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)

Motor activity has been followed in rats during an experimental allergic encephalomyelitis (EAE). The disease was produced by transfer of lymph node cells from sensitized syngenic donors. Small and large movements were permanently registered by an electric activity meter. It could be demonstrated that a decrease of the motility is an early symptome of the disease. Therefore the measurement of the motoric activity might be a useful parameter in the classification of EAE.
Experientia 1979 Sep 15
PMID:Decrease in motor activity - an early symptom in the course of experimental allergic encephalomyelitis (EAE). 31 8

Intraneural injection of sera from rabbits with experimental allergic encephalomyelitis, induced by sensitization with bovine brain white matter in complete Freund's adjuvant, produced focal primary demyelinative lesions in rat sciatic nerves. Demyelinating activity was removed by prior incubation of antisera with central (CNS) and peripheral nervous system (PNS) myelin but not with liver or kidney, and was heat-labile and complement-dependent. Recipient animals developed a sensorimotor disturbance of their toes and ankles on the side injected with antiserum. Twenty minutes after antiserum injection, Schwann cells showed focal cytoplasmic outpouching and their external mesaxons opened. Between 1 and 8 hours after injection vacuolation, splitting and vesiculation of myelin became increasingly prominent at Schmidt-Lanterman clefts and paranodal regions, with concomitant degenerative changes in Schwann cell cytoplasm. Polymorphonuclear cell infiltration and endoneurial edema were apparent at this time. Substantial demyelination occurred before the appearance of phagocytic cells. Between 8 hours and 3 days many nerve fibers were surrounded and attacked by invading macrophages. Axons became demyelinated progressively over several internodes by macrophage phagocytosis. Early signs of remyelination were observed by 5 days. These findings suggest that antibodies directed against antigens common to both CNS and PNS myelin can produce in vivo peripheral nerve demyelination.
J Neuropathol Exp Neurol 1979 Sep
PMID:Peripheral nerve demyelination induced by intraneural injection of experimental allergic encephalomyelitis serum. 46 69

Suppurative meningitis should be recognized as being a complication of varicella. The clinician must assiduously exclude suppurative meningitis that at times may be clinically indistinguishable from the typical postinfectious encephalomyelitis of varicella. Misdiagnosis of the cause of CNS alterations during the course of varicella is possible.
Am J Dis Child 1979 Sep
PMID:Postvaricella suppurative meningitis. Case reports and review of the literature. 47 44

The effect of X-irradiation on experimental vaccinia infection of BALB/c mice was studied. As compared with nonirradiated controls, the X-irradiated animals exhibited (i) a time lag in virus replication (delayed, but protracted replication); (ii) a delayed and repressed immune response: (iii) more severe acute cytocidal infection of leptomeninges, choroid plexus, ependyma, and vessels, with extensive damage to the brain-barrier system; and (iv) noncytocidal, latent infection of glial cells and neurons. Several animals developed acute or subacute demyelination disease, resembling experimental allergic encephalomyelitis or postinfectious encephalomyelitis.
Infect Immun 1979 Sep
PMID:Vaccinia virus infection of the central nervous system in X-irradiated mice. 50 Jan 84

The clinical and pathological features of a fourth patient with progressive encephalomyelitis with rigidity are reported and compared with those previously described. It is suggested that the muscular rigidity, abnormal postures, painful muscular spasms, and myoclonus are a product of excessive and abnormal discharges of alpha motor neurones caused by their release from control by spinal internuncial neurones. A count of neuronal perikarya in the ventral horns confirmed that the disease selectively destroyed small and medium sized neurones, most of which were spinal internuncial neurones. Experimental, clinical, and pathological evidence concerning spinal internuncial neurones is reviewed and found to conform to this theory. The pathogenesis of opsoclonus may be similar.
J Neurol Neurosurg Psychiatry 1979 Sep
PMID:Spinal internuncial neurones in progressive encephalomyelitis with rigidity. 50 76

Epsilon aminocaproic acid, an inhibitor of plasminogen and trypsinogen activators, can decrease the severity of experimental allergic encephalomyelitis (EAE) in rats. The drug was tried because of a number of observations suggesting that neutral proteases, such as plasmin, might be chemical mediators of demyelination. The highest concentrations of plasminogen activator are found in the walls of veins and venules, around which demyelination is common in many demyelinating diseases, including MS. Indeed, the earliest lesion in MS is often demyelination with little cellular infiltration. In vitro studies have shown that neutral proteases secreted by activated macrophages selectively lyse myelin basic protein.
Neurology 1978 Sep
PMID:The modification of experimental allergic encephalomyelitis with epsilon aminocaproic acid. 56 43

Sxteen pure metals were implanted as pellets of powder or as wires into the brains of rats. Al, Be, Cr, Fe, Pb, Sn, and W were relatively innocuous. Mg and Mn produced local necrosis. Bi, Cd, Co, Cu and Ni produced more severe local necrosis. Viable tissue adjacent to Co and Ni necrotic lesions had some perivascular lymphocytic infiltrates. Zn implants caused very little necrosis but adjacent areas had prominent perivascular lymphocytic cuffs. The infiltrates persisted for at least 4 weeks but disappeared as soon as the zinc was removed. Some compounds of zinc were also capable of inducing infiltrates. The perivascular infiltrates resembled the lesions of allergic encephalomyelitis, but there was no correlation between the ability of metal powders to induce lymphocytic infiltrates after intracerebral implantation and their adjuvancy after intraperitoneal injection with neural antigen.
J Neuropathol Exp Neurol 1978 Sep
PMID:Lymphocytic inflammation produced by intracerebral implantation of zinc and other metals. 69 Jun 68

Since 1962, when Jamaica experienced its first and only outbreak of eastern equine encephalomyelitis (EEE), surveillance for the causative virus has been in progress. Wild birds, rodents, mosquitoes, sandflies and sentinels (domestic chickens, guinea pigs, mice and hamsters) have been constantly examined for EEE virus and serological conversion. In essence, only negative results have been obtained. Since June 1976, domestic chickens have been investigated as a possible reservoir and several have been found to have haemagglutinating antibodies, with titres ranging from 1:10 to 1:160. These titres fell rapidly, eg, from 1:160 to 1:10 within 60 days. These results incriminate the domestic fowl as a major reservoir for the virus, and suggest that the life of immunoglobulins against EEE is short in birds. Thus, the large number of negative serological tests found in previous investigations might be misleading since positive sera might have been missed between intervals of capture and recapture of the birds. The results indicate that investigators could usefully modify their procedure by bleeding wild birds as early as one to two weeks after initial capture. The importance and duration of the dominant avian anti-EEE virus immunoglobulins should be investigated.
Res Vet Sci 1978 Sep
PMID:The role of chickens in the epidemiology of eastern equine encephalomyelitis virus in Jamaica. 72 35

The changes in the glial cell reactivity depended on the phase and severity of the pathological process in the experimental allergic encephalomyelitis induced in guinea pigs by injection of Mycobacteria tuberculosis in a mixture of arlacel and vaselin. These reactivity changes measured by the method of inhibition of the glial cell migration in the tissue culture was specific of the nervous tissue antigens. The same changes in the reactivity could be induced in the tissue culture of the glial cells from the intact animals by the addition of sera or the lymph node cells from the actively sensitized guinea pigs. The present data did not allow to attribute the changes in the glial cell reactivity to the products of destruction of the nervous tissue only to the action of the humoral or the cell factors (elements) penetrating into the CNS from the blood vessels or the lymphatic tissue.
Biull Eksp Biol Med 1975 Sep
PMID:[Reactivity of the neuroglia in guinea pigs sensitized with Mycobacteria tuberculosis]. 81 99

In this work we demonstrate a suppressive activity on the induction of experimental allergic encephalomyelitis (EAE) in Lewis rats, transferable to syngeneic animals, challenged with encephalitogenic mixture (myelin basic protein, complete Freud's adjuvant plus Bordetella pertussis organisms) 24 h later. This activity is probably effected by T cells and not by (an) inhibitory serum factor(s). The induction of this specific protection could be due to the penetration of the myelin basic protein antigen into the thymus where we first found suppressive cells. From the thymus, suppressor cells could then emigrate to spleen (on day 15) and to nondraining lymph nodes (on day 17). In the course of normal EAE in Lewis rats and especially at the time of self cure, this suppression is not demonstrated, but possible.
Eur J Immunol 1977 Sep
PMID:Evidence for suppressor cells in Lewis rats' experimental allergic encephalomyelitis. 92 33


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