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 microbial agent was isolated previously from a case of Viluy encephalomyelitis and named the 'KPN agent' after the initials of the patient. Here a detailed characterization of nucleic acids extracted from the purified KPN agent is presented. The agent contains both DNA and RNA, and has its own tRNAs and some other low-Mr RNAs, including 5S RNA. These findings, and the isolation of eukaryotic-type ribosomes, suggest that the KPN agent is not a virus, as believed before, but a more complex micro-organism, with protein-synthesizing capacity. The nucleotide sequence of the 5S RNA in the ribosomes of the KPN agent is identical with the sequence of 5S RNA of Acanthamoeba castellanii. The novel protozoan nature of the KPN agent is discussed in relation to other unusual properties of this micro-organism. Some implications of these results for the aetiology of Viluy encephalomyelitis are also discussed.
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PMID:Preliminary characterization of an organism isolated from a case of Viluy encephalomyelitis indicates a protozoal, rather than viral, aetiology. 242 25

Gliotoxin is a fungal metabolite belonging to the class of epipolythiodioxopiperazines which possesses both immunomodulating and anti-phagocytic activities. We have examined the effect of gliotoxin on passively induced allergic encephalomyelitis and report here that pulse treating activated experimental allergic encephalomyelitis (EAE) effector lymphocytes with gliotoxin inhibits, in a dose-dependent manner, their ability to transfer disease. Cells treated with 300 ng/ml are unable to replicate in vitro in response to concanavalin A stimulation, nor did they produce interleukin-2 (IL-2) following stimulation. Furthermore this concentration of gliotoxin also causes complete fragmentation of genomic DNA in treated cells, yet these cells are still capable of transferring clinical EAE. These data suggest that replication of donor lymphocytes in the recipient is not essential for the development of EAE.
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PMID:Replication of donor lymphocytes in recipients is not essential for the passive transfer of allergic encephalomyelitis. 245 57

DNAs from eight Chlamydia psittaci isolates (koala conjunctivitis, avian psittacosis, avian ornithosis, ovine abortion, ovine polyarthritis, sporadic bovine encephalomyelitis, and feline conjunctivitis) and one Chlamydia trachomatis isolate (lymphogranuloma venereum) were compared by restriction endonuclease and DNA probe analyses. Digestion with HindIII yielded a series of discrete fragments which allowed the differentiation of most isolates. A gene probe, pFEN207, which encodes the chlamydia-specific component of the lipopolysaccharide group antigen was used in Southern hybridizations. The probe was chlamydia specific and hybridized to a single BamHI fragment and multiple HindIII fragments in each isolate. The variation in size of the hybridizing fragments allowed easy differentiation of the isolates and may eventually lead to a meaningful subgrouping of the diverse group of disease agents presently included in the species C. psittaci.
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PMID:Comparison of Chlamydia psittaci isolates by restriction endonuclease and DNA probe analyses. 282 36

Defined DNA fragments of cloned Theiler's murine encephalomyelitis virus genome were used to construct procaryotic recombinant plasmids expressing viral genes 3C and 3D. In these plasmids (pEX-EMBL vectors), viral sequences are fused in-phase behind the Escherichia coli lac Z' gene which is under the control of the inducible lambda Pr promoter. Partially purified fusion proteins were used to immunize Balb/c mice. Sera monospecific for the viral protease 3C and polymerase 3D were obtained. These sera detected their corresponding antigens in situ in infected BHK cells using immunocytochemical reactions.
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PMID:Expression of Theiler's murine encephalomyelitis virus protease 3C and polymerase 3D in Escherichia coli and characterization of monospecific sera. 284 4

Cyclosporine is an 11 aminoacid cyclic peptide of fungal origin endowed with potent immunosuppressive activity. Unlike the conventional immunosuppressants, cyclosporine does not interfere with DNA metabolism, but it selectively and reversibly inhibits lymphocyte T-helper activation by inhibiting the production of interleukin-2 which plays a role in immune response development. Cyclosporine has little effect on lymphocytes B and does not modify the production of antibodies when it is in progress. The drug is effective in preventing spontaneous or autoantigen-induced auto-immune diseases in animals. The best studied models are experimental allergic encephalomyelitis, uveitis in the rat and spontaneous diabetes of BB rats. However, cyclosporine has no effect on diseases exclusively due to the pathogenic action of antibodies, such as spontaneous thyroiditis of the obese chicken. It is also possible to obtain a curative effect, this type of model being nearer to therapeutic conditions in humans than the previous models.
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PMID:[Cyclosporin and autoimmune diseases. 1: Experimental bases]. 355 Sep 87

Prazosin, an antagonist of the alpha 1-adrenoceptor, has been found to suppress the clinical and histologic expression of experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. This effect appears to be specific for the alpha 1-receptor. To determine the effect of this drug on vascular permeability to serum proteins and inflammatory cells, leakage of serum proteins into the central nervous system (CNS) was measured with [125I]albumin, and quantitation of cellular inflammation was determined by an estimation of total DNA. The results show that in both actively induced and passively transferred models of the disease, treatment with prazosin significantly suppresses leakage of serum proteins into the CNS but does not significantly suppress the increase of DNA. The results of the [125I]albumin studies additionally support the conclusion that the extent of vascular permeability to serum proteins in the spinal cord is a significant correlate of clinical disease. The results of the DNA estimation were at variance with the histologic evidence of cellular infiltration. We conclude that treatment with prazosin has a significant effect on the development of vascular edema in EAE. These results additionally validate a role for the adrenergic receptor in the development of EAE, and support the hypothesis that the primary site of action of prazosin is on the vascular alpha 1-adrenoceptor.
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PMID:Prazosin treatment suppresses increased vascular permeability in both acute and passively transferred experimental autoimmune encephalomyelitis in the Lewis rat. 378 88

A 37-year-old homosexual man with the acquired immune deficiency syndrome (AIDS) developed progressive, ultimately fatal, neurological deficits 12 weeks after a course of cutaneous zoster. Premortem radiological procedures and cerebrospinal fluid analyses were nondiagnostic. At postmortem examination, several opportunistic infections associated with AIDS were recognized. Throughout the brain, necrotic and demyelinative lesions were present, suggestive of progressive multifocal leukoencephalopathy. However, light microscopical examination showed numerous Cowdry type A intranuclear inclusions in astrocytes, oligodendrocytes, and neurons near the periphery of the lesions. Herpes zoster encephalomyelitis was diagnosed and confirmed by electron microscopy, peroxidase-antiperoxidase staining, and by Southern blot analysis of DNA extracted from brain tissue. This case provides insight into the pathogenesis of zoster-associated encephalomyelitis and suggests another agent to be considered in the differential diagnosis of encephalopathy in patients with AIDS and other disorders of immunological impairment.
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PMID:Progressive encephalitis three months after resolution of cutaneous zoster in a patient with AIDS. 396 60

In 2-mo-old Lewis rats immunized with bacterial lipopolysaccharides (LPS) precomplexed to guinea pig myelin basic protein (BP), the clinical and histologic manifestations of experimental allergic encephalomyelitis (EAE) were diminished compared with BP-treated controls. Similarly, in animals immunized with BP and challenged with BP-LPS at the same time or as long as 5 days after, the immunization with BP also inhibited the disease. That this capacity to reduce the incidence of BP-induced EAE is a unique property of LPS was suggested by the fact that other negatively charged molecules, such as DNA, RNA, and dextran sulphate, were not effective in inhibiting the clinical signs of EAE. After recovery from EAE induced by BP, some animals develop a recurrence of the disease if challenged with BP at appropriate intervals. However, after recovery from mild EAE induced by BP-LPS and after challenges with EAE-initiating BP antigens, secondary EAE was inhibited significantly.
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PMID:Experimental allergic encephalomyelitis in Lewis rats: inhibition by bacterial lipopolysaccharides and acquired resistance to reinduction by challenge with myelin basic protein. 616 59

DNA levels were measured in the spinal cords of Lewis rats during the development of and recovery from experimental allergic encephalomyelitis (EAE). Spinal cord DNA was first increased 11 days after immunizing the rats with guinea pig myelin and rose to levels four times that of the Freund's adjuvant controls at day 14, then subsided after day 22. Spinal cord DNA was still 150% of control levels 60 days after immunization. These DNA changes were compared with fluctuations in spinal cord acid proteinase in the same animals. Acid proteinase activity in EAE spinal cord increased later than the rise in DNA and attained a level of 170% of control at days 15-17, then subsided. Spinal cord DNA was higher in rats immunized with whole myelin than in those administered equivalent amounts of purified myelin basic protein. Furthermore DNA was higher in spinal cords of rats immunized with a larger dose of myelin (1.0 mg) than with a lower amount (0.5 mg). Various protease inhibitors including pepstatin, nitrophenyl p-guanidino benzoate, polylysine, and dipropionyl rhein, previously shown to protect Lewis rats against EAE, suppressed the increase of DNA in the spinal cord. Measurement of DNA increases in the spinal cord of EAE animals provides a convenient reproducible measurement of the severity of inflammation in the CNS and provides an objective criterion for assessment of the efficacy of various agents screened as possible therapeutic treatment for multiple sclerosis.
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PMID:DNA changes in spinal cords of rats with experimental allergic encephalomyelitis. 620 37

Pigeon herpes encephalomyelitis virus (PHEV) was stable at -70 C for at least 4 months. When stored at -20 C, the virus lost 80% of its infective titers in 4 months. When stored at -10 C, however, the titers decreased rapidly; no detectable virus remained within 12 weeks. PHEV was thermolabile: it was completely inactivated at 56 and 60 C for 10 and 2 min respectively. It was also killed by 1% cresol and 2% sodium hydroxide for two hr and 2% septol for 24 hr. Two-percent phenol or formaline for 2 hr, however, significantly decreased virus infective titers. Phenol-purified DNA extracted from PHEV showed an ultraviolet spectrum of typical nucleic acids that had ratios of absorbancies at 265 nm/280 nm between 2 and 2.3. The extracted viral DNA was infectious in chorioallantoic membrane and chick embryo fibroblast cell cultures, but it was not noninfectious when given to pigeons. DNA infectivity was destroyed by DNAse but not RNAse treatment. Extracted DNA was not neutralized by antiserum against the intact virus, and it lost its infectivity property when heated at 70 C for 10 min.
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PMID:Viral encephalomyelitis of pigeons. VI. Some physico-chemical properties of the virus and extracted viral DNA. 626 86


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