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)

Chick embryo fibroblast cultures of the C/O phenotype (leukemia--free) infected with eastern equine encephalomyelitis (EEE) virus were incubated in the presence of 15 micrograms/ml N-methyl-N-nitro-N-nitrosoguanidine in the culture medium. Seven (5%) temperature-sensitive mutants were isolated from cell homogenates only in those cases where cell cultures before infection had been treated with actinomycin D. The recovered ts mutants are characterized by the marked ts- phenotype and genetic stability. The method of obtaining EEE virus ts mutants under the effect of N-methyl-N-nitro-N-nitrosoguanidine in C/O phenotype (leukemia-free) chick embryo fibroblast cultures treated before virus inoculation with actinomycin D is discussed.
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PMID:[Ts mutants of the Eastern equine encephalomyelitis virus. Their generation, isolation and preliminary characterization]. 300 84

A case of an encephalomyelitis in a child with acute lymphoblastic leukemia is reported. The patient was a 5-year-old boy who developed seizures, progressive confusion, and coma after radiation and intrathecal methotrexate therapy. Computed tomography (CT) of the brain showed bilateral hypodensities in the posterior parietal and temporal regions. At autopsy, perivascular inflammation, microglial nodules without intranuclear viral inclusions, and bilateral necrosis of the temporoparietal and hippocampal regions were seen in the brain and spinal cord. Paraneoplastic encephalomyelitis is generally recognized in adult patients with underlying malignancy but, to our knowledge, has not been reported in children with leukemia. This report should alert the clinicians to an entity that must be included in the differential diagnosis of leukemic children with progressive neurologic disorder.
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PMID:Encephalomyelitis associated with leukemia in a child. 347 99

The perivascular spaces of the central nervous system are involved in various pathological situations. The aim of this paper is to focus on the histopathological lesions of the perivascular spaces which commonly occur in the infectious (bacterial, viral, parasitic), tumoral (carcinoma, lymphoma, leukemia), demyelinating (multiple sclerosis, allergic encephalomyelitis) and vascular diseases of the brain. According to their apparent function in each of these situations an attempt was made to classify the main physiopathological processes involving the perivascular spaces into 3 distinct groups. The perivascular spaces may be considered as follows: (1) double way route between the parenchyma and the leptomeningeal space (extension to the brain of a meningeal pathological process, drainage of parenchymal wastes); (2) elective location of the inflammatory reaction partly as a result of the presence of connective tissue; (3) site of particular lesions such as dilatation, the pathogenesis of which remains unclear.
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PMID:[Pathology of perivascular spaces in the central nervous system]. 650 82

A case report of a 53 year old male with hairy cell leukaemia is presented in whom encephalomyelitis caused by toxoplasmosis resulted in an influx of hairy cells into the cerebrospinal fluid following disruption of the blood-brain barrier. These cells subsequently disappeared as the barrier reformed. It is suggested that the presence of hairy cells in the cerebrospinal fluid is a secondary self-limiting phenomenon.
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PMID:Hairy leukaemic cell influx into the cerebrospinal fluid secondary to encephalomyelitis. 823 15

A patient with acute lymphoblastic leukaemia was mistakenly given vincristine intraventricularly, as part of an intensified course of chemotherapy. Despite a CNS washout and supportive treatment, the patient developed progressive ascending paralysis, gradually lapsed into coma and died some 10 days later. Autopsy and post-mortem histological examination showed evidence of brain death caused by florid encephalomyelitis, apparently induced by the intraventricular administration of vincristine.
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PMID:Accidental intraventricular vincristine administration: an avoidable iatrogenic death. 891 96

Bilateral facial paralysis is an unusual clinical entity that occurs in less than 1% of patients with facial paralysis. In children bilateral facial paralysis is even more rare, and establishing its etiology can be challenging. Four pediatric patients ranging in age from 3 to 17 years are presented who developed bilateral facial paralysis as a result of acute otitis media, Lyme disease, recurrent central nervous system leukemia, and acute disseminated encephalomyelitis. The diagnosis and treatment of pediatric bilateral facial paralysis are reviewed, as well as the pertinent literature.
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PMID:Pediatric bilateral facial paralysis. 954 63

Since Morton and Siegel's epochal experiments 30 years ago animal models have been successfully utilized both for transfer and resolution of autoimmune diseases (AID). More recently human lymphocyte xenografts have reproduced clinical AID in SCID mice. Allogeneic stem cell transplantation demonstrated therapeutic potential in fully developed autoimmune disease. Mixed allogeneic chimerism induced by a sublethal approach has also been shown to prevent and even reverse autoimmune insulitis in nonobese diabetic (NOD) mice. More unexpectedly it was found that experimental adjuvant arthritis (AA) and experimental allergic encephalomyelitis (EAE) could be cured by means of total body irradiation (TBI) followed by autologous hemolymphopoietic stem cell (HSC) transplantation. It was postulated that the newly developing T cells might be tolerant to self antigens. The transfer of AID from affected donors to recipients of allogeneic HSC transplants has been reported for many organ-specific AID, including diabetes (IDDM), thyroiditis, myasthenia gravis and thrombocytopenic purpura (AITP); rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) were not transferred. Conversely patients with the combination of AID and a severe blood disease (leukemia, aplasia) were cured of both diseases following allogeneic BMT, with the notable exception of a relapse in a patient with RA despite full donor engraftment. Allogeneic transplants are certainly more promising as far as concerns a resolution of AID, because they may also exert a graft-versus-autoimmunity effect by gradually eradicating the recipient's lymphopoiesis, but transplant related mortality (TRM) is considered still too high to employ this procedure consistently. New non-myeloablative conditioning regimens, designed to allow the donor's immune system to take over, are already utilized for malignant and non-malignant hematologic diseases, and may become an attractive option for severe, refractory AID. For the time being, however, autologous procedures are still safer, and are being utilized in many projects worldwide. The EBMT/EULAR Registry has collected over 70 patient reports. The more numerous and favorable results have been obtained up to now in multiple scleosis and in systemic lupus erythematosus; the worst in refractory autoimmune thrombocytopenic purpura. No definite conclusions as to the efficacy of autologous HSC transplantation, from marrow or from blood, with or without T-cell depletion, may be drawn at this time, but the feeling is that real cures will be very difficult to obtain by this approach, and that corticosteroid-free remissions and a general lowering of the autoimmune potential will be more realistic goals. Accurate comparisons with already existing aggressive immunosuppressive protocols will become necessary, if possible by means of prospective randomized clinical studies.
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PMID:Stem cell transplantation for severe autoimmune diseases: progress and problems. 979 58

The treatment of severe autoimmune diseases has been recently revitalized by the increasing utilization of clinical interventions aimed at ablating/abrogating autoimmune lymphoid clones followed (but not in certain procedures) by transplantation of allogeneic, but also autologous, hematopoietic stem cells. Two different investigative avenues have paved the way to specific clinical studies. The first originates from the epochal murine experiments of the '70s, and has been greatly expanded in the last decade. A graft-versus-autoimmunity effect could also be demonstrated. In addition, it could also be shown that induced experimental autoimmune diseases such as adjuvant arthritis and autoimmune encephalomyelitis could, surprisingly, be cured following autologous transplantation. The first results in humans were observational and derived from studies including patients with coincidental diseases (severe autoimmune diseases plus leukemia/aplasia) treated with allogeneic hematopoietic stem cell transplants. Although the concept of an allogeneic transplant is indisputably more appealing, very few patients with an isolated severe autoimmune disease have been treated using such a therapeutic approach. Reduced intensity conditioned transplants relying on subsequent graft-versus-autoimmunity effects strengthened by donor lymphocyte infusions are being explored cautiously. On the other hand, autologous transplants are being performed quite extensively. To date, transplanted severe autoimmune diseases include multiple sclerosis, connective tissue diseases (systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis) and many others. It is uncertain if the main mechanism is solely immunoablative, or whether tolerized lymphocytes may also develop during a postulated "window of opportunity" following the transplant.
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PMID:[Immunoablation or otherwise followed by hematopoietic cell stem as intensive treatment of severe autoimmune diseases]. 1197 10

Tissue plasminogen activator (tPA) is expressed by many types of neurons in the developing and adult rodent brain. We have now mapped tPA transcripts and protein in the human central nervous system using tissue arrays and find widespread expression, in particular in neocortical mantle, thalamus, amygdala, and hippocampal pyramidal neurons. The abundant presence of tPA protein in cellular vesicles implies that its acute release, e.g. upon ischaemic stroke or trauma, could play a role in neuronal damage. We also found in patients with multiple sclerosis (MS), and to a lesser extent patients with leukaemia and encephalitis, prominently elevated tPA activity in the cerebrospinal fluid and in MS in neurons in the proximity of areas of demyelination elevated tPA mRNA and antigen levels. In addition, we observed up-regulation of tPA expression in a mouse model of MS, experimental autoimmune encephalomyelitis. Accumulating evidence implies roles for tPA in normal neural function, as well as in neurodestructive processes in humans, such as occur in MS and brain tumours and warrant further studies on expression of tPA and its regulatory molecules in neurodegenerative diseases.
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PMID:Tissue plasminogen activator as a key effector in neurobiology and neuropathology. 1202 48

The A8 virus is a molecular clone of the neuropathogenic FrC6 virus derived from the Friend murine leukemia virus (F-MuLV). To elucidate the effects of A8 virus-infection on immune-mediated diseases in the central nervous system, we investigated the development of acute and monophasic experimental autoimmune encephalomyelitis (EAE) in A8 virus-infected Lewis rats. In EAE rats after A8 virus infection (A8-EAE), many inflammatory cells were found in the gray matter including the frontal lobe, where almost no inflammatory cells were found in rats with EAE alone. The modified distribution of inflammatory cells was not dependent on the ages of A8 virus-infected rats, although the frequency of the modified distribution was reduced in older rats. The chimeric virus Rec2, which contains the pol and env genes of 57 virus on the background of A8 and does not induce spongiform degeneration in the CNS, caused the same distributional modification of inflammatory cells in the rats with EAE as in A8-EAE rats. Furthermore, the incidence and intensity of spongiform degeneration, thymoma and splenomegaly caused by A8 virus were reduced by the induction of EAE.
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PMID:Neuropathology of experimental autoimmune encephalomyelitis modified by retroviral infection. 1256 68


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