Dissertations / Theses on the topic 'GDNF'
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Ivanchuk, Stacey M. "Expression of RET, GDNF and GDNFR-Ã in human development and disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq20655.pdf.
Full textDHALIWAL, PARVIN. "PARKINSON'S GDNF THERAPY AND OXIDATIVE STRESS." Thesis, The University of Arizona, 2008. http://hdl.handle.net/10150/190438.
Full textRoxo, Tiago Filipe Dias Santos. "Efeito anti-inflamatório do GDNF: qual a sua contribuição para a neuroprotecção dopaminérgica?" Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1625.
Full textAs microglias são os macrófagos residentes do Sistema Nervoso Central e actuam como a principal forma de defesa imunitária. Podem assumir um estado denominado activado, tendo a sua capacidade fagocítica aumentada e produzindo espécies reactivas de oxigénio, com o propósito de proteger as células do Sistema Nervoso Central. No entanto, este estado activado tem sido também relacionado com um processo neurodegenerativo. Aumentos dos níveis de interleucinas e citocinas têm sido descritos em doenças neurodegenerativas, nomeadamente na doença de Parkinson, onde a perda de neurónios dopaminérgicos tem sido associada a uma excessiva activação microglial. Factores solúveis libertados pelos astrócitos mostraram ser capazes de modular a reactividade microglial. Destes factores, o factor derivado de uma linha de células da glia (GDNF) destacou-se pela sua capacidade em proteger os neurónios dopaminérgicos, tanto in vitro como in vivo. Alguns estudos têm também demonstrado uma acção anti-inflamatória do GDNF, mediada pelo receptor GFR1, sugerindo que possa existir uma relação entre estes dois efeitos. No entanto, até ao momento, não foi ainda demonstrada uma relação de causaefeito entre eles. Assim, este trabalho tem como objectivo elucidar a importância do controlo da reactividade microglial pelo GDNF na sobrevivência dos neurónios dopaminérgicos. A estratégia principal será impedir a acção do GDNF especificamente na microglia, através do silenciamento do receptor GFR1, e avaliar o efeito deste silenciamento na acção neuroprotectora do GDNF após aplicação de um estímulo inflamatório. A expressão de GFR1 em culturas primárias de microglia do mesencéfalo ventral e numa linha celular de microglia N9 foi confirmada por imunocitoquímica e Western Blot. O silenciamento do receptor GFR1 na linha celular de microglia N9 foi alcançado com sucesso e resultados preliminares sugerem que o silenciamento deste receptor em culturas primárias de microglia é também possível. A exposição de co-culturas de microglia N9 e culturas mistas de neurónios e glia do mesencéfalo ventral a diferentes concentrações de LPS induziu a morte selectiva de neurónios dopaminérgicos. Paralelamente, foi possível observar um aumento da reactividade microglial. Experiências adicionais serão necessárias para atingir o objectivo principal deste trabalho. No entanto, estes resultados servirão de base para, em futuras experiências, elucidar a relevância do efeito anti-inflamatório do GDNF na neuroprotecção dopaminérgica.
Trupp, Miles. "Neurotrophic signalling by GDNF and its receptors /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980602trup.
Full textFink, Erin Nicole. "GM1 signaling through the GDNF receptor complex." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1198013799.
Full textChermenina, Maria. "GDNF and alpha-synuclein in nigrostriatal degeneration." Doctoral thesis, Umeå universitet, Histologi med cellbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-91811.
Full textOliveira, Julieta Conceição Mendes Borges. "GDNF e GPER: novas ferramentas no controlo da neuroinflamação?" Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1628.
Full textMicroglial cells, the macrophages resident in the central nervous system, are responsible for the innate immune response. When moderately activated, these cells perform vital functions such as phagocytosing dead cells and removing cell debris and toxins. However, a persistent activation of these cells may result in deregulation of its activity. They can become reactive and contribute to neuronal death. Increasing evidences suggests that inflammation and oxidative stress mediated by reactive microglia play a key role in the progression of various neurodegenerative diseases such as Parkinson's disease. Both the glial cell line derived neurotrophic factor (GDNF) and estrogens are reported to play a role in this process and to control excessive activation of microglia. A previous study from our group that used a primary culture of ventral midbrain microglia showed that GDNF present in medium conditioned by astrocytes can inhibit microglial reactivity induced by Zymozan A. The first objective of the present study was to verify if the presence of neurons, injured or not, could influence this anti-inflammatory effect exerted by GDNF. Using the same culture we found that media conditioned by both astrocytes and neurons was no longer capable of inhibiting NO production on LPS-stimulated microglia. The different effects of the two media may be related to the fact that the media conditioned by cultures of neurons and astrocytes presented lower levels of GDNF as compared with media conditioned only by astrocytes. On the other hand, studies using primary cultures and microglia cell lines demonstrated the ability of estrogen to attenuate parameters of microglial activation such as phagocytic activity, production of reactive oxygen and nitrogen, as well as other factors inflammatory cascade. The ability of estrogens to regulate estrogen receptors α and β present in microglia was previously described. However, more recently a transmembrane estrogen receptor, the G-protein coupled estrogen receptor (GPER) was identified. The objective of the second part of the present work was to clarify the involvement of GPER in the control microglial reactivity mediated by estradiol. Using the N9 microglial cell line, an agonist and an antagonist of GPER receptor, we found that GPER activation promoted the migration of microglial cells and significantly reduced the various parameters of microglial reactivity evaluated. Taken together these results suggest that GPER can be an important therapeutic target for neurodegenerative and neuroinflammatory diseases, especially in males, for whom estrogen therapy is not feasible.
Fonseca, Ana Paula da Silva. "Contribuição do GDNF para a neuroprotecção exercida pelo estrogénio." Master's thesis, Universidade da Beira Interior, 2010. http://hdl.handle.net/10400.6/799.
Full textParkinson´s disease is the second most common neurodegenerative disorder after Alzheimer and is mainly characterized by a progressive and selective depletion of dopamine neurons in the Substantia Nigra. Numerous studies have reported a greater prevalence and incidence of PD in men than in women. Studies involving estrogen treatment of ovariectomised rodents attribute this largely to the neuroprotective effets of estrogen. However, a neuroprotective role for physiologic levels of circulating estrogen in females is less clear. Estrogens have also been shown to regulate the expression of neurotrophic factors, like glial cell line-derived neurotrophic factor (GDNF), which might mediate their neuroprotective effects. GDNF produces neuroprotective and regenerative effects in the nigrostriatal pathways, acting as a potent survival factor for dopaminergic neurons that degenerate in Parkinson’s disease. In order to clarify the role of endogenous levels of estrogens in protecting the nigrostriatal pathway, we used the 6-hydroxydopamine (6-OHDA) model of Parkinson’s disease and tested how the removal of ovaries in fertile females interferes with extent of the dopaminergic lesion induced by 6-OHDA. Female Wistar rats were ovariectomised and 3 weeks after the surgery the animals were stereotaxically injected in the striatum with 6-OHDA. The extent of the lesion was assessed by counting the cells expressing the dopaminergic marker tyrosine hydroxylase by imunohistochemistry and also the expression levels of this protein by Western blot in both the Substantia Nigra and the striatum. The plasma levels of estradiol were also quantified. To determine if there was a relationship between estradiol levels, the expression of GDNF and the extent of the dopaminergic lesion, we also studied the expression of the neurotrophic factor GDNF. Our findings strongly suggest that endogenously produced estrogens and GDNF are associated with increased levels of striatal tyrosine hydroxylase, a marker of dopaminergic cell survival.
Wartiovaara, Kirmo. "GDNF and p75 neurotrophin receptor in development and disease." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/laa/biola/vk/wartiovaara/.
Full textÅkerud, Peter. "GDNF family ligands and neural stem cells in Parkinson's disease /." Stockholm : [Karolinska Univ. Press], 2001. http://diss.kib.ki.se/2001/91-7349-042-3/.
Full textBatista, Carla Isabel Soares. "Regulação dos níveis de GDNF na substantia nigra pelo estradiol." Master's thesis, Universidade de Aveiro, 2007. http://hdl.handle.net/10773/731.
Full textO stress oxidativo ao nível da via nigroestriatal é reconhecido como uma das causas da degeneração dos neurónios dopaminérgicos da substantia nigra na doença de Parkinson (DP), sendo o efeito protector do estradiol recorrentemente associado à protecção contra o stress oxidativo. A acção protectora do estradiol na via nigroestriatal pode ainda envolver outros efeitos, tais como modulação da expressão de factores neurotróficos cuja capacidade de promover a sobrevivência neuronal é sobejamente conhecida. Neste trabalho analisámos a regulação dos níveis do factor neurotrófico derivado de uma linha de células da glia (GDNF) pelo 17β-estradiol na substantia nigra e determinámos qual a contribuição específica deste efeito para a acção neuroprotectora da hormona. Adicionalmente, estudámos a modulação do efeito do 17β-estradiol na expressão de GDNF por agentes oxidantes, levodopa (L-DOPA) e H2O2. Para determinar os níveis de GDNF procedemos a análise de Western-Blot em extractos de células pós-natais de substantia nigra em cultura após incubação com 17ß-estradiol. Realizámos estudos in vivo para determinar de que forma o 17ß-estradiol afecta a acção da toxina dopaminérgica 6-hidroxidopamina (6-OHDA), quer ao nível da viabilidade das células dopaminérgicas, como ao nível da expressão dos níveis de GDNF. Os resultados obtidos permitiram concluir que, em células pós-natais de substantia nigra em cultura, o 17ß-estradiol promoveu o incremento da expressão do GDNF pelos astrócitos, provavelmente via ligação a receptores membranares. Verificámos ainda que os efeitos do estradiol parecem ser potenciados pela a exposição a L-DOPA e H2O2. In vivo, o estradiol protegeu as células dopaminérgicas da substantia nigra da lesão causada por 6-OHDA, possivelmente através da estimulação da síntese de GDNF observada nestas condições. ABSTRACT: Estradiol is currently considered a neuroprotector agent of nigral dopaminergic neurons. Oxidative stress in the nigrostriatal pathway has been associated with the development of Parkinson disease and the protective effect of estradiol is thought to be associated with a defence against oxidative stress. The protection promoted by estradiol in nigrostriatal pathway may also be coupled to the expression of neurotrophic factors, molecules recognized by its capability to promote neuron survival. In this study we analysed how 17ß-estradiol regulates nigral glial cell line deriv GDNF levels and evaluated the contribution of this effect to the neuroprotective action of this hormone. We also assessed how levodopa (L-DOPA) and H2O2 modulated the effect of estradiol on GDNF expression. Western-Blot analysis was used to determine GDNF levels in cultured substantia nigra cells after incubation with 17ß-estradiol. Using in vivo studies we evaluated how 17ß-estradiol affects the action of the dopaminergic toxin - 6- hidroxydopamine (6-OHDA) on the dopaminergic cell viability and the expression of GDNF. Taken together the results showed that, in cultured postnatal substantia nigra cells, 17ß-estradiol promoted the increase of GDNF expression by astrocytes through activation of putative membrane receptors. Exposure to the oxidative agents L-DOPA and H2O2 augmented the effect of estradiol. In vivo, estradiol protected nigral dopaminergic cells from 6-OHDA induced injury, possibly through stimulation of GDNF synthesis.
Cameron, Nicholas John. "Developing Olfactory Ensheathing Cells for ex vivo Delivery of GDNF." Thesis, Griffith University, 2010. http://hdl.handle.net/10072/365205.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
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Nevalainen, Nina. "Dysfunction in the nigrostriatal system : effects of L-DOPA and GDNF." Doctoral thesis, Umeå universitet, Histologi med cellbiologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-64149.
Full textBoucher, Timothy John. "The GDNF family of neurotrophic factors : effects on adult sensory neurons." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272413.
Full textHohmeier, Tim [Verfasser]. "Die enterische Muskulatur als Quelle des neurotrophen Faktors GDNF / Tim Hohmeier." Gießen : Universitätsbibliothek, 2015. http://d-nb.info/1080661387/34.
Full textKlein, Pontus. "Functions of GDNF/Ret signaling in models of autosomal recessive Parkinson’s disease." Diss., Ludwig-Maximilians-Universität München, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-166901.
Full textMikaels, Åsa. "Expression and function of GDNF family ligands and receptors in the nervous system /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4885-2/.
Full textDoxakis, Epaminondas. "Regulation of expression and role of the GDNF family receptors in neuronal development." Thesis, University of St Andrews, 1999. http://hdl.handle.net/10023/14779.
Full textRossi, Jari. "Roles of GDNF family receptor GFRa[alpha]2 in the peripheral nervous system." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/eri/biote/vk/rossi/.
Full textCharlet-Berguerand, Nicolas. "Etude de la régulation de l'épissage alternatif des pré-messagers RET, GFRalpha1, cTNT et C1C1." Paris 7, 2003. http://www.theses.fr/2003PA077023.
Full textVargas, Vivian. "Expression and function of GDNF family ligands and their receptors by human immune cells." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-22922.
Full textBrodbeck, Stephan [Verfasser]. "Charakterisierung des Transkriptionsfaktors SIX2 und seiner Bindungsstellen im GDNF- und Six2-Promotor / Stephan Brodbeck." Karlsruhe : KIT-Bibliothek, 2003. http://d-nb.info/1198221607/34.
Full textYAMADA, KIYOFUMI. "PRO-ADDICTIVE AND ANTI-ADDICTIVE FACTORS FOR DRUG DEPENDENCE." Nagoya University School of Medicine, 2008. http://hdl.handle.net/2237/10542.
Full textNevalainen, Nina. "Effects of glial cell line-derived neurotrophic factor (GDNF) on mouse fetal ventral mesencephalic tissue." Thesis, Mälardalen University, Department of Biology and Chemical Engineering, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-615.
Full textThe symptoms of Parkinson's disease occur due to degeneration of dopamine neurons in substantia nigra. It has been demonstrated that glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor when it comes to protect and enhance survival of dopamine neurons in animal models of Parkinson's disease. The aim of this study was to evaluate short- and long-term effects of GDNF on survival and nerve fiber outgrowth of dopamine cells and astrocytic migration in mouse fetal ventral mesencephalic (VM) tissue. Primary tissue cultures were made of mouse fetal VM tissue and evaluated at 7 and 21 days in vitro (DIV) in terms of dopaminergic nerve fiber outgrowth and astrocytic migration when developed with GDNF present, partially, or completely absent. The results revealed that VM tissue cultured in the absence of GDNF did not exhibit any significant differences in migration of astrocytes or dopaminergic nerve fiber outgrowth neither after 7 DIV nor after 21 DIV, when compared with tissue cultured with GDNF present. Migration of astrocytes and dopaminergic nerve fiber outgrowth reached longer distances when tissue was left to develop for 21 DIV in comparison with 7 DIV. In order to study the long-term effects of GDNF, mouse fetal dopaminergic tissue was transplanted into the ventricles of adult mice and evaluated after 6 months. No surviving dopamine neurons were present in the absence of GDNF. In contrast dopamine neurons developed with GDNF did survive, indicating that GDNF is an essential neurotrophic factor when it comes to long-term dopamine cell survival. More cases have to be assessed in the future in order to strengthen the findings. Thus, transplanted dopamine neurons will be assessed after 3 and 12 months in order to map out when dopamine neurons deprived of GDNF undergo degeneration.
Veit, Christine. "Charakterisierung der Regulation der gerichteten Migration und Invasion humaner Pankreaskarzinomzellen durch den neuronalen Wachstumsfaktor GDNF." [S.l. : s.n.], 2002. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10283627.
Full textBasu, Shubhayu. "Effects of three dimensional structure of tissue scaffolds on animal cell culture." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1092689986.
Full textTitle from first page of PDF file. Document formatted into pages; contains xviii, 236 p.; also includes graphics (some col.). Includes bibliographical references (p. 194-211). Available online via OhioLINK's ETD Center
Fuqua, Joshua Lee. "STUDIES OF THE EFFECTS OF DOPAMINE NEURON STIMULATING PEPTIDES IN RODENT MODELS OF NORMAL AND DYSFUNCTIONAL DOPAMINERGIC SYSTEMS." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/90.
Full textCristofaro, Rosalba. "GENETICA MOLECOLARE, EPIDEMIOLOGIA, PATOGENESI DEL RENE MIDOLLARE A SPUGNA." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3426283.
Full textIL Rene con Midollare a Spugna (MSK) riconosciuto per la prima volta a Padova, da Lenarduzzi nel 1939 grazie all’impiego dell’allora nuova tecnica dell’urografia e successivamente descritto nel 1949 da Cacchi e Ricci, rispettivamente urologo e patologo dell’Università patavina può essere annoverato tra le nefropatie congenite malformative per la presenza di ectasie precaliceali dei dotti collettori e per la sua frequente associazione con altre malformazioni congenite renali ed extrarenali. La funzione renale e la durata della vita nei pazienti MSK è normale; spesso si complica con lo sviluppo di nefrocalcinosi e nefrolitiasi. La patogenesi di MSK non è stata completamente chiarita ma la maggior parte degli autori concorda che si tratta di una patologia congenita con espressione ritardata. Che la causa di MSK potesse essere di natura genetica era suggerito dalla descrizione di alcuni casi familiari, dall’appartenenza di MSK al gruppo delle patologie malformative e dalla sua associazione con altre malattie ereditarie. La scoperta del gene/i responsabili della patologia è stato negli ultimi anni obiettivo del nostro gruppo di lavoro ed in particolare del mio lavoro di dottorato. L’ipotesi che ha dato inizio allo studio è che MSK sia la conseguenza di un disturbo durante lo sviluppo renale dell’interfaccia “gemma ureterale- mesenchima metanefrico” a causa di mutazioni/polimorfismi di RET, GDNF, o di altri geni coinvolti nell’embriogenesi renale, o in particolare a causa dell’interazione GDNF/RET. I risultati del sequenziamento diretto e test RFLP di GDNF su una casistica veneta di 112 pazienti, ben selezionata sulla base di stretti criteri urografici hanno permesso di identificare 1 variante rara della regione del promotore di GDNF (-27+18G>A) significativamente associata a MSK (p=0.02). Inoltre, la possibilità di estendere lo screening di GDNF su alcuni familiari di pazienti MSK ci ha permesso di scoprire che le varianti erano ereditate e che nelle famiglie erano associate al fenotipo MSK. Nella seconda parte del lavoro di dottorato è stata posta l’attenzione sui casi familiari di MSK. In collaborazione con la Clinica Nefrologica di Verona sono stati indagati 50 gruppi famigliari scelti random dalla coorte di 112 pazienti con MSK . Dall’’analisi mediante ecografia e/o Uro-TC estesa ai consanguinei della stessa generazione, e di 1, se possibile, 2 generazioni precedenti e/o successive è emerso che in 27 famiglie MSK segregava come carattere autosomico dominante, con espressività variabile e ridotta penetranza. Sui probandi di queste famiglie è stato fatto lo screening per il gene GDNF. Inoltre, in collaborazione con il laboratorio di Nefrologia Pediatrica dell’Università di Padova è stato fatto, lo screening di Six1, Spry1 e Pax2 che sono geni coinvolti nel processo di nefrogenesi renale e con un importante ruolo nei meccanismi di regolazione di GDNF, per un totale di 19 casi famigliari. Lo screening di GDNF mediante sequenziamento diretto delle regioni esoniche e delle giunzioni introne-esone non ha evidenziato nessuna variante rare né altre sostituzioni nucleotidiche. Allo stesso modo nessuna mutazione causativa è stata evidenziata per Six1, Spry1 e Pax2. Per Spry1 e Pax2 solo polimorfismi noti ma senza alcuna significatività statistica nelle frequenze alleliche confrontata con quella di popolazioni di controllo riportate in letteratura. Un altro obiettivo del mio lavoro di dottorato è stato quello di aver cercato di capire come varianti rare di GDNF possano essere associate al fenotipo MSK, in un sottogruppo di pazienti con nefrolitiasi, nefrocalcinosi ed MSK bilaterale. L’asportazione di un carcinoma renale in una paziente con MSK e mutazione di GDNF (-27+18G/C) ha dato l’opportunità di studiare per la mutazione di GDNF il suo significato funzionale e di verificare che cellule papillari renale prelevate da polo indenne al carcinoma renale e con bassi profili di espressione per GDNF, differenziavano spontaneamente verso un lineaggio osteogenico con la sintesi di proteine tipiche della matrice osteoide. Per cercare di approfondire se la down regolazione di GDNF, molto probabilmente dovuta alla mutazione che cade nella regione del promotore, possa avere avuto un coinvolgimento nel fenomeno di calcificazione osservato si è cercato di ottenere su cellule epiteliali renali (HK2), attraverso la tecnica di RNA interference, un silenziamento stabile di GDNF. I dati preliminari di questi ultimi esperimenti hanno mostrato che nelle cellule HK2 silenziate per GDNF vi era la presenza di depositi di Ca2PO4, confermati sia dalla colorazione von Kossa sia dall’analisi SEM. la presenza dei depositi di calcio fosfato non sono state osservate né nel controllo negativo né nei cloni silenziati in normali condizioni di coltura, mentre nel controllo negativo in condizione osteogenica i depositi erano presenti, seppur in minore quantità rispetto al clone silenziato. Sebbene preliminari, i nostri suggeriscono che la down regolazione di GDNF potrebbe favorire la deposizione di Ca2PO4 attraverso un meccanismo non ancora identificato. La nostra ipotesi è che l’apoptosi potrebbe essere la chiave.
Knott, Laura. "Cooperation between GDNF/Ret and EphrinA/EphA4 signals for motor axon pathway selection in the limb." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-78380.
Full textWang, Ruizhong. "Therapeutic Effects of Neurotrophic Factors GDNF and Artemin on Experimental Neuropathic Pain and Dorsal Root Injury." Tucson, Arizona : University of Arizona, 2006. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1461%5F1%5Fm.pdf&type=application/pdf.
Full textChen, Yan. "EFFECTS OF GLIAL CELL LINE-DERIVED NEUROTROPHIC FACTOR (GDNF) ON STEM/PROGENITOR CELL PROLIFERATION AND DIFFERENTIATION." UKnowledge, 2005. http://uknowledge.uky.edu/gradschool_diss/233.
Full textFORREST, Shelley Lynne. "Effects of visceral inflammation and nerve injury on nociceptors expressing receptors for the GDNF family ligands." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/9832.
Full textSchindler, Cora [Verfasser], Astrid [Akademischer Betreuer] Weyerbrock, and Nadja [Akademischer Betreuer] Osterberg. "GDNF moduliert die Sensitivität humaner Glioblastoma multiforme Zellen gegenüber dem Stickstoffmonoxid-Donor JS-K in vitro." Freiburg : Universität, 2018. http://d-nb.info/1153335530/34.
Full textWang, Ruizhong. "Therapeutic Effects of Neurotrophic Factors GDNF and Artemin on Experimental Neuropathic Pain and Dorsal Root Injury." Diss., The University of Arizona, 2005. http://hdl.handle.net/10150/195103.
Full textKlein, Pontus [Verfasser], and Rüdiger [Akademischer Betreuer] Klein. "Functions of GDNF/Ret signaling in models of autosomal recessive Parkinson’s disease / Pontus Klein. Betreuer: Rüdiger Klein." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2011. http://d-nb.info/1048014614/34.
Full textRémy, Sévérine. "Les neurones dopaminergiques : le gdnf et la neurturine comme facteurs de survie la xenotransplantation comme approche restauratrice." Nantes, 2001. http://www.theses.fr/2001NANT2020.
Full textJezierski, Anna. "Characterization and Therapeutic Potential of Human Amniotic Fluid Cells in Mediating Neuroprotection." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26157.
Full textBrizard, Mara. "Stratégies de transfert du gène codant le GDNF en vue d'une thérapie génique de la maladie de Parkinson." Paris 5, 2004. http://www.theses.fr/2004PA05N083.
Full textGlial cell line-derived neurotrophic factor (GDNF) gene transfer has protective and survival-promoting effects on nigrostriatal dopamine neurons which degenerate in the Parkinson's disease (PD). In order to improve gene transfer systems, we developed "gutless" adenoviral vectors. Their production proved inadequate, what led us to opt for lentiviral vectors. We then showed that lentiviral vectors pseudotyped with two different viral envelopes allow an efficient and sustained gene transfer in mouse brain. Moreover, they can be administered successfully several times, even with high titers of neutralizing antibodies directed against the pseudotyping envelope protein. We finally found that reproduces the early stage of PD, lentivirus-mediated intrastriatal GDNF delivery can promote reinnervation of the partially deafferated striatum accompanied by functional recovery
Barbosa, Izabela Guimaraes. "Estudo da concentração plasmática de fatores neurotróficos (BDNF,NGF e GDNF) em pacientes com transtorno bipolar do humor." Universidade Federal de Minas Gerais, 2009. http://hdl.handle.net/1843/BUBD-8AEM62.
Full textIntrodução: O transtorno bipolar do humor (TBH) é uma síndrome psiquiátrica de prevalência elevada, curso crônico, associada com grande morbidade. Evidências na literatura sugerem quealterações nos fatores neurotróficos, principalmente fator neurotrófico derivado do cérebro (BDNF), tem um importante papel na fisiopatologia do TBH. Objetivo: O objetivo deste estudo é avaliar a concentração plasmática dos níveis de fatores neurotróficos (BDNF, NGF e GDNF) em pacientes com TBH tipo I, comparando-os com controles saudáveis e correlacionando com a presença de comorbidades e medicações em uso. Métodos: Foram realizados análises das concentrações plasmáticas de fatores neurotróficos (BDNF, NGF e GDNF), através do método de ELISA, em 74 sujeitos, incluindo 21 controlessaudáveis e 53 pacientes bipolares (34 pacientes em mania e 19 pacientes em eutimia). No momento da entrada no estudo nenhum dos sujeitos estava em uso de corticosteróides, antibióticos ou antiinflamatórios pelo menos há 4 semanas. Resultados: Comparado com controles saudáveis, as concentrações plasmáticas de GDNF(p=0,395) e NGF (p=0,795) não diferenciaram do grupo controle. As concentrações plasmáticas de BDNF, comparado com o grupo controle, foram significativamente elevadas nos pacientes, tanto em episódios maníacos quanto em eutimia (p=0,001). Elevações nos níveis circulantes de BDNF não foram associadas com tratamento medicamentoso, comorbidades psiquiátricas, comorbidades clínicas, idade, escolaridade, intensidade de sintomas maníacos ou presença depsicose. Pacientes que apresentaram o primeiro episodio de humor há pelo menos 10 anos, mostraram elevações mais significativas nos níveis plasmáticos de BDNF (p=0,049). Conclusões: Observamos, pela primeira vez, elevações nos níveis plasmáticos de BDNF empacientes com TBH tipo I, especialmente nos com evolução de doença superior a 10 anos. Nossos achados corroboram dados da literatura que sugerem papel do BDNF na fisiopatologia do TBH.
Kelps, Kristen. "Molecular and Cellular Characterization of Dopamine Neuron Stimulating Peptides." UKnowledge, 2013. http://uknowledge.uky.edu/neurobio_etds/6.
Full textMahesh, Gajanan Sahare. "Establishment of Long-Term Culture and Elucidation of Self-Renewal Mechanisms of Primitive Male Germ Cells in Cattle." Kyoto University, 2015. http://hdl.handle.net/2433/200509.
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新制・課程博士
博士(農学)
甲第19243号
農博第2140号
新制||農||1036(附属図書館)
学位論文||H27||N4947(農学部図書室)
32242
京都大学大学院農学研究科応用生物科学専攻
(主査)教授 今井 裕, 教授 祝前 博明, 教授 松井 徹
学位規則第4条第1項該当
Nidadavolu, Prakash [Verfasser]. "Parkin cooperates with GDNF/Ret signaling during the development and maintenance of the dopaminergic system in mice / Prakash Nidadavolu." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2017. http://d-nb.info/1234658348/34.
Full textBuj-Bello, Anna. "Neurotrophic actions of GDNF and neurturin in the developing avian nervous system and cloning and expression of their receptors." Thesis, University of St Andrews, 1997. http://hdl.handle.net/10023/14781.
Full textMammeri, Hamid. "CIBLAGE ASTROCYTAIRE DE L'EXPRESSION DU GDNF PAR DES LENTIVECTEURS POUR UNE THERAPIE GENIQUE DE PROTECTION DE LA MALADIE DE PARKINSON." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2006. http://tel.archives-ouvertes.fr/tel-00184121.
Full textDans la perspective d'un traitement visant à protéger les neurones de la SN, de nombreuses études ont été centrées sur l'utilisation du glial cell-line derived neurotrophic factor (GDNF), facteur neurotrophique et neuroprotecteur des neurones dopaminergiques. Son efficacité thérapeutique a été démontrée par de nombreuses études dans des modèles animaux de la MP et lors d'essais cliniques.
Depuis une dizaine d'années, de nombreux travaux ont démontré l'efficacité de la thérapie génique (TG) comme méthode d'administration du GDNF et un effort particulier est entrepris pour optimiser cette approche. Cependant, malgré des résultats très encourageants obtenus dans les modèles murins et de primates de la MP, il s'est révélé que l'utilisation des vecteurs viraux se confrontait à une limite majeure. En effet, le ciblage préférentiellement neuronal de ces vecteurs entraîne la dispersion de la protéine dans la voie striatonigrale provoquant ainsi la formation massive de collatérales dans des zones non désirées.
Afin d'éviter la dispersion du GDNF, nous avons étudié la restriction de sa localisation au striatum en ciblant préférentiellement les astrocytes striataux via un vecteur lentiviral.
Une première partie du travail porte sur la caractérisation d'un vecteur pseudotypé par l'enveloppe Mokola. Chez la souris, l'enveloppe permet un ciblage spécifique des astrocytes quel que soit le promoteur utilisé, contrairement aux rat et primate, chez lesquels un ciblage préférentiellement astrocytaire est obtenu en combinaison avec le promoteur CMV.
Dans une seconde partie, le vecteur pseudotypé par Mokola a été utilisé pour étudier l'effet d'une expression restreinte de GDNF aux astrocytes striataux sur la protection de la voie nigrostriée. L'injection d'un vecteur permettant la synthèse de GDNF (Mok-GDNF) dans un modèle de rat de la MP permet une forte et stable synthèse de GDNF pendant au moins un an. Bien que le GDNF soit très majoritairement retrouvé au niveau du striatum et du globus pallidus, un très faible transport du GDNF dans les zones de projection est détecté. Cette dispersion résiduelle ne permet pas la génération de collatérales ectopiques. L'injection du vecteur Mok-GDNF permet une protection du système dopaminergique de la voie nigrostriée ainsi que le rétablissement d'un turn-over de la DA normal, traduit par une restauration complète du comportement moteur. Ces résultats indiquent que l'utilisation du vecteur pseudotypé par Mokola pour exprimer le GDNF se révèle optimale pour la TG de protection de la MP.
Stark, Robert Stefan [Verfasser], and Johanna [Akademischer Betreuer] Anneser. "Genetisch modifizierte Knochenmarkstammzellen als Therapieansatz bei Amyotropher Lateralsklerose : lentivirale Transduktion von GDNF und BDNF / Robert Stefan Stark. Betreuer: Johanna Anneser." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1047762072/34.
Full textMeka, V. V. Durga Praveen [Verfasser], and Edgar [Akademischer Betreuer] Kramer. "Parkin cooperates with GDNF/Ret signaling to prevent dopaminergic neurodegeneration in mice / V. V. Durga Praveen Meka ; Betreuer: Edgar Kramer." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2017. http://d-nb.info/1144485592/34.
Full textDolatshad, Nazanin Fatima. "Expression analysis of GDNF family of neurotrophic factors and their receptors in the postnatal, adult and ageing gut and bladder of rats." Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288967.
Full textChi, L. (Lijun). "Sprouty and Cerberus proteins in urogenital system development." Doctoral thesis, University of Oulu, 2007. http://urn.fi/urn:isbn:9789514284540.
Full textGoodison, Tavia. "Capacity of Neurotrophic Factors of the GDNF Family in Supporting the Survival of Dopaminergic Neurons in the Central Nervous System of the Aging Mouse." Thesis, Griffith University, 2013. http://hdl.handle.net/10072/367684.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Griffith University School of Biomolecular and Physical Sciences
Science, Environment, Engineering and Technology
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Brown, Russell W., Seth L. Kirby, Adam R. Denton, John M. Dose, Elizabeth D. Cummins, Wesley Drew Gill, and Katherine C. Burgess. "An Analysis of the Rewarding and Aversive Associative Properties of Nicotine in the Neonatal Quinpirole Model: Effects on Glial Cell Line-Derived Neurotrophic Factor (GDNF)." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/940.
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