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1.
Neurol Sci ; 2024 May 04.
Artigo em Inglês | MEDLINE | ID: mdl-38704479

RESUMO

BACKGROUND: Juvenile myoclonic epilepsy (JME) is characterized by altered patterns of brain functional connectivity (FC). However, the nature and extent of alterations in the spatiotemporal characteristics of dynamic FC in JME patients remain elusive. Dynamic networks effectively encapsulate temporal variations in brain imaging data, offering insights into brain network abnormalities and contributing to our understanding of the seizure mechanisms and origins. METHODS: Resting-state functional magnetic resonance imaging (rs-fMRI) data were procured from 37 JME patients and 37 healthy counterparts. Forty-seven network nodes were identified by group-independent component analysis (ICA) to construct the dynamic network. Ultimately, patients' and controls' spatiotemporal characteristics, encompassing temporal clustering and variability, were contrasted at the whole-brain, large-scale network, and regional levels. RESULTS: Our findings reveal a marked reduction in temporal clustering and an elevation in temporal variability in JME patients at the whole-brain echelon. Perturbations were notably pronounced in the default mode network (DMN) and visual network (VN) at the large-scale level. Nodes exhibiting anomalous were predominantly situated within the DMN and VN. Additionally, there was a significant correlation between the severity of JME symptoms and the temporal clustering of the VN. CONCLUSIONS: Our findings suggest that excessive temporal changes in brain FC may affect the temporal structure of dynamic brain networks, leading to disturbances in brain function in patients with JME. The DMN and VN play an important role in the dynamics of brain networks in patients, and their abnormal spatiotemporal properties may underlie abnormal brain function in patients with JME in the early stages of the disease.

2.
Chin J Integr Med ; 17(4): 296-301, 2011 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-21509674

RESUMO

OBJECTIVE: To establish a retinal vein occlusion (RVO) animal model and observe the therapeutic effect of a Chinese herbal composition (Fufang Xueshuantong Capsule, , FXC)inischemicinischemic) in ischemic retinal disease. METHODS: Fifteen adult male Sprague-Dawley rats underwent laser photothrombosis to induce RVO on their right eyes and were subsequently randomized to receive FXC (the intervention group, n=7) or placebo treatment (the control group, n=8). Fundus fluorescein angiography was performed after 2, 4 and 8 weeks of treatment. Real-time reverse transcription-PCR was used to quantify the mRNA expression of vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (SDF-1). The main outcomes were the mRNA copies of VEGF and SDF-1 and the counts of RVO signs. RESULTS: Laser photothrombosis procedure induced typical lesions of RVO, including hemorrhage, leakage, retinal detachment, capillary non-perfusion, filling defect of retinal vessels, and lateral circulation/dilation of small vessels. The retinal lesions were associated with an increased expression of VEGF (P<0.05). No significant change of SDF-1 expression was noticed. Compared with the control group, the intervention group had numerically fewer RVO lesions at week 2 (1.71±0.76 vs. 3.50±1.51, t=-2.82, P<0.05). The benefit of intervention remained at weeks 4 and 8. CONCLUSIONS: A rat model of laser photothrombosis-induced RVO was established and an increase in the VEGF expression was observed in the retinal lesion. The FXC had therapeutic benefit in improving retinal lesions in the rat model of RVO.


Assuntos
Modelos Animais de Doenças , Medicamentos de Ervas Chinesas/uso terapêutico , Oclusão da Veia Retiniana/terapia , Animais , Sequência de Bases , Quimiocina CXCL12/genética , Quimiocina CXCL12/metabolismo , Primers do DNA , Angiofluoresceinografia , Expressão Gênica , Masculino , Ratos , Ratos Sprague-Dawley , Oclusão da Veia Retiniana/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fator A de Crescimento do Endotélio Vascular/genética , Fator A de Crescimento do Endotélio Vascular/metabolismo
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