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Titlebook: Neuroimmunological Diseases; Susumu Kusunoki Book 2016 Springer Japan 2016 Guillain-Barré Syndrome.Multiple Sclerosis.Neuroimmunology.Neur

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樓主: Daguerreotype
11#
發(fā)表于 2025-3-23 09:52:47 | 只看該作者
Animal Models for the Study of Neuroimmunological Diseasehanisms of disease and provided robust and reliable models to test novel therapeutic strategies. However, few preclinical studies of therapeutic treatments have demonstrated efficacy in the clinic, possibly because of the biological differences between humans and other animals. Although animal model
12#
發(fā)表于 2025-3-23 17:35:15 | 只看該作者
Blood–Brain Barrier and Blood–Nerve Barrierbarriers, including blood–brain barrier, blood–cerebrospinal fluid (CSF) barrier, blood–spinal cord barrier, and blood–nerve barrier, tightly seal off the central and peripheral nervous systems from the continuously changing milieu within the bloodstream. These neural barriers inhibit the free parac
13#
發(fā)表于 2025-3-23 18:36:17 | 只看該作者
Multiple Sclerosis: Etiology and Mechanism, with Special Reference to Asianst yet proven. Genome-wide association studies have revealed many susceptibility genes for MS, and the functions of these genes are mostly immune-related, supporting the autoimmune hypothesis. Increased numbers of T cells showing inter- and intramolecular epitope spreading against myelin proteins; in
14#
發(fā)表于 2025-3-23 23:26:01 | 只看該作者
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發(fā)表于 2025-3-24 04:10:37 | 只看該作者
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發(fā)表于 2025-3-24 06:50:32 | 只看該作者
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發(fā)表于 2025-3-24 14:39:11 | 只看該作者
18#
發(fā)表于 2025-3-24 18:31:51 | 只看該作者
Autoantibodies in Guillain-Barré Syndrome (GBS)hysiology of antibody-mediated nerve injury in GBS. The major target antigens in GBS and FS are sialic acid-containing glycolipids, gangliosides such as GM1 or GQ1b. The frequency of IgG antiglycolipid antibodies (subclass IgG1 or IgG3) is approximately 60?%. The heterogeneity of ganglioside express
19#
發(fā)表于 2025-3-24 19:56:32 | 只看該作者
20#
發(fā)表于 2025-3-24 23:24:06 | 只看該作者
POEMS Syndromemulti-organ involvement, associated with plasma cell dyscrasia and upregulation of serum levels of vascular endothelial growth factor (VEGF). The pathogenesis of the disorder is not well understood, but increased vascular permeability and neovascularization mediated by VEGF and other inflammatory cy
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