Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new method of pulsed Z-spectroscopic imaging is proposed for in vivo visualization and quantification of the parameters describing cross-relaxation between protons with liquid-like and solid-like relaxation properties in tissues. The method is based on analysis of the magnetization transfer (MT) effect as a function of the offset frequency and amplitude of a pulsed off- resonance saturation incorporated in a spoiled gradient-echo MRI pulse sequence. The theoretical concept of the method relies on an approximated analytical model of pulsed MT that provides a simple three-parameter equation for a pulsed steady-state Z-spectrum taken far from resonance. Using this model, the parametric images of cross-relaxation rate constant, content, and T(2) of the semisolid proton fraction can be reconstructed from a series of MT-weighted images and a coregistered T(1) map. The method was implemented on a 0.5 T clinical MRI scanner, and it provided high-quality 3D parametric maps within an acceptable scanning time. The estimates of cross-relaxation parameters in brain tissues were shown to be quantitatively consistent with the literature data. Clinical examples of the parametric images of human brain pathologies (multiple sclerosis and glioma) demonstrated high tissue contrast and clear visualization of the lesions.
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PMID:Pulsed Z-spectroscopic imaging of cross-relaxation parameters in tissues for human MRI: theory and clinical applications. 1197 72

We present a case of sudden-onset aphasia due to a single pathological lesion, which at neuroradiological imaging studies was suggestive of glioma, while on biopsy proved be of demyelinating nature. Every cause of demyelinating lesions of the central nervous system was considered in the differential diagnosis, concluding for a primary demyelinating disease. The clinical and radiological differences between multiple sclerosis and acute disseminated encephalomyelitis are discussed. Although aphasia has already been described in demyelinating diseases, we underline its rarity as onset symptom.
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PMID:Aphasia as a rare presentation of monosymptomatic demyelinating disease: case report and review of the literature. 1223 96

Alteration in the isoprenoid metabolites--digoxin, ubiquinone, and dolichol--have been reported in neuronal degeneration (Parkinson's disease), oncogenesis (central nervous system glioma), functional neuropsychiatric disorders (schizophrenia and epilepsy), and immune-mediated disorders (multiple sclerosis). The coexistence of these disorders has been documented in literature and a central dysfunction related to digoxin and the isoprenoid pathway may underlie all these disorders. A family with a high prevalence of Parkinson's disease, schizophrenia, neoplasms, syndrome X, rheumatoid arthritis, and epilepsy has been described. The psychological behavioral patterns of the family were: creativity and high IQ, hypersexual behavior, reduced appetite and eating behavior, insomnia and reduced sleep patterns, increased tendency for spirituality, increased tendency for addiction, less bonding and affectionate behavior, and left handedness/right hemispheric dominance. Digoxin, an endogenous Na(+)-K+ ATPase inhibitor secreted by the hypothalamus, was found to be elevated and red blood cell (RBC) membrane Na(+)-K+ ATPase activity was found to be reduced in all the disorders and in the indexed family studied. Hypothalamic digoxin can modulate conscious perception and its dysfunction may lead to schizophrenia. Digoxin can also preferentially upregulate tryptophan transport over tyrosine, resulting in increased levels of depolarizng tryptophan catabolites, serotonin, quinolinic acid, strychnine, and nicotine, and decreased levels of hyperpolarizing tyrosine catabolites, dopamine, noradrenaline, and morphine, contributing to membrane Na(+)-K+ ATPase inhibition in all the above disorders and the indexed family. Digoxin-induced membrane Na(+)-K+ ATPase inhibition can result in increased intracellular Ca2+ and reduced Mg2+ levels, leading on to glutamate excitotoxicity, oncogene activation, and immune activation. Digoxin-induced altered Ca2+/Mg2+ ratios, reduced ubiquinone, and increased dolichol can affect glycoconjugate metabolism, membrane formation and structure, and mitochondrial function, leading to the diverse disorders described above, including those in the indexed family. The isoprenoid pathway and neurotransmitter patterns were compared in right-handed/LH dominant and left-handed/RH dominant individuals. The left-handed/RH dominant individuals compared to right-handed/LH dominant individuals had elevated hydroxymethylglutarylcoenzyme A reductase activity, with increased serum digoxin and dolichol levels. The serum ubiquinone, serum Mg2+ and RBC Na(+)-K+ ATPase activity were reduced in left-handed/RH dominant individuals. The left-handed/RH dominant individuals compared to right-handed/LH dominant individuals had elevated levels of serum tryptophan, quinolinic acid, serotonin, nicotine, and strychnine. The levels of tyrosine, dopamine, noradrenaline, and morphine were low in left-handed/RH dominant compared to right-handed/LH dominant individuals. The hyperdigoxinemic state indicates right hemispheric dominance. Hypothalamic digoxin can thus function as the master conductor of the neuroimmunoendocrine orchestra and coordinate the functions of various cellular organelles.
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PMID:Central role of hypothalamic digoxin in conscious perception, neuroimmunoendocrine integration, and coordination of cellular function: relation to hemispheric dominance. 1232 12

Upregulation of the cAMP/protein kinase A (PKA) pathway has been shown to result in decreased proliferation, increased differentiation, and subsequent apoptosis of malignant glioma cells. Conventional cAMP analogs, however, are difficult to use in a clinical setting. Therefore, we investigated the effects of rolipram, a drug that has undergone clinical trials as an antidepressant and has also been proposed as a treatment for multiple sclerosis. Rolipram acts as a specific inhibitor of type IV phosphodiesterase (PDE4), leading to increased intracellular levels of cAMP. We report that the inhibition of PDE4 by rolipram results in the activation of the cAMP/PKA pathway, with potent stimulation of a reporter gene containing a cAMP-responsive element in its promoter region. Further, treatment of the human glioma cell line A-172 with rolipram results in increased expression of the cell cycle inhibitors p21(Cip1) and p27(KiP1), and decreased activity of cdk2, a cyclin-dependent kinase essential for cell cycle progression. As a result, the proliferation of A-172 cells is inhibited, with induction of a Gl block. Eventually, rolipram-treated A-172 cells undergo differentiation, which is followed by apoptotic cell death. As we observe this effect with other glioma cell cultures as well, our results suggest that rolipram could prove useful as a novel differentiating agent with both cytostatic and cytotoxic potential in the treatment of malignant gliomas.
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PMID:The type IV phosphodiesterase inhibitor rolipram induces expression of the cell cycle inhibitors p21(Cip1) and p27(Kip1), resulting in growth inhibition, increased differentiation, and subsequent apoptosis of malignant A-172 glioma cells. 1243 76

This study was undertaken to assess the contribution of the combination of (201)Tl SPECT and (99m)TcO(4)(-)SPECT to the differential diagnosis of brain tumors and tumor-like lesions. In the 8 patients selected for this study, both (201)Tl SPECT and (99m)TcO(4)(-) SPECT were performed because of clinical or radiological suspicion of brain tumor, no therapy was initiated before either SPECTs, diagnosis was based on biopsy, and MRI findings were stable in the interval between SPECTs. Histological diagnoses consisted of low grade glioma (n=1), high grade glioma (n=2), lymphoma (n=1), metastasis (n=1), multiple sclerosis (n=2) and cavernous angioma (n=1). Two high grade astrocytomas, one malignant lymphoma and one metastatic tumor showed (201)Tl accumulation and were diagnosed as tumor. The combination of (201)Tl and (99m)TcO(4)(-) did not change the diagnosis. One cavernous angioma showed no (201)Tl accumulation and was diagnosed as non-tumor. The combination of (201)Tl and (99m)TcO(4)(-) did not change the diagnosis. One low grade astrocytoma showed faint (201)Tl accumulation and was diagnosed as non-tumor. As (201)Tl uptake was higher than (99m)TcO(4)(-) uptake, the combination of (201)Tl and (99m)TcO(4)(-) changed the diagnosis to tumor. Two multiple sclerosis showed (201)Tl accumulation and were diagnosed as tumor. As (99m)TcO(4)(-) uptake was higher than (201)Tl uptake, the combination of (201)Tl and (99m)TcO(4)(-) changed the diagnosis to non-tumor. In three of the eight patients (38%), the combination of (201)Tl SPECT and (99m)TcO(4)(-) SPECT altered the diagnosis made by (201)Tl SPECT alone. In all of these three cases, the diagnosis made by the combination of (201)Tl SPECT and (99m)TcO(4)(-) SPECT was correct.
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PMID:Contribution of the combination of (201)Tl SPECT and (99m)T(c)O(4)(-) SPECT to the differential diagnosis of brain tumors and tumor-like lesions. A preliminary report. 1271 94

Monoclonal antibody J1-31 was raised against plaque materials taken from brains of patients who had suffered from multiple sclerosis (MS). Preliminary characterization of the antigen revealed it to be a protein of M(w) 68-70 kDa with both a cytoplasmic and nuclear localization. Here we report the results of isolation and peptide sequencing of the antigen from human brains, and immunocytochemical analysis of the antigen in F98 glioma cells. Purification and peptide sequencing indicate that the antibody recognizes a form of glial fibrillary acidic protein, possibly a phosphorylated variant. However, confocal immunocytochemistry and western analysis of F98 glioma cells raise the possibility that it also recognizes a phosphorylated epitope found in nuclear lamins. Analysis of the expression of the J1-31 epitope in F98 cells with respect to time in culture, cell density, and DNA synthesis showed a developmental relationship: cells that were engaged in rapid growth and DNA synthesis exhibited strong J1-31 staining in nuclei, whereas quiescent cells did not. We conclude that mAB J1-31 remains a useful antibody for studying multiple sclerosis, and is likely to prove useful in studies of the dynamics of nuclear lamins, particularly in models for wound-healing.
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PMID:GFAP and nuclear lamins share an epitope recognized by monoclonal antibody J1-31. 1276 17

We report on the use of serial proton MR spectroscopy ((1)H MRS) to differentiate between glioma and tumefactive plaque in a known multiple sclerosis (MS) patient who developed a symptomatic cerebral space occupying lesion. Gliomas and acute MS plaques may have indistinguishable chemical resonance spectra, whereas that of chronic plaque is distinct. In our case (1)H MRS demonstrated elevated concentrations of choline, lactate and lipid, with reduced N-acetyl aspartate, a pattern consistent with either low grade glioma or acute demyelinating plaque. A repeat study 4 months later showed no change, this was felt to be incompatible with the natural history of an acute plaque and low grade glioma was diagnosed. Surgical removal of the lesion revealed an oligodendroglioma, confirming the imaging findings.
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PMID:Use of serial proton magnetic resonance spectroscopy to differentiate low grade glioma from tumefactive plaque in a patient with multiple sclerosis. 1548 9

The membrane composition and the isoprenoid pathway metabolites important in maintaining cell membrane integrity was studied in neurological and psychiatric disorders. The results indicate alteration in cholesterol:phospholipid ratio of the RBC membrane which is increased in glioma, schizophrenia, and bipolar mood disorder (MDP); decreased in multiple sclerosis and Parkinson's disease; and not significantly altered in epilepsy. The concentration of total glycosaminoglycans (GAG), hexose, and fucose decreased in the RBC membrane and increased in the serum. The RBC membrane Na+-K+ ATPase activity was reduced and serum HMG CoA reductase activity was increased. There were increased serum levels of digoxin, cholesterol, and dolichol and decreased levels of ubiquinone. The serum magnesium and tyrosine levels were reduced and tryptophan increased. The results indicate a defect in membrane formation and a decreased membrane Na+-K+ ATPase activity in all the disorders studied. The results are discussed, and a hypothesis regarding the relationship between these disorders and defective membrane architecture and membrane Na+-K+ ATPase inhibition is presented.
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PMID:Isoprenoid pathway-related membrane dysfunction in neuropsychiatric disorders. 1458 55

Psychiatric abnormalities have been described in primary neurological disorders like multiple sclerosis, primary generalized epilepsy, Parkinson's disease, subacute sclerosing panencephalitis (SSPE), central nervous system glioma, and syndrome X with vascular dementia. It was therefore considered pertinent to compare monoamine neurotransmitter pattern in schizophrenia with those in the disorders described above. The end result of neurotransmission is changes in membrane Na(+)-K+ ATPase activity. Membrane Na(+)-K+ ATPase inhibition can lead to magnesium depletion, which can lead to an upregulated isoprenoid pathway. The isoprenoid pathway produces three important metabolites--digoxin, an endogenous membrane Na(+) -K+ ATPase inhibitor; ubiquinone, a membrane antioxidant and component of mitochondrial electron transport chain; and dolichol, important in N-glycosylation of protein. The serum/plasma levels of digoxin, dolichol, ubiquinone, magnesium, HMG CoA reductase activity, and RBC Na(+)-K+ ATPase activity were estimated in all these disorders. The result showed that the concentration of serum tryptophan and serotonin was high and serum tyrosine, dopamine, adrenaline, and noradrenaline low in all the disorders studied. The plasma HMG CoA reductase activity, serum digoxin, and serum dolichol levels were high and serum ubiquinone levels, serum magnesium, and RBC Na(+)-K+ ATPase activity were low in all the disorders studied. The significance of these changes in the pathogenesis of syndrome X, multiple sclerosis, primary generalized epilepsy, schizophrenia, SSPE, and Parkinson's disease is discussed in the setting of the interrelationship between these disorders documented in literature.
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PMID:Schizoid neurochemical pathology-induced membrane Na(+)-K+ ATPase inhibition in relation to neurological disorders. 1460 43

We report a 39-year-old female patient known to have multiple sclerosis (MS), who later developed cerebral glioblastoma. The tumor was documented on the brain-magnetic resonance imaging (MRI) during the work-up for an apparent relapsing MS, and was subsequently confirmed pathologically by stereotactic biopsy and the postmortem brain examination. Our case, as well as others, re-emphasizes the need to evaluate the symptoms and brain MRI carefully, even in well-documented MS subjects. The concurrence of MS and intracranial glioma is uncommon. The possible relationship between the 2 diseases was discussed, and related literature reviewed.
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PMID:Concurrence of multiple sclerosis and intracranial glioma. Report of a case and review of the literature. 1467 9


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