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Biomedical subjects

J Sedlák

Publications and source records attributed to J Sedlák.

At least 19 recordsLinked to original sources
PubMed1995

Sialylated Lewis(x) and Lewis(a) determinants expression on human neoplastic cell lines: immunocytometric study with the 5th workshop monoclonal antibodies.

The reactivity of monoclonal antibodies from the 5th workshop Selectins/Selectin Ligands panel, directed to the sialylated Lewis(x) and sialylated Lewis(a) determinants, with the human breast carcinoma (BT-20, ZR-75-1 and MDA-MB-468) cell lines, human ovarian carcinoma cell line A2780, fibrosarcoma (HT-1080, B-6FS) and hematopoietic neoplastic (U-937, HL-60, K-562) cell lines were determined with the aid of flow immunocytofluorometry. The examined monoclonal antibodies to sialylated Lewis determinants reacted with examined breast carcinoma, but not with the examined ovarian carcinoma and fibrosarcoma cell lines.

Antibodies, Monoclonal↗
PubMed1995

Differential effect of protein kinase inhibitors (staurosporine and CGP 41,251) on TPA-induced homotypic aggregation and cell surface adhesion antigen expression in human monoblastoid cell line U-937.

The phorbolester (TPA)-induced homotypic aggregation of human monoblastoid U-937 cells was completely abolished by staurosporine, but not by a new selective protein kinase C inhibitor, benzoylated staurosporine derivative CGP 41,251, a compound with known anti-tumor and drug resistance modulating activity. Staurosporine, a protein kinase inhibitor with broad profile of inhibitory activity on diverse protein kinases, but not CGP 41,251 substantially inhibited the TPA-induced up-regulation of intercellular adhesion molecule-1 (ICAM-1, CD54) and to a lesser extent also its ligand CD11a. These results suggest that protein kinase C-independent mechanisms, inhibited by staurosporine but not by the selective PKC inhibitor CGP 41,251 are involved in the TPA-induced homotypic adhesion and modulation of cell surface adhesion antigens in the human monoblastoid cell line U-937.

Alkaloids↗
PubMed1995

Phorbol ester (TPA)-induced differential modulation of cell surface antigens in human pluripotential leukemia (K-562) cell line: effects of protein kinase inhibitors with broad- and PKC selective inhibitory activity.

Phorbol ester (TPA)-induced increase in cell surface expression of adhesion structures, i.e. intercellular adhesion molecule-1 (ICAM-1, CD54), beta 2 integrin LFA-1 (CD11a), complement-regulatory cell membrane protein-protein (CD59) and leukocyte common antigen (CD45) in human erythroid/myeloid leukemia cell line K-562 was inhibited by staurosporine, an inhibitor with broad, non-selective protein kinase inhibitory profile, but not by CGP 41,251, a benzoylated staurosporine derivative with the selective protein kinase C (PKC) inhibitory activity. Neither staurosporine nor CGP 41,251 modulated TPA-induced down-regulation of transferrin receptor (CD71). These data suggest that phorbol ester-induced cell surface antigen modulations in K-562 cells are predominantly mediated by PKC-independent signalling pathways.

Alkaloids↗
PubMed1995

[Density of adhesive proteins after oral administration of proteolytic enzymes in multiple myeloma].

The authors present information on the presence of adhesive proteins on membranes of myeloma and precursor cells isolated from bone marrow and blood from a group of 33 patients examined by fluorescent flow cytometry. They also compare the density of integrins (CD29, CD49e, CD41, CD51 and CD61) and adhesive proteins from the group of "homing" receptors (CD44) and IgG "superfamily" (LFA-1, LFA-3, ICAM-1, N-CAM) and their changes after a single oral dose of a mixture of proteolytic enzymes (Wobe Mugos, Wobenzym, MUCOS Pharma, FRG). The authors observed a significant drop of CD29, CD54 (ICAM-1), CD58 (LFA-3) after Wobe Mugos, CD49, CD51, CD58 after Wobenzyme. The insignificant decline of density of CD44 on cells, as well as of the soluble receptor of CD44 after oral administration of proteolytic enzymes in serum, incl. the mentioned changes of integrins and other adhesive proteins, indicate the importance of enzyme preparations in the supporting treatment of malignant processes.

Adjuvants, Immunologic↗
PubMed1994

Tyrosine kinase inhibitor-induced differentiation of K-562 cells: alterations of cell cycle and cell surface phenotype.

Protein tyrosine kinase (PTK) inhibitor herbimycin A inhibited proliferation, induced accumulation of cells in the G0/G1 phase of the cell cycle and a marked increae of hemoglobin-producing human leukemic K-562 cells in vitro. The isoflavonoid PTK- and topoisomerase II inhibitor genistein produced a similar effect with the accumulation of cells in the G2/M phase of cell cycle. Genistein potentiated the effect of herbimycin A on the cell cycle (i.e. decreased the proportion of S-phase cells) and induced an increased proportion of hemoglobin-producing cells. Genistein, but not herbimycin A induced a marked increase in cell surface expression of CD15 (LewisX) antigen. Both of these agents down-regulated CD45 (leukocyte common antigen) and monocyte-associated CD14 antigen on K-562 cells. Neither genistein nor herbimycin A induced increased cell surface expression of glycophorin.

Animals↗
PubMed1994

[Transesophageal ventricular stimulation and ventricular tachycardia in the period before implantation of a cardioverter-defibrillator].

The administration of an implantable cardioverter-defibrillator (ICD) is the method of choice in life-threatening ventricular tachyarrhythmias. This effective non-pharmacological intervention was a great advance in the prevention of sudden cardiac death. As to ventricular tachycardias, relapsing ventricular tachycardias based on ischaemic alone need not influence ventricular tachycardia. The mechanism of ventricular tachycardia in ischaemic heart disease is reentry and therefore this arrhythmia can be terminated not only by a defibrillation discharge but also by antitachycardiac stimulation. Various types of antitachycardiac stimulation are part of modern types of ICD. Evidence of the effectiveness of antitachycardiac stimulation (electrophysiological examination) permits to use it also by the transoesophageal approach. This treatment can be very effective and we can thus overcome the period before the definite administration of an ICD, as indicated by the case described.

Aged↗
PubMed1994

Drug-resistance associated alterations of cell surface antigen expression in a human anthracycline-resistant ovarian carcinoma cell line.

The anthracycline uptake and cell surface expression of plasma membrane antigens (HLA class I, c-erbB-2, protectin-CD59, integrin beta 1-chain-CD29, etc.) were compared on a parental anthracycline sensitive and an anthracycline-resistant subline of the human ovarian carcinoma cell line A2780. The anthracycline-resistant (A2780/ADR) subline incubated for 30 min in the presence of daunomycin displayed two subpopulations with different anthracycline cell content as determined by flow cytometry. The subpopulation with lower daunomycin cell content was absent in the parental anthracycline sensitive cell line. The most predominant antigenic changes on the resistant subline as compared with the sensitive one were as follow: Loss of HLA class I and a twofold increase in the expression of CD59 antigen and a slight decrease of integrin beta 1-chain on the cell surface of the resistant subline.

Antibiotics, Antineoplastic↗
PubMed1994

Modulation of cell surface EGF receptor and HLA expression on glioma cell lines induced with cytokines and differentiation promoters.

Alterations of cell surface expression of HLA (class I, class II DR, DP and DQ) and EGF-receptor on two malignant glioma cell lines (U-343MG and U-563MG) induced with cytokines (IFN-gamma, TNF-alpha, IL-1 alpha) and differentiation promoters (all-trans retinoic acid, phorbol ester TPA) were analyzed with the aid of flow cytometry. IFN-gamma induced a 10-15fold increase of HLA class I. TNF-alpha alone induced a two- to fivefold increase of HLA class I cell surface density and increased the IFN-gamma induced upregulation of HLA class I to approximately 20-24 times the antigen density of uninduced cells. TNF-alpha was able to increase HLA class II DR and DP cell surface expression on glioma lines, but it enhanced only the IFN-gamma-induced HLA class II DR upregulation. All-trans retinoic acid and TPA regulated in the opposite way the EGF-receptor cell surface expression on U-563MG cells.

Antigens, Surface↗
PubMed1994

Myeloid activation antigen CD66/67: immunochemical and immunocytometric characterization with the Vth workshop monoclonal antibodies.

Flow cytometric and immunochemical studies performed with the CD66/67 panel antibodies from the Vth International Workshop on Leukocyte Antigens allowed to subdivide these antibodies into five groups, according to the molecular weights of polypeptides recognized by these antibodies on pooled healthy donor granulocytes. Although some monoclonal antibodies recognized either 95-110 kDa, or 160-180 kDa polypeptides, majority of the examined antibodies reacted with epitopes shared by both 95-110 kDa and 160-180 kDa polypeptides. Differential TPA-induced modulation of recognized antigens was observed with HL-60 and U-937 leukemia/lymphoma cell lines.

Antibodies, Monoclonal↗
PubMed1993

[The effect of aminophylline on the sinoatrial node].

The objective of the submitted prospective study was to assess the influence of intravenously administered aminophylline on the sinoatrial node. The authors examined by electrophysiological methods 20 patients (16 without dysfunction of the sinoatrial node and 4 with dysfunction of the sinoatrial node). From the investigation patients were eliminated with an apparent and obvious cause of elevated uric acid serum levels and patients where on electrophysiological examination limited values of the corrected recovery time of the sinoatrial node were found (from 650 ms to 999 ms). To all 20 patients 240 mg aminophylline were administered by the i.v. route with in 2 mins. The following parameters were recorded: age, serum level of uric acid, basal heart rate in ms, corrected recovery time of the sinoatrial node in ms, heart rate and corrected recovery time of the sinoatrial node 5 min after completed administration of aminohpylline in ms. As regards age and uric acid serum levels there was no significant difference between dysfunction of the sinoatrial node and normal function of the sinoatrial node. Intravenously administered aminophylline hastened significantly the heart rate in patients without dysfunction of the sinoatrial node (p < 0.05). The value of the corrected recovery time of the sinoatrial node was shorter but the difference was not statistically significant. In patients with dysfunction of the sinoatrial node aminophylline did not affect the heart rate and corrected recovery time of the sinoatrial node.

Adult↗
PubMed1993

Modulation of protectin (CD59 antigen) cell surface expression on human neoplastic cell lines.

The ability of cytokines (IFN alpha, IFN gamma, TNF alpha, IL-1 alpha, IL-6), all-trans retinoic acid, 1,25(OH)2-vitamin D3 and the tumor promoting phorbol ester TPA to regulate cell surface expression of protectin (CD59 antigen) on human hematopoietic and non-hematopoietic neoplastic cell lines was examined with the aid of immunocytofluorometric measurements. The tumor promoting phorbol ester TPA induced a marked up-regulation of protectin in all examined cell lines with the exception of promyelocytic leukemia HL-60, where TPA significantly decreased protectin cell surface expression. All-trans retinoic acid weakly down-regulated cell surface protectin on K-562, while 1,25(OH)2-vitamin D3 produced such effect on HL-60 cells. None of the examined cytokines induced a significant protectin down-regulation in the examined cell lines.

Antigens, CD↗
PubMed1993

Phorbol ester-induced modulation of cell surface antigens on U-937 cells in protein-free medium: effect of protein kinase and calmodulin inhibitors.

Phorbol ester (PMA) induced decrease in cell surface expression of CD4 antigen was potentiated on human monoblastoid cell line U-937 cultured and induced in protein-free culture medium. Down-regulation of the CD4 antigen was partially inhibited by the isoquinoline protein kinase inhibitor H7 and unaffected by the calmodulin inhibitor R24571 (calmidazolium). PMA-induced increase of the monocyte-associated CD14 antigen was dependent the presence of fetal bovine serum (FBS) in culture medium and partially abolished by calmodulin inhibitor R24571. H7 inhibitor partially abrogated this up-regulation in 4 out of 8 induction experiments. PMA-induced down-regulation of MHC class I antigen was found in both FBS-supplemented and protein-free culture media. This effect was partially inhibited by both H7 and R24571 inhibitors.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Modulation of leukosialin (sialophorin, CD43 antigen) on the cell surface of human hematopoietic cell lines induced by cytokins, retinoic acid and 1,25(OH)2-vitamin D3.

Cell surface expression of leukosialin (sialophorin, CD43 antigen) on human neoplastic hematopoietic cell lines K-562, U-937, HL-60 and REH was determined with the aid of a new CD43 monoclonal antibody (Bra7G) by the immunochemical (radioimmunoprecipitation, immunoblotting) and immunocytofluorometric techniques. Interferon-gamma and TNF-alpha were utilized as the "physiological" inducers of differentiation-associated markers. The "non-physiological" inducer phorbol ester PMA induced down-regulation of leukosialin cell surface expression on immature erythroid-myeloid leukemia cell line K-562, but up-regulation of CD43 antigen on the promyelocyte leukemia cell line HL-60 and, to a lesser extent on the monocyte-like U-937 and CALLA+ ALL cell line REH. Retinoic acid down-regulated leukosialin on both U-937 monocyte-like cells and the CALLA+ ALL cell line REH. In contrast to these data, interferon-gamma, TNF-alpha, retinoic acid and 1,25(OH)2-vitamin D3 induced the up-regulation of leukosialin in a promyelocytic leukemia cell line HL-60.

Antigens, CD↗
PubMed1993

[Sick sinus syndrome and permanent cardiac pacing].

The authors submit a retrospective analysis of 140 patients with an affection of the sinoatrial node who had a permanent cardiac pacemaker. The analysis comprises an 18-month period; the patients were from the eastern Slovakian region. The authors emphasize different affections of the sinoatrial node and discuss various ways of permanent cardiac pacing and other types of non-pharmacological treatment (e.g. electric ablation). Diseases of the sinoatrial node account for as much as 40% of implantations of a permanent pacemaker on account of bradyarrhythmia. At the clinic this implies a quantitative increase of cardiac pacing on account of diseases of the sinoatrial node by 18%, as compared with a previous period (e.g. the average for 1978-1987). A qualitative change is the introduction of physiological permanent cardiac pacing.

Aged↗
PubMed1993

IL-1 alpha induced, TNF alpha mediated HLA class II (DR) antigen up-regulation in a human ductal breast carcinoma cell line ZR-75-1.

The IL-1 alpha induced up-regulation of HLA class I and HLA class II (DR) antigen expression on the cell surface of the human breast cancer cell line ZR-75-1 was demonstrated. This was associated with a concomitant increase in TNF alpha production. Coincubation with an anti-TNF alpha neutralizing antibody partially inhibited the IL-1 alpha induced up-regulation of HLA DR antigen but had no effect on IL-1 alpha induced HLA class I up-regulation. These data indicate that IL-1 alpha induced HLA class II (DR) antigen up-regulation in ZR-75-1 cells is partially mediated by TNF alpha and that IL-1 alpha induced HLA class I and class II (DR) antigen up-regulation in ZR-75-1 human breast cancer cells in vitro are mediated by different mechanisms.

Breast Neoplasms↗
PubMed1992

Monoclonal antibodies to two adhesive cell surface antigens (CD43 and CD59) with different distribution on hematopoietic and non-hematopoietic tumor cell lines.

Two new murine monoclonal antibodies were prepared by hybridoma technique after immunization with the immature pluripotent leukemia cell line K562. The monoclonal antibody Bra10G (IgG2b) reacted in a non-lineage pattern with all examined hematopoietic neoplastic cell lines and peripheral blood cells (granulocytes, lymphocytes, erythrocytes) of healthy donors, with the exception of monoblastoid cell line U-937 and B lymphoma cell line Daudi. This monoclonal antibody immunoprecipitated an 18-20 kDa cell surface protein expressed also on the cell surface of examined non-hematopoietic (malignant glioma, melanoma and breast carcinoma) cell lines. These properties and the efficient inhibition of Bra10G binding to the cell surface of K562 cells by the reference CD59 monoclonal antibody (MEM-43) indicated that Bra10G belongs to the CD59 cluster of monoclonal antibodies which identify the human protectin molecule. The monoclonal antibody Bra7G (IgM) reacted with a 95 kDa cell surface protein expressed on hematopoietic cells (with the exception of erythrocytes) and was absent on the examined non-hematopoietic neoplastic cell lines. These data together with a partial inhibition of Bra7G binding by the reference CD-43 monoclonal antibody suggested the CD43 (leukosialin, sialophorin) specificity of this monoclonal antibody.

Animals↗