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  1. 27 Acta Neurobiologiae Experimentalis

  2. 3 Postępy Biologii Komórki

  3. 2 Atest

  4. 2 Folia Histochemica et Cytobiologica

  5. 2 Gospodarka Mięsna

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  1. 56 Adamczyk A.

  2. 12 Czapski G. A.

  3. 9 Wilkaniec A.

  4. 8 Cieslik M.

  5. 8 Jesko H.

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  1. 6 2019

  2. 2 2018

  3. 4 2017

  4. 8 2015

  5. 7 2013

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1

Inwestycje w badania i rozwój przedsiębiorstw w świetle badań ankietowych

100%
Adamczyk A.
Wiadomości Statystyczne
|
2013
|
tom 58
|
nr 01
2

Rola oddziału krakowskiego Centrum Doradztwa Rolniczego we wdrażaniu Programu LEADER na Spiszu

100%
Adamczyk A.
Wieś i Doradztwo. Pismo Małopolskiego Stowarzyszenia Doradztwa Rolniczego
|
2011
|
nr 3-4
3

Nowe stanowisko hederyki Rydera na zbiorniku Grabownia w Rybniku

100%
Adamczyk A.
Przyroda Górnego Śląska
|
2010
|
nr 59
12-13
4

Pas zieleni izolacyjnej w Parku "Wioski Świata" w Krakowie

100%
Adamczyk A.
Aura
|
2015
|
nr 01
5

Zbiorowe zatrucie w oczyszczalni sciekow

88%
Adamczyk A.
Atest
|
1997
|
nr 01
40-43
6

The association between maternal immune activation and mitochondrial failure in adulthood: relevance to neurodevelopmental disorders

63%
Cieslik M., Adamczyk A.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
Evidence suggests that maternal immune activation (MIA) during pregnancy is a risk factor for neurodevelopmental disturbances including autism spectrum disorders (ASDs). Animal models support this linkage and demonstrate that MIA in rodents leads to behavioral alterations in offspring that are characteristic of autism. However, the mechanism by which MIA causes long‑term behavioral deficits is unknown. Investigation of the links between maternal infection during pregnancy, mitochondrial dysfunction, and behavioral alterations in offspring. To induce MIA, pregnant Wistar rats were injected with lipopolysaccharide (LPS; 0.1mg/kg, intraperitoneally) on gestational day 9.5, a time point analogous to the first trimester of human gestation. Brains from adolescent offspring were evaluated for mitochondrial outcomes. Prenatal exposure to MIA led to anxiety and repetitive behavior. Adolescent offspring of MIA dams exhibited up-regulation of pro-inflammatory cytokines, oxidative stress, and disturbances in redox homoeostasis. Moreover, substantial mitochondrial abnormalities were observed. A significant decrease in mitochondrial membrane potential and changes in ATP production could be attributed to a downregulation of complex I and IV. Deregulated bioenergetics of mitochondria were accompanied by impaired mitochondrial dynamics, altered expression of fusion/fission machinery proteins including mitofusin 1 and 2 (Mfn1, Mfn2), Opa1, dynamin related protein‑1 (Drp1), and fission protein 1 (Fis1). We also demonstrated lower expression of the genes coding for PGC1α and TFAM (PPARGC1A and TFAM, respectively) that are responsible for mitochondrial biogenesis. MIA at early gestation leads to long-lasting effects on the mitochondrial bioenergetics, dynamics, and biogenesis in the offspring which can lead to synaptic dysfunction and behavioral abnormalities similar to ASD. FINANCIAL SUPPORT: Supported by the NSC grant 2016/23/D/NZ4/03572.
7

Ocena mieszanek pelnoporcjowych dla swin z udzialem nasion lubinu i bobiku srutowanych lub platkowanych

63%
Niedzwiadek T., Adamczyk A.
Biuletyn Informacyjny Przemysłu Paszowego
|
1993
|
tom 32
|
nr 3
3-20
8
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Content available

Regeneracja kolumn chromatograficznych wchodzących w skład zestawu Glyco Test 100 firmy Pierce do oznaczania zawartości hemoglobiny glikozylowanej we krwi

63%
Kaminska E., Adamczyk A.
Diagnostyka Laboratoryjna
|
1989
|
tom 25
|
nr 4-5
9

Paliwa alternatywne do silnikow wysokopreznych na bazie innych niz rzepak roslin oleistych

63%
Adamczyk A., Podlaska J.
Problemy Inżynierii Rolniczej
|
1994
|
tom 02
|
nr 2
57-64
Celem badań było określenie przydatności oleju uzyskanego z lnianki, katranu abisyńskiego i gorczycy białej do produkcji biopaliwa napędowego do wysokoprężnych silników spalinowych lub innych zastosowań technicznych. Do przetworzenia badanych olejów na biopaliwo wykorzystano reakcję estryfikacji tłuszczów. Syntezę przeprowadzono według metody niskotemperaturowej z oczyszczeniem fazy paliwowej na adsorbencie, (rozwiązanie zgłoszone do Urzędu Patentowego RP).
10

Extracellular alpha-synuclein and its neurotoxic fragment NAC peptide induce cell death by different molecular pathways

63%
Kazimierczak A., Adamczyk A.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 1
Extracellular alpha-synuclein (ASN, NACP ñ NAC Precursor Protein) was suggested to play a crucial role in the pathogenesis of various neurodegenerative diseases such as Parkinsonís disease and Alzheimerís disease. The fragment corresponding to the region 61-95 of the protein, originally termed NAC (non-amyloidbeta component), has been found in amyloid plaques associated with Alzheimerís disease, and several reports suggest that this region is responsible for the toxicity of alpha-synuclein. However, the precise mechanism of ASN and NAC action remains unclear. The aim of the present study was to investigate the signaling events in ASN and NAC mediated apoptosis of neuronal PC12 cells. Immunochemical, spectrophotometrical and spectrofl uorometrical methods were used in this study. Our data evaluated by MTT assay and Hoechst 33342 showed that soluble ASN and NAC peptide, in concentration dependent manner, induce enhancement of free radicals level and apoptotic death of PC12 cells by 50% and 70%, respectively. ASN induced caspase-3 activation by 40% with concomitant decrease in poly(ADP-ribose) polymerase (PARP) immunoreactivity and had no effect on AIF release from mitochondria. On the contrary, NAC peptide had no effect on caspase-3 activity and PARP protein level, but enhanced PARP activity and induce AIF release. Inhibitor of caspase-3 (Z-DEVD-FMK, 100 microM) prevented large population of cells against ASN-evoked cell death, but had no signifi cant protective effect on cells treated with NAC peptide. These fi ndings indicate that ASN and its liberated neurotoxic fragment induce different signaling pathways of programmed cell death. Supported by the MS&HE Grant No 2PO5A4129 and MS&HE Scientifi c Network No 28/E-32/SN-0053/2007
11

Nowa pomoc dydaktyczna

63%
Adamczyk A.
Parki Narodowe
|
2008
|
nr 2
12

Zastosowanie skorek wieprzowych i drobiowych w produkcji kielbas drobnorozdrobnionych. Czesc II. Wplyw dodatku oraz sposobu wprowadzania skorek i izolatu bialka sojowego na wybrane wlasciwosci farszow miesnych oraz wytworzonych z nich kielbas modelowych

51%
Slowinski M., Grochalska D., Adamczyk A.
Gospodarka Mięsna
|
1997
|
tom 49
|
nr 05
48-51
13

The role of alpha-synuclein in regulation of cyclin dependent kinase 5

51%
Czapski A. G., Gassowska M., Kazmierczak A., Adamczyk A.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr 1
Alpha-Synuclein (ASN), a small cytosolic protein enriched in synaptic terminals, was implicated in the pathomechanism of several neurodegenerative disorders called alpha-synucleinopathies. ASN was shown to be a main component of characteristic intraneuronal protein aggregates called Lewy bodies (LB) and Lewy neurites (LN), observed i.a. in Parkinson’s disease, dementia with LBs and in the LB variant of Alzheimer’s disease. Recent studies demonstrated that ASN may exist also in the extracellular space. Low-molecular ASN aggregates distributed in the brain parenchyma likely may be more toxic than ASN in LB, however, the exact mechanism of cytotoxicity of extracellular ASN is not fully understood. Our previous studies demonstrated the significant impact of extracellular ASN on calcium homeostasis. ASN evoked deregulation of intracellular calcium concentration leading in consequence to enhancement of nitric oxide synthesis. Deregulation of calcium homeostasis affects other calcium-dependent enzymes, including Calpains. The aim of the present study was to investigate the involvement of Calpaindependent activation of Cyclin Dependent Kinase 5 (Cdk5) in molecular mechanism of extracellular ASN cytotoxicity. The activation of Cdk5 is regulated by binding of regulatory subunits p35 and p39. Deregulation of calcium homeostasis may induce the Calpainmediated breakdown of Cdk5/p35 into Cdk5/p25 leading to overactivation of Cdk5. In our studies we used rat Pheochromocytoma PC12 cells incubated with exogenous ASN (10 µM) in the presence of Calpain inhibitor Calpeptin (10 µM) and Cdk5 inhibitors Roscovitine (10 µM) and BML-259 (10 µM). Our results indicated that incubation of PC12 cells in the presence of extracellular ASN (10 µM) for 48 h evoked cell death, and Cdk5 inhibitors efficiently prevented ASN toxicity, indicating an important role of Cdk5 in molecular mechanism of ASN toxicity. The level of Cdk5 protein was unchanged, but phosphorylation of Cdk5 at Tyr15 was significantly increased, suggesting that the enzymatic activity of Cdk5 is increased in ASN-treated cells. The presence of p25 protein was observed, what suggests that Calpain-dependent proteolysis of p35 occurred in ASN-treated cells. Calpeptin, an inhibitor of Calpains, prevented ASN-induced cell death, confirming the important role of Calpain activation in mechanism of ASN toxicity. In summary, our results demonstrated that alteration of calcium homeostasis evoked by extracellular ASN induce Calpain-dependent overactivation of Cdk5. These molecular processes may be involved in ASN-evoked cell death in vitro and probably also in neurodegenerative disorders.
14

Selol protects PC12 cells against sodium nitroprusside-induced apoptosis through activation of Se-dependent antioxidative enzymes

51%
Dominiak A., Wilkaniec A., Wroczynski P., Adamczyk A.
Acta Neurobiologiae Experimentalis
|
2015
|
tom 75
|
nr Supl.
BACKGROUND AND AIMS: It has been hypothesized that Se depletion followed by decreased activity of Se-dependent enzymes may be responsible for the development of oxidative stress observed in various neurodegenerative diseases. Thus, Se-dependent protection strategy to reduce neuronal oxidative injuries, can contribute to attenuation of neurodegeneration. The compound Selol is an organic mixture of selenitetriglycerides, which was previously shown to exhibit antitumor properties. The aim of the present study was to investigate the cytoprotective effect of Selol against sodium nitroprusside (SNP) induced oxidative stress and PC12 cells death. METHODS: The study was carried out using spectrophotometric and spectrofluorometric methods as well as real-time PCR analysis. RESULTS: We found that treatment with SNP (0.5 mM) induced significant elevation of free radicals, decreased the reduced glutathione (GSH) level as well as increased the formation of oxidized glutathione (GSSG). In addition, the significant alteration in the activities of antioxidative enzymes, such as glutathione peroxidase (GPx), glutathione reductase (GR) and thioredoxin reductase (TrxR) were observed after SNP treatment. Selol, at low molecular range neutralized SNP-induced free radicals generation and modulated GSH homeostasis. Moreover, Selol significantly elevated the activities of GPx, GR and TrxR, thus preventing cell death evoked by SNP. The involvement of Selol on the intracellular antioxidative defence system was further confirmed by using a GPx and TrxR inhibitor, sodium aurothiomalate, that abolished its cytoprotective effect. CONCLUSIONS: Taken together, these findings suggest that treatment with Selol protects cells from oxidative stress via enhancement of the intracellular antioxidant potential. The Selol’s efficacy in combating free radical damage suggests that it can be a valuable therapeutic agent in the treatment of neurodegenerative disorders. Supported from MUW FW27/PM34D/14 and MMRC statutory theme 8.
15

Zastosowanie skorek wieprzowych i drobiowych w produkcji kielbas drobnorozdrobnionych. Czesc I. Wplyw dodatku izolatu bialka sojowego na jakosc emulsji z modyfikowanych skorek

51%
Grochalska D., Slowinski M., Adamczyk A.
Gospodarka Mięsna
|
1997
|
tom 49
|
nr 04
32-33
16

alpha-Synuclein stimulates nitric oxide synthase (NOS) by activation of NMDA receptor

51%
Adamczyk A., Czapski G. A., Kazmierczak A., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
17

Nowoczesny sposób natleniania basenów hodowlanych

51%
Tarnogrodzki A., Szummer A., Adamczyk A.
Magazyn Przemysłu Rybnego
|
2013
|
nr 3
18

NAC peptide evoked oxidative stress leads to p53 mediated apoptosis

51%
Kazmierczak A., Czapski G. A., Adamczyk A., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr 1
The non-Aβ component of Alzheimer’s disease (AD) amyloid (NAC) is a highly amyloidogenic peptide consisting of 35 amino acids which was first identified associated with senile plaques in AD brain. It is a fragment of the presynaptic protein alpha-synuclein and, as such, it is implicated in the etiologies of both Alzheimer’s and Parkinson’s (PD) disease. However the molecular mechanisms of NAC toxicity is not fully understood. Our present study focused on the role of oxidative stress mediated p53 pathway in apoptotic cell death evoked by NAC peptide. Here we found that exposure of PC12 cells to exogenous NAC peptide (10 µM) enhanced free radical generation, induced mitochondria dysfunction and cell death. We also observed free radicals-dependent enhancement of Tp53 gene expression after NAC treatment. The inhibition of p53 by pifithrin significantly protected PC12 cells against NAC peptide - evoked mitochondria failure and death. In addition, exposure to NAC peptide resulted in the higher expression of cyclin-dependent kinase 5 (Cdk5), one of the enzymes responsible for p53 phosphorylation and activation. Concomitantly, we observed the increase of expression of Cdk5r1 and Cdk5r2 genes, coding p35 and p39 peptides, that are essential co-factors in regulation of Cdk5 activity. Moreover, the specific Cdk5 inhibitor (BML-259, 10µM) protected large population of cells against NAC-evoked cell death. Our findings indicate that NAC peptide exerts its toxic effect by activation of p53/Cdk5 - dependent apoptotic signaling pathway. This study was supported by MSHE Grant NN 401024236 and statutory theme no 7.
19
Content available remote

Non-Abeta component of Alzheimer's disease amyloid and amyloid beta peptides evoked poly(ADP-ribose) polymerase-dependent release of apoptosis-inducing factor from rat brain mitochondria

51%
Adamczyk A., Czapski G. A., Jesko H., Strosznajder R. P.
Journal of Physiology and Pharmacology. Supplement
|
2005
|
tom 56
|
nr 2
5-13
Amyloid beta peptide (Aß) and non-Aß component of Alzheimer’s disease amyloid (NAC) are involved in pathomechanism of Alzheimer's Disease (AD) and are deposited in the AD brain in the form of senile plaques. However, the mechanism of their neurotoxicity is not fully understood. In this study the sequence of events involved in NAC and Aß peptides evoked toxicity was investigated in brain slices, synaptosomes and in subcellular fractions. Radio-, immunochemical, spectrophotometrical methods and DNA electrophoresis were used in this study. Our data indicated that Aß 1-40 (25 µM) and NAC (10 µM) peptides induced liberation of free radicals and massive DNA damage that lead to activation of DNA bound enzyme poly(ADP-ribose) polymerase-1 (PARP-1). In consequence of these processes apoptosis-inducing factor (AIF) was released from mitochondria and was translocated to nucleus. The inhibitor of PARP, 3-aminobenzamide significantly decreased AIF release from mitochondria and its translocation. Both peptides under the investigated conditions had no effect on caspase-3 activity. Our data indicated that Aß and NAC peptides stimulate AIF-dependent apoptotic pathway that seems to be caspase independent process. The inhibition of PARP-1 may protect the brain against Aß and NAC toxicity.
20

Inhibitory effect of alpha-synuclein and non-amyloid beta component of Alzheimer's disease amyloid on dopamine transporter function in rat striatal synaptosoines:relationship to oxidative stress

51%
Adamczyk A., Kazmierczak A., Cakala M., Strosznajder J. B.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
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