neuromyelitis optica/albumin

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The clinical value of the albumin quotient in patients with neuromyelitis optica spectrum disorder.

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The disruption of the blood-brain barrier (BBB) is common in patients with neuromyelitis optica spectrum disorder (NMOSD), causing pro-inflammatory immune cells to migrate into the central nervous system (CNS) and active demyelinating lesions. Albumin quotient is commonly used as an

Low antioxidant status of serum uric acid, bilirubin and albumin in patients with neuromyelitis optica.

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BACKGROUND Oxidative stress plays a central role in neuropathology of multiple sclerosis (MS). The patients with MS have low antioxidant status. Antioxidant therapy may represent an attractive treatment of MS. However, the relationship between neuromyelitis optica (NMO), a distinct nosologic entity

Increased cerebrospinal fluid metalloproteinase-2 and interleukin-6 are associated with albumin quotient in neuromyelitis optica: Their possible role on blood-brain barrier disruption.

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BACKGROUND Inflammation in neuromyelitis optica (NMO) is triggered by a serum antibody against the aquaporin-4 (AQP4). This process requires antibody penetration of the blood-brain barrier (BBB), but the mechanisms for BBB disruption in NMO remain unknown. OBJECTIVE We examined whether changes in

Cerebrospinal fluid/serum gradient of IgG is associated with disability at acute attacks of neuromyelitis optica.

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Increased blood-brain barrier (BBB) disruption can be found in patients with neuromyelitis optica (NMO); however, its clinical implication and association with disability at acute attack remains obscure. The purpose of the study was to evaluate the clinical significance of BBB disruption and the

Markedly elevated soluble intercellular adhesion molecule 1, soluble vascular cell adhesion molecule 1 levels, and blood-brain barrier breakdown in neuromyelitis optica.

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OBJECTIVE To evaluate the degree of blood-brain barrier disruption in patients with neuromyelitis optica (NMO) and to clarify whether the levels of soluble intercellular adhesion molecule 1 (sICAM-1) and soluble vascular cell adhesion molecule 1 (sVCAM-1) in patients with NMO can be useful

Clinical and immunological differences between MOG associated disease and anti AQP4 antibody-positive neuromyelitis optica spectrum disorders: Blood-brain barrier breakdown and peripheral plasmablasts.

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Patients with anti-aquaporin-4 (AQP4) water channel antibody-positive neuromyelitis optica spectrum disorders (AQP4-NMOSD) and myelin oligodendrocyte glycoprotein (MOG) associated disease (MOGAD) often present with similar clinical symptoms, and some cases are hard to differentiate at

Impact of blood-brain barrier disruption on newly diagnosed neuromyelitis optica spectrum disorder symptoms and prognosis.

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Blood-brain barrier (BBB) disruption and ensuing immune activation are central to the pathogenesis of central nervous system (CNS) inflammatory diseases. However, the influence of BBB permeability on the clinical signs and prognosis of newly diagnosed neuromyelitis optica spectrum

Neuromyelitis optica (NMO) antibody positivity in patients with transverse myelitis and no visual manifestations.

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OBJECTIVE To describe a subgroup of patients with IgG antibody to Aquaporin 4 Protein (AQP4) specific to neuromyelitis optica (NMO), who did not have clinical manifestations of optic nerve involvement at the time of diagnosis. METHODS Assessment of five patients (four African Americans and one

Clinical characteristics, course and prognosis of relapsing Devic's Neuromyelitis Optica.

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OBJECTIVE To evaluate the clinical characteristics, course and prognosis of Devic's neuromyelitis optica (DNO), to evaluate the prognostic role of demographic and clinical features, to evaluate the current DNO diagnostic criteria. METHODS Demographic, clinical, CSF and MRI data of patients affected

Anti-C1q autoantibodies in patients with neuromyelitis optica spectrum disorders.

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We examined anti-complement C1q (C1q) autoantibody levels in serum and cerebrospinal fluid (CSF) samples of patients with neuromyelitis optica spectrum disorders (NMOSD). We analyzed the correlations between anti-C1q autoantibody levels and the clinical and other CSF characteristics of NMOSD. Serum

Blood Brain Barrier Permeability Could Be a Biomarker to Predict Severity of Neuromyelitis Optica Spectrum Disorders: A Retrospective Analysis.

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Background: Blood-brain barrier (BBB) pathology exists in neuromyelitis optica spectrum disorders (NMOSD). However, the clinical use of BBB permeability, such as predicting disease severity of NMOSD, has rarely been studied in a large cohort of patients. Objectives: The current study explored the

Proteomic analysis of the cerebrospinal fluid in multiple sclerosis and neuromyelitis optica patients.

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The present study aimed to compare the 2-dimensional (2D) electrophoresis pattern of the cerebrospinal fluid (CSF) in multiple sclerosis (MS), neuromyelitis optica (NMO) and control individuals, to identify the proteins with differential expression and to examine their significance. CSF samples from

Therapeutic plasma exchange for neuromyelitis optica spectrum disorder: A multicenter retrospective study by the ASFA neurologic diseases subcommittee.

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Neuromyelitis optica/neuromyelitis optica spectrum disorder patients' response to therapeutic plasma exchange (TPE) is currently incompletely characterized.Our study aims to understand the clinical status improvement of neuromyelitis optica/neuromyelitis

GRP 78 antibodies are associated with clinical phenotype in neuromyelitis optica.

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We previously reported the association between blood-brain barrier (BBB) dysfunction and glucose-regulated protein 78 (GRP 78) autoantibodies in neuromyelitis optica (NMO).We clarify whether the BBB-endothelial cell activation induced by immunoglobulin G

Markedly increased IP-10 production by blood-brain barrier in neuromyelitis optica.

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OBJECTIVE Severe damage to the blood-brain barrier (BBB) allows anti-aquaporin 4 (AQP4) antibodies to access the astrocytic endfeet in neuromyelitis optica (NMO). In the current study, we identified the pathogenic cytokines/chemokines that are responsible for the BBB malfunction induced by NMO

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