Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 26

Liczba wyników na stronie
first rewind previous Strona / 2 next fast forward last
Wyniki wyszukiwania
help Sortuj według:

help Ogranicz wyniki do:
first rewind previous Strona / 2 next fast forward last
EN
The aim of this paper is to create a research methodology that allows a quick analysis of the structural state of high alloy austenitic steels using non-destructive ultrasonic tests, in contrast to destructive standard methods. Electromagnetic acoustic transducers (EMAT) are used to generate and receive the ultrasonic wave and detect the microstructural changes caused by sample sensitization in elevated temperature, even after 0.5 h in high temperature exposition. Different acoustic response for reference sample and sensitized samples were recorded. In this work, changes in share wave amplitude were measured.
EN
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.
EN
The roles of 12/15-lipoxygenase(s) (LOX), poly(ADP-ribose) polymerase (PARP-1) activity and mitochondrial apoptosis inducing factor (AIF) protein in the molecular processes evoked by amyloid β (Aβ) toxicity were investigated in PC12 cells that express either wild-type (APPwt) or double Swedish mutation (APPsw) forms of human Aβ precursor protein. Different levels of Aβ secretion characterize these cells. The results demonstrated a relationship between the Aβ levels and LOX protein expression and activity. High Aβ concentration in APPsw cells correlated with a significant increase in free radicals and LOX activation, which leads to translocation of p65/NF-κB into the nucleus. An increase in AIF expression in mitochondria was observed concurrently with inhibition of PARP-1 activity in the nuclear fraction of APPsw cells. AIF accumulation in mitochondria may be involved in adaptive/protective processes. However, inhibition of PARP-1 may be responsible for the disturbances in transcription and DNA repair as well as the degeneration of APP cells. Under conditions of increased nitrosative stress, evoked by the nitric oxide donor, sodium nitroprusside (SNP, 0.5 mM), 70-80 % of all cells types died after 24 h, significantly more in APPsw cells. There was no further significant change in mitochondrial AIF level and PARP-1 activity compared to corresponding nontreated with SNP cells. Only one exception was observed in PC12 control, where SNP significantly inhibits PARP-1 activity. Moreover, SNP significantly activated gene expression for 12/15-LOX in all types of investigated cells. Inhibitors of all LOX isoforms and specific inhibitor of 12-LOX enhanced the survival of cells that were subjected to SNP. We conclude that the LOX pathways may play a role in Aβ toxicity and in nitrosative-stress-induced cell death and that inhibition of these pathways offers novel protective strategies. Supported by MS&HE grant NN40113938 and MRC statutory theme No 7.
EN
Ceramide and sphingosine-1-phosphate (S1P) are very active sphingolipid messengers which play a crucial role in regulation of neuronal cells survival and death. Alternation of ceramide/S1P rheostat is related to several pathological disorders including Alzheimer’s disease. Ceramides are involved in cells proliferation, differentiation and apoptotic death, while S1P enhances cell proliferation and antagonizes apoptosis. S1P regulates cellular processes by binding to five specific G protein coupled-receptors (S1PR1-5). The aim of the study was to investigate the molecular processes of neuronal death evoked by ceramide and the role of S1P in neuroprotection. Our study indicated that ceramide enhanced significantly the level of free radicals and decreased neuronal cells (SHSY5Y) viability through inhibition of PI3-K/Akt pathway. Ceramide also decreased anti-apoptotic (Bcl-2) and increased pro-apoptotic (Bax, Hrk) gene expression. Exogenously added S1P increased the viability of cells through S1PR (1-3) receptors-dependent mechanism. S1P also increased Bcl-2 gene expression and decreased the gene expression of Hrk protein. Summarizing, our study indicated that the action of ceramide and S1P on mitochondria may control neuronal fate and may play a crucial role in neurodegeneration and neuroprotection.
EN
Poly(ADP-ribose)polymerase (PARP-1) plays a key role in DNA repair but its over activation has been proposed to be important in pathogenesis of brain ischemia and in neurodegenerative diseases. PARP catalyzes the conversion of bNAD+ to polymers of poly(ADP-ribose) (PAR) and is fully responsible for producing of PAR polymers during genotoxic stress. The last data indicated that PAR act at the mitochondria to induce cell death through stimulation of apoptosis inducing factor (AIF) release. However, the role of PAR in cell death seems to be complex and not fully elucidated. To better understand the role and relationship between AIF and PARP/PAR in death signaling the hippocampal neuronal (HT22) cells in culture were subjected to different concentration of DNA alkylating agent, 1-methyl-3-nitro-1-nitrosoguanidine (MNNG). The immunochemical and spectrophotometrical methods were applied. Consequently, HT22 cells treated with MNNG at 50ñ 500 mM demonstrated concentration dependent mitochondria failure and death. 24 h after 500 mM MNNG treatment only 15% of cells survive. PARP-1 inhibitors: 3-aminobenzamide (3AB) and PJ34 at 5 mM and 20 mM, respectively, protect most of the cells against MNNG induced death signaling. At lethal MNNG concentration PARP/PAR dependent AIF translocation from mitochondria is observed and the caspase independent death signaling is activated. Concomitantly PARP inhibitors affect the endogenous pathway regulated by PI-3K/AKT PKB/GSK-3 and infl uence the level of GSK-3β active form phosphorylated on Tyrosine 216. Summarizing our data indicated that inhibitors of PARP have positive effect on neuroprotective pathway regulated by PI-3K/AKT and on mitochondria function. Supported by Scientifi c Network of MS&HE No 28/E-32/SN0053/2007
EN
Amyloid β (Aβ) is responsible for mitochondrial failure and biochemical alterations linked to Alzheimer`s disease (AD). To better understand mechanisms of Aβ toxicity we investigated its mitochondrial and nuclear targets, apoptosis-inducing factor (AIF) and Poly(ADP-ribose) polymerase-1 (PARP-1) in PC12 cells transfected with wild type (APPwt) or double Swedish-mutated human Amyloid Precursor Protein gene (APPsw) characterized by different Aβ concentrations. We found close relationship between Aβ level and cyclooxygenase (COX)- and lipoxygenase (LOX)-related free radical formation leading to p65/NF-κB nuclear translocation. COX and LOX inhibitors protected APPsw cells against p65 translocation. Aβ-evoked oxidative stress enhanced mitochondrial AIF level and inhibited PARP-1 in APPsw cells. Nitrosative stress evoked by 0.5 mM sodium nitroprusside (SNP) had no further effect on Aβ-altered PARP-1 activity and mitochondrial AIF level in APPsw cells. However, SNP evoked death of 70–80% of all cell types after 24 h. COX and LOX inhibitors had ameliorating effect in these conditions. Our data indicated that double Swedish mutation in APP signifi cantly increased cell vulnerability to oxidative stress. Enhanced mitochondrial AIF level and PARP-1 inhibition might be responsible for cell survival under oxidative stress evoked by accumulating Aβ in APPsw cells. COX and LOX inhibitors protected the cells against death caused by simultaneous Aβ toxicity and nitrosative stress.
EN
INTRODUCTION: Prenatal exposure to infection and subsequent inflammatory responses, as well as, mitochondrial dysfunction has been implicated in the pathogenesis of autism spectrum disorders (ASDs). However, the molecular links between infection-induced fetal brain changes, mitochondrial deregulation, and the autistic phenotype remain obscure. AIM(S): Analysis of maternal immune activation (MIA)-induced changes in the expression of mitochondrial dynamics markers in the brain of the neonatal and adolescent rat offspring. METHOD(S): The MIA model was induced by single intraperitoneal injection of lipopolysaccharide (100 μg/kg b.w.) to pregnant rats at embryonic day 9.5. On the 7th or 52-53rd post-natal day, rat offspring were decapitated, and the brains isolated. Transmission electron microscopy (TEM), quantitative real‑time PCR (qPCR), and immunoblotting were used to determine mitochondrial ultrastructure and mRNA/protein expression, respectively. RESULTS: The electron microscopic study demonstrated altered mitochondrial morphology, including fragmented cristae, expanded matrix compartment, and membrane disruption in both the cerebral cortex and hippocampus of adolescent MIA offspring. Moreover, changes were noted in the expression of proteins involved in the maintenance of mitochondrial morphology. We observed upregulated fusion machinery proteins – mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and Opa1 – as well as mitochondrial fission proteins – dynamin related protein‑1 (Drp1) and fission protein 1 (Fis1) – in the neonatal MIA brains. However, in adolescent animals exposed to prenatal infection, the expression of Mfn1, Mfn2 and Opa1 was significantly reduced; nevertheless, Drp1 and Fis1 remained increased CONCLUSIONS: MIA-evoked perturbations in the proteins regulating mitochondrial dynamics reveal potentially important aspects of the mechanism linking neuroinflammation, impaired mitochondrial function, and ASD. FINANCIAL SUPPORT: Supported by the POWER Och!Doc Program and NSC grant 2016/23/D/NZ4/03572.
EN
α-Synuclein (ASN) secreted from neurons into the extracellular space affects the homeostasis of neighboring cells, but the pathophysiology of extracellular ASN remains largely unknown. The aim of the present study was to analyze the role of cyclin dependent kinase 5 (Cdk5) in molecular mechanism of extracellular ASN toxicity. We found that exogenously applied ASN evoked apoptotic cell death in a significant population of dopaminergic PC12 cells. ASN induced rapid and long-lasting calcium influx and activation of calciumdependent enzymes, including caspase-3, nitric oxide synthase and calpain. ASN-induced calpain activation leads to cleavage of Cdk5 activator p35, and subsequently to formation of p25 and Cdk5 overactivation. Moreover, we showed that exposure of PC12 cells to ASN increased Cdk5 activity by enhancement of its phosphorylation at Tyr15. Calpeptin, an inhibitor of calpains, and inhibitors of Cdk5, Roscovitine and BML-259, prevented ASN-evoked apoptosis and cell death, indicating the involvement of Cdk5 in mechanism of ASN toxicity. Our data showed that alterations in calcium homeostasis and modulation of calcium-dependent enzymes by extracellular ASN may contribute to the early stages of pathogenesis in Parkinson’s disease and other synucleinopathies.Supported by a grant from The National Science Centre 2012/05/B/NZ3/02047.
PL
Tani import oraz notowane przez ostatnie lata wysokie ceny skupu żywca są jedną z ważniejszych przyczyn nierentowności przedsiębiorstw przemysłu mięsnego. Dodatkowym problemem dla właścicieli firm z tej branży są powstające w produkcji mięsnej odpady, które powinny zostać odpowiednio zagospodarowane, co z reguły generuje wysokie koszty. Optymalnym rozwiązaniem wydaje się zastosowanie w tym celu fermentacji metanowej. Substraty, takie jak gnojowica świńska oraz treść przewodu pokarmowego, mogą być wykorzystane jako substrat dla biogazowni bez wstępnej obróbki termicznej, natomiast odpady poubojowe, w myśl Rozporządzenia Parlamentu Europejskiego i Rady (WE) nr 1069/2009 z dnia 21 października 2009 r., wymagają wcześniejszej higienizacji. W Pracowni Ekotechnologii, działającej przy Instytucie Inżynierii Biosystemów Uniwersytetu Przyrodniczego w Poznaniu, przeprowadzono badania wydajności biogazowej tych odpadów z Zakładu Mięsnego „Paszak” w Olszówce (gmina Przykona). Analizę wykonano zgodnie z obowiązującą niemiecką normą DIN 38 414/S8. Na podstawie otrzymanych wyników stwierdzono, że substraty te mają bardzo duży potencjał energetyczny. Wykazano, że racjonalne zagospodarowanie uciążliwych odpadów rzeźnych (treści przewodu pokarmowego świń i gnojowicy) może generować zysk ekonomiczny wynikający ze sprzedaży energii elektrycznej i ciepła, a także wyeliminowania kosztów związanych z utylizacją generowanych odpadów.
EN
The inexpensiveness of import and high prices of livestock noted in the last few years are one of the most significant reasons for the lack of profitability of meat industry companies. An additional problem for the entrepreneurs in this sector is the production of meat waste which needs to be properly managed, which usually generates high costs. Methane fermentation seems to be the optimal solution for this problem. Such substrates as swine slurry and digestive tract content can be used as a substrate for biogas plants without heat pretreatment, while slaughterhouse waste requires prior hygienisation in accordance with the Regulation of the European Parliament and Council Regulation (EC) No 1069/2009 of 21 October 2009.In the Laboratory of Eco-technology functioning at the Institute of Biosystems Engineering at the University of Life Sciences in Poznan research on biogas efficiency of waste from a meat processing plant “Paszak” in Olszowka (municipality of Przykona) was conducted. The analysis was performed on the basis of the German standard DIN 38 414/S8. On a base of achieved results it was concluded that these substrates have a very high energy potential. It was also shown that rational waste management burdensome slaughterhouse waste such as swine slurry and digestive tract cane generate economic profit resulting from the sale of electricity and heat production, but also in the avoidance of costs of proper waste utilization.
first rewind previous Strona / 2 next fast forward last
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.