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Výsledky testování nanomateriálů pro ošetření kožných ran
Juhás, Štefan ; Juhásová, Jana
Pomocí experimentů na miniprasatech jsme testovali hojení čerstvé rány ošetřené pomocí různých nanovlákenných materiálu a porovnávali se standardním ošetřením. Z předem definovaných ran se v pravidelných intervalech odebírali vzorky na histologickou analýzu, mikrobiologii, provádělo se měření ran a fotodokumentace. Z miniprasat se taky odebírala krev pro stanovení prozánětlivých cytokinů.
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Following the phenotype development of TgHD minipigs by invasive and noninvasive approach
Ellederová, Zdeňka ; Baxa, Monika ; Vidinská, Daniela ; Bohuslavová, Božena ; Vochozková, Petra ; Šmatlíková, Petra ; Klíma, Jiří ; Valeková, Ivona ; Ardan, Taras ; Juhás, Štefan ; Juhásová, Jana ; Konvalinková, R. ; Klempíř, J. ; Pokorný, M. ; Krupička, R. ; Kauler, J. ; Hansíková, H. ; Motlík, Jan
Recent promising treatments for Huntington’s disease (HD) may require pre-clinical testing in large animals. In 2009, we generated HD transgenic (TgHD) minipigs with one copy encoding the N-terminal part (548 aa) of human huntingtin (HTT) with 124 CAG/CAA repeats integrated into chromosome 1 q24-q25. The successful germ line transmission occurred through four successive generations.
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Mitochondrial phenotype in minipig model transgenic for N-terminal part of human mutated huntingtin
Hansíková, H. ; Rodinová, M. ; Křížová, J. ; Dosoudilová, Z. ; Štufková, H. ; Bohuslavová, Božena ; Klíma, Jiří ; Juhás, Štefan ; Ellederová, Zdeňka ; Motlík, Jan ; Zeman, J.
Huntington’s disease (HD) is neurodegenerative disorder caused by an abnormal expansion of CAG repeat encoding a polyglutamine tract of huntingtin (htt). It has been postulated that mitochondria dysfunction may play significant role in the pathophysiology of the HD. But it is still not known yet in detail how mitochondria are able to cover energy needs of the cells during the progression of the HD.
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Establishing preclinical proof-of-concept of gene therapy for Huntington disease
Miniariková, J. ; Juhás, Štefan ; Caron, N. ; Spronck, L. ; Vallés, A. ; De Haan, M. ; Blits, B. ; Ellederová, Zdeňka ; van Deventer, S. ; Petry, H. ; Southwell, A. ; Déglon, N. ; Motlík, Jan ; Konstantinová, P. ; Evers, M.
Huntington disease (HD) is an autosomal dominant neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the HTT gene. The translated expanded polyglutamine repeat in the huntingtin protein is known to cause toxic gain-of-function, affecting numerous cellular processes. Our approach involves a new therapeutic modality by developing a single (one-time) treatment for HD based on a gene therapy lowering the expression of the toxic huntingtin using the RNA interference (RNAi) mechanism. Huntingtin lowering is achieved using gene transfer of a cassette encoding an engineered microRNA targeting human HTT, delivered via adeno-associated viral vector serotype 5 (AAV5-miHTT).
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Potent anti-spasticity and anti-nociceptive effect of subpial GAD65 and VGAT gene delivery in rat and mice
Maršala, M. ; Tadokoro, T. ; Hernandez, M. B. ; Navarro, M. ; Maršala, S. ; Miyanohara, A. ; Juhás, Štefan ; Juhásová, Jana ; Platoshyn, O.
In previous studies we have developed a novel spinal subpial (SP) AAV delivery technique in adult mice, rats and minipigs. Using this technique we have demonstrated potent and wide-spread transgene (GFP) expression in spinal white and gray matter after a single SP bolus of AAV9-UBI-GFP.
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