Wyniki wyszukiwania - Biblioteka Nauki

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Stanowisko laboratoryjne do reflektometrycznych pomiarów światłowodów

100%

Grabiec W. , Parobczak K.

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2008

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tom Vol. 57, nr 4

387-399

PL

W artykule opisano stanowisko pomiarowe znajdujące się w Laboratorium Techniki Światłowodowej Instytutu Telekomunikacji Wydziału Elektroniki WAT, przeznaczone do reflektometrycznych pomiarów włókien optycznych. Podano przyczyny powstawania strat w torze optycznym oraz metodę ich pomiaru za pomocą reflektometru. Przedstawiono budowę, zasadę pracy oraz najistotniejsze parametry eksploatacyjno-techniczne reflektometru, będącego na wyposażeniu laboratorium. Zwrócono uwagę na wybrane problemy występujące przy pomiarach tłumienności światłowodów metodą reflektometryczną.

EN

In this paper, the measurement test bed placed in the Fibre-optic Technique Laboratory of Tele-communication Institute Faculty of Electronics MUT is described. This test bed is devoted to reflectometric fibre-optic measurements. The reasons for coming out the losses in the optical channel as well as the method of losses measurement using reflectometer are shown. The structure of the MUT's laboratory reflectometer as well as principles of work and the most important operatingtechnical parameters were presented. The selected problems occurring in measurements of the fibre optic losses using reflectometric method are described.

2

Activity-dependent rearrangement of the neuronal cell nucleus

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Szczepankiewicz A. A. , Walczak A. , Parobczak K. , Wilczynski G. M.

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nr Suppl.1

EN

It is now firmly established that long-lasting synaptic plasticity involves dramatic changes in gene expression occurring under the influence of specific signaling pathways and transcription factors. Numerous studies have shown that DNA and histone epigenetic modifications play key roles in neuronal plasticity. Recent studies in non-neuronal cells, indicated the existence of epigenetic mechanism of yet another class, related to the nuclei structural remodeling and very poorly understood in neurons. Therefore, we decided to study the ultrastructure of the cell nuclei in the hippocampal dentate gyrus granule neurons upon seizures induced by kainic acid, an analog of glutamate. Under these conditions the granular neurons instead of degradation, undergo an intensive plasticity phenomena. We found that seizures led to rapid and dramatic enlargement and striking reorganization of internal component-structures of interchromatin granule clusters (IGCs) in granular cell’s nucleus. Moreover, unlike IGCs of control animals, the reorganized IGCs contained activated RNA polymerase II CTD phosphoepitopes. These observations may suggest involvement of IGC in activity-dependent transcription events in neurons.

3

RNA-binding proteins in dendritogenesis

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Perycz M. , Parobczak K. , Jaworski J.

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nr 3

EN

Proper development of dendritic arbor is a precisely orchestrated process in which translation is shown to play pivotal role. RNA binding proteins such as ZBP1 (beta-actin zipcode binding protein 1), Staufen1 and Staufen2 bind to and transport their target mRNAs, enabling their local translation in dendrites and taking part in regulation of this process. ZBP1 knockdown with short interfering RNAs in developing rat hippocampal neurons in vitro, resulted in decrease in total number of dendrites and dendritic tree complexity, which was reversed both with siRNA-resistant ZBP1 rescue mutant and jasplakinolide treatment that prevents depolymerisation of actin cytoskeleton. In contrast, mature neurons with stable dendritic arbors, did not lose dendrites upon ZBP1 depletion, which suggests ZBP1 plays role in formation of new dendrites as opposed to maintenance of mature ones. We also show that both Staufen1 and Staufen2 knockdown in developing neurons results in impoverishment in dendritic arbors complexity and decrease in total number of dendrites. RNA-binding proteins can be subject to phosphorylation, which modulate their activity, and one possibility for a common regulator of their role in dendritogenesis would be Src kinase, which we show to phosphorylate ZBP1 and Staufen1. Taken together, presented data demonstrate that mRNA transport and possibly local protein synthesis play a prominent role in development of dendritic arbor. Ministry of Science and Higher Education Grant NN301314733.

4

Sieć smartfonów IEEE 802.11ac w trybie ad-hoc z VoIP w sytuacjach kryzysowych

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Jarmakiewicz J. , Maślanka K. , Parobczak K.

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2015

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tom nr 4

149--152

PL

Dokonano analizy możliwości wykorzystania urządzeń mobilnych pracujących pod kontrolą systemu Android, do pracy w sieci Wi-Fi, w trybie doraźnym dla usług telefonicznych w sytuacji kryzysowe.j Przedstawiono przegląd rozwoju techniki Wi-Fi z uwzględnieniem zagadnień technicznych oraz stanu rynku, ze wskazaniem dalszego kierunku rozwoju. Opisano ograniczenia systemowe dla łączności w trybie ad-hoc w systemie Android. Wykonano badania wydajności sieci 802 11ac ad-hoc podczas operacji ratownicze) dla usługi telefonicznej.

EN

The article covers analysis of Android-based mobile devices application in an ad-hoc Wi-Fi operation during a crisis situation scenario. The Wi-Fi standard development survey, with regard to technical issues and mobile market review was performed, with an indication of further evolution. System limitations concerning the Ad-Hoc connectivity in the Android operating system were described. The evaluation of 802 11ac Ad-Hoc network efficiency during realization of telephony service in a rescue.

5

How neurons become giant-identification of proteins regulated by mTOR kinase in etiopathology of tuberous sclerosis

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Malik A. , Swiech L. , Perycz M. , Urbanska M. , Blazejczyk M. , Wulf P. , Parobczak K. , Pietruszka P. , Zarebska M. , Rutowicz K. , Jaworski J.

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nr 3

EN

mTOR is a serine-threonine protein kinase for several aspects of neuronal function. Increased mTOR signaling has been implicated in tuberous sclerosis (TS), a multiorgan disease affecting brain. TS is caused by mutations in genes encoding for hamartin and tuberin that lead to increase of the mTOR activity and subsequent abnormal cell growth and proliferation, leading to brain lesions containing giant cells. It is unclear how mTOR contributes to observed changes. Our aim was to identify downstream mTOR effectors important for the disease related abnormal cell growth. To model TS giant cells, rat cortical neurons cultured in vitro were transfected with short interfering RNA (siRNA) targeting tuberin that caused a Rapamycin-sensitive increase of neuron soma size. Next, we designed a siRNA library directed against 140 mRNAs encoding potential mTOR targets, selected based on published data. To select siRNAs decreasing soma size of enlarged cells, cortical neurons were contransfected with tuberin siRNA together with siRNAs from the library. Our screen revealed over 20 genes, whose expression downregulation reversed the giant-cell like phenotype and 6 siRNAs that further increased size of cells with tuberin knockdown. Among proteins contributing to abnormal neuron growth upon mTOR overactivation, we identifi ed those involved in actin cytoskeleton dynamics, vesicular transport and cellular signaling. This work has been fi nanced by PBZ-MNiI-2/1/2005 and PNRF-96- AI-1/07 grants.