Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of neuropsychiatric systemic lupus erythematosus (NP-SLE) is clinical and one of exclusion. Brain cross-reactive lymphocytotoxins or neuronal antibodies have been proposed as a mechanism underlying NP-SLE. We assessed the clinical relevance of neuronal cell binding antibodies using a standardized clinical definition of NP-SLE. Serum from 54 SLE patients and 77 controls were tested for binding to 3 neuroblastoma and 3 glioblastoma cell lines. Thirty-three SLE patients (61%) fulfilled clinical criteria for the diagnosis of NP-SLE; of these, 55% had serum binding activity to both neuroblastoma and glioblastoma cell lines, compared with 33% of the other SLE patients. When reactivity to neuroblastoma cell lines only was assessed, 43% of NP-SLE patient sera demonstrated binding activity, versus 14% of sera from the remaining SLE patients. Control subjects' reactivity to neuroblastoma cell lines was positive in 12% of sera. Analysis of serum reactivity using non-neuronal cell lines revealed that neuroblastoma, but not glioblastoma, cell binding was specific. NP-SLE patients with evidence of diffuse symptomatology had a higher mean titer of neuroblastoma cell line binding than those with focal symptomatology. Using a panel of substrates, one can identify a significant proportion of patients who are independently defined as having NP-SLE, who demonstrate specific serum neuronal antibodies.
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PMID:Antineuronal antibodies in neuropsychiatric systemic lupus erythematosus. 401 26

There are three types of interferons (IFN), alpha, beta and gamma. IFN-alpha is produced in the leukocytes infected with virus, while IFN-beta is from fibroblasts infected with virus. IFN-gamma is induced by the stimulation of sensitized lymphocytes with antigen or non-sensitized lymphocytes with mitogens. It is believed that IFN-alpha and beta originated from the same ancestral gene, whereas IFN-gamma did not. IFN has not only an antiviral activity, but also various kinds of biological activities including cell growth inhibition, immunosuppressive effects, enhancement of macrophage, natural killer (NK) cell, killer (K) cell and neutrophil functions, and cell differentiation-inducing activity. IFN also shows the antitumor activity resulting from the integration of the above-mentioned biological activities. IFN is also deeply involved in the pathogenesis of various diseases, e.g., collagen diseases such as SLE and rheumatoid arthritis, insulin-dependent diabetes mellitus, fulminant hepatitis, severe pancreatitis, nephritis, multiple sclerosis, allergic diseases, and atherosclerosis. At present, IFN is clinically used in therapy against virus infections such as hepatitis B and C, and for malignancies such as renal cell carcinoma, multiple myeloma, malignant melanoma, glioblastoma, skin cancers, malignant lymphoma and chronic myelogenous leukemia.
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PMID:[Interferon-alpha, beta, gamma]. 799 28