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1.
Acta Radiol ; 64(2): 690-697, 2023 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-35171064

RESUMO

BACKGROUND: Synthetic magnetic resonance imaging (SyMRI) enables to reformat various images by adjusting the MR parameters. PURPOSE: To investigate whether customization of the repetition time (TR), echo time (TE), and inversion time (TI) in SyMRI could improve the visualization of subthalamic nucleus (STN). MATERIAL AND METHODS: We examined five healthy volunteers using both coronal SyMRI and quantitative susceptibility mapping (QSM), seven patients with Parkinson's disease (PD) using coronal SyMRI, and 15 patients with PD using coronal QSM. Two neuroradiologists reformatted SyMRI (optimized SyMRI) by adjusting TR, TE, and TI to achieve maximum tissue contrast between the STN and the adjacent brain parenchyma. The optimized MR parameters in the PD patients varied according to the individual. For regular SyMRI (T2-weighted imaging [T2WI] and STIR), optimized SyMRI, and QSM, qualitative visualization scores of the STN (STN score) were recorded. The contrast-to-noise ratio (CNR) of the STN was also measured. RESULTS: For the STN scores in both groups, the optimized SyMRI were significantly higher than the regular SyMRI (P < 0.05), and there were no significant differences between optimized SyMRI and QSM. For the CNR of differentiation of the STN from the substantia nigra, the optimized SyMRI was higher than the regular SyMRI (volunteer: T2WI P = 0.10 and STIR P = 0.26; PD patient: T2WI P = 0.43 and STIR P = 0.25), but the optimized SyMRI was lower than the QSM (volunteer: P = 0.26; PD patient: P = 0.03). CONCLUSIONS: On SyMRI, optimization of MR parameters (TR, TE, and TI) on an individual basis may be useful to increase the conspicuity of the STN.


Assuntos
Estimulação Encefálica Profunda , Doença de Parkinson , Núcleo Subtalâmico , Humanos , Núcleo Subtalâmico/diagnóstico por imagem , Núcleo Subtalâmico/patologia , Estimulação Encefálica Profunda/métodos , Imageamento por Ressonância Magnética/métodos , Encéfalo/patologia , Doença de Parkinson/diagnóstico por imagem
2.
Neurosci Res ; 94: 10-6, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-25591911

RESUMO

Although iron is essential in physiological processes, accumulation of iron in central nervous system is associated with various neurological diseases including Alzheimer's disease and Parkinson's disease. Innate immune reactions are involved in the pathogenesis of those diseases, but roles of iron in innate immunity are not known well. In the present study, pretreatment of U373MG human astrocytoma cells with an iron chelator desferrioxamine (DFX) inhibited the expression of CXCL10 induced by a Toll-like receptor 3 (TLR3) agonist polyinosinic-polycytidylic acid (poly IC). Induction of interferon-ß (IFN-ß) was not affected, but phosphorylation of signal transducer and transcription 1 (STAT1) was decreased by DFX. We have previously reported that various IFN-stimulated genes (ISGs) are involved in CXCL10 induction by poly IC. Pretreatment with DFX also decreased the expression of these ISGs. Pretreatment of cells with FeSO4 counteracted inhibitory effects of DFX on ISG56, retinoic acid-inducible gene-I (RIG-I), CXCL10 and phosphorylation of STAT1. These results suggest that iron may positively regulate STAT1 phosphorylation and following signaling to express ISG56, RIG-I and CXCL10 in U373MG cells treated with poly IC. Iron may contribute to innate immune and inflammatory reactions elicited by the TLR3 signaling in astrocytes, and may play an important role in neuroinflammatory diseases.


Assuntos
Quimiocina CXCL10/metabolismo , Desferroxamina/farmacologia , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Indutores de Interferon/farmacologia , Quelantes de Ferro/farmacologia , Poli I-C/farmacologia , Astrocitoma/patologia , Linhagem Celular Tumoral , Quimiocina CXCL10/genética , Relação Dose-Resposta a Droga , Interações Medicamentosas , Ensaio de Imunoadsorção Enzimática , Humanos , RNA Mensageiro/metabolismo , RNA Interferente Pequeno/farmacologia , Fator de Transcrição STAT1/metabolismo , Transdução de Sinais/efeitos dos fármacos , Fator A de Crescimento do Endotélio Vascular/genética , Fator A de Crescimento do Endotélio Vascular/metabolismo
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