Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A pelvic limb paresis of 6 weeks duration in a yearling sheep resulted from protozoan encephalomyelitis involving the spinal cord at the thoracolumbar junction. An elevated lumbosacral cerebrospinal fluid protein concentration but normal cisternal cerebrospinal fluid protein concentration indicated the presence of a thoracolumbar inflammatory lesion resulting in cord compression which obstructed the rostral flow of the cerebrospinal fluid. Under general anaesthesia, myelography at the lumbo-sacral site demonstrated blockage to the rostral flow of contrast medium at T13/L1. At necropsy, there were no gross pathological changes at T13/L1, but histopathology revealed non-tract specific lymphocytic perivascular cuffing, axonal swelling and oedema in the spinal cord, characteristic of a protozoal encephalomyelitis. No parasites were detected in the multiple spinal cord sections examined but immunocytochemistry identified antigens cross-reactive with Sarcocystis spp. antigens in glial cells in these lesions.
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PMID:Protozoan encephalomyelitis causing pelvic limb paresis in a yearling sheep. 1603 13

Experimental autoimmune encephalomyelitis (EAE) in adult rodents is the standard experimental model for studying autonomic demyelinating diseases such as multiple sclerosis. Here we present a low-cost and reproducible glass window implantation protocol that is suitable for intravital microscopy and studying the dynamics of spinal cord cytoarchitecture with subcellular resolution in live adult mice with EAE. Briefly, we surgically expose the vertebrae T12-L2 and construct a chamber around the exposed vertebrae using a combination of cyanoacrylate and dental cement. A laminectomy is performed from T13 to L1, and a thin layer of transparent silicone elastomer is applied to the dorsal surface of the exposed spinal cord. A modified glass cover slip is implanted over the exposed spinal cord taking care that the glass does not directly contact the spinal cord. To reduce the infiltration of inflammatory cells between the window and spinal cord, anti-inflammatory treatment is administered every 2 days (as recommended by ethics committee) for the first 10 days after implantation. EAE is induced only 2-3 weeks after the cessation of anti-inflammatory treatment. Using this approach we successfully induced EAE in 87% of animals with implanted windows and, using Thy1-CFP-23 mice (blue axons in dorsal spinal cord), quantified axonal loss throughout EAE progression. Taken together, this protocol may be useful for studying the recruitment of various cell populations as well as their interaction dynamics, with subcellular resolution and for extended periods of time. This intravital imaging modality represents a valuable tool for developing therapeutic strategies to treat autoimmune demyelinating diseases such as EAE.
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PMID:Implanting glass spinal cord windows in adult mice with experimental autoimmune encephalomyelitis. 2437 39