Karol Jastrzębski
Medical University of Łódź
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Featured researches published by Karol Jastrzębski.
Neurologia I Neurochirurgia Polska | 2016
Izabela Jatczak-Pawlik; Dominika Książek-Winiarek; Dagmara Wójkowska; Krzysztof Jóźwiak; Karol Jastrzębski; Mirosława Pietruczuk; Andrzej Głąbiński
UNLABELLED Migration of inflammatory cells from the blood to the central nervous system (CNS) is crucial for development of multiple sclerosis (MS). Inhibition of this process would allow to control disease activity. The first step confirming this approach would be the analysis of the impact of effective MS relapse therapy on migration of effector T cells. The aim of the study was to analyze the influence of methylprednisolone (MP) on the migratory activity of effector CD4+ T cells from MS patients. Moreover, to study the potential mechanism of this process we studied expression of chemokine receptors on migrating cells. MATERIAL AND METHODS Peripheral blood samples were obtained from relapsing-remitting MS (RR-MS) patients during relapse (n=23) and from control group (n=23). After isolation CD4+ T cells were incubated with various concentrations of MP. Then they were stimulated in chemotaxis assay with chemokines CCL3 or CXCL10 or were used to CCR1 and CXCR3 expression analysis. RESULTS CXCL10- and CCL3-stimulated migration of CD4+ T cells was significantly increased in MS. MP was able to reduce in vitro migration of effector T cells induced by CXCL10, but not by CCL3. Inhibition by MP was dose-dependent. Expression of analyzed chemokine receptors was unaltered after MP incubation. CONCLUSIONS MP reduced CD4+ T cells migration induced by CXCL10 without affecting CXCR3 expression. These observations demonstrate one of the potential mechanisms of MP action in MS, distinct from inducing cell apoptosis, and suggests the new targets for development of more effective MS treatments.
Neurologia I Neurochirurgia Polska | 2017
Alicja Kozera-Kępniak; Karol Jastrzębski; Jakub Walenczak; Andrzej Klimek; Andrzej Głąbiński
INTRODUCTION AND OBJECTIVES Recent research has suggested that genetic factors may play an important role in the development of drug resistance in epilepsy. It is not clear which gene loci are responsible for the drug-resistant phenotype. Studying certain nuclear receptors may be helpful in predicting drug response, as they regulate drug transporting proteins and enzymes involved in their metabolism. This study focuses on one of these receptors, the human pregnane X receptor (hPXR). The objective was to examine the link between selected single nucleotide polymorphisms (SNPs) 69789A/G rs 7643645 and 66034T/C rs 13059232 hPXR and the lack of response to epilepsy treatment. MATERIALS AND METHODS 73 patients diagnosed with drug-resistant epilepsy were included in the study. The diagnoses were made according to the criteria published by The International League Against Epilepsy (ILAE) in 2010. The control group was comprised of a group of 122 healthy volunteers. Genetic material isolated from the peripheral blood of the participants was analyzed with TagMan Genotyping Assays in search of the selected hPXR polymorphisms. RESULTS The distribution of genotypes of the 66034T/C rs 13059232 hPXR polymorphism was significantly different in the group with drug-resistant epilepsy and the control group. In the drug-resistant group the CC genotype was significantly more common compared to the control group (50.7% vs 35.2%) p=0.0339. The distribution of 69789 A/G rs 7643645 hPXR genotypes was comparable in both groups. CONCLUSIONS There is potential association between hPXR and drug resistance but its relevance for the development of drug-resistant phenotype remains to be studied.
Aktualności Neurologiczne | 2017
Karol Jastrzębski
Karol Jastrzębski
Aktualności Neurologiczne | 2015
Karol Jastrzębski
© Medical Communications Sp. z o.o. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (CC BY-NC-ND). Reproduction is permitted for personal, educational, non-commercial use, provided that the original article is in whole, unmodified, and properly cited. Czy punkcja lędźwiowa może spowodować zakrzepicę zatok żylnych mózgowia? Komentarz redakcyjny do artykułu Mariny Baszkiewicz pt.: Zakrzepica zatok żylnych mózgu. Opis przypadku Can lumbar puncture be the cause of cerebral venous sinus thrombosis? Editorial Comment on Marina Baszkiewicz Cerebral venous sinus thrombosis. Case report
Journal of Molecular Neuroscience | 2015
Magdalena Justyna Kacperska; Karol Jastrzębski; Bartłomiej Tomasik; Jakub Walenczak; Maria Konarska-Król; Andrzej Glabinski
Neurologia I Neurochirurgia Polska | 2015
Karol Jastrzębski; Magdalena Justyna Kacperska; Agata Majos; Magdalena Grodzka; Andrzej Głąbiński
Aktualności Neurologiczne | 2014
Karol Jastrzębski; Magdalena Justyna Kacperska; Małgorzata Figlus
Neurologia I Neurochirurgia Polska | 2013
Maciej Radek; Karol Wiśniewski; Marek Grochal; Karol Jastrzębski; Piotr Gębski; Dorota Snopkowska-Wiaderna; Andrzej Radek
Aktualności Neurologiczne | 2018
Karol Jastrzębski; Magdalena Obrembska; Łukasz Kępczyński; Katarzyna Turoboś; Agnieszka Sobczyńska-Tomaszewska; Elżbieta Miller; Andrzej Głąbiński; Centrum Medyczne MedGen, Warszawa, Polska
Aktualności Neurologiczne | 2017
Karol Jastrzębski