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1
Content available remote Nanostruktury węglowe i błony lub powłoki polimerowe z ich udziałem. Cz. I. Charakterystyka ogólna, funkcjonalizacja oraz metody badań kompozycji z nanorurkami lub grafenami
100%
Kugler S. , Spychaj T.
Polimery
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2013
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tom T. 58, nr 2
93-99
PL
Artykuł stanowi przegląd literaturowy. Cz. I obejmuje charakterystykę nanostruktur węglowych oraz sposoby ich funkcjonalizacji w celu wykorzystania w charakterze napełniaczy w matrycach polimerowych. Opisano również metody badań kompozycji i nanokompozytów zawierających struktury węglowe.
EN
In this study, we present a literature review on the polymer films and coatings with carbon nanoparticles. The first part of the article describes the characteristics of carbon nanostructures and methods used for their functionalization (noncovalent and covalent) with the aim of using them as fillers in polymeric matrices. The methods used to examine the compositions and nanocomposites with carbon nanostructures are also discussed.
2
Content available remote Nanostruktury węglowe i błony lub powłoki polimerowe z ich udziałem
100%
Kugler S. , Spychaj T.
Polimery
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2013
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tom T. 58, nr 3
177-180
PL
W cz. II. artykułu przedstawiono najnowsze osiągnięcia w dziedzinie otrzymywania błon i powłok polimerowych z nanostrukturami węglowymi, użytymi w roli zarówno napełniaczy, jak i odrębnych błon z materiału węglowego.
EN
In the second part of the article, the latest developments in the field of preparation of polymer films and coatings with carbon nanostructures, used both as fillers and separate layers of carbon material, have been presented.
3
Lack of prodomain abolishes BDNF constitutive secretion by HEK 293 cells
70%
Ziemlinska E. , Skup M. , Czarkowska-Bauch J. , Bahr M. , Kugler S.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
EN
Brain-derived neurotrophic factor (BDNF) and its proBDNF precursor are released both in constitutive and activity-dependent manner. Prodomain itself proved to be necessary for BDNF targeting to regulated secretory pathway [Egan et al. (2003) Cell, Chen et al. (2005) J Neurosci] but its role in constitutive secretion is elusive. As mature BDNF (mBDNF) conveys trophic and prosurvival signals whereas proBDNF may convey growth inhibiting and death signals, an important issue arises: can we control the type of signal being triggered by BDNF? To verify this we cut off the prodomain and generated plasmid coding only for rat mBDNF. To test the constitutive mBDNF construct secretion we have chosen HEK 293 cell line. Two other plasmids coding either for proBDNF (template for both BDNF forms) or proBDNF protected from prodomain cleavage (source of proBDNF only), served as controls. BDNF secretion was evaluated with WB technique using antibodies detecting (1) both BDNF forms, (2) HA tag (mBDNF construct) and (3) MYC tag (proBDNF constructs). We found all three constructs being stably expressed in HEK cells. However, in contrast to both proBDNF constructs, which were secreted and detected in media fraction, mBDNF construct was revealed only in the cell lysate fraction, not being released to the media. This is the fi rst observation showing that mBDNF can be constitutively released only when accompanied by prodomain. Support: ASTF 211-00-2007 for EZ, Polish-German grant to MS and SK.
4
The effect of AAV1/2-mediated BDFN transgene overexpression on trkbFL and trkbTK receptor transcripts and on TrkBFL cellular lokalization in the transected spinal cord of the rat
61%
Ziemlinska E. , Wiewior I. , Grygielewicz P. , Czarkowska-Bauch J. , Kugler S. , Skup M.
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nr S
EN
Brain-derived neurotrophic factor (BDNF) regulates its fulllength TrkB (TrkBFL) receptor. BDNF administration to the brain or spinal cord after injury stimulates neuronal plasticity and brings some improvement of impaired functions, but a prolonged exposure of neurons to BDNF in vitro and BDNF infusions to the brain downregulate TrkBFL protein and reduce its downstream signaling, thus limiting BDNF effectiveness. In our recent study we used AAV-mediated transfer of BDNF transgene to cause long-term delivery of BDNF to isolated spinal cord transected at Th11 – Th12 segments. Three groups of rats were used: intact, spinal PBS (spPBS), and spinal AAV-BDNF (spBDNF) injected. The treatment resulted in substantial improvement of treadmill locomotion at two weeks after spinalization, but its effect weakened in time (7 weeks). The mechanism underlying this effect may arise from decreased abundance and availability of TrkBFL and its truncated forms. To verify it, we compared levels of trkbFL/trkbTK transcripts (qPCR) and evaluated TrkBFL segmental distribution (immunohistochemistry). Both transcripts decreased in the scar and in L1 – L2 segments in spPBS rats, but tended to increase in L1 – L2 in spBDNF rats (p<0.07). In L3 – L6 segments no group differences in transcripts were found. Comparison of TrkBFL and c-Myc labeling of transgene-derived BDNF revealed that: (1) caudally to the transection, TrkBFL was abundant in neurons and white matter oligodendroglia (2) c-Myc (+) or (-) neurons showed comparable intensity of TrkBFL labeling (3) neuronal TrkBFL labeling was higher in segments with BDNF excess. In summary, BDNF overproduction in isolated spinal network does not downregulate TrkB transcripts, either it alters cellular abundance and pattern of TrkBFL segmental expression. Data suggest that other aspects of TrkB-mediated signaling are responsible for weakening of functional effect of BDNF. Supported by S007/PolishGerman/2007/01 grant and EMBO fellowship (for EZ).
5
L1 overexpression in rats with complete spinal cord transection downregulates phosphacan and upregulates synaptophysin, GAP43 and Adcy1 expression
61%
Platek R. , Grycz K. , Wieckowska K. , Czarkowska-Bauch J. , Kugler S. , Schachner M. , Skup M.
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tom 73
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nr Suppl.1
EN
Recovery after spinal cord injury requires neuronal remodeling which is regulated by cell adhesion molecules (CAMs) and chondroitin sulfate proteoglycans (CSPGs). CSPG may be potentially both inhibitory and supportive of regenerative plasticity. To verify whether chronic (5 weeks) L1 CAM overexpression in transected spinal cord of the rat, proven to promote recovery in mice, affects CSPG phosphacan and markers of synaptic plasticity, adeno-associated viral vector encoding L1 protein (AAV5-L1) was injected into L1 lumbar segment, immediately after transection at Th10/11. Control group received AAV5-EGFP. AAV5-L1 transduced neurons and astrocytes below the lesion, resulting in 170-fold increase in L1 mRNA level at low thoracic segments (Th
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