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)

We reported a case of acute disseminated encephalomyelitis (ADEM) after Streptococcus infection. Brain MRI (T2-weighted image) showed high intensity lesion in the gray matter in the acute phase. The high intensity pattern of the lesion was different from those in previously reported cases. The boy, aged 14, had fever late in August 1993. He had lumbago and back pain since September 3 and also leg weakness developed since September 7. He became unable to urinate on September 10 and was admitted on September 12. His consciousness became indistinct. We considered ADEM on the basis of high CSF level of myelin basic protein, clinical course, symptoms and MRI findings and began to administer steroid hormone on the second day after admission. He rapidly recovered. We reported here an atypical case of ADEM as to the antecedent infection and MRI lesion.
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PMID:[A case of acute disseminated encephalomyelitis with lesions in the cerebral gray matter on MRI in the acute phase]. 766 10

The lymphokine production of two T-cell clones, which both recognize epitopes within the encephalitogenic 139-151 sequence of myelin proteolipid protein, was examined after stimulation with immobilized antibodies to the CD3 moiety of the T-cell-receptor complex. Clone A1 produced interleukin (IL)-2 and interferon (IFN)-gamma, but no IL-4, while clone D5 produced IL-4, but no IL-2 or IFN-gamma. A1 therefore belongs to the T-helper type 1 (Th1) subset, while D5 is a Th2 clone. In addition, the Th1 clone induced severe experimental allergic encephalomyelitis (EAE), while the Th2 clone did not induce any signs of EAE. Synthetic peptides were used to demonstrate that these clones recognized slightly different epitopes within the 139-151 sequence. Histidine 139 was shown to be optimal for the stimulation of the Th2 clone, while the presence of this residue inhibited the stimulation of the Th1 clone. Th2 cells specific for an encephalitogenic peptide may be important in the regulation of encephalitogenic Th1 cells.
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PMID:Fine-specificity differences in the recognition of an encephalitogenic peptide by T helper 1 and 2 cells. 769 54

We report a 63-year-old man with progressive gait disturbance and dysarthria. The patient was apparently well until the age of 62 (February, 1990) when he noted unsteadiness of gait. Two months later, dysarthria appeared. He was admitted to Juntendo Izunagaoka Hospital on April 23, 1990. Neurologic examination revealed a mentally sound man with normal higher cerebral functions. Cranial nerves were unremarkable except for scanning speech. His gait was ataxic with positive Romberg sign. No motor weakness was noted, however, he had hypotonia and cerebellar ataxia. Deep tendon reflexes were retained and the plantar response was flexor. Pain, touch and vibration senses were diminished in the distal parts of the lower extremities. Laboratory examination revealed a 2.5 cm mass in the left lung field. Cranial MRI revealed a small T1-low and T2-high signal intensity lesion in the left temporal lobe. Abdominal CT scan revealed multiple low density lesions in the liver. His subsequent course was complicated by progressive deterioration in his gait and loss of deep tendon reflexes. He expired on November 24, 1990. The patient was discussed in the neurological CPC and the chief discussant arrived at the conclusion that the patient had anti-Hu associated paraneoplastic encephalomyelitis and sensory neuropathy. Some other participants thought that the patient had carcinomatous cerebellar degeneration. Postmortem examination revealed a 4x4 cm mass lesion involving the left S4-S5 segments. Histologic examination of the tumor was small cell carcinoma. Many metastatic foci were found in the liver. The cerebral hemispheres were unremarkable except for a small wedge-shaped tissue defect in the left temporal lobe which appeared to have been caused by old head trauma which the patient had received. The cerebellar vermis showed slight enlargement of cortical sulci, however, the cerebellar hemispheres appeared unremarkable. Upon histologic examination, marked loss of Purkinje cells was noted, particularly in the cerebellar anterior lobe. The dentate nucleus showed slight cell loss with increase in fat granule cells. The inferior olive was normal. The histologic characteristics were consistent with the pathologic diagnosis of carcinomatous cerebellar degeneration. No evidence of limbic encephalitis was seen. The peripheral nerve was not examined.
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PMID:[A 63 year-old man with progressive gait disturbance and dysarthria]. 888 38

Proton magnetic resonance imaging enables non-invasive monitoring of lesion formation in multiple sclerosis and has an important role in assessing the potential effects of therapy. T2-weighted and short tau inversion recovery magnetic resonance imaging were used to assess the effect of a neurotrophic adrenocorticotrophic hormone analogue [H-Met(O(2))-Glu-His-Phe-D-Lys-Phe-OH] on the volume of lesions in the brains of rats suffering from chronic experimental allergic encephalomyelitis, an animal equivalent of multiple sclerosis. Lesion volume was monitored during a five-month period. Magnetic resonance imaging indicated that treatment with the adrenocorticotrophic hormone analogue significantly reduced the lesion volume by 84 and 85% 10 and 20 weeks after lesion induction, respectively. Furthermore, peptide treatment significantly reduced chronic experimental allergic encephalomyelitis-related neurological symptoms during the chronic phase of the disease (week 3 until week 20 after lesion induction). Both functional and morphological recovery were considerably advanced by peptide treatment. Twenty weeks after lesion induction rats with chronic experimental allergic encephalomyelitis were killed for histological analysis, to correlate magnetic resonance imaging findings with morphological changes. The regions of abnormally high signal intensities on T2-weighted magnetic resonance images coincided with areas of demyelination and concomitant widespread inflammatory infiltration, oedema formation and enlarged ventricles. The improved neurological status and the 84% reduction in the lesion volume in the cerebrum of rats chronic experimental allergic encephalomyelitis point to the potential value of trophic peptides in the development of strategies for limiting the damage caused by central demyelinating lesions in syndromes such as multiple sclerosis.
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PMID:Longitudinal in vivo magnetic resonance imaging studies in experimental allergic encephalomyelitis: effect of a neurotrophic treatment on cortical lesion development. 913 Jul 95

Demonstration of the direct involvement of cranial blood vessels by varicella zoster virus (VZV) is facilitated by immunohistochemistry (IHC), in situ hybridization (ISH) and polymerase chain reaction (PCR) techniques. The extent to which an inflammatory vasculitis serves as the pathogenic mechanism for VZV encephalomyelitis (VZVE) is still, however, debated. Most VZVE patients are immunocompromised and show little inflammation, either pre-mortem in cerebrospinal fluid (CSF) or at autopsy. We describe an HIV-positive patient with a moderately depressed CD4 count (304) who presented with massively elevated CSF protein (1800 mg/dl), bloody CSF and pleocytosis (1300 white blood cells (WBC)/mm3). His CSF was positive for VZV DNA by PCR. He was treated with acyclovir and foscarnet, but died. At autopsy, an unusually widespread, inflammatory, transmural vasculitis caused by VZV affected meningeal vessels at virtually all brain stem and spinal cord levels, causing multiple subpial hemorrhages and necrosis. Virus DNA in multiple areas of brain, brainstem and spinal cord was readily revealed by PCR, but not by the presence of viral inclusions, IHC or ISH. This case, with a clinically confusing presentation for VZVE, illustrates the extensive, albeit infrequent, degree of necrotizing vasculitis and CSF abnormalities that VZV is capable of producing. Antiviral therapy may have inhibited VZV genome replication and subsequent antigen production, resulting in negative ISH and IHC studies, but generated increased VZV genomic fragments that were detectable by the more sensitive PCR technique.
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PMID:Profound cerebrospinal fluid pleocytosis and Froin's Syndrome secondary to widespread necrotizing vasculitis in an HIV-positive patient with varicella zoster virus encephalomyelitis. 974 10

Chronic experimental allergic encephalomyelitis (CEAE) is an established experimental model for multiple sclerosis (MS). The demyelinating lesions in the white matter of the central nervous system observed in CEAE and in MS are accompanied by various neurophysiological alterations. Among the best defined electrophysiological abnormalities are the changes in event-related potentials, in particular evoked potentials involving the spinal cord, i.e. motor and sensory evoked potentials. Less familiar are the changes observed in the electroencephalogram of CEAE-affected animals, which are also encountered in the human equivalent, MS. In the present experiment we evaluated the therapeutic value of a neurotrophic peptide treatment [H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH, an ACTH4-9 analogue] and its effect on the delayed flash visual evoked potentials (VEP) and power spectra of the electroencephalogram, during a 17-week follow-up of CEAE. CEAE animals treated with the neurotrophic peptide were protected against the development of neurological symptoms during the course of the demyelinating syndrome. VEPs of animals suffering from CEAE showed a delay of the latencies of the late components which was significantly counteracted by peptide treatment. The peak-to-peak amplitude of the VEP afterdischarge recorded from CEAE animals was significantly increased during the course of CEAE and correlated closely with the progression of the myelinopathy. Furthermore, CEAE animals showed an increase of electroencephalogram (EEG) beta activity of up to 500% as compared with the age-matched control group. This increase in beta power mainly consisted of a prevailing 20-21 Hz peak, a frequency that normally is not dominant in control EEG recordings of the rat during passive wakefulness. All these electrophysiological phenomena were absent in ACTH4-9 analogue-treated animals. The present findings underscore the potential importance of a neurotrophic peptide treatment in the pharmacotherapy of central demyelinating syndromes, and possibly of MS.
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PMID:Neurotrophic ACTH4-9 analogue therapy normalizes electroencephalographic alterations in chronic experimental allergic encephalomyelitis. 987 50

The 2A protein appears to be diverse among picornaviruses, in contrast to the other non-structural proteins, which have homologous structures and functions. In enteroviruses and rhinoviruses, 2A is a trypsin-like protease involved in protein processing and in shut-off of host-cell macromolecular synthesis. The aphthovirus and cardiovirus 2A is associated with an unusual processing event at the 2A/2B junction. It is shown here that the 2A protein of several diverse picornaviruses, the human parechoviruses, Aichi virus and avian encephalomyelitis virus, possess previously unrecognized conserved motifs and are likely to have a common function. Moreover, these motifs, a conserved histidine and flanking amino acids, an asparagine-cysteine dipeptide and a putative transmembrane domain, are characteristic of a family of cellular proteins, at least two of which are involved in the control of cell growth. These observations have important implications for an understanding of picornavirus genome structure and evolution, as well as pointing to possible functions of 2A in these viruses.
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PMID:The 2A proteins of three diverse picornaviruses are related to each other and to the H-rev107 family of proteins involved in the control of cell proliferation. 1064 May 59

Experimental autoimmune encephalomyelitis (EAE) is an inflammatory and demyelinating disease of the central nervous system and is an animal model of multiple sclerosis (MS). In the present report, a linear analogue and a series of cyclic semi-mimetic peptides were designed and synthesized based on the human myelin basic protein (MBP(87-99)) epitope (Val87-His-Phe-Phe-Lys-Asn-Ile-Val-Thr-Pro-Arg-Thr-Pro90) and on Copolymer I (a mixture of random polymers of Ala, Gln, Lys and Tyr used to treat MS). These analogues were designed looking for suppressors of EAE induced by guinea pig MBP(72-85) epitope (Gln-Lys-Ser-Gln-Arg-Ser-Gln-Asp-Glu-Asn-Pro-Val) in Lewis rats. The linear analogue [Arg91,Ala96]MBP(87-99), in which Arg substitutes Lys91 and Ala substitutes Pro96, was found to be a strong inhibitor which when administered to Lewis rats together with the encephalitogenic agonist MBP(72-85) completely prevented the induction of EAE. In contrast, three N- and C-termini amide-linked cyclic semi-mimetic peptides, [cyclo-Phe-Arg-Asn-Ile-Val-Thr-Ala-Acp (1), cyclo-Phe-Ala-Arg-Gln-Acp (2), cyclo-Tyr-Ala-Lys-Gln-Acp (3)] as well as a Lys side chain and C-terminous cyclic semi mimetic peptide cyclo(Lys, Acp)-Phe-Lys-Asn-Ile-Val-Thr-Ala-Acp (4) which contain segments of MBP(87-99) or are constituted from immunophoric residues of copolymer 1, were ineffective in inducing or inhibiting EAE in Lewis rats. However co-injection of cyclic analogues with MBP(72-85) delayed the onset of EAE indicating a modulatory effect on the EAE activity of MBP(72-85). These findings suggest that molecule length, size of cyclic moiety and backbone conformation are important elements for immunogenic activity. Moreover blockade of MBP(72-85) induced EAE by the unrelated peptide [Arg91,Ala56]MBP(87-99) could indicate that the mechanism of inhibition is not due to binding competition but rather due to the delivery of a negative signal by the antagonist which overcomes the agonist response possibly through the activation of antigen specific regulatory T cells.
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PMID:Treatment of experimental allergic encephalomyelitis (EAE) induced by guinea pig myelin basic protein epitope 72-85 with a human MBP(87-99) analogue and effects of cyclic peptides. 1100 34

The MHC class II molecule H2-A(s), expressed in the SJL mouse strain, is the principle restriction element of autoreactive CD4(+) T cells mediating experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. We deduced the H2-A(s) ligand motif from the analysis of naturally processed self peptides and from peptide binding studies. Major anchor residues were identified using various sets of substituted and truncated peptides, derived from natural peptide ligands and known H2-A(s) binders like myelin basic protein 81 - 99. The nine-residue H2-A(s) core binding motif comprises an arrangement of anchors in relative positions P1, P4, P6, P7, and P9. The P1 pocket is relatively unspecific and the P6 pocket favors hydrophobic-aliphatic side chains. The P1 pocket contributes little to peptide binding. Primary anchors were identified in P4, P7, and in particular in P9. The preferred anchor residues are Lys (P4), His/Arg (P7), and Pro (P9), respectively. Ala-polysubstituted peptides containing only one of these dominant anchor residues still retain the capacity to bind to H2-A(s). Thus, the presence of only one suitable anchor side chain in P4, P7, or P9 is sufficient for high-affinity peptide binding, at least in the absence of negatively charged side chains nearby. The identified ligand motif facilitates the analysis of immunogenic peptides interacting with H2-A(s) and will allow a better prediction of pathogenetically relevant peptide antigens in the autoimmune mouse model.
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PMID:Ligand motif of the autoimmune disease-associated mouse MHC class II molecule H2-A(s). 1118 Jan 20

A child with acute disseminated encephalomyelitis (ADEM) developed after acute herpetic gingivostomatisis was described. Inspite of the improvement of his gingivostomatitis, his consciousness gradually deteriorated and he was admitted to Nakadori General Hospital. His consciousness level was drowsiness and increased bilateral patellar reflexes were shown. Because magnetic resonance imaging (MRI) T2-weighted scan showed areas of high signal intensity disseminated in superior portion of medulla oblongata, dorsal portion of pons, basal nuclei and thalamus, he was suspected as having ADEM. Anti-herpes simplex virus (HSV) 1 IgG and IgM antibodies elevated in both blood and cerebrospinal fluid. From these results, HSV1 infection was thought to be the preceding infection of ADEM. Methylprednisolone therapy (20 mg/kg daily) for 3 days, followed by prednisolone (2 mg/kg) was started, with an excellent response. In addition, administration of acyclovir was also continued, considering the complication of HSV encephalitis. MRI T2-weighted scan performed at 2 months later after the onset of ADEM revealed disappearance of the lesions. He was discharged without remaining disorders. It is difficult to distinguish between ADEM and HSV encephalitis because both of these diseases show various neurological symptoms. In our case, MRI was the most useful method for correct diagnosis of ADEM. We concluded that ADEM is important as a disease of central nervus system due to HSV1 infection, in addition to encephalitis.
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PMID:Acute disseminated encephalomyelitis developed after acute herpetic gingivostomatitis. 1121 14


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