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1.
J Integr Neurosci ; 21(6): 159, 2022 Sep 21.
Artículo en Inglés | MEDLINE | ID: mdl-36424739

RESUMEN

BACKGROUND: Currently, case studies or clinical trials in different patient populations remain the main resource underlying the understanding of disorder of consciousness (DoC). This provides a low efficacy for the derivation of data and the implementation of associated controlled experimental designs. Preclinical models provide precise controls, reduced variability, rich data output and limited ethical complexity. Nonhuman primates are suitable model animals for disorders of consciousness due to their brain structure being very similar to that of humans. Behavioral tests remain the primary standard for assessing the consciousness status of humans. However, there is currently no behavioral assessment scale available for evaluation of the state of consciousness disorder in nonhuman primates. This presents a significant challenge for the establishment of different models of consciousness disorder. Therefore, there is considerable motivation to focus on the development of a proper tool for assessment of the state of consciousness associated with nonhuman primate models that are based on clinically common consciousness assessment scales. METHODS: It is assumed that the Delphi and level analysis methods based on clinical consciousness disorder assessment scales may provide an effective way to select and include assessment indexes for levels of consciousness in nonhuman primates. RESULTS: 8 first-level indicators with 41 second-level indexes were selected preliminary as a pool of evaluation entries of state of consciousness of nonhuman primates. CONCLUSIONS: It may be practicable to extract appropriate indicators for non-human primates from the clinical consciousness disorder assessment scales. Besides, a combination of Delphi method, behavioral analysis, electroencephalography, neuroimaging (such as positron emission tomography-computed tomography) and functional magnetic resonance imaging is necessary to test the reliability and validity of the novel scale reported here.


Asunto(s)
Trastornos de la Conciencia , Primates , Animales , Humanos , Trastornos de la Conciencia/diagnóstico , Reproducibilidad de los Resultados , Encéfalo/diagnóstico por imagen , Imagen por Resonancia Magnética
2.
Aging (Albany NY) ; 13(8): 11877-11888, 2021 04 23.
Artículo en Inglés | MEDLINE | ID: mdl-33893248

RESUMEN

BACKGROUND: Cerebral ischemia-reperfusion injury (CIRI) can cause brain tissue inflammation, neuronal degeneration, and apoptosis. There is increasing evidence that microRNAs (miRNA) exert neuroprotective effects by regulating the inflammatory process during cerebral ischemia-reperfusion injury. Additionally, it is increasingly acknowledged that neuroinflammation is regulated by Toll-like receptor 4 (TLR4). However, it is unclear whether miRNA can exert its neuroprotective effects by regulating TLR4-mediated inflammation. METHODS: The effects of BMSCs over-expressing miR-202-3p on CIRI, angiogenesis in midbrain tissue, and the release of inflammatory factors (IFs) in the serum were measured using in vivo rat models. We also used SH-SY5Y cells to establish an ischemia-reperfusion in vitro cell model. The interaction between miR-202-3p and TLR4 was analyzed by overexpressing miR-202-3p and knocking down TLR4. Knockdown of TLR4 was performed using siRNA. RESULTS: Overexpression of miR-202-3p in BMSCs could significantly improve brain function and reduce brain damage. Simultaneously, miR-202-3p could significantly promote angiogenesis, increase the expression of vWF and VEGF, and reduce the expression of IFs. When the expression of TLR4 was significantly reduced in SH-SY5Y cells, the expression of IFs increased. Therefore, miRNA-202-3p may interact with TLR4 to modulate inflammation. CONCLUSION: Our data indicated that miR-202-3p potentially exerts its neuroprotective effects and protects against CIRI by regulating TLR4-mediated inflammation.


Asunto(s)
Isquemia Encefálica/terapia , Trasplante de Células Madre Mesenquimatosas , Neovascularización Fisiológica/genética , Daño por Reperfusión/prevención & control , Animales , Apoptosis/genética , Isquemia Encefálica/sangre , Isquemia Encefálica/complicaciones , Isquemia Encefálica/inmunología , Línea Celular Tumoral , Modelos Animales de Enfermedad , Técnicas de Silenciamiento del Gen , Vectores Genéticos/genética , Humanos , Inflamación/sangre , Inflamación/genética , Inflamación/inmunología , Mediadores de Inflamación/sangre , Mediadores de Inflamación/metabolismo , Lentivirus/genética , Masculino , Mesencéfalo/irrigación sanguínea , Mesencéfalo/inmunología , Mesencéfalo/patología , Células Madre Mesenquimatosas/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Cultivo Primario de Células , Ratas , Daño por Reperfusión/sangre , Daño por Reperfusión/inmunología , Daño por Reperfusión/patología , Receptor Toll-Like 4/genética , Transfección
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