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1.
Chinese Medical Journal ; (24): 270-274, 2012.
Article in English | WPRIM | ID: wpr-333503

ABSTRACT

<p><b>BACKGROUND</b>Despite the large scale technical innovations that have been made, a number of patients with neuromyelitis optica (NMO) are lacking NMO-IgG in both serum and cerebrospinal fluid. Longitudinally extensive spinal cord (LESC) lesions and linear lesions are associated with NMO. However, differences of spinal cord magnetic resonance imaging (MRI) features, including LESC lesions and linear lesions, between NMO-IgG positive and negative patients still remain unknown. The aim of the present study was to analyze the relationship between NMO-IgG status and spinal cord MRI features in NMO patients, particularly concerned about LESC lesions and linear lesions.</p><p><b>METHODS</b>Clinical data and spinal cord MRI of 52 NMO patients were retrospectively analyzed. Eight patients were NMO-IgG negative in both serum and cerebrospinal fluid, while 44 were NMO-IgG positive. Quantitative data between the two cohorts were compared by the Student's t test or Mann-Whitney U test, the chi-square test or Fisher's exact test was used to evaluate qualitative data.</p><p><b>RESULTS</b>NMO-IgG negative patients had a higher sex ratio (male/female) (P = 0.014). On axial MRI, lesions in the NMO-IgG negative group were mostly located in the peripheral cord (50%), and central lesions (55%) were more common in the NMO-IgG positive group (P = 0.051). LESC lesions were common in both cohorts. None of linear lesions was found in NMO-IgG negative patients, while the NMO-IgG positive cohort had significantly more linear lesions (48%) (P = 0.016).</p><p><b>CONCLUSIONS</b>Patients with NMO-IgG negativity may have different spinal cord lesion features compared to NMO-IgG positive patients. Diagnosis of NMO cannot be excluded even when NMO-IgG negativity and non-specific spinal lesions occur.</p>


Subject(s)
Adult , Female , Humans , Male , Middle Aged , Young Adult , Immunoglobulin G , Blood , Cerebrospinal Fluid , Magnetic Resonance Imaging , Neuromyelitis Optica , Blood , Cerebrospinal Fluid , Pathology , Retrospective Studies , Spinal Cord , Pathology
2.
Journal of Southern Medical University ; (12): 600-602, 2008.
Article in Chinese | WPRIM | ID: wpr-280138

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the changes in the activity of nuclear factor-kappaB (NF-kappa B) in mice with dextran sulphate sodium (DSS)-induced rat colitis and its modulalorg effect on intercellular adhesion molecule-1 (ICAM-1) expression.</p><p><b>METHODS</b>Twenty normal male mice were randomized into DSS group and normal saline (NS) control group according to a matched-pair design. From days 1 to 7, the mice in DSS group were subjected to oral administration of 5%DSS solution, and from days 8 to 20, NS was given instead, for a total of 3 cycles. In the control group, only NS was administered. The colonic pathology was observed using HE staining and the mucosa 1 damage was scored for each mouse. The DNA-binding activity of NF-kappa B was tested by electrophoretic mobility shift assay, and the expressions of ICAM-1 and NF-kappa B p65 were detected using immunohistochemistry.</p><p><b>RESULTS</b>The DNA-binding activity of NF-kappa B was significantly increased in DSS group as compared with NS group. ICAM-1 and p65 expressions were detected in the nuclei of the vascular endothelial and inflammatory cells, especially in the mucosa and submucosa, but such positive cells were seldom observed in NS group. A positive correlation was found between the DNA-binding activity of NF-kappa B and ICAM-1 expression.</p><p><b>CONCLUSION</b>NF-kappa B activation is an important event in the development of DSS-induced colitis in that activated NF-kappa B upregulates ICAM-1 expression during colonic inflammation.</p>


Subject(s)
Animals , Male , Mice , Colitis , Metabolism , DNA , Metabolism , Dextran Sulfate , Electrophoretic Mobility Shift Assay , Immunohistochemistry , Intercellular Adhesion Molecule-1 , Mice, Inbred BALB C , NF-kappa B , Metabolism , Protein Binding , Random Allocation , Transcription Factor RelA , Metabolism
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