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

Changes in a posttranslational modification of tubulin, which accompany differentiation, have been studied in neuroblastoma-glioma hybrid cultured cells. The modification consists of the reversible enzymatic addition of a tyrosine to the COOH terminus of the alpha chain. Cytoplasmic tubulin purified from undifferentiated cells resembled that from adult mammalian brain in that half was in a form which can not accept tyrosine; of the remainder, which is a substrate for tubulin-tyrosine ligase, a higher proportion had COOH-terminal tyrosine. In the tubulin from differentiated cells, in which there had been extensive assembly of axonal microtubules from a preformed pool of subunits, the nonsubstrate tubulin was almost entirely replaced by the species with COOH-terminal tyrosine. In living cells, in the absence of protein synthesis, there was fixation of labeled tyrosine into cytoplasmic alpha chains which was extensive enough to be consistent with turnover, during the course of an hour, of the pre-existing COOH-terminal tyrosine. The alpha chain in the particulate fraction of the cells was comparably labeled, along with some unidentified low molecular weight components.
 ...
PMID:Tubulin tyrosylation in vivo and changes accompanying differentiation of cultured neuroblastoma-glioma hybrid cells. 50 Jun 54

Brain samples were taken in macroscopically oedematous zones during 21 operations for malignant glioma, and studied with the electron microscope. Oedema was found in 17 cases, mostly as serous extracellular fluid. Vascular changes in the oedema region are mostly as serous extracellular fluid. Vascular changes in the oedema region are mostly secondary to oedema: the origin of oedema fluid ought to be found in the tumour proper. Cellular reaction is slight; neuronal lesions may be ascribed mostly to a perturbation of axonal flow. Oedema round malignant gliomas and oedema round other malignant or benign tumours are morphologically distinct.
 ...
PMID:The brain surrounding malignant gliomas: an ultrastructural study. 69 43

Secondary mediator compounds are postulated to have a role in vasogenic oedematogenesis. They may also cause focal brain dysfunction due to their neuronal, axonal and glial modulating properties. Using the feline model of infusion brain oedema the effects of right frontal intracerebral infusion (200 microliters/hr for 3 hrs) of saline, bradykinin (10(-4) to 10(-6) M), arachidonic acid (10(-2) to 10(-3) M), 20% protein and four human glioma cyst fluids were evaluated. Somatosensory evoked potentials (SSEP), motor evoked potentials (MEPs), rCBF and rCBF CO2 reactivity (Hydrogen clearance). ICP, craniospinal compliance, local brain tissue water content (microgravimety), brain histology and BBB function (Evans Blue 2%) were measured. Brain water content increased locally from 69% to 79%, ICP increased (by mean 14 mmHg) and compliance decreased (mean 70%) and there were the histological features of brain oedema with all infusates. BBB opening occurred with Bradykinin (+), arachidonic acid (++), 20% protein ( ) and glioma cyst fluid (4+). Polymorphic and macrophage infiltrates were seen with all infusions but rCBF and MEPs remained normal. SSEPs changed with high dose bradykinin and some glioma cyst infusates whilst CBF CO2 reactivity was locally impaired by all infusates except saline and arachidonic acid. This study suggests that certain compounds in brain oedema fluid could mediate local brain dysfunction.
 ...
PMID:The contribution of secondary mediators to the etiology and pathophysiology of brain oedema: studies using a feline infusion oedema model. 212 86

Glia-derived nexin (GDN), also known as protease nexin I, is a serine protease inhibitor of deduced relative molecular mass 41,700, identified in conditioned media of glioma cells by its neurite-promoting activity. GDN can promote neurite outgrowth in vitro from neuroblastoma cells, sympathetic neurons and hippocampal neurons (L. Farmer et al., manuscript in preparation). In vivo, GDN is constitutively expressed in all parts of the olfactory system, where axonal regeneration and neurogenesis occur continuously throughout life. This observation indicates that GDN could be important for axonal regeneration in vivo. To investigate this possibility, we have taken advantage of the fact that damage to nerves in the peripheral nervous system leads to their regeneration, whereas in the central nervous system no such regeneration can occur. Here we report that after lesion of the rat sciatic nerve there is a large transient increase in the amount of GDN messenger RNA and of released GDN. The cells showing GDN immunoreactivity are mainly localized distal to the lesion site. These results further support the suggestion that GDN is important for axonal regeneration in vivo, and indicate that protease inhibitors could have a role in Wallerian degeneration and peripheral nerve regeneration.
 ...
PMID:Induction of glia-derived nexin after lesion of a peripheral nerve. 268 11

Three patients developed the sudden onset of total blindness several months after treatment with oral CCNU and low-dose whole-brain radiation. The anterior visual system was included in the radiation field in all patients. Radiotherapy was given for a frontal-lobe glioblastoma multiforme, for central nervous system prophylaxis in a patient with oat cell carcinoma of the lung, and for a parietal-lobe glioblastoma multiforme. None of the neoplasms involved the anterior visual system. The radiation dose ranged from 3000 to 4650 rad and the oral CCNU dosage from 300 mg to 1050 mg. Patients 1 and 2 also received other chemotherapeutic agents. Patient 3 who was treated only with oral CCNU and cranial irradiation died. At autopsy the brain showed a widely infiltrating residual high-grade glioma as well as patchy coagulative necrosis with swollen axons and dystrophic calcifications. The optic chiasm showed severe demyelination, axonal loss, and hyalinized vessels. Synergism between oral CCNU and radiation may account for the blindness produced.
 ...
PMID:Sudden onset of blindness in patients treated with oral CCNU and low-dose cranial irradiation. 302 94

This paper describes the immunohistochemical staining properties of four monoclonal antibodies (MAbs) (CF, EB, AD, and KB) which had been previously shown to be specific for purified neuron-specific enolase (NSE) by a solid-phase radioimmunoassay. In this study, the authors immunostained a spectrum of normal and neoplastic neuronal, "neuroendocrine," and nonneuronal tissues fixed in formalin and embedded in paraffin. Positivity was generally restricted to normal neuronal structures and neuronal tumors, including adrenal neuroblastoma, ganglioneuroblastoma, olfactory neuroblastoma, pheochromocytoma, carotid body paraganglioma, duodenal gangliocytic paraganglioma, and teratoma with neuroepithelial components. Three staining patterns of the normal or neoplastic neuronal structures were observed: two MAbs (CF and EB) stained predominantly the nerve fibers (axoplasm); one (AD) stained predominantly the cell bodies (perikaryon); and one (KB) stained both the axoplasm and the perikaryon. "Neuroendocrine" tumors such as pulmonary small cell carcinoma, pancreatic islet cell tumor, thyroid medullary carcinoma, and carcinoid tumors from various locations showed a variable staining pattern. Tumor cells undergoing mitotic division were usually positive regardless of type. Normal structures other than neuronal or "neuroendocrine," including normal glial cells, were negative. The authors also studied a range of glial cell tumors with MAbs CF and AD as well as with Dako polyclonal antiserum to NSE. The results showed that CF stained the axonal fibers in the normal white matter surrounding these tumors; it did not stain the tumor cells or the perikarya of neurons in the surrounding normal gray matter. AD stained the glioma cells as well as the perikarya and dendrites of neurons in the surrounding normal gray matter; it did not stain the axonal fibers in the surrounding normal white matter. By contrast, the polyclonal antiserum stained all of these structures. The high degree of staining specificity of the MAbs should prove them to be valuable in immunohistochemical diagnosis of tumors as well as in further understanding the role of NSE in neuronal differentiation.
 ...
PMID:Immunohistochemical characterization of a set of monoclonal antibodies to human neuron-specific enolase. 328 44

A number of neural and nonneural tumor cell lines of rat and human origin were assayed for neuron-specific enolase (NSE) by radioimmunoassay. Most neural tumor cell lines had appreciably higher levels of NSE than did the nonneural tumor cell lines, the highest levels being found in two anaplastic rat glioma lines ( F98 and T24). These two lines contained more than twice the amount of NSE found in a rat pheochromocytoma line (PC12) and in neuroblastoma lines derived from rats ( B35 and B50 ) or humans (IMR-32 and SHSY - 5Y ). Several of the rat glioma and schwannoma lines were inoculated intracerebrally into syngeneic rats. In the resulting tumors, NSE was demonstrable by immunohistochemistry only in those from the F98 and T24 cell lines. A number of ethylnitrosourea-induced rat tumors were also examined immunohistochemically for NSE: NSE was demonstrated in three anaplastic gliomas; three astrocytomas; and two mixed gliomas. Reactive astrocytes were also positive. Fibroadenomas of apocrine and mammary glands in rats were weakly positive, but other extraneural tumors tested were negative. Since normal neuronal elements, axonal swellings, and amine precursor uptake and decarboxylation cells are strongly positive for NSE, whereas glia and most other normal cells are negative, we hypothesize that the elevated metabolic demands imposed on neoplastic and reactive glial cells and on some extraneural tumors necessitate the opening up of metabolic pathways that are normally operative only in neurons and neuroendocrine cells, therefore resulting in the synthesis of the more stable neuron-specific form of enolase.
 ...
PMID:Immunoradiometric and immunohistochemical demonstration of neuron-specific enolase in experimental rat gliomas. 672 96

To test the hypothesis that glial-derived factors exert differential effects on neurons in developing and aged brain, we treated NB2a/d1 neuroblastoma cells with conditioned medium (CM) obtained from C6 glioma cells. Undifferentiated NB2a/d1 cells rapidly (< 4 h) elaborated neurites in response to CM. Cells previously differentiated by 14 days treatment with 1 mM dbcAMP, which induces outgrowth of axonal neurites, exhibited no obvious effects when exposed to CM. By contrast, CM was toxic to cells that were treated with 1 mM dbcAMP for 7 days followed by 7 days in which dbcAMP had been reduced to 0.1 mM or withdrawn. These results highlight the potential of glial-derived factors to exert trophic and toxic effects depending upon neuronal differentiation state.
 ...
PMID:Toxic and trophic effects of glial-derived factors on neuronal cultures. 801 52

'Reactive' astrocytes and 'activated' microglial cells are the major cellular components of gliotic tissue, one of the most serious obstacles to axonal regeneration in mammalian central nervous system grey and white matter. The appearance of reactive glial cells after a lesion in the CNS correlates with the expression of molecules, like proteoglycans, capable of preventing neurite outgrowth. Co-cultures of embryonic neurones with glial cells and glial cell lines, that might share characteristics with reactive astrocytes and microglial cells, show that while cultured astrocytes promote neurite outgrowth, plasma membranes of C6 glioma and microglial cells express neurite inhibitory activities with proteoglycan-like characteristics, similar to those expressed by the gliotic tissue associated inhibitors. These results suggest that in vivo microglial cells might be at least one of the sources of proteoglycans with neurite outgrowth inhibitory properties.
 ...
PMID:Neurite outgrowth inhibitors associated with glial cells and glial cell lines. 829 1

In vitro and animal studies have identified molecules in mammalian CNS myelin which inhibit neuritic extension and which may be responsible, at least in part, for the lack of axonal regeneration after injury in the injured brain, optic nerve and spinal cord. To determine whether such inhibitory activity may be present in human CNS myelin, we used a bioassay to characterize neurite outgrowth on this substrate. Human CNS myelin strongly inhibited neuritic outgrowth from newborn rat dorsal root ganglion neurons and NG-108-15 cells, a neuroblastoma-glioma hybrid cell line. Similar but less potent inhibitory activity was identified in human gray matter. The CNS myelin inhibition of neuritic outgrowth appeared to be dependent on direct contact between the myelin substrate and neurites. The inhibitory activity in human CNS myelin closely resembled that described in adult rodents. Inhibition of neurite growth by human CNS myelin in this in vitro bioassay mirrors the lack of regeneration in vivo and can be used as a model to develop strategies designed to enhance axonal regeneration and neural recovery.
 ...
PMID:Human central nervous system myelin inhibits neurite outgrowth. 878 92


1 2 3 4 5 6 7 Next >>