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Carbon nanoparticles as transporters of melittin to glioma grade IV U87 cells in in vitro model

100%
Biniecka P., Jaworski S., Bugajska Z., Daniluk K.
Annals of Warsaw University of Life Sciences - SGGW. Animal Science
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2017
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tom 56[1]
Carbon nanoparticles as transporters of melittin to glioma cells in in vitro model.Substances derived from nature have natural cytotoxic properties, melittin, the main component of bee venom is one of them. It has the ability to destroy any lipid bilayer, therefore to be used in a cancer treatment it needs to be targeted. The aim is to create the drug delivery system, which would efficiently deliver the active substance to glioma cells. Carbon nanoparticles are considered to be a good agent in biomedical applications, due to their biocompatibility and small sizes. In this study five types of nanoparticles were used: pristine graphene (GN), nanographene oxide (nGO), graphite (G), nanodiamond (UDD) and hierarchical nanoporous carbons (HNCs) to target the melittin to cancer cells. The visualization of the drug delivery complexes of melittin and nanoparticles was done with transmission electron microscopy, the influence of the complexes on cell morphology and structure was pictured with scanning electron microscope. Moreover, in order to check the viability of the cells treated with melittin and the complexes of melittin and nanoparticles the PrestoBlueTM assay was done, also to specify the way of the cell death the annexin V/PI assay was carried out. The results indicate that various nanoparticles behave differently in a complex with melittin. The UDD, GN and nGO nanoparticles resulted in higher mortality than the melittin itself. Creating and applying such complexes of melittin with nanoparticles in glioma cancer treatment may be a promising solution in the therapy.
2

Pathofunctional roles of glutamine transporters in neurotransmission, insulin secretion and pH regulation

100%
Chaudhry F. A.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Glutamine is involved in many metabolic pathways such as generation of amino acids, nucleotides and glutathione. Glutamine also serves in pH homeostasis, urea formation, immune response and wound healing. In addition, glutamine is considered to be the primary precursor of the fast neurotransmitters glutamate and GABA in the central nervous system (CNS). The prevailing hypothesis of a glutamate/GABA-glutamine cycle suggests that a large amount of released glutamate and GABA are translocated into perisynaptic astroglial cells, converted into glutamine, and subsequently shuttled back to neurons for regeneration of the neurotransmitters. This mechanistic view is supported by differential localization of glutamate and GABA transporters on perisynaptic glial processes, and demonstration of the key glutamine metabolizing enzymes glutamine synthetase (GS) and phosphate-activated glutaminase (PAG) in glial cells and nerve terminals, respectively. However, the molecular mechanisms involved in glutamine extrusion from glial cells and its transport into neurons have until recently eluded characterization. We have molecularly identified a family of amino acid transporters (Slc38) with isoform specific characteristics. We show that the system A transporters (SATs) mediate neuronal transport of glutamine. SAT1 is enriched in GAD67 expressing GABAergic neurons suggesting a role in GABA formation. SAT2 expression is pronounced in the somatodendritic domains of glutamatergic neurons where it sustains formation of glutamate and is intrinsic for retrograde signaling. Activity of the homologous system N transporter SN1 – expressed exclusively on astroglial cell membranes – is dynamically regulated by intracellular protein kinases and may fine-tune extracellular levels of glutamine accessible for neuronal uptake. SN2 – also expressed in the astroglial cells, but with differential subcellular localization – mediates glutamine release for neurotransmitter synthesis and glycine release to regulate NMDA receptors. Finally, we have shown that these transporters also contribute to pH restoration during chronic metabolic acidosis and regulation of insulin secretion. Recently, I have also contributed to the investigation of a child with congenital glutamine synthetase deficiency, who developed generalized hypotonia and hyperreflexia and treatment-resistant seizures postpartum and had very low serum and cerebrospinal fluid concentrations of glutamine and glutamate (Häberle et al. 2012). Glutamine supplementation restored serum levels of glutamine and glutamate, while corresponding values in the CNS approached normal. Ammonia toxicity was also prevented. The frequency of seizures abated and EEG showed significant improvement. Altogether, our data show the importance of glutamine and glutamine transporters in normal physiology and pathophysiology and bolster existence of a glutamate/GABA-glutamine cycle.
3

Change in the level of liver organic anion transporting polypeptide 1 after repeated exposure to aromatic bromine derivatives in rats

100%
Lisiecka M., Szymanska J. A., Frydrych B.
Acta Toxicologica
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2005
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tom 13
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nr 2
4
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Effects of hyperthyroidism on lipid content and composition in oxidative and glycolytic muscles in rats

80%
Miklosz A., Chabowski A., Zendzian-Piotrowska M., Gorski J.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 4
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