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1.
Int Orthop ; 45(2): 401-410, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-32621139

RESUMO

PURPOSE: The biological action of platelet-rich plasma (PRP) could slow down the osteoarthritis progression, resulting in a delay of joint replacement. This work aims to evaluate the ability of PRP to postpone and even avoid knee replacement in patients with knee osteoarthritis (KOA) analyzing, on the one hand, the time of delay and on the other hand the percentage of patients without undergoing total knee arthroplasty (TKA). METHODS: A retrospective analysis and a survival analysis were conducted. KOA patients who underwent knee replacement between 2014 and 2019 and previously received PRP infiltrations were included in the retrospective analysis. Regarding survival analysis, KOA patients who received PRP treatment during 2014 and with follow-up until 2019 were included. The dates of PRP treatment and TKA, KOA severity, age of the patients, number of PRP cycles, and administration route were analyzed. RESULTS: This work included 1084 patients of which 667 met the inclusion criteria. 74.1% of the patients in the retrospective study achieved a delay in the TKA of more than 1.5 years, with a median delay of 5.3 years. The survival analysis showed that 85.7% of the patients did not undergo TKA during the five year follow-up. The severity degree, age, PRP cycles, and administration route had a statistically significant influence on the efficacy of PRP in delaying surgery. CONCLUSION: These data suggest that the application of PRP in KOA patients is a treatment that could delay TKA, although further studies are needed to understand and improve this therapy.


Assuntos
Artroplastia do Joelho , Osteoartrite do Joelho , Plasma Rico em Plaquetas , Artroplastia do Joelho/efeitos adversos , Humanos , Injeções Intra-Articulares , Osteoartrite do Joelho/cirurgia , Estudos Retrospectivos , Análise de Sobrevida , Resultado do Tratamento
2.
Food Funct ; 15(13): 7214-7223, 2024 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-38817211

RESUMO

Parkinson's disease is the neurodegenerative motor disorder with the highest incidence worldwide. Among other factors, Parkinson's disease is caused by the accumulation of α-synuclein aggregates in a patient's brain. In this work, five molecules present in the diet are proposed as possible nutraceuticals to prevent and/or reduce the formation of α-synuclein oligomers that lead to Parkinson's disease. The olive oil polyphenols tyrosol, hydroxytyrosol (HT), hydroxytyrosol acetate (HTA) and dihydroxyphenyl acetic acid (DOPAC) besides vitamin C were tested using a cellular model of α-synuclein aggregation and a Caenorhabditis elegans Parkinson's disease animal model. Levodopa was included in the assays as the main drug prescribed to treat the disease as well as dopamine, its direct metabolite. HTA and DOPAC completely hindered α-synuclein aggregation in vitro, while dopamine reduced the aggregation by 28.7%. The Parallel Artificial Membrane Permeability Assay (PAMPA) showed that HTA had the highest permeability through brain lipids among the compounds tested. Furthermore, the C. elegans Parkinson's disease model made it possible to assess the chosen compounds in vivo. The more effective substances in vivo were DOPAC and HTA which reduced the αS aggregation inside the animals by 79.2% and 76.2%, respectively. Moreover, dopamine also reduced the aggregates by 67.4% in the in vivo experiment. Thus, the results reveal the potential of olive oil tyrosols as nutraceuticals against α-synuclein aggregation.


Assuntos
Caenorhabditis elegans , Azeite de Oliva , Doença de Parkinson , Álcool Feniletílico , alfa-Sinucleína , Animais , Humanos , alfa-Sinucleína/metabolismo , Caenorhabditis elegans/efeitos dos fármacos , Suplementos Nutricionais , Modelos Animais de Doenças , Azeite de Oliva/química , Azeite de Oliva/farmacologia , Doença de Parkinson/tratamento farmacológico , Doença de Parkinson/metabolismo , Álcool Feniletílico/análogos & derivados , Álcool Feniletílico/farmacologia , Álcool Feniletílico/química , Agregados Proteicos/efeitos dos fármacos
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