Results 201 to 210 of about 15,097 (295)

Extension of the fluidics NTF-Biobank of polytraumatized patients with extracellular vesicles: improved vesicle preservation through local processing. [PDF]

open access: yesEur J Trauma Emerg Surg
Weber B   +11 more
europepmc   +1 more source

Diffusion Basis Spectrum Imaging of Tissue Microstructure and Early Treatment in Multiple Sclerosis

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective Conventional MRI cannot resolve the coexisting pathological processes within multiple sclerosis tissue. Diffusion Basis Spectrum Imaging decomposes the diffusion signal into fiber, cell, and hindered ratios indexing axonal integrity, cellularity, and extracellular space, respectively.
Apisit Kaewsanit   +10 more
wiley   +1 more source

Glucagon‐Like Peptide‐1 Receptor Agonists in Multiple Sclerosis: A Topical Narrative Review

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT The glucagon‐like peptide‐1 (GLP‐1) receptor agonists (RAs) are a relatively new class of drugs that were initially approved by the US Food and Drug Administration to improve glycemic control in patients with type 2 diabetes mellitus and, subsequently, weight reduction in patients with obesity.
Audrey Y. Chang, Farrah J. Mateen
wiley   +1 more source

Author Correction: Acoustic metamaterials-driven transdermal drug delivery for rapid and on-demand management of acute disease. [PDF]

open access: yesNat Commun
Xu J   +14 more
europepmc   +1 more source

Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective Aquaporin‐4‐IgG seropositive neuromyelitis optica spectrum disorder (AQP4+ NMOSD), myelin oligodendrocyte glycoprotein antibody‐associated disease (MOGAD), and multiple sclerosis (MS) are pathophysiologically distinct neuroinflammatory disorders. Complement activation is a major mechanism of injury in AQP4+ NMOSD, whereas its role in
Angeliki G. Filippatou   +23 more
wiley   +1 more source

Juvenile Huntington Disease With Cerebellar‐Predominant Atrophy Identified by Genome Sequencing

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Juvenile Huntington disease accounts for a small fraction of Huntington disease cases and is driven by the largest trinucleotide repeat expansions. We describe a 6‐year‐old boy with progressive global regression, generalized dystonia, and epilepsy, in whom serial imaging showed striking cerebellar‐predominant atrophy with an initially normal ...
Enrique Gonzalez Saez‐Diez   +5 more
wiley   +1 more source

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