Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015674 (chronic fatigue syndrome)
2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with intracranial tumors (ICT) and acute cerebral infarctions (CI), both necrosis and reversible changes occur in central nervous system (CNS) tissue. The damaged CNS cells release specific substances into the cerebrospinal fluid (CFS). Radioimmunoassay (RIA)-determined myelin basic protein (MBP) and RIA-determined creatine kinase BB (CK-BB) are markers of damage to CNS specific structures. The elevated CSF level of MBP is considered a marker of myelin damage and the increased concentration of CSF CK-BB may be of combined neuronal and astrocytic origin. CSF was collected from 57 patients with the diagnosis of CI (n = 30) and ICT (n = 27) and the concentration of MBP and CK-BB were measured by RIA. Our study shows increased CSF levels of MBP and CK-BB in patients with CI and patients with ICT. We have also found a linear correlation between MBP and CK-BB in both CI and ICT, and for a given CK-BB level, MBP was significantly higher in patients with ICT than in patients with CI. These facts suggest that lesion markers behave differently in the different pathologic processes affecting the CNS.
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PMID:Myelin basic protein and creatine kinase BB isoenzyme as CSF markers of intracranial tumors and stroke. 242 41

We examined 100 symptomatic Gulf War veterans (patients) and 100 controls for immunologic assays. The veterans and controls were compared for the percentage of T cells (CD3); B cells (CD19); helper:suppressor (CD4:CD8) ratio; natural killer (NK) cell activity; mitogenic response to phytohemagglutin (PHA) and pokeweed mitogen (PWM); level of immune complexes; myelin basic protein (MBP) and striated and smooth muscle autoantibodies; and antibodies against Epstein-Barr virus, cytomegalovirus, herpes simplex virus type 1 (HSV-1), HSV-2, human herpes Type 6 (HHV-6), and Varicella zoster virus (VZV). The percentage of T cells in patients versus controls was not significantly different, whereas a significantly higher proportion of patients had elevated T cells compared with controls. The percentage of B cells was significantly elevated in the patients versus the controls. The NK cell (NK) activity was significantly decreased in the patients (24.8 +/- 16.5 lytic units) versus the controls (37.3 +/- 26.4 lytic units). The percentage of patients with lower than normal response to PHA and PWM was significantly different from controls. Immune complexes were significantly increased in the patients (53.1 +/- 18.6, mean +/- SD) versus controls (34.6 +/- 14.3). Autoantibody titers directed against MBP and striated or smooth muscle were significantly greater in patients versus controls. Finally, the patients had significantly greater titers of antibodies to the viruses compared with the controls (p < 0.001). These immune alterations were detected 2-8 years after participation in the Gulf War. The immune alterations are consistent with exposure to different environmental factors. We conclude that Gulf War syndrome is a multifaceted illness with immune function alterations that may be induced by various factors and are probably associated with chronic fatigue syndrome.
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PMID:Cellular and humoral immune abnormalities in Gulf War veterans. 1517 70