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This study focuses on presenting the investment in the renewable energy installations and the legal form of beneficiaries aided by the EU funds to show the effects of undertakings consistent with the sustainable development as reflected in Corporate Social Responsibility implemented in rural areas of the Podlaskie Voivodeship. CSR is closely linked to the sustainable development because of its overriding goal that such development satisfies needs of this generation without jeopardizing the possibility of satisfying needs of future generations. Most projects related to renewable energy installations were realised by beneficiaries qualified as partnerships and natural persons conducting business activity (54 entities). In the Podlaskie Voivodeship, solar energy installations were most commonly funded (84) through the end of 2015. In the years 2007-2013, a total of PLN 356 853 658 was allocated to the issues connected with renewable energy development, including 45% for solar energy. The level of EU subsidy totalled PLN 174 575 220, including 55% spent on solar energy use projects.
Celem analizy było zbadanie związku między wzrostem lesistości a gruntami rolnymi w latach 2010-2015 oraz korelacją pomiędzy lesistością a migracją wewnętrzną mieszkańców poszukujących zatrudnienia poza rolnictwem (m.in. przez rejestrację mikroprzedsiębiorstw) na przykładzie województwa podlaskiego. Zastosowano metodę opisową, którą poszerzono o wyliczenie współczynnika korelacji Pearson’a dla zbadania kluczowych współzależności. Obliczone współczynniki korelacji sugerują silne powiązanie wielkości środków UE z wielkością obszarów zalesionym w trzech wydzielonych powiatach – Białystok, Łomża, Suwałki. Ponadto, stwierdzono wysoką korelację między migracją wewnętrzną a działalnością przedsiębiorców odzwierciedloną w liczbie zarejestrowanych podmiotów gospodarczych w powiatach białostockim i łomżyńskim oraz przeciętnych powiązań w przypadku powiatu suwalskiego. Na transfer użytków rolnych pod zalesiania ma wpływ lokalny rozwój infrastruktury technicznej, np. budowa dróg w powiecie suwalskim i oddziaływuje na uzyskane współczynniki korelacji.
BACKGROUND AND AIMS: Most of the current antidepressants modulate levels of monoamines just after administration, however, only after prolonged therapy the clinical effect may be observed. Myriad attempts tried to identify molecular factors responsible for such a delayed response, the prominent example being the cyclic AMP response element binding protein (CREB). Many research suggest that chronically given antidepressants enhance CREB levels and activity. On the other hand, CREB knock-out mice showed rather antidepressant-like behavior, however, the compensatory effects of cAMP response element modulator (CREM) in absence of CREB were not taken into account. In our study we evaluated transgenic mice with selective ablation of CREB in noradrenergic cells, maintained in CREM deficient background (CrebDBHCreCrem-/-) for elucidation of the role of CREB in antidepressant treatment. METHODS: mRNA levels of neurotrophins and α1-adrenoceptors in CrebDBHCreCrem-/- mice were investigated in hippocampus and prefrontal cortex using qPCR method. Next mice were screened in behavioral tests like: open field (OF), tail suspension test (TST) and rotarod. Preliminary TST after acute desipramine (DMI) administration (20 mg/kg, ip) was executed. RESULTS: CrebDBHCreCrem-/- mutant mice did not show any abnormalities in their basal phenotype, moreover the mRNA levels of studied genes were not changed either. However, preliminary experiments revealed that CrebDBHCreCrem-/- show a treatment-resistant phenotype after acute DMI administration in TST, (effect absent in single mutants). CONCLUSIONS: Our results provide further evidence for the important role of CREM as a compensatory factor and indicate that these mice may represent an unique tool to dissect the role of CREB in the mechanism of antidepressants. Supported by statutory funds of the Institute of Pharmacology and 2014/13/B/NZ7/02293 grant. K. Rafa-Zabłocka is a holder of scholarship from the KNOW sponsored by MSHE, Poland.
BACKGROUND AND AIMS: In neural cells, autophagy is proposed to serve as a surveillance mechanism which helps to clear protein aggregates, and loss of autophagy leads to neurodegeneration in mice. Our previous experiments, performed on genetically engineered mice with conditional and progressive neurodegeneration of medial spiny neurons (TIF-IAD1RCre mice) mimicking the typical progression of Huntington’s disease (HD), showed that the delayed onset of neurodegeneration observed in these mutants might be associated with temporary increased autophagy. The aim of current study was to evaluate a new strategy proposed recently for the anti-HD treatment, based on enhancing autophagy by administration of trehalose, a natural alpha-linked disaccharide. METHODS: Trehalose (2%) was dissolved in water and presented to the mice as a replacement for their water bottles for 1 or 2 months prior the experiments. The effects of trehalose were compared with groups receiving maltose (2%) as well as water (vehicle). The autophagy was determined by Western blot (WB) and immunohistochemistry (IHC) with use of anti-LC3B antibody. The animals were screened for their motor coordination by accelerated rotarod, and post-mortem for selected neurodegenerative markers by WB and IHC. RESULTS: Both control and mutant mice showed enhanced autophagy after trehalose administration as revealed by WB and IHC staining. Nevertheless, further analysis of quantitative assessment of several neurodegenerative markers by WB did not reveal any significant effects in attenuating the neurodegenerative process. There have been also no differences in behavioral phenotype. CONCLUSIONS: Our results provide additional evidence for stimulation of autophagy evoked by chronic administration of trehalose. However further study is needed, the enhancement of autophagy has not yet been proved to be neuroprotective in investigated model. Supported by 2011/03/B/NZ7/05949 grant financed by National Science Center (NCN).
Parkinson’s Disease (PD) is characterized by an increased production of oxygen free radicals leading to alteration of the cellular constituents and subsequent dopaminergic cell loss within the region of substantia nigra (SN) and ventral tegmental area (VTA). However, it is well known that PD is not only associated with dopaminergic transmission. Involvement of extranigral structures in PD includes the noradrenergic system as well. Post-mortem studies of human brains revealed that neuronal loss associated with PD may proceed and is even greater in the region of locus ceruleus (LC) than SN/ VTA. In PD animal models, the loss of noradrenaline made worse the dopamine nigrostriatal damage and, in opposite, an enhanced noradrenaline level may have a neuroprotective role. The aim of this study was to determine whether genetically evoked, selective loss of noradrenergic neurons may have any long-term, negative impact on the dopaminergic system. We applied the conditional inactivation of the gene encoding transcription factor TIF-IA (essential for the regulation of rRNA synthesis) by the Cre-loxP system to induce the progressive and selective loss of noradrenergic neurons which was achieved by expressing Cre recombinase under dopamine beta-hydroxylase (DBH) promoter. Resulting TIFIADBHCre mice were born at expected rates, viable but showed clear signs of noradrenergic innervations failure e.g. ptosis, reduced locomotor activity, growth retardance and shorten life span. The animals were analyzed at 8 and 12 weeks of age. The selective loss of noradrenergic neurons was confirmed by immunofluorescent staining with the anti-tyrosine hydroxylase (TH) antibody. We observed approx. 90% reduction of TH positive cells in the LC of 8 weeks TIF-IADBHCre mice. The number of TH+ cells was not changed in the region of SN/VTA, neither in 8 nor 12 week old mutants. However, our preliminary data indicate that lack of the noradrenergic transmission may lead to enhanced expression of selected markers associated with neurodegeneration within the region of SN/VTA. Namely, we have found 1.4 fold up-regulation of mRNA encoding for glial fibrillary acidic protein (GFAP) as revealed by quantitative real-time PCR and increased level of oxidative stress shown by immunoblot detection of carbonyl groups by Western Blot in the SN/VTA of 12 weeks TIF-IADBHCre mice compared to control animals. If we provide additional evidences that selective noradrenergic degeneration affects functioning of dopaminergic neurons, TIF-IADBHCre mice may became a valuable, new model for study possible anti-PD treatment at early stages of the disease as dopaminergic neurons in these mice are not directly affected by the mutation. As for today, there are no experimental studies on a possible long-term negative impact of progressive noradrenergic degeneration on other neurotransmitter systems despite of clinically observed concomitant loss of SN/VTA and LC neurons in PD. This study was supported by the grant no 2011/03/B/NZ7/05949 financed by National Science Centre and statutory funds of the Institute of Pharmacology, Polish Academy of Sciences.
Parkinson’s disease (PD) is characterized by an inevitable loss of dopaminergic cells.However, examination of human brain tissues revealed that noradrenergic cell loss in the region of the locus coeruleus (LC) may proceed and may be even greater than dopaminergic degeneration. AIM(S): The aim of this study was to determine whether genetically evoked, selective loss of LC noradrenergic neurons in a progressive manner may negatively influence the dopaminergic system. Our mice models have progressive degeneration of the noradrenergic system, based on deletion of the gene Rrn3 encoding transcription factor TIF-IA, which is essential for the regulation of rRNA synthesis. METHOD(S): First, we applied the conditional inactivation of the Rrn3 by the Cre-loxP system expressing Cre recombinase under DBH promoter. TIF‑IADBHCre mice revealed ptosis, reduced locomotor activity, and a shortened life span associated with enhanced expression of various neurodegenerative markers within the dopaminergic system, including upregulation of micro- and astroglia, pro-inflammatory proteins, and enhanced level of oxidative stress. To limit mutations to the CNS, in a second model a Cre-dependent lentiviral vector carrying the Rrn3 deletion created by the CRISPR/Cas9 system was directly delivered to LC of DBHCre mice. RESULTS: Our construct was first successfully tested in vitro on primary dopamine neurons followed by in vivo stereotactic application. This approach seems to be successful as, in preliminary data, we observed the disintegration of nucleoli in transduced noradrenergic neurons in LC, which is the determinant of the functional impairment of the targeted TIF‑IA. CONCLUSIONS: To-date, there are no experimental studies on possible long-term negative impacts of progressive noradrenergic degeneration on other neurotransmitter systems, despite the clinically observed concomitant loss of SN/VTA and LC neurons in PD. If we provide additional evidence, mice with ongoing neurodegeneration of LC neurons may became a valuable tool for studying the presymptomatic phase of PD.
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