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Biomedical subjects

Mirosława Koronkiewicz

Publications and source records attributed to Mirosława Koronkiewicz.

6 recordsLinked to original sources
PubMed2006

High dose of intravenously given glucocorticosteroids decrease IL-8 production by monocytes in multiple sclerosis patients treated during relapse.

The aim of our study was to determine whether high doses of intravenous methylprednisolone have significant impact on immune parameters during the multiple sclerosis (MS) exacerbations. Peripheral blood of 32 MS patients was evaluated, using two-color flow cytometry before glucocorticosteroids and after 7 days from starting therapy. Significant increase of B cells, decrease of NK cells and monocytes producing IL-8 were observed after treatment. IL-8 is one of the cytokines responsible for blood-brain-barrier disruption and migration of immune cells to the central nervous system; in this aspect, explaining glucocorticosteroid effects during MS exacerbations.

Adult↗
PubMed2004

Synthesis and preliminary evaluation of the new water-soluble radioactive platinum(IV) complexes.

A novel class of water-soluble Pt(IV) complexes with histamine (Hist) and radioiodinated histamine ([(125)I/(131)I]Hist) has been synthesised with the goal of potential application for concomitant anticancer radio-chemotherapy of solid tumours. The prepared complex of 1:2 metal:ligand stoichiometry ([Pt(IV)(Hist)(2)(OH)(2)]Cl(2)) was characterised by microanalysis, mass spectrometry, and chromatographic methods. Cytotoxic/cytostatic activities of the complex were examined by flow cytometry method using the MCF-7 cells line. A slightly lower cytotoxicity of the Pt(IV) complex comparing to cisplatin was found (IC(50) 59 and 48 microM, respectively). Both cisplatin and the histamine complex show a cytostatic activity by blocking MCF-7 cells in S-phase of cell cycle. Biodistribution studies in normal rats revealed the highest accumulation of the (131)I-labelled complex in liver and kidneys (41.3% and 12.4% ID after 24 h post-intravenous injection (p.i.v.)). The similar pharmacokinetics was observed in tumour-bearing C3H/W mice, however, a lower accumulation in liver was observed following an intraperitoneal comparing to an intravenous administration. A concentration of the complex in tumour increased with time post-intraperitoneal injection (1.2 and 2.5%ID/g after 2 and 24 h (p.i.), respectively). An increasing tumour/muscle ratio was also observed (2.2 and 4.5 after 2 and 24 h p.i., respectively), and that suggests a penetration of the complex into the tumour cells, and a permanent binding with some cellular components, probably with the DNA.

Animals↗
PubMed2003

Changes of percentages in immune cells phenotypes and cytokines production during two-year IFN-beta-1a treatment in multiple sclerosis patients.

OBJECTIVE: The aim of the study was to find out whether INF-beta-1a influences the immune profile of peripheral blood (PB) leukocytes in MS patients. METHOD: We have studied 20 patients with relapsing-remitting form of MS treated with INF-beta-1a using twocolor cytometry. We determined immune cells phenotypes and production of some cytokines: IL-4, IL-10, IL-12, IFN-gamma, before drug administration and after starting the treatment. RESULTS: In MS patients an increased percentage of CD14(+)CD86(+) cells and CD3(+)CD25(+) cells was noticed after 6, 9 and 12 months of INF-beta-1a therapy. Among cytokine-producing cells we noted an increased fraction of CD3(+)IL-4, CD14(+)IL-10 and CD14(+)IL-12 cells after 12 months, which decreased to the level observed before treatment after 24-month therapy. CONCLUSIONS: IFN-beta-1a treatment was associated with significant changes in immune response. This effect was mostly evident within the first year of treatment.

Adjuvants, Immunologic↗
PubMed2002

Biological investigation of the platinum(II)-[*I]iodohistamine complexes of potential synergistic anti-cancer activity.

Cisplatin chemotherapy in combination with external irradiation or with low-dose continuous internal radiotherapy produces significant supra-additive treatment effects towards several tumor cells. The purpose of our research is to develop a new class of platinum-based anticancer drugs containing moieties of synergistic potency such as platinum core and a radiotherapeutic isotope which, delivered directly to the tumorous cells by a specifically designed vectors, should produce a local enhancement of therapeutic dose. Thus, we have synthesized a new platinum-iodohistamine complex and its radioactive analogues labeled with I-125 and I-131. In the present study some biological properties of those compounds have been investigated. The in vitro screening study pointed out that non-radioactive platinum-iodohistamine complex possesses high cytostatic activity against COLO-205 cells, and moderate activity against HL-60 cell line. No cytotoxicity was observed against MOLT-4 and L-1210 cells, as well as against VERO normal cells. The biodistribution of intravenously administered radioactive platinum-[131I]-iodohistamine complex to normal rats revealed the highest accumulation in the liver (c.a. 40%ID). Intraperitoneal injections of the complex to tumor-bearing C3H mice resulted in scattering of the dose in the organs (mainly in GIT, liver, kidney). The retention of radioactive complex in neoplastic tissue was 3-4 times higher than in normal muscular tissue, although exhibited the tendency to decrease with time post injection. The results of the present study show promising features of the newly developed platinum-iodohistamine complexes and justify prospective investigation of in vivo anticancer potency on animal models of solid tumors.

Adenocarcinoma↗
PubMedDate not supplied

Tezacitabine blocks tumor cells in G1 and S phases of the cell cycle and induces apoptotic cell death.

Tezacitabine (FMdC) is a new cytostatic/cytotoxic agent widely investigated in clinical trials and on the cellular level. In a previous paper (3) we worked on human and murine leukemia (L-1210, HL-60, and MOLT-4) cells, and in this paper we investigated the influence of FMdC on the cell cycle and apoptosis in vitro of three other leukemias (CCRF-SB, KG-1, and Jurkat), and human solid tumor (carcinoma) cell lines (COLO-205, MCF-7, and PC-3). We found that FMdC induces the G1 (at concentrations higher than 10 nM). and S-phase (at low concentration) leaky block of the cell cycle. FMdC also effectively induces apoptotic death of cells by the caspase 3/7 pathway. We found also that FMdC induces intensive changes in the protein metabolism. These changes are correlated with the cell death.

Animals↗