with concomitant vascular changes. The findings suggest impaired monoamine oxidase (MAO) activity in scleroderma with consequent accumulation in the organism of biogenic amines derived from tryptophan. An increased T/IAA ratio seems to be of prognostic significance in scleroderma, suggesting an adverse course of the disease.

Colorimetry↗
PubMed1977

5-Hydroxytryptamine and tryptamine pathways in scleroderma.

Levels of 5-hydroxyindoleacetic acid, indoleacetic acid and total indoles were determined in the urine of 23 patients with systemic scleroderma and 7 patients with cutaneous scleroderma, before and after peroral loading with L-tryptophan (0-1 g/kg body weight). Before loading, 5-hydroxyindoleacetic acid levels were normal in nearly all cases of systemic scleroderma as well as of cutaneous scleroderma; however after loading, in nearly one half of cases there was no normal increase of this metabolite. These results suggest impaired transformation of serotonin into 5-hydroxyindoleacetic acid. A disproportionately high ratio of total indoles to indoleacetic acid suggests the presence of excess of tryptamine. The results of the study may indicate that in scleroderma metabolism of biogenic amines derived from tryptophan is abnormal, probably as a result of impaired activity of monoamine oxidase.

Adolescent↗
PubMed1976

Intestinal absorption of L-tryptophan in scleroderma.

The purpose of this investigation was to study the intestinal absorption of L-tryptophan and to assess the absorptive function of the intestine in scleroderma. The oral L-tryptophan loading test was performed in 31 cases of systemic scleroderma (progressive systemic sclerosis, PSS) and 3 cases of localized scleroderma. Serum levels of tryptophan and urinary excretion of indole-acetic acid (IAA) and indican (IS) were determined in order to assess intestinal absorption of tryptophan. In 10 cases the D-xylose test and in 4 cases Schilling's test was also performed. Furthermore, in vitro binding of L-tryptophan by plasma proteins in PSS and in other skin diseases as controls was studied. The normal increase in serum tryptophan after loading was noted in 17 cases (in 14 cases of PSS with a mild, slow progression in 3 cases of PSS with a severe, rapidly progressing course). In 10 of these cases, urinary excretion of IAA was higher than normal and in normal and in 3 cases excretion of urinary IS was also above normal. On the other hand, in 14 cases of severe, rapidly progressing PSS and in 2 of 3 cases of widespread linear scleroderma, serum levels of tryptophan were markedly depressed after loading, while urinary excretion of IAA and IS was normal. In all 4 cases studied, Schilling's test was normal, and only in 2 of 10 cases of PSS was the D-xylose test abnormal. It is concluded that in the majority of cases of PSS, intestinal absorpiton of tryptophan is normal as also is the absorptive function of the intestine. The slight rise in serum tryptophan after loading in some cases of PSS may be a result of increased binding of tryptophan by albumin.

Adolescent↗
PubMedDate not supplied

[Studies of the role of cellular immunity and angiogenetic changes in the pathogenesis of circumscribed scleroderma].

The studies were performed in 48 patients with morphea and included evaluation of 1) antinuclear antibodies 2) lymphocyte induced angiogenesis 3) natural killer (NK) cell activity and 4) T cell subpopulations in peripheral blood. The presence of antinuclear antibodies was found in 44.4% (8/18) patients with scleroderma linearis and in 21% (4/19) patients with morphea disseminata. Lymphocyte induced angiogenesis was increased in 41.5% (17/41) morphea patients, mainly in cases with pronounced vascular changes. The E rosette forming test showed a decreased percentage of active rosette forming cells (ARFC) and total rosette forming cells (TRFC) in peripheral blood and the NK cell activity was lowered in patients with morphea. These results obtained in patients with morphea show some similarities and differences in comparison to cellular immunity disturbances in patients with systemic scleroderma.

Angiogenesis Inducing Agents↗
PubMedDate not supplied

[Studies of the mechanism of disorders of the natural killer cell activity in patients with systemic scleroderma].

The NK activity of peripheral blood mononuclear cells (PBMC) was evaluated in 90 patients with various subsets of systemic scleroderma (SSc). The NK activity, as performed with K-562 as target cell, was found to be significantly lowered in patients with diffuse scleroderma, but did not differ from the healthy control in patients with acrosclerosis. The lowest values in the NK activity assay were obtained in patients with most extensive skin involvement and severe internal organ changes. The NK activity of healthy donors' PBMC was significantly decreased by addition of SSc patients PBMC (50:1) to the cytotoxicity assay, but was not influenced by the patients sera.

Cytotoxicity, Immunologic↗