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)

Treatment of SJL/J mice with myelin components prior to infection with Theiler's picornavirus did not effect the development of inflammatory demyelinating lesions characteristic of Theiler's mouse encephalomyelitis. These results suggest that the pathogenesis of this disease differs from experimental autoimmune encephalomyelitis, which can be suppressed by such a treatment.
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PMID:Theiler's virus encephalomyelitis is unaffected by treatment with myelin components. 400 34

Every experiment with the contents of one, or with those pooled from two to five of the normal stock of Rockefeller Institute strain of albino mice, 1 to 2 months of age, revealed the presence of a virus which, after intracerebral inoculation into normal mice, induced characteristic paralytic encephalomyelitis, indistinguishable from Theilerapos;s disease. No difference was seen in this effect of intestinal contents deriving from animals paralyzed during the course of spontaneous encephalomyelitis and from normal mice. The influence of age on carriage of virus, as well as on the persistence of the carrier state, is discussed. The present, as well as previous work has shown that the virus found in normal (or paralyzed) mice is similar to that of Theiler's disease in all of its properties thus far investigated; among the strains of the latter now at hand it can be classified with those having a low degree of invasiveness after peripheral inoculation. The virus has thus far been recovered from intestinal contents, intestinal walls, and mesenteric glands but not from the central nervous system of normal mice; from these sites, as well as from the central nervous system, in paralyzed mice. In order of concentration of virus, the contents have more, the walls less, and the glands least.
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PMID:A TRANSMISSIBLE AGENT (THEILER'S VIRUS) IN THE INTESTINES OF NORMAL MICE. 1987 Oct 11

A specific complement fixation test can be obtained in various central nervous system virus infections by using as antigens emulsions of infected brain tissue, freezing and thawing the brain emulsion, and then centrifuging it in an angle head centrifuge at 3500 R.P.M. for 1 hour. The method has proved reliable in the case of rabies, St. Louis encephalitis, Japanese B encephalitis, lymphocytic choriomeningitis, Eastern equine encephalomyelitis, Western equine encephalomyelitis, louping ill, and spontaneous encephalomyelitis of mice (Theiler's disease). The specificity of the reaction, regardless of the virus involved, requires different temperatures of inactivation of the sera according to animal species: 56 degrees C. for guinea pig, 60 degrees C. for mouse, and 65 degrees C. for rabbit and dog sera, all heated for 20 minutes. For human sera a temperature of inactivation of 60 degrees C. also for 20 minutes has been adopted; at this temperature the reaction is in general specific. Complement-fixing antibodies in high titre were found in the sera of rabbits, guinea pigs, mice, and dogs immunized with rabies virus. Complement-fixing antibodies were present in high titre in sera drawn from two persons 8 years after an attack of louping ill, from five persons 2(1/2) years after an attack of Eastern equine encephalomyelitis, and from two persons 2(1/2) years after Western equine encephalomyelitis. In cases of St. Louis encephalitis and lymphocytic choriomeningitis, complement-fixing antibodies have been found shortly following infection but not after long periods.
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PMID:THE COMPLEMENT FIXATION TEST IN THE DIAGNOSIS OF VIRUS INFECTIONS OF THE CENTRAL NERVOUS SYSTEM. 1987 Nov 44