Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

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Tytuł oryginału: Free radicals-mediated induction of oxidized DNA bases and DNA-protein cross-links by nickel chloride.
Autorzy: Woźniak Katarzyna, Błasiak Janusz
Źródło: Mutat. Res 2002: 514 (1/2) s.233-243, il., tab., bibliogr. 50 poz.
Sygnatura GBL: 304,952

Hasła klasyfikacyjne GBL:
  • toksykologia
  • genetyka

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • dorośli 19-44 r.ż.
  • płeć męska
  • in vitro

    Streszczenie angielskie: Using the comet assay, we showed that nickel chloride at 250-1000 ćM induced DNA damage in human lymphocytes, measured as the change in comet tail moment, which increased with concentration up to 500 ćM and then decreased. Observed increase might follow from the induction of strand breaks or/and alkali-labile sites (ALS) by nickel, whereas decrease from its induction of DNA-DNA and/or DNA-protein cross-links. Proteinase K caused an increase in the tail moment, suggesting that nickel chloride at 1000 ćM might cross-link DNA with nuclear proteins. Lymphocytes exposed to NiCl2 and treated with enzymes recognizing oxidized and alkylate bases: endonuclease III (Endo III), formamidopyrimidine-DNA glycosylase (Fpg) and 3-methyladenine-DNA glycosylase II (AlkA), dusplayed greated extent of DNA damege than those not treated with these enzymes, indicating the induction of oxidized and alkylated bases by nickel. The incubation of lymphocytes with spin traps, 5,5-dimethyl-pyrroline N-oxide (DMPO) and PBN decreased the extent of DNA damage which might follow from the production of free radicals by nickel. The pre-treatment with Vitamin C at 10 ćM and Vitamin E at 25 ćM decreased the tail moment of the cells exposed to CiCl2 at the concentrations of the metal causing strand breaks or/and ALS. The results obtained suggest that free radicals may be involved in the formation of strand breaks or/and ALS in DNA as well as DNA-protein cross-links induced by NiCl2. Nickel chloride can also alkulate DNA bases. Our results support thesis on multiple, free radicals-based genotoxicity pathways of nickel.


    2/9

    Tytuł oryginału: Antigen levels of the urokinase-type plasminogen activator and its gene polymorphisms in colorectal cancer.
    Autorzy: Przybyłowska K., Smolarczyk K., Kulig A., Romanowicz-Makowska H., Dziki A., Ulańska J., Pander B., Błasiak J.
    Źródło: Cancer Lett. 2002: 181 (1) s.23-30, il., tab., bibliogr. 18 poz.
    Sygnatura GBL: 306,023

    Hasła klasyfikacyjne GBL:
  • gastroenterologia
  • onkologia
  • genetyka
  • immunologia

    Typ dokumentu:
  • praca kliniczna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • płeć męska
  • płeć żeńska

    Streszczenie angielskie: We analysed the distribution of genotypes of two polymorphisms in the urokinas-type plasminogen activator (uPA) gene: C - T substitution in exon 6 and T - C substitution in intron 7 in 52 subjects with colorectal cancer. Genotypes were determined in tumour tissue and distant mucosa samples by allele-specific polymerase chain reaction. The antigen levels of uPA in cancer tissue were higher than in distant mucosa as measrued by enzyme-linked immunosorbent assay. The level of uPA antigens in cancer samples with the C/C genotype of C - T polymorphism in exon 6 was higher than in samples with C/T and T/T genotypes. No differences in the level of uPA antigens between the alleles of the intron 7 T - C polymorphism were found. As uPA can be involved in cancer invasion and metastasis, C/C genotype in exon 6 of uPA gene can be further considered as being related to colorectal cancer progression.


    3/9

    Tytuł oryginału: Dyspersja odstępu Q-T a restenoza po zabiegu przezskórnej angioplastyki tętnic wieńcowych.
    Tytuł angielski: QT dispersion and restenosis after percutaneous transluminal coronary angioplasty.
    Autorzy: Bryniarski Leszek, Czarnecka Danuta, Stolarz Katarzyna, Styczkiewicz Marek, Rachwał Katarzyna, Błasiak Artur, Oruba Bartłomiej, Rajtar Renata, Kawecka-Jaszcz Kalina
    Źródło: Folia Cardiol. 2002: 9 (1) s.21-28, tab., bibliogr. 24 poz., sum.
    Sygnatura GBL: 313,196

    Hasła klasyfikacyjne GBL:
  • kardiologia

    Wskaźnik treści:
  • ludzie

    Streszczenie polskie: Wstęp: Obecnie stosowane kryteria oceny elektrokardiograficznej próby wysiłkowej nie wykazują pełnej skuteczności w rozpoznawaniu restenozy. Dyspersja odstępu Q-T jest miarą niejednorodności repolaryzacji komór i stwierdza się jej zwiększenie u pacjentów z chorobą niedokrwienną serca. Celem pracy jest ocena dyspersji odstępu Q-T w elektrokardiograficznej próbie wysiłkowej u pacjentów z restonozą po zabiegu przezskórnej angioplastyki tętnic wieńcowych (PTCA). Materiał i metody: Badaniem objęto 50 pacjentów, których obserwowano przez 6 miesięcy po wykonaniu PTCA. Grupę I stanowiło 24 pacjentów, z nawrotem zwężenia do 6 miesięcy po zabiegu, zaś grupę II (kontrolną) dobraną pod względem płci, wieku i ilości naczyń zajętych procesem chorobowym - 26 pacjentów bez restenozy. Wykonywano standardowy 12-odprowadzeniowy zapis EKG przed PTCA, a następnie elektrokardiograficzne testy wysiłkowe: do 7 dni, po 1 i po 3 miesiącach obserwacji. Odtęp Q-T oceniano manualnie, a wartość skorygowanego odstępu Q-T (Q-Tc) obliczono na podstawie formuły Bazetta. Za miarę dyspersji QT przyjęto różnicę między maksymalną a minimalną wartością Q-T w 12 odprowadzeniach EKG. Na podstawie zapisu elektrokardiograficznego próby wysiłkowej oceniano wartość dyspersji w spoczynku i na szczycie wysiłku. Wyniki: Wyjściowo grupa I i II nie różniły się wartością dyspersji QT w EKG spoczynkowym. Po 3 miesiącach stwierdzono istotne różnice dyspersji odstępu Q-T w zapisach EKG przed testem wysiłkowym w ...

    Streszczenie angielskie: Electrocardiographic exercise stress test assessed by the currently used criteria has not proven to be an absolutely presise method in the diagnosis of the restenosis after percutaneous transluminal coronary angioplasty (PTCA). QT dispersion is used as an index of heterogeneity of the ventricular repolarization and increases in patients with ischaemic heart disease. The aim of the study was to assess the influence of the restenosis on QT dispersion during exercise testing in patients after PTCA. Material and methods: The study included 50 patients, observed during 6 months after PTCA. Group I - 24 pts. with restenosis till 6 months after PTCA. Group II (controls) was recruited according to age, gender and the number of diseased coronary vessels and included 26 pts. without restenosis. The standard 12 lead ECG was done before PTCA, and ECG exercise tests were performed in 7 days, 1 and 3 months after PTCA. The measurement of QT interval was done manually. The QT dispersion was calculated as the difference between maximal and minimal duration of QT interval in all 12 leads. In exercise ECG recordings the QT dispersion was assessed at pre-test and at the peak exercise. Results: At the baseline groups did not differ in terms of the QT dispersion in resting conditions. Three months after PTCA significant differences in values of QT dispersion were observed during treadmill exercise test in resting conditions (57.5 ń 21 ms vs. 39.3 ń 15 ms; p = 0.002) and at the peak ...


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    Tytuł oryginału: Erupcyjna aktywność neuronalna wybranych struktur mózgu ssaków.
    Tytuł angielski: Slow bursting activity in the selected structures of mammalian brain.
    Autorzy: Błasiak Tomasz
    Źródło: Post. Hig. 2002: 56 (3) s.323-330, il., bibliogr. [28] poz., sum. - Konferencja pt. Blaski i cienie elektrofizjologii mózgu in vitroKonferencja pt. Techniki elektrofizjologiczne w badaniach zjawisk bioelektrycznych - od kanałów jonowych po sieci neuronalne KrakówŁódź 24.10.07-08.06. 20012002
    Sygnatura GBL: 301,727

    Hasła klasyfikacyjne GBL:
  • neurologia

    Typ dokumentu:
  • praca związana ze zjazdem

    Wskaźnik treści:
  • zwierzęta

    Streszczenie angielskie: Slow bursting activity of the cells in the hypothalamus of the mammalian brain is described, with a special emphasis on the vasopressinergic neurons of the supraoptic and paraventricular nuclei (SON/PVN). This patterned activity is compared to the one observed in the thalamic structure - the intergeniculate leaflet of the lateral geniculate nucleus (IGL). Histograms of activity, bimodal distributions of the frequencies, averaged bursts and a few other characteristic properties of the oscillatory activity observed in SON/PVN and IGL are shown. Slow bursting activity of the intergeniculate leaflet cells is suggested to have a same function as has patterned firing of hypothalamic cells. Peptidergic contents of IGL cells, possibly attenuated blood - brain barrier in the area of this structure and its role in the adjustment of the circadian rhythms are some of the arguments to support this hypothesis.


    5/9

    Tytuł oryginału: Are ultra-slow isoperiodic oscillations in rat intergeniculate leaflet neurons dependent on reciprocal connection with its contralaterally located counterpart?
    Autorzy: Lewandowski Marian H., Błasiak Tomasz, Błasiak Anna
    Źródło: Neurosci. Lett. 2002: 330 (3) s.243-246, il., bibliogr. 13 poz.
    Sygnatura GBL: 305,936

    Hasła klasyfikacyjne GBL:
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: We investigated effects of the electrical lesion and/or chemical inactivation of intergeniculate leaflet (IGL) neurons on the ultra-slow isoperiodic neuronal oscillation of the contralaterally located IGL. The spontaneous extracellular activity of neurons, recorded simultaneously in both leaflets of the lateral geniculate nucleus, showed an ultradian oscillatory patern. In all our experiments, both the electrical lesion and the inactivation of neurons via the blockade of action potential generation did not cause any changes in the neuronal activity pattern in the contralaterally located geniculate leaflet. The obtained results show that a bilateral IGL connection is not necessary for the pattern of neuronal oscillation in the IGL. Hence the functional significance of a reciprocal connection between both lateral geniculate nucleus leaflets is still an open question.


    6/9

    Tytuł oryginału: TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine.
    Autorzy: Gloc Ewa, Warszawski Mariusz, Młynarski Wojciech, Stolarska Małgorzata, Hoser Grażyna, Skorski Tomasz, Błasiak Janusz
    Źródło: Acta Bioch. Pol. 2002: 49 (1) s.121-128, il., bibliogr. 30 poz. - 8 Międzynarodowe Sympozjum pt. Aspekty molekularne chemioterapii Gdańsk 09. 2001
    Sygnatura GBL: 303,116

    Hasła klasyfikacyjne GBL:
  • toksykologia
  • genetyka
  • hematologia
  • onkologia

    Typ dokumentu:
  • praca związana ze zjazdem
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • in vitro

    Streszczenie angielskie: The TEL/JAK2 chromosomal translocation (t(9;12)(p24;p13) is associated with T cell childhood acute lymphoblastic leukemia. The TEL/JAK2 fusion protein contains the JAK2 catalytic domain and the TEL-specific oligomerization domain. TEL-mediated oligomerization of the TEL/JAK2 proteins results in the constitutive activation of the tyrosine kinase activity. Leukemia cells expressing TEL/JAK2 tyrosine kinase become resistant to anti-neoplastic drugs. Amifostine is a pro-drug which can selectively protect normal tissues against the toxicity of anticancer drugs and radiation. We investigated the effects of amifostine on idarubicin-induced DNA damage and repair in murine pro-B lymphoid BaF3 cells and BaF3-TEL/JAK2-transformed cells using alkaline single cell gel electrophoresis (comet assay). Idarubicin induced DNA damage in both cell types but amifostine reduced its extent in control non-transformed BaF3 cells and enhanced it in TEL/JAK2-transformed cells. The transformed cells did not show measurable DNA repair after exposure to amifostine and idarubicin, but cells treated only with idarubicin were able to recover within a 60-min incubation. Because TEL/JAK2-transformed cells can be considered as model cells for certain human leukemias and lymphomas we anticipate an enhancement of idarubicin cytotoxicity by amifostine in these diseases. Moreover, TEL/JAK2 tyrosine kinase might be involved in cellular response to DNA damage. Amifostine could promote apoptosis or lower the threshold for apoptosis induction dependent on TEL/JAK2 activation.


    7/9

    Tytuł oryginału: A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.
    Autorzy: Błasiak Janusz, Gloc Ewa, Warszawski Mariusz
    Źródło: Acta Bioch. Pol. 2002: 49 (1) s.145-155, il., bibliogr. 38 poz. - 8 Międzynarodowe Sympozjum pt. Aspekty molekularne chemioterapii Gdańsk 09. 2001
    Sygnatura GBL: 303,116

    Hasła klasyfikacyjne GBL:
  • toksykologia
  • onkologia

    Typ dokumentu:
  • praca związana ze zjazdem
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • in vitro

    Streszczenie angielskie: Idarubicin is an anthracycline antibiotic used in cancer therapy. Mitoxantrone is an anthracycline analog with presumed better antineoplastic activity and lesser toxicity. Using the alkaline comet assay we showed that the drugs at 0.01 - 10 ćM induced DNA damage in normal human lymphocytes. The effect induced by idarubicin was more pronounced than by mitoxantrone (P 0.001). The cells treated with mitoxantrone at 1 ćM were able to repair damage to their DNA within a 30-min incubation, whereas the lymphocytes exposed to idarubicin needed 180 min. Since anthracyclines are known to produce free redicals, we checked whether reactive oxygen species might be involved in the observed DNA damage. Catalase, an enzyme inactivating hydrogen peroxide, decreased the extnt of DNA damage induced by idarubicin, but did not affect the extent evoked by mitoxantrone. Lymphocytes exposed to the drugs and treated with endonuclease III or formamidopyrimidine-DNA glycosylase (Fpg), enzymes recognizing and nicking oxidized bases, displayed a higher level of DNA damage than the untreated ones. 3-Methyladenine-DNA glycosylase II (AlkA), an enzyme recognizing and nicking mainly methylated bases in DNA, increased the extent of DNA damage caused by idarubicin, but not that induced by mitoxantrone. Our results indicate that the induction of secondary malignancies should be taken into account as side effects of the two drugs. Direct strand breaks, oxidation and methylation of the DNA bases can underlie the DNA-damaging effect of idarubicin, whereas mitoxantrone can induces strand breaks and modification of the bases, including oxidation. The observed in normal lymphocytes much lesser genotoxicity of mitoxantrone compared to idarubicin should be taken into account in planning chemotherapeutic strategies.


    8/9

    Tytuł oryginału: Amifostine differentially modulates DNA damage evoked by idarubicin in normal and leukemic cells.
    Autorzy: Błasiak Janusz, Gloc Ewa, Młynarski Wojciech, Drzewoski Józef, Skórski Tomasz
    Źródło: Leuk. Res. 2002: 26 (12) s.1093-1096, il., bibliogr. 8 poz.
    Sygnatura GBL: 306,151

    Hasła klasyfikacyjne GBL:
  • toksykologia
  • genetyka
  • farmacja
  • hematologia
  • onkologia

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • in vitro

    Streszczenie angielskie: Human lymphocytes, p53 protein-deficient acute promyelocytic leukemia cell line HL-60, murine pro-B lymphoid cell line BaF3 and its TEL/ABL-transformed clone cells were exposed to idarubicin with and without pre-treatment with amifostine. Idarubicin at 0.5 - 5ćM evoked DNA damage measured by the Comet assay. Amifostine at 14 mM decreased DNA-damaging effect of idarubicin in human lymphocytes and BaF3 cells, but increased the effect in TEL/ABL-transformed cells. Amifostine had no influence on the action of idarubicin in HL-60 cells. Our results suggest that the reaction of the cell to DNA damage may contribute to its diverse response to amifostine combined with anticancer drugs and that p53 and fusion tyrosine kkinases may be involved in this diveristy.


    9/9

    Tytuł oryginału: Recognition and repair of DNA-cisplatin adducts.
    Autorzy: Woźniak Katarzyna, Błasiak Janusz
    Źródło: Acta Bioch. Pol. 2002: 49 (3) s.583-596, il., tab., bibliogr. [100] poz.
    Sygnatura GBL: 303,116

    Hasła klasyfikacyjne GBL:
  • onkologia
  • genetyka
  • farmacja

    Typ dokumentu:
  • tytuł obcojęzyczny

    Streszczenie angielskie: Anticancer activity of cisplatin (cis-diamminedichloroplatinum) is believed to result from its interaction with DNA. The drug reacts with nucleophilic sites in DNA forming monoadducts as well as intr-and interstrand crosslinks. DNA-cisplatin adducts are specifically recognized by several proteins. They can be divided into two classes. One constitutes proteins which recognize DNA damage as an initial step of the nucleotide excision and mismatch repari pathways. The other class contains proteins stabilizing cellular DNA-protein and protein-protein complexes, including non-histone proteins stabilizing cellular DNA-protein and protein-protein complexes, including non-histone proteins from the HMG (high-mibility-group) family. They specifically recognize 1,2-interstrand d(GpG0 and d(ApG) crosslinks of DNA-cisplatin adducts and inhibit their repair. Many HMG-domain proteins can function as transcription factors, e.g. UBF, an RNA polymerase I transcription factor, the mamalian testis-determining factor SRY and the human mitochondrial transcription factor mtTFA. Moreover, it seems that some proteins, which probably recognize DNA-cisplatin adducts non-specifically, e.g. actin and other nuclear matrix proteins, can disturb the the structural and functional organization of the nucleus and whole cell. The formation of complexes between DNA and proteins in the presence of cisplatin and the changes in the cell architecture may account for the drug cytotoxicity.

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