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1

Ogólnopolska konferencja naukowa pt. "Aktualne problemy prawa konstytucyjnego"

100%
Czapski G.
Zeszyty Naukowe Uniwersytetu Przyrodniczo-Humanistycznego w Siedlcach. Seria: Administracja i Zarządzanie
|
2014
|
nr 27[100]
2

Prawo do informacji publicznej na przykładzie Biuletynu Informacji Publicznej Urzędu Miasta w Białej Podlaskiej

100%
Czapski G.
Zeszyty Naukowe Uniwersytetu Przyrodniczo-Humanistycznego w Siedlcach. Seria: Administracja i Zarządzanie
|
2014
|
nr 27[100]
3
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Content available

Labour migration of Poles

100%
Czapski G.
Economic and Regional Studies
|
2020
|
tom 13
|
nr 3
Subject and purpose of work: The contemporary labour market in Poland is characterised by a large scale of migration of people, caused by the desire to find a good job. This situation is facilitated by the possibility of free movement within the European Union. The purpose of this study is to present the concept of migration, its types, causes and effects. Statistics related to the labour migration of Poles are also presented. The subject of the study is the migration activity of Poles abroad. The obtained data are presented using the descriptive method and graphical methods. Materials and methods: National literature and statistical data were used during the work on the research problem. Results: Statistics showing the scale of the migration phenomenon in Poland are presented. The research period covered the years 2013-2018. Conclusions: Over the period under consideration, the number of Poles travelling abroad for work purposes decreased. This may be due to the decreasing number of unemployed people and the lower unemployment rate in Poland. At the same time, an increasing number of job offers in the national labour market can be observed.
4

Effect of myloid Beta peptides on DNA degradation

51%
Zambrzycka A., Czapski G., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
5

Expression of poly(ADP-ribose) polymerases in hippocampus during systemic inflammatory response. The role of PARP-1 protein interactions in cognition

51%
Czapski G., Adamczyk A., Strosznajder R. P., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2011
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tom 71
|
nr 1
Poly(ADP-ribosyl)ation is covalent modification of proteins responsible for the alterations of their function. This process is catalyzed by poly(ADP-ribose)polymerases (PARP) family, consisted of 18 isoforms. Among target proteins, there are many DNA-related proteins and PARP-1 itself. In the brain, PARP-1 is responsible for more than 90% of poly(ADP-ribosyl)ation. PARP-1 plays a significant role in regulation of several transcription factors including NF-kB and p53. Our previous data indicated an important impact of PARP-1 in brain ischemia and in systemic inflammatory response (SIR). In this study we have analyzed the expression of PARP family genes in hippocampus of mice subjected to lipopolysaccharide (LPS)- evoked SIR. Moreover, the effect of SIR on PARP-1/PAR protein interaction and on memory function was evaluated. Mice C57BL6 were injected i.p. with LPS (1 mg/kg b.w.) alone or together with PARP inhibitors 3-aminobenzamide (30 mg/kg b.w.). The studies were carried out by using immunochemistry, microarray, real-time RT-PCR, and behavioral analysis. Our data indicated the small effect of SIR on PARP-1 gene expression level, however, expression of genes for PARP-3, -9, -12 and -14 was significantly increased 12 h after LPS administration. The level of PAR in hippocampus was elevated during SIR indicating activation of protein poly(ADP-ribosyl)ation. Moreover, further analysis of LPS-affected genes indicated that among 83 proteins known for their direct interaction with PARP-1, genes for 21 are present in SIR-related interactome, along with several genes for transcription factors and proteins involved in signal transduction. The enhancement of gene expression in hippocampus for several members of PARP family during SIR may be responsible for the alteration of PARPs function, higher level of PAR formation and for the modification of PARP/PAR protein interaction, transcription, cell signaling and memory. Our data indicated that SIR significantly decreases object recognition but has small effect on spatial memory. PARP-1 inhibitor protects against SIR induced molecular alteration in hippocampus and against SIR-evoked cognition impairment. Moreover, PARP-1 inhibitors significantly enhanced spatial memory in LPS treated mice. Our results indicate that inhibition of PARP-1 is a promising protective strategy during overactivation of inflammatory reaction. The role of other PARP family members in SIR is a target of our future investigation.
6

The molecular network between amyloid Beta peptide, sphingosine kinase and sirtuins in cell survival and death implication in Alzheimer's disease

51%
Strosznajder J., Czapski G., Cieslik M.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: Deregulation of the sphingolipid metabolism plays an important role in the pathogenesis of Alzheimer’s disease (AD). Mitochondrial function and mitochondrial deacetylases, i.e. sirtuins (Sirt3,-4,-5), are also affected in AD. The aim of this study was to analyse the interaction between amyloid-β1-42 (Aβ1-42), sphingosine kinases (SphKs) and mitochondrial sirtuins in cell survival/death. METHODS: The spectrofluorometrical, immunochemical and QRT-PCR methods were applied. RESULTS: PC12 cells were subjected to Aβ1-42 oligomers and SphK inhibitor (SKI II) for 24–96 h.Aβ1-42 enhanced SphK1 expression and activity after 24 h, but down-regulated them after 96 h and had no effect on SphK2. Aβ1-42 and SKI II induced oxidative stress, disturbed the balance between pro- and anti-apoptotic proteins and evoked cell death. Simultaneously, up-regulation of anti-oxidative enzymes catalase and superoxide dismutase 2 occurred. Moreover, the total protein level of glycogen synthase kinase-3β (Gsk-3β) was reduced. Aβ1-42 significantly increased the level of mitochondrial proteins: AIF and Sirt3, -4, -5. Additional analysis demonstrated a significant role of p53 protein at very early stages of Aβ1-42 toxicity. However, during prolonged exposure to Aβ1-42, the activation of caspases, MEK/ERK, and alterations in mitochondrial permeability transition pores were also involved in mechanism responsible for cell death. Moreover, SphK product, sphingosine-1-phosphate (S1P), and Sirt activators and antioxidants, effectively prevented toxicity of Aβ1-42. CONCLUSIONS: Our data indicated that p53 protein and SphKs may be involved at early stage of molecular mechanisms of Aβ toxicity. We suggest the important role of interactions between Aβ peptide, SphKs and Sirts in pathomechanism of AD. The activation of S1P-dependent signalling and Sirts may offer a promising cytoprotective strategy. This study was supported by The National Science Centre Grant 2013/09/B/NZ3/01350 to J.B.S.
7
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The situation of graduates and students in the Polish labour market

51%
Czapski G., Nazaruk S., Sokolowska B.
Economic and Regional Studies
|
2023
|
tom 16
|
nr 4
8

Effect of lipopolysaccharide induced inflamation on neuropeptide Y neurons in mouse hippocampus

45%
Smialowska M., Domian H., Zieba B., Czapski G., Strosznajder L.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Neuropeptide Y (NPY), a 36 amino acid neurotransmitter, is involved in the regulation of emotional behavior and its role in the central responses to peripheral immune challenge is postulated. Plasma NPY levels rises in human sepsis and NPY improved survival in the experimental endotoxic shock induced by lipopolysaccharide (LPS) injection. Some of the behavioral effects of LPS, anorexia, depression and anxiety-like behavior are also modulated by NPY. Therefore, in the present study tried to fi nd out if LPS affected NPY neurons in mouse hippocampus, a structure most susceptible to damage and involved in the regulation of emotion. Male C57BL/6 mice were injected with LPS (1 m/kg, i.p.) and their brains were taken after 6 or 24 h. The brains were fi xed with paraformaldehyde, cut into frontal sections containing the dorsal hippocampus and processed by immunohistochemistry using an NPY antibody. NPY-immunoreactive neurons were counted stereologically in hippocampal subregions CA1+2, CA3 and DG+hilus, and results were statistically analysed. It was found that after 24 h LPS decreased by ca. 38% the number of NPY-positive neurons in the hippocampal CA regions. The effect was particularly signifi cant in the CA3 area. Moreover, staining intensity was diminished. The obtained results indicate a decrease in NPY expression in the hippocampus, which may be due to the peptide release induced by LPS infl ammatory action. Supported by MS&HE.28/E32/ BWSN-0053/2008.
9

Systemic inflammation leads UP-regulation of prooxidative genes and to activation of death signalling

39%
Czapski G., Chalimoniuk M., Jacewicz M., Gajkowska B., Smialowska M., Strosznajder J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Our recent data have shown that systemic infl ammation evoked by lipopolysaccharide (LPS) stimulates NO-mediated signalling pathways in the midbrain. The aim of the present study was to investigate the dynamics of proinfl ammatory genes expression in mouse hippocampus during 4 days after intraperitoneal injection of LPS (1 mg/kg b.w.). Moreover, the selected biochemical processes involved in cell death pathways were analysed. Real-time PCR analysis indicated the signifi cant time-dependent alteration of several prooxidative genes expression. During fi rst 3 h posttreatment the level of mRNA for COX-2, iNOS and TNFα was increased, then after 6–24 h for cPLA2, TLR4, 5-LOX and 12- LOX, respectively. Immunohistochemical analysis showed an appearance of many activated microglia cells, confi rming activation of local infl ammatory reaction in hippocampus. The biochemical and molecular studies demonstrated the signifi cant activation of apoptosis inducing factor (AIF)-mediated, caspase-3 -independent death signalling and cathepsin B-related autophagy. These data were confi rmed by electron-microscopic examination of cell ultrastructure. The presented genetic, biochemical and morphologic alterations induced by systemic infl ammation could be responsible for impairment of learning and memory. This study was supported by Scientifi c Network 28/E-32/BWSN-0053/2008.
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