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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Efeitos neuroprotetores do Edaravone na hidrocefalia experimental induzida em ratos Wistar / Neuroprotective effects of edaravone in experimentally induced hydrocephalus in Wistar rats

Garcia, Camila Araújo Bernardino 30 January 2015 (has links)
Introdução: Hidrocefalia é uma síndrome caracterizada pelo acúmulo de líquido cérebroespinal no interior das cavidades ventriculares. Considerando a sua fisiopatologia de caráter multifatorial um dos fatores envolvidos é o estresse oxidativo desencadeado pela peroxidação lipídica e formação de radicais livres. O Edaravone é um novo fármaco antioxidante com efeitos neuroprotetores, que ainda não foi testado em pacientes com hidrocefalia. Objetivo: Avaliar a resposta neuroprotetora do Edaravone na hidrocefalia experimental em ratos jovens. Metodologia: A hidrocefalia foi induzida em ratos filhotes, injetando uma porção de caulim na cisterna magna. Os animais foram divididos em três grupos: controle (C) (n=10); hidrocefalia não tratada (HNT) (n=20); hidrocefalia tratado com 20mg/kg Edaravone (HTE) (n=20). O grupo tratado com a droga recebeu todos os dias, a partir do primeiro dia após a indução, uma injeção intraperitoneal com o Edaravone. Os animais foram pesados diariamente, avaliados por testes comportamentais e exame de ressonância magnética, análise histopatológica, imunoistoquímica e bioquímica. Todos os animais foram sacrificados, 14 dias após a indução de hidrocefalia. Resultados: Do terceiro ao oitavo dia após a indução de hidrocefalia, os animais ganharam menos peso do que os controles. No entanto, a partir do nono dia pós-indução, o ganho de peso foi similar nos três grupos experimentais. No teste de campo aberto e no labirinto aquático, o desempenho dos animais do grupo HTE foi melhor, quando comparado com os animais do grupo HNT. Na imunoistoquímica para GFAP, os animais do grupo HNT demonstravam astrócitos intensamente marcados com extensões grossas, enquanto que os animais do grupo de HTE tinham astrócitos mais delicados e com extensões finas. Na análise por caspase-3 os animais tratados com Edaravone mostraram um número menor de células em processos de apoptose. Conclusões: O uso do Edaravone evidenciou uma tendência a diminuir células em processo de apoptose, melhorou a resposta comportamental, e atividade dos astrócitos ligeiramente reduzida evidenciado por GFAP imunomarcação no corpo caloso de ratos jovens com hidrocefalia / Background: Hydrocephalus is a syndrome resulting from the current unbalance between the formation and absorption of cerebrospinal fluid (CSF), and consequent accumulation within the cerebral ventricles. Clinically, hydrocephalic children can present several neurological disorders, not always reversed with treatment, even after the development of more and more sophisticated shunt systems (1). Although lesions of hydrocephalus be multifactorial, it is known that oxidative stress is one of the mechanisms involved. The Edaravone is a new antioxidant drug with neuroprotective effects but has not been tested in hydrocephalus (2). Objectives: To evaluate the neuroprotective response of Edaravone on experimental hydrocephalus in young rats. Methodology: Hydrocephalus was induced in pup rats by injecting kaolin into the cisterna magna. The animals were divided into three groups with 10 rats each one: control (C); untreated hydrocephalus (HNT); hydrocephalus treated with 20mg/kg Edaravone (HTE). The treated group receive the drug every day from the first day after induction. The animals were weighed daily, assessed by behavioral tests and magnetic resonance examination. All animals were sacrificed 14 days after hydrocephalus induction and the brains processed for histological, immunohistochemical and biochemical analysis. In the analysis of caspase-3 treated animals showed Edaravone a smaller number of cells in the process of apoptosis. Results: From the third to the eighth day after the hydrocephalus induction, the animals gained less weight than controls. However, from the ninth day of induction, weight gain was similar in the 3 experimental groups. In the open field test the performance of hydrocephalic rats receiving Edaravone was better than those who did not receive the drug. In immunohistochemistry for GFAP in the corpus callosum, the control rats did not exhibit reactive astrocytes. On the other hand, the animals of HNT group showed intensely labeled astrocytes with thick extensions, while the animals in the HTE group the astrocytes were more delicate and with thin extensions. Conclusion: The use of Edaravone showed a tendency to decrease in cell apoptosis improved the behavioral response and slightly reduced astrocyte activity evidenced by GFAP immunostaining in the corpus callosum of young rats with hydrocephalus
2

Efeitos neuroprotetores do Edaravone na hidrocefalia experimental induzida em ratos Wistar / Neuroprotective effects of edaravone in experimentally induced hydrocephalus in Wistar rats

Camila Araújo Bernardino Garcia 30 January 2015 (has links)
Introdução: Hidrocefalia é uma síndrome caracterizada pelo acúmulo de líquido cérebroespinal no interior das cavidades ventriculares. Considerando a sua fisiopatologia de caráter multifatorial um dos fatores envolvidos é o estresse oxidativo desencadeado pela peroxidação lipídica e formação de radicais livres. O Edaravone é um novo fármaco antioxidante com efeitos neuroprotetores, que ainda não foi testado em pacientes com hidrocefalia. Objetivo: Avaliar a resposta neuroprotetora do Edaravone na hidrocefalia experimental em ratos jovens. Metodologia: A hidrocefalia foi induzida em ratos filhotes, injetando uma porção de caulim na cisterna magna. Os animais foram divididos em três grupos: controle (C) (n=10); hidrocefalia não tratada (HNT) (n=20); hidrocefalia tratado com 20mg/kg Edaravone (HTE) (n=20). O grupo tratado com a droga recebeu todos os dias, a partir do primeiro dia após a indução, uma injeção intraperitoneal com o Edaravone. Os animais foram pesados diariamente, avaliados por testes comportamentais e exame de ressonância magnética, análise histopatológica, imunoistoquímica e bioquímica. Todos os animais foram sacrificados, 14 dias após a indução de hidrocefalia. Resultados: Do terceiro ao oitavo dia após a indução de hidrocefalia, os animais ganharam menos peso do que os controles. No entanto, a partir do nono dia pós-indução, o ganho de peso foi similar nos três grupos experimentais. No teste de campo aberto e no labirinto aquático, o desempenho dos animais do grupo HTE foi melhor, quando comparado com os animais do grupo HNT. Na imunoistoquímica para GFAP, os animais do grupo HNT demonstravam astrócitos intensamente marcados com extensões grossas, enquanto que os animais do grupo de HTE tinham astrócitos mais delicados e com extensões finas. Na análise por caspase-3 os animais tratados com Edaravone mostraram um número menor de células em processos de apoptose. Conclusões: O uso do Edaravone evidenciou uma tendência a diminuir células em processo de apoptose, melhorou a resposta comportamental, e atividade dos astrócitos ligeiramente reduzida evidenciado por GFAP imunomarcação no corpo caloso de ratos jovens com hidrocefalia / Background: Hydrocephalus is a syndrome resulting from the current unbalance between the formation and absorption of cerebrospinal fluid (CSF), and consequent accumulation within the cerebral ventricles. Clinically, hydrocephalic children can present several neurological disorders, not always reversed with treatment, even after the development of more and more sophisticated shunt systems (1). Although lesions of hydrocephalus be multifactorial, it is known that oxidative stress is one of the mechanisms involved. The Edaravone is a new antioxidant drug with neuroprotective effects but has not been tested in hydrocephalus (2). Objectives: To evaluate the neuroprotective response of Edaravone on experimental hydrocephalus in young rats. Methodology: Hydrocephalus was induced in pup rats by injecting kaolin into the cisterna magna. The animals were divided into three groups with 10 rats each one: control (C); untreated hydrocephalus (HNT); hydrocephalus treated with 20mg/kg Edaravone (HTE). The treated group receive the drug every day from the first day after induction. The animals were weighed daily, assessed by behavioral tests and magnetic resonance examination. All animals were sacrificed 14 days after hydrocephalus induction and the brains processed for histological, immunohistochemical and biochemical analysis. In the analysis of caspase-3 treated animals showed Edaravone a smaller number of cells in the process of apoptosis. Results: From the third to the eighth day after the hydrocephalus induction, the animals gained less weight than controls. However, from the ninth day of induction, weight gain was similar in the 3 experimental groups. In the open field test the performance of hydrocephalic rats receiving Edaravone was better than those who did not receive the drug. In immunohistochemistry for GFAP in the corpus callosum, the control rats did not exhibit reactive astrocytes. On the other hand, the animals of HNT group showed intensely labeled astrocytes with thick extensions, while the animals in the HTE group the astrocytes were more delicate and with thin extensions. Conclusion: The use of Edaravone showed a tendency to decrease in cell apoptosis improved the behavioral response and slightly reduced astrocyte activity evidenced by GFAP immunostaining in the corpus callosum of young rats with hydrocephalus
3

The effect of Edaravone on Amyloid beta aggregation

Berntsson, Elina January 2019 (has links)
Alzheimer’s disease (AD) is a devastating neurodegenerative disease that affect millions of people worldwide. Aggregation of Amyloid-β (Aβ) monomers create toxic oligomers that can interact with cellular membranes and disturb cellular functions, resulting in cell death and neurological dysfunction. Increased levels of oxidative stress have been shown in the brains of AD patients, something that besides the obvious cell and tissue toxicity, also favors the amyloidogenic pathway and generates more Aβ monomers. Here we show that Edaravone, a free radical scavenger can affect the aggregation rate of different lengths of Aβ. We show that Aβ-40 that is more commonly found in vivo aggregates faster with addition of Edaravone, while Aβ-42 aggregates slower or not at all. These findings add up to previous findings where free radical scavengers and antioxidants such as Edaravone have been suggested as a potential treatment in Alzheimer’s disease.
4

Descriptors for Edaravone; Studies on its Structure, and Prediction of Properties

Liu, Xiangli, Aghamohammadi, Amin, Afarinkia, Kamyar, Abraham, R.J., Acree, W.E. Jr, Abraham, M.H. 15 March 2021 (has links)
Yes / Literature solubilities and NMR and IR studies have been used to obtain properties or descriptors of edaravone. These show that edaravone has a significant hydrogen bond acidity so that it must exist in solution partly as the OH and NH forms, as found by Freyer et al. Descriptors have been assigned to the keto form which has a low hydrogen bond acidity, and which is the dominant form in nonpolar solvents. Physicochemical properties of the keto form can be been calculated such as solubilities in nonpolar solvents, partition coefficients from water to nonpolar solvents, and partition coefficients from air to biological phases.
5

The Use of MM/QM calculations of 13C chemical shifts in the analysis of Edaravone tautomers

Abraham, R.J., Cooper, M.A., Aghamohammadi, Amin, Afarinkia, Kamyar, Liu, Xiangli 07 March 2024 (has links)
Yes / The 13C NMR chemical shifts of the three Edaravone tautomers (keto, enol, and amine) were calculated using a combined molecular mechanics (Pcmod 9.1/MMFF94) and ab initio (GIAO (B3LYP/DFT, 6–31 + G(d)) model. This method gave such good agreement with experiment that the assignment of the complex spectrum of Edaravone in solution, which is a mixture of the three tautomers could be made. This has been attempted previously by various methods with diverse results. In CDCl3 solution, the observed spectra show only one form, the keto tautomer, and this is also the case with acetonitrile solvent. Acetone solvent reacts with Edavarone in the NMR tube. In the other solvents studied, methanol, pyridine, DMSO, trifluoroethanol (TFE), there is a mixture of the tautomers with populations which vary with the solvent. The application of the shift predictions allows the assignment of the 13C spectra to the three tautomers and from this the proportions of the tautomers in the solution. The results at times differ significantly from previous studies, and this is discussed.
6

Amyotrofisk lateralskleros och effekten av behandling med riluzol. Kan masitinib och edaravone bli ett alternativ eller komplement till riluzolbehandling?

Klintborg, Alla January 2018 (has links)
Amyotrofisk lateralskleros (ALS) är en grupp motorneuronsjukdomar som leder till degenerering och död av centrala och perifera motoriska neuroner. ALS patienter drabbas av muskelsvaghet, muskelförtvining i skelettmuskulatur och förlamning. Överlevnaden efter diagnosen är ca två år i de flesta fall. I Sverige insjuknar årligen drygt 200 personer i ALS. Komplexa genetiska faktorer till exempel ALS-kopplade gener är avgörande för utvecklingen av ALS. Några miljöfaktorer har föreslagits som riskfaktorer för sporadisk ALS. På grund av en mycket komplex etiologi i sjukdomsuppkomst och utveckling saknas det än idag effektiv terapi för ALS. Vad gäller primära läkemedel som används i ALS-terapi är endast riluzol godkänd i Sverige idag. Edaravone och masitinib som har visat svag till moderat effekt och utifrån kontrollerade kliniska studier har de en neuroprotektiv roll som förlänger överlevnadstiden något. Syftet med föreliggande examensarbete var att undersöka den senaste utvecklingen kring behandlingar av ALS samt att utvärdera effekten av edaravone och masitinib samt jämföra deras respektive effektivitet med standardpreparatet riluzol. Totalt valdes och analyserades 6 kliniska studier, där 3 studier utvärderade effektiviteten av behandling med olika doser riluzol, i en klinisk studie undersöktes biverkningsspektrumet av riluzol, samt en klinisk studie med masitinib och en med edaravone. Behandling med riluzol resulterade i ökad överlevnad hos ALS patienter med 20 % (Studie 1) och 35 % (Studie 2) efter 12 månader. Resultaten från en stor klinisk studie (Studie 3) som inkluderade ett stort antal ALS-patienter visade att riluzol tolereras mycket väl vid dosen 100 mg/dag (50 mg x 2 per dag). Resultaten från Studie 4 visade att behandling med 100 mg/dag riluzol förlängde fas 4 hos patienter med ALS oavsett i vilken fas av sjukdomen behandlingen påbörjades. Behandling med masitinib i dosen 4,5 mg/kg/dag + riluzol (100 mg/dag) visade signifikant effekt för ALS patienter med baseline av ALSFRS-R utveckling ˂1,1 poäng/månad och visade 27% effekt efter 48 veckor behandling. Effekten visade sig vara högre, 35% i patienter med sjukdomsutveckling kortare än 18 månader efter diagnos (Studie 5). Utifrån resultat från Studie 6 visade behandling med edaravone effekt endast i en begränsad grupp av ALS patienter, identifierade med hjälp av post-hoc analys av en tidigare fas III RCT. Däremot fanns det ingen indikation att behandling med edaravone skulle vara effektiv för en bredare grupp ALS patienter. Det är möjligt att masitinib är ett nytt läkemedel för behandling av ALS patienter som skulle kunna användas som komplement till riluzolbehandling, dock behövs fler kliniska studier för att utvärdera effekten av masitinib.  Riluzol har känd effekt – förlänger överlevnaden med 2 till 3 månader i vanliga fall av ALS. Edaravone visade svag effekt vid behandling av ALS.
7

Time-related Aspects of Otoprotection : Experimental Studies in Rat

Lidian, Adnan January 2013 (has links)
Intratympanic injection of various otoprotectants through the round window membrane (RWM) might become available in the near future as an alternative to the currently available medical and surgical methods used to treat several inner ear diseases. The most common outcome of such diseases is sensorineural hearing loss (SNHL). Two examples of  these otoprotectants are Edaravone and Brain-Derived Neurotrophic Factor (BDNF), both of which have already proved effective against  noise-induced hair cell loss, barotrauma  and ototoxicity caused by cisplatin. In four different studies we used two electrophysiological methods, auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE), to study the effects of tobramycin and Pseudomonas aeruginosa exotoxin A (PaExoA) on the inner ears of 129 male Sprague-Dawley rats. In two investigations, not only the otoprotective effects of Edaravone on tobramycin-induced ABR threshold shifts and PaExoA-induced DPOAE  threshold changes, were studied but even different application times, in order to establish in which interval it was still possible to achieve effective otoprotection.We found that Edaravone gave otoprotection from tobramycin when injected simultaneously or within 7 days, but it had only a limited effect on the changes in DPOAE thresholds caused by PaExoA when injected 1, 2, or 4 hours after the exotoxin. The effect of BDNF on PaExoA-induced ABR threshold shifts was investigated in two studies, where different doses of intratympanically injected PaExoA were used and where BDNF was applied simultaneously, 12 or 72 hours efter exotoxin instillation. We found that BDNF had an otoprotective effect on SNHL induced by different doses PaExoA when injected simultaneously or with no more than 12 hours delay.

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