Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper reports the effects of supplementation of the diet with linoleic acid on the severity of experimental allergic encephalomyelitis (EAE) in guinea pigs. Clinical signs of disease (e.g. paresis, paraplegia, urinary incontinence), weight loss, frequency of perivascular lesions in the central nervous system and ability of isolated lymph node cells to respond to myelin basic protein in vitro were all reduced by linoleic acid supplementation. Linoleic acid was effective when fed at a dose of 0.5 ml/day from 7 to 21 days after sensitization of the animals with basic protein, i.e., before and during the time in which clinical signs normally appeared. The same daily dose fed from 7 days before to 7 days after sensitization, i.e., ceasing about 7 days before the normal time of appearance of clinical signs, produced no significant effect. Feeding linoleic acid to normal guinea pigs significantly altered the fatty acid composition of their serum and lymph nodes, but not of their brain. Of several possible explantations for the protective effect of lineolic acid in EAE, we considered action by this essential fatty acid on the immune system most likely.
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PMID:Reduction by linoleic acid of the severity of experimental allergic encephalomyelitis in the guinea pig. 63 36

Prophylactic administration of Piroxicam (Feldene), a reversible inhibitor of prostaglandin biosynthesis, significantly reduced the occurrence of paralytic signs and the amount of antibodies against myelin basic protein in the model of mild acute experimental allergic encephalomyelitis in the Lewis rat. Mononuclear infiltration of the central nervous system remained unaffected. A therapeutic intervention with piroxicam, however, increased paresis and CNS pathology. Immunohistochemical studies revealed an increased proportion of ED1-positive macrophages and monocytes in the infiltrates of the spinal cord in animals treated with piroxicam. Possible reasons for the different effects of the prophylactic and therapeutic treatment are discussed in the study.
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PMID:Experimental allergic encephalomyelitis-prophylactic and therapeutic treatment with the cyclooxygenase inhibitor piroxicam (Feldene). 193 15

The identification of radiation myelopathy using biochemical assays and imaging techniques has not previously been accomplished but has clear clinical application. Measurement of myelin basic protein (MBP) in the cerebrospinal fluid (CSF) and visualization of the spinal cord using magnetic resonance imaging (MRI) gives a potentially accurate diagnosis of radiation myelopathy. Female New Zealand white rabbits were irradiated to the thoracic spinal cord with single doses of 15-45 Gy. Animals receiving higher doses (greater than or equal to 22 Gy) generally demonstrated an early paresis (4-8 weeks) that temporarily improved, and then progressed to complete paralysis by 14-18 weeks. MBP levels in the CSF became strikingly elevated to 100-1000 times the normal value. Subsequent, experiments in which rabbits were serially assessed for MBP levels demonstrated a transient elevation, which corresponded to the transient paresis, followed by dramatic elevations concurrent with the onset of paralysis. Magnetic resonance imaging (MRI) of the irradiated spinal cord showed a geographically distinct region of abnormality that corresponded to the radiation field. Histopathology demonstrated demyelination, focal astrocytosis, erythrodiapedesis, and perineuronal edema in the irradiated sections. It appears that MBP levels in the CSF reflect not only radiation-induced myelopathy but also transient demyelination, and that MRI may have the potential to indicate the region of damage.
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PMID:Myelin basic protein and magnetic resonance imaging for diagnosing radiation myelopathy. 246 19

The immunotherapeutic potential of three anti-rat CD2 monoclonal antibodies (mAb) (OX34, OX54, OX55) and the combination of OX54 with OX55 was tested in Lewis rat experimental autoimmune encephalomyelitis (EAE). In actively induced EAE, a single injection of OX34 2 days before immunization with myelin basic protein (MBP) in complete Freund's adjuvant (CFA) completely prevented or greatly attenuated EAE in all animals. Injection of OX54 acted moderately suppressive while OX55 or OX54/55 did not affect disease severity. Abrogation of EAE by OX34 was not restricted to its application before immunization. Therapeutic administration of all three mAb and the Ab combination from onset of first clinical signs efficiently blocked progression of disease and prevented all animals from developing hind limb paresis. In adoptive transfer EAE induced with in vitro activated cells of an encephalitogenic T helper line, clinical and histological signs were completely prevented by injection of OX34 on the day of cell transfer and 4 days later, underlining the strong impact of anti-CD2 mAb on the effector phase of disease. Immunocytofluorometric analysis of peripheral blood lymphocytes after a single Ab injection demonstrated that all mAb induced a variable degree of transient reduction in T cell numbers and modulation of CD2 antigens. In contrast to the other mAb, OX34 persisted on lymphocytes for at least 11 days, which may explain its unique suppressive effect on EAE after a single injection before immunization. The assumption that prophylactic administration of OX34 also inhibits MBP-induced EAE, due to persistence into the effector phase, was substantiated by the finding that none of the mAb prevented generation of an antigen-specific cellular response in MBP/CFA-immunized animals. Since none of the Ab induced T cell unresponsiveness or inhibited T cell activation by antigen- or Ab-mediated stimulation of the T cell receptor, we suggest that their marked action on the effector phase of EAE may rely on inhibition of T cell infiltration into the central nervous system. The demonstrated efficacy of these anti-CD2 mAb in EAE suggests a potential therapeutic role that may be equal to that of anti-CD4 or anti-T cell receptor Ab.
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PMID:Suppression of experimental autoimmune encephalomyelitis in Lewis rats by antibodies against CD2. 753 58

Paralytic tremor (pt) is a neurological sex-linked recessive mutation in rabbits which is characterized by a coarse body tremor and limb paresis. Morphological studies showed that this mutation affects CNS myelination. Although the number of oligodendrocytes is not reduced, myelination is slower, irregular and defective. We have made a biochemical and molecular analysis of 4-wk-old mutant and normal rabbits. The amount of myelin in the mutant represents only approximately 25% of the normal level. Radioimmunoassay for myelin basic protein showed a reduction to approximately 40% in pt whole-brain homogenate but the difference was not significant in purified myelin. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of brain homogenates followed by immunoblotting showed that all major myelin proteins are affected by the pt mutation, although to different degrees. While most of the myelin proteins are reduced to approximately 60-80% of the normal level, an important reduction to approximately 30%, was measured for the proteolipid protein (PLP). In purified myelin, the difference in PLP concentration was significant while the other specific proteins were less affected. A similar reduction in myelin-protein gene expression was detected at the mRNA level. Sex-linked transmission, low concentrations of PLP and its specific mRNA in the CNS indicate that the pt mutation primarily affects the expression of the Plp gene.
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PMID:Paralytic tremor (pt) rabbit: a sex-linked mutation affecting proteolipid protein-gene expression. 827 12

Cytokine production by T cells in the cerebrospinal fluid (CSF) and central nervous system (CNS) of SJL/J mice during myelin basic protein (MBP)-induced experimental allergic encephalomyelitis (EAE) was examined. Reverse transcriptase/polymerase chain reaction (RT/PCR) was used to measure interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) mRNA levels from perfused CNS tissue (brain and spinal cord) and from cells isolated from CSF. Animals were grouped according to EAE severity, ranging from asymptomatic (adjuvant only) to severe disease (paralysis or severe paresis). Cytokine signals, normalized to actin, were almost undetectable in control tissues, and only slightly elevated in whole CNS tissue from animals with mild EAE. Both cytokine messages were strongly upregulated in CNS tissues derived from severely affected animals, consistent with previous observations correlating disease progression with infiltration by memory/effector CD4+ T cells, the major source of these cytokines. This cytokine upregulation was specific to the CNS, since other organs from the same animals did not express significant levels of IL-2 and IFN-gamma. CSF was obtained from the cisterna magna of unperfused mice and verified as such by absence of red blood cells (RBCs) and by immunoglobulin concentration orders of magnitude lower than in serum. Cytokine message was measured in RNA isolated from cells in CSF. Levels of IL-2 and IFN-gamma mRNA in CSF cells were significantly elevated in mild EAE and strongly upregulated in severe disease, correlating with those in total CNS tissue. These results confirm the CSF as representative of the immune status of the CNS and indicate a role for IL-2 and IFN-gamma in inflammatory CNS disease.
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PMID:Cytokine production by cells in cerebrospinal fluid during experimental allergic encephalomyelitis in SJL/J mice. 829 48

Oral administration of acetylcholine receptor (AChR) or myelin basic protein (MBP) to Lewis rat prior to immunization with AChr or MBP and complete Freund's adjuvant (CFA) has previously been shown to prevent or delay the onset of experimental autoimmune myasthenia gravis (EAMG) or experimental allergic encephalomyelitis (EAE), which represent animal models of myasthenia gravis and multiple sclerosis, respectively. Here we show that Lewis rats immunized with AChr+MBP+CFA developed both signs of muscular weakness seen in EAMG and paresis characteristic for EAE. This disease was associated with high levels of anti-AChR and anti-MBP antibody secreting cells and of AChR- and MBP-reactive INF-gamma secreting Th1-like cells in lymph nodes. The diseased rats also showed upregulation of AChR- and MBP-induced mRNA expression of IFN-gamma in lymph node cells. Oral tolerization with AChR and MBP in combination prior to immunization with AChR+MBP+CFA alleviated clinical disease as well as AChR- and MBP-specific B cell node cells. The results implicate that oral tolerization simultaneously to more than one autoimmune disease-related autoantigen is feasible, and that suppression of autoantigen-induced IFN-gamma and augmentation of TGF-beta are pivotal in tolerance induction.
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PMID:Suppression of experimental autoimmune myasthenia gravis and experimental allergic encephalomyelitis by oral administration of acetylcholine receptor and myelin basic protein: double tolerance. 855 28

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa
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PMID:[A 76-year-old man with loss of vision and dementia]. 928 74

Experimental autoimmune encephalomyelitis (EAE) is a T cell-mediated autoimmune disease of the CNS and an animal model for the human demyelinating disease, multiple sclerosis. In the Lewis rat, myelin basic protein (MBP)-CFA-induced EAE is an acute monophasic disease from which animals recover fully, do not relapse, and develop a robust long-term resistance to further active reinduction of disease. In this paper, we report that rats recovering from MBP-CFA-induced EAE have significantly increased serum levels of reactive nitrogen intermediates indicative of increased NO production. These levels remain elevated after the recovery period and increase even further early after a rechallenge with MBP-CFA, and all animals are totally refractory to a second episode of disease. Oral treatment of rats with N-methyl-l -arginine acetate (l -NMA), beginning at peak disease on day 11 postimmunization, results in significant prolongation of disease and an alteration in the presentation of clinical symptoms from that of solely hind limb paresis/paralysis to severe fore limb involvement as well. Treatment of fully recovered rats with l -NMA 24 h before a rechallenge with MBP-CFA leads to decreased serum reactive nitrogen intermediate levels and results in a second episode of EAE in 100% of animals. Furthermore, l -NMA treatment of fully recovered rats in the absence of a rechallenge immunization leads to spontaneous relapse of disease.
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PMID:Nitric oxide plays a critical role in the recovery of Lewis rats from experimental autoimmune encephalomyelitis and the maintenance of resistance to reinduction. 1058 85

A 4-year-old boy showed two episodes of encephalitis/encephalopathy involving disturbed consciousness, convulsion, and paresis associated with the elevated levels of protein and myelin basic protein of the cerebrospinal fluid. MRI studies of the brain revealed symmetrical lesions in the brain stem and thalami at the first episode, and additional lesions were found in the cerebellum involving both the gray and white matter in the second episode. The intensities of MRI lesions were low in T I and high in T2. These episodes were followed by an elevation of the anti-viral antibody titers, for influenza A virus during the first episode and for adenovirus during the second. In the second episode, intravenous methylprednisolone therapy resulted in rapid improvement of his neurological signs.
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PMID:Acute relapsing encephalopathy mimicking acute necrotizing encephalopathy in a 4-year-old boy. 1059 58


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