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    Wyświetlanie 1-9 z 9
    Tytuł:
    Patogeneza proliferacyjnej witreoretinopatii
    Pathogenesis of Proliferative Vitreoretinopathy
    Autorzy:
    Bogatko, Joanna
    Kędzierski, Tomasz
    Cisiecki, Sławomir
    Pietras, Tadeusz
    Łyszcz, Weronika
    Szemraj, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/30148725.pdf
    Data publikacji:
    2023
    Wydawca:
    Uczelnia Łazarskiego. Oficyna Wydawnicza
    Tematy:
    proliferacyjna witreoretinopatia
    przedarciowe odwarstwienie siatkówki
    przejście nabłonkowo-mezenchymalne
    proliferative vitreoretinopathy
    rhegmatogenous retinat detachment
    epithelial-mesenchymal transition
    Opis:
    Witreoretinopatia proliferacyjna (PVR) uznawana jest za najczęstszą przyczynę niepowodzenia operacyjnego leczenia przedarciowego odwarstwienia siatkówki. Obecnie PVR porównuje się z procesem nieprawidłowego gojenia ran, powstawaniem i obkurczaniem błon komórkowych po obu stronach powierzchni siatkówki i w komorze ciała szklistego, a także zwłóknieniami śródsiatkówkowymi. W rozwoju PVR wyodrębnia się kilka etapów: fazę niedokrwienia, stan zapalny, apoptozę, fazę migracji, proliferacji i transformacji, obkurczania się błon. Kluczową rolę w całym procesie odgrywają komórki nabłonka barwnikowego siatkówki, które (stymulowane m.in. przez czynniki zapalne) ulegają transformacji, tracąc cechy komórek nabłonkowych na rzecz cech komórek mezenchymatycznych, przypominających fibroblasty. Trwają badania molekularne, mające na celu lepsze zrozumienie patofizjologii PVR, oraz badania kliniczne środków zapobiegających powstawaniu PVR.
    Proliferative vitreoretinopathy (PVR) is considered the most common cause of failure in the surgical treatment of rhegmatogenous retinal detachment. Currently, PVR is compared to the process of abnormal wound healing characterized by the formation and shrinking of cell membranes on both sides of the retinal surface and in the vitreous body chamber, as well as intraretinal fibrosis. Several phases can be distinguished, i.e. the ischemic phase, inflammation, apoptosis, the phase of migration, proliferation and transformation, and the phase of membrane shrinking. A key role in the whole process is played by retinal pigment epithelial cells, which, stimulated, among other things, by inflammatory factors, undergo a transformation, losing the characteristics of epithelial cells in favor of those of fibroblast-like mesenchymal cells. Laboratory studies are underway for a better understanding of the pathophysiology of PVR, as well as clinical trials of various agents to prevent PVR.
    Źródło:
    Review of Medical Practice; 2023, XIX, 4; 20-26
    2956-4441
    2956-445X
    Pojawia się w:
    Review of Medical Practice
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Impaired base excision repair is related to the pathogenesis of non-alcoholic fatty liver disease
    Autorzy:
    Ziółkowska, Sylwia
    Czarny, Piotr
    Szemraj, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1024273.pdf
    Data publikacji:
    2020-12-30
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Tematy:
    DNA repair
    non-alcoholic fatty liver
    base excision repair
    Opis:
    Non-alcoholic fatty disease (NAFLD) is a liver disorder that affects up to 30% of the population, mainly in Western countries. It is estimated that up to 75% of NAFLD patients will develop a more aggressive form of the disease, non-alcoholic steatohepatitis (NASH). NAFLD can lead to fibrosis and liver failure; however, it is difficult to diagnose NAFLD due to its non-specific symptoms. Unfortunately, there is no treatment available for this disease. The risk factors of NAFLD are obesity and insulin resistance (IR). The molecular factors that seem to play an important role in the pathogenesis of NAFLD are oxidative stress as well as impaired DNA damage repair processes; a great body of evidence confirms an association with the base excision repair (BER) pathway. The activity of BER is decreased in patients with NAFLD and in animal models of this disease. In order to better understand the underlying basis of the disease, knowledge should be broadened in the area of DNA repair in NAFLD.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biologica et Oecologica; 2020, 16; 5-11
    1730-2366
    2083-8484
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biologica et Oecologica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Is there a link between TNF gene expression and cognitive deficits in depression?
    Autorzy:
    Bobińska, Kinga
    Gałecka, Elżbieta
    Szemraj, Janusz
    Gałecki, Piotr
    Talarowska, Monika
    Powiązania:
    https://bibliotekanauki.pl/articles/1038686.pdf
    Data publikacji:
    2017
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    depressive disorder
    TNF-α
    TNFRSF1A
    TNFRSF1B
    cognitive impairment
    Opis:
    Neuroinflammation is a known factor in the pathogenesis of recurrent depressive disorders. Depression is accompanied by activated immune-inflammatory pathways including increased levels of TNFα, sTNFR1and sTNFR2.The purpose of this study was to analyse the TNF-α, TNFRSF1A and TNFRSF1B genes on both mRNA and protein levels in patients with rDD, and to investigate the relationship between TNF-α,TNFRSF1A and TNFRSF1B gene expression and cognitive performance. The study comprised 158 subjects: patients with recurrent depressive disorder (n=89) and healthy subjects (n=69). Cognitive function assessment was based on: Trail Making Test, The Stroop Test, Verbal Fluency Test and Auditory Verbal Learning Test. Both mRNA and protein expression levels of all genes were significantly higher in rDD subjects when compared to healthy controls. No statistically significant correlations were observed between the analysed variables in both the rDD group and the HS test group. The only exception was noticed in the HS test group, where increased expression of TNFRSF1A and TNFRSF1B gene negatively affected the performance of the AVLT test. However, statistically significant correlations between TNF, TNFRSF1A, TNFRSF1B mRNA gene expression levels and all the neuropsychological tests used in the survey for the entire group were observed. Conclusions: 1.The results of our study show increased expression of the TNF, TNFRSF1A and TNFRSF1B genes on both mRNA and protein levels in depression. 2. Elevated expression of TNF-α, TNFRSF1A and TNFRSF1B negatively correlates with cognitive efficiency: working memory, executive functions, attention, auditory-verbal memory, effectiveness of learning processes and verbal fluency.
    Źródło:
    Acta Biochimica Polonica; 2017, 64, 1; 65-73
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Association of the DIO2 gene single nucleotide polymorphisms with recurrent depressive disorder
    Autorzy:
    Gałecka, Elżbieta
    Talarowska, Monika
    Orzechowska, Agata
    Górski, Paweł
    Bieńkiewicz, Małgorzata
    Szemraj, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1039107.pdf
    Data publikacji:
    2015
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    depressive disorder
    iodothyronine deiodinase type II
    polymorphism
    haplotype
    Opis:
    Genetic factors may play a role in the etiology of depressive disorder. The type 2 iodothyronine deiodinase gene (DIO2) encoding the enzyme catalyzing the conversion of T4 to T3 is suggested to play a role in the recurrent depressive disorder (rDD). The current study investigates whether a specific single nucleotide polymorphism (SNP) of the DIO2 gene, Thr92Ala (T/C); rs 225014 or ORFa-Gly3Asp (C/T); rs 12885300, correlate with the risk for recurrent depression. Genotypes for these two single nucleotide polymorphisms (SNPs) were determined in 179 patients meeting the ICD-10 criteria for rDD group and in 152 healthy individuals (control group) using a polymerase chain reaction (PCR) based method. The specific variant of the DIO2 gene, namely the CC genotype of the Thr92Ala polymorphism, was more frequently found in healthy subjects than in patients with depression, what suggests that it could potentially serve as a marker of a lower risk for recurrent depressive disorder. The distribution of four haplotypes was also significantly different between the two study groups with the TC (Thr-Gly) haplotype more frequently detected in patients with depression. In conclusion, data generated from this study suggest for the first time that DIO2 gene may play a role in the etiology of the disease, and thus should be further investigated.
    Źródło:
    Acta Biochimica Polonica; 2015, 62, 2; 297-302
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Cloning and expression of a new recombinant thrombolytic and anthithrombotic agent - a staphylokinase variant
    Autorzy:
    Kowalski, Michał
    Brown, George
    Bieniasz, Magdalena
    Oszajca, Katarzyna
    Chabielska, Ewa
    Pietras, Tadeusz
    Szemraj, Zofia
    Makandjou-Ola, Eusebio
    Bartkowiak, Jacek
    Szemraj, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1040615.pdf
    Data publikacji:
    2009
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    K2 domain of t-PA
    thrombolytic and antithrombotic agents
    thrombolysis
    staphylokinase
    recombinant protein
    hirulog
    antiplatelet activity
    Opis:
    To develop a more potent antithrombin agent with thrombolytic and antiplatelet properties, a new staphylokinase (SAK) variant was constructed. The kringle 2 domain (K2) of tissue type-plasminogen activator (t-PA) containing a fibrin-specific binding site (i), the RGD sequence (Arg-Gly-Asp) for the prevention of platelet aggregation (ii) and the antithrombotic agent - hirulog (iii) was assembled to the C-terminal part of recombinant staphylokinase (r-SAK). cDNA for the hybrid protein SAK-RGD-K2-Hirul was cloned into Pichia pastoris pPIC9K yeast expression vector. The introduction of K2 t-PA, the RGD sequence and hirulog into the C-terminus of r-SAK did not alter the staphylokinase activity. We observed a higher clot lysis potency of SAK-RGD-K2-Hirul as evidenced by a faster and more profound lysis of 125I-labeled human fibrin clots. The potency of thrombin inhibition by the hirulog C-terminal part of the recombinant fusion protein was almost identical to that of r-Hir alone. These results suggest that the SAK-RGD-K2-Hirul construct can be a more potent and faster-acting thrombolytic agent with better antithrombin and antiplatelet properties compared to r-SAK and SAK-RGD-K2-Hir.
    Źródło:
    Acta Biochimica Polonica; 2009, 56, 1; 41-53
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Antigen levels of urokinase-type plasminogen activator receptor and its gene polymorphism related to microvessel density in colorectal cancer
    Autorzy:
    Przybylowska, Karolina
    Szemraj, Janusz
    Kulig, Andrzej
    Dziki, Adam
    Ulanska, Joanna
    Blasiak, Janusz
    Powiązania:
    https://bibliotekanauki.pl/articles/1040754.pdf
    Data publikacji:
    2008
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    plasminogen activation system
    urokinase type plasminogen activator receptor (uPAR)
    gene polymorphism
    colorectal cancer
    cancer progression
    angiogenesis
    microvessel density
    Opis:
    We determined the distribution of genotypes and frequencies of alleles of the (CA)n repeat polymorphism in intron 3 of the urokinase plasminogen activator receptor (uPAR) gene, uPAR antigen levels and microvessel density (MVD) in tumour and distant mucosa samples from 52 patients with colorectal cancer. The uPAR level was higher for patients with high MVD comparing to patients with lower MVD which may suggest that uPAR can be correlated with progression of colorectal cancer. The significant relationship between the high MVD and uPAR antigen level appeared to be independent of the (CA)n repeat polymorphism because no differences in the level of uPAR antigen between carriers of alleles were found. The received results, indicate that uPAR might be considered as a target in colorectal cancer patients' therapy.
    Źródło:
    Acta Biochimica Polonica; 2008, 55, 2; 357-363
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Tissue distribution of a menthyl-conjugated oligodeoxyribonucleotide antisense to PAI-1 mRNA
    Autorzy:
    Szemraj, Janusz
    Al-Nedawi, Khalid
    Chabielska, Ewa
    Buczko, Wlodzimierz
    Pawlowska, Zofia
    Powiązania:
    https://bibliotekanauki.pl/articles/1041329.pdf
    Data publikacji:
    2005
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    PAI-1
    antisense oligonucleotides
    tissue distribution
    Opis:
    The inhibitory effect of numerous analogues of PO-16, an hexadecadeoxyribonucleotide antisense to sequences -22 to -17 of PAI-1 mRNA coding for a fragment of the signal peptide, on the expression of PAI-1 in endothelial cells, and physiological consequences of the subsequently reduced PAI-1 activity tested in vitro and in vivo, were described in our previous studies. Of particular interest was PO-16 5'-O-conjugated with menthyl phosphorothioate (MPO-16R). In this work, tissue localisation of MPO-16R labelled with [35S] phosphorothioate at the 3'-end, was determined. [35S]MPO-16R and control [35S]MPO-16R-SENSE oligonucleotides were administered intravenously into 22 rats and organ distribution of the labelled bioconjugates was assessed after 24 and 48 h. For this purpose, tissue sections were subjected to autoradiography, and quantitated by liquid scintillation after solubilisation. Overall clearance of radioactivity was already seen after 24 h, with the radioactivity recovered mainly in the kidney and liver. A smaller fraction of radioactivity was also retained in the spleen and heart. The kidney concentration of the labelled probe was higher than that of liver by 50%. The distribution of PAI-1 mRNA in untreated rat kidney, liver, spleen and heart established by two independent techniques: Ribonuclease Protection Assay and Real-Time PCR, shows the same pattern as that observed for [35S]MPO-16R antisense.
    Źródło:
    Acta Biochimica Polonica; 2005, 52, 4; 849-855
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Genetyczne uwarunkowania funkcjonowania mechanizmu hemostazy w chorobach układu krążenia rola polimorfizmu regionów promotorowych
    Genetic determinants of haemostasis in cardiovascular diseases the role of gene promotor regions
    Autorzy:
    Pietrucha, Tadeusz
    Szemraj, Janusz
    Chiżyński, Krzysztof
    Powiązania:
    https://bibliotekanauki.pl/articles/945056.pdf
    Data publikacji:
    1999
    Wydawca:
    Uniwersytet Łódzki. Wydawnictwo Uniwersytetu Łódzkiego
    Opis:
    In this review the potential role of polymorphism gene promoter regions of beta-chain fibrinogen and plasminogen activator inhibitor type I (PAI-1) in cardiovascular disease is discussed. The thorough discussion covers the potential mechanisms of their effect.
    Źródło:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica; 1999, 14
    0208-614X
    Pojawia się w:
    Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-9 z 9

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