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)

The intracellular volume of neoplastic brain cells was investigated with regard to the effects of hypo-osmolality and hyperosmolality utilizing double isotopic labeling with 3-0-methyl-D-glucose or tritiated water to measure the total volume of the pellet and inulin or polyethyleneglycol to measure the extracellular volume of the pellet. The cellular pellets were rapidly separated from the incubation medium by centrifugation after addition of an oil mixture. After 60 minutes incubation in Hanks balanced salt medium, the intracellular volume was 7.50 +/- 0.64, 8.48 +/- 0.19, and 2.97 +/- 0.18 ml H2O per 10(6) packed cells for C-6 glioma cells, N18TG-2 neuroblastoma cells, and NG108-15 neuroblastoma X glioma hybrid cells, respectively. The extracellular trapped space of these cultured cells was about one third of the intracellular volume. The intracellular volume of C-6 glioma cells was increased in hypotonic environment, whereas it was decreased with hyperosmolality. Both intracellular sodium and potassium were increased with increased osmolality of the incubation media. These data indicate iso-osmotic regulation by tumor cells, i.e., there is a good correlation between the intracellular volume, intracellular cations and lactate levels of C-6 glioma cells under various osmotic conditions.
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PMID:Intracellular volume of osmotically regulated C-6 glioma cells. 717 79

In 27 pentobarbital-anesthetized cats cerebral blood flow and regulation of cerebral blood flow was measured one to 3 weeks following stereotactical xenotransplantation of a rat glioma clone into the internal capsula. Tumor growth was accompanied by severe vasogenic peritumoral edema in the white matter of the tumor-bearing hemisphere. White matter water content in the vicinity of the tumor increased from 69.1 +/- 0.9 to 0.5 +/- 0.7 ml/100 g wet weight (means +/- SE) which corresponds to an increase in tissue volume of about 60%. Intracranial pressure after 3 weeks was 12 +/- 2.6 mm Hg. Blood flow in the peritumoral white matter decreased from 32.2 +/- 5.6 to 18.6 +/- 1.9 ml/100/g/min but it did not change in the peritumoral grey matter or the opposite hemisphere. The decrease in blood flow was due to the volume expansion of the swollen edematous tissue and not to a compression of the microcirculation because neither flow nor vascular resistance changed when referred to dry rather than to wet weight of the edematous tissue. Flow regulation in the peritumoral edematous white matter was disturbed. CO2 reactivity of blood flow was 5.4% mm Hg change in aPCO2 (non-edematous contralateral white matter 6.4%/mm Hg), and the autoregulatory capacity between 40 and 170 mm Hg was 0.7%/mm Hg (non-edematous white matter 1.0% mm Hg). It is concluded that in the absence of significant intracranial hypertension, even severe degrees of vasogenic peritumoral edema do not interfere with blood flow and flow regulation. This is in contrast to the cytotoxic type of edema, and indicates that microcirculatory compression by edema, when present, is the consequence of pericapillary glial hydrops and not of an accumulation of extravasated edema fluid.
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PMID:Blood flow and regulation of blood flow in experimental peritumoral edema. 723 66

The penetration of [3H]thymidine, [3H]D-leucine, [125I]albumin, and the drugs [3H]5-fluorouracil and [3H]vinblastine into human glioma spheroids (in vitro tumor models) was studied by a method based on rapid freezing, freeze drying, vapor fixation, wax embedding, dry sectioning, and contact autoradiography. No significant disturbances in the distribution of water soluble substances were observed. Thymidine and D-leucine penetrated the whole spheroids relatively fast, whereas albumin showed reduced penetration. The concentration of albumin was highest at the periphery of the spheroids, but only smaller amounts were detected in the deeper regions. A significant difference between the penetration patterns of the drugs studied was also observed. Fluorouracil penetrated rather freely, but the penetration of vinblastine was limited.
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PMID:Penetration of substances into tumor tissue--a methodological study on cellular spheroids. 723 41

Six-month-old Fischer rats (F344) were given the carcinogen methylnitrosourea in their drinking water. Of the induced brain tumors, four were established in culture and propagated as 78FR-G-219 (pleomorphic glioma), 78FR-G-299 (astrocytoma), 78FR-G-284 and 78FR-G-344 (mixed glioma) permanent lines. All cell lines produced S-100 protein and grew as tumors when inoculated s.c. or i.c. in syngeneic hosts. A comparative study of the antigenicity of these lines at different passage levels was carried out using native and chemically modified cells. Syngeneic rats were immunized with cells conjugated with dimethylsulfate and trinitrobenzene sulfonic acid. The immune response was characterized and quantified by an indirect immunofluorescence method and by a complement-dependent microcytotoxicity test. Chemical modification of the tumor cells enhanced antigenicity of the treated cells. The best results were attained with trinitrobenzene sulfonic-acid-treated cells and constituted a two-fold increase in the cytotoxicity index. Cytotoxicity values varied in the different cell lines. Antisera raised with trinitrobenzene sulfonic-acid-modified cells of all lines cross-reacted with cells of all lines. Cytotoxicity values were insignificantly reduced by absorbing the antisera with a variety of syngeneic tissues. Antisera raised against native syngeneic brain cells showed virtually no cytotoxicity for glioma cells. Antisera raised against syngeneic brain cells treated with trinitrobenzene sulfonic acid, however, were slightly cytotoxic for normal brain cells and glioma cells as well. The results of the present studies show that antigenicity of glioma cells can be definitely raised with trinitrobenzene sulfonic acid treatment. Furthermore, it would seem that haptenization of glioma-associated antigens may be a promising approach ot the study of glioma-host interactions.
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PMID:The humoral antibody response of rats immunized with chemically modified syngeneic brain cells and glioma cells. 723 19

In some cases of glioma, it may be relatively difficult to demonstrate by computed tomography (CT), or even by contrast enhancement technique (CE). Studying a series of delayed CT scans, it seems that one of the main factors of delayed CE effect is due to extravascular components of iodine. So for getting better CE effect in these gliomas, we tried to increase the extravascular iodine concentration with utilizing the returning water of intravenously administrated Glycerol. By this method of drip injection of contrast material following the Glycerol, we could get an increase of CE effect of 40 or 70% comparing to the usual drip injected CE scans in two benign gliomas, but we couldn't find the difference in one malignant glioma and in the high vascular area of the benign gliomas. Though the mechanism was not completely explained in this article, we thought that CE effect in malignant gliomas or high vascular tumors was mainly by intravascular component of iodine. This malignant glioma a big cyst, and with the use of intravenous contrast material and delayed CT scanning, we had been able to know that contrast media entered cystic collections, which progressively increased in density and were maximally enhanced on delayed, 180 minutes after injection of contrast material.
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PMID:[A role of glycerol in contrast enhancement (author's transl)]. 724 92

Capillary permeability of rat brains bearing ethylnitrosourea induced rat glioma was measured with quantitative autoradiography. In the small tumors (less than 2mm in diameter), no changes in capillary permeability was noted. When tumors became larger and neovascularization of the tumor occurred, increase in capillary permeability was evident. This change was more prominent in the center of the tumor than in the periphery. In the large tumors, the capillary permeability was markedly increases, and the value was similar to that in the choroid plexus. This indicates that blood-brain barrier(BBB) completely disappeared in the large tumors. This BBB change may be the main cause of tumor induced brain edema. The data also provide the information about pharmacokinetics of water soluble drugs in the brain tumors.
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PMID:[Changes of blood-brain barrier in the ethylnitrosourea induced rat glioma (author's transl)]. 732 57

Experimental brain tumours were produced in cats by stereotactic implantation of 4 million suspended cells of a rat glioma clone into the internal capsule. Three weeks after implantation a spherical tumour developed with a diameter of up to 10 mm which was surrounded by vasogenic white matter oedema. In untreated animals water content in the peritumoural white matter increased form 69.1 +/- 0.9 to 80.0 +/0 0.8 ml/100 g w. w., and regional blood flow reciprocally decreased from 32.2 +/- 5.6 to 18.9 +/- 0.05 ml/100 g/min. A single injection of a crystalline suspension of 10 mg/kg dexamethasone given intramuscularly one week before the animals were killed, led to a significant amelioration of brain oedema. Peritumoural white matter water content decreased to 73.0 +/- 0.5 ml/100 g w w. and blood flow rose to 35.7 +/- 2.8 ml/100 g/min. These changes were accompanied by parallel shifts of electrolyte content buy did not correlate with EEG activity, as assessed by Fourier frequency analysis. Corticosteroids did not prevent extravasation of peroxidase or Evans blue across the tumour vessels. The beneficial effect, therefore, is attributed to either an acceleration of resorption or an inhibition of the spread of oedema from tumour into the peritumoural brain tissue.
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PMID:Corticosteroid therapy of experimental tumour oedema. 732 60

Brain tumors were induced in inbred Fischer rats (F344) by administration of methylnitrosourea in the drinking water. One of the induced tumors, a pleomorphic glioma (78-219), was established in vitro and propagated as 78FR-G-219 permanent cell line. The tumorigenicity of the established line was investigated by intracerebral or subcutaneous inoculation of 1X10 (6) - 10X10(6) cells. Lymphocytes infiltrating secondary tumors (TIL) were enriched by a single step centrifugation on different discontinuous Percoll density gradients, while blood lymphocytes (PBL) and lymphocytes from spleen and lymph node (SL and LNL) were enriched by Ficoll - Isopaque flotation. The reactivity spectrum of the isolated lymphocytes raised against cultured 78FR-G-219 cells was monitored by means of two different assays: Lymphocyte microcytotoxicity test (LMC) and colony inhibition assay (CIA). Reactivity of PBL, SL and LNL of glioma-bearing animals was clearly reduced, while TIL showed no natural killer (NK) activity, no cytotoxicity against syngeneic 78FR-G-219 pleomorphic glioma cells and no colony inhibition in mixed lymphocyte/target cell cocultivation. NK activity of TIL was only slightly reduced against target cells of a non-cross-reacting syngeneic astrocytoma line (78FR-G-299).
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PMID:Reactivity of tumor-infiltrating, blood, spleen and lymph node lymphocytes against syngeneic glioma target cells. 734 50

Diffusion-weighted magnetic resonance imaging was performed to determine the changes in water diffusion and to investigate the detectability of diffusion anisotropy in patients with intracranial disorders. Diffusion maps of the apparent diffusion coefficient (ADC) were created of 19 patients with cerebral infarction, five with intracerebral hematoma, four with glioma, four with meningioma, four with hydrocephalus, and five with subdural hematoma. ADC was increased in chronic cerebral infarction and glioma, and decreased in acute cerebral infarction, meningioma, and the marginal area of glioma compared with the ADC of the normal gray matter. There was a significant difference in ADC between the marginal and internal areas of glioma. Increased ADC may be due to increased vasogenic edema in infarction and a lack of significant restriction of diffusion within glioma. Decreased ADC can be attributed to restricted diffusion caused by cytotoxic edema in infarction and the underlying histological pattern of densely packed tumor cells in glioma. Diffusion anisotropy of the internal capsule was less detectable in pathological than normal hemispheres. Diffusion anisotropy was less detectable in patients with hydrocephalus and subdural hematoma. Intracranial lesions were thought to have influenced the compression of the brain structures and cells, resulting in decreased diffusion. The measurement of ADC by diffusion-weighted magnetic resonance imaging has the potential for greater understanding of the biophysical changes in various intracranial disorders, including correct diagnosis of cerebral infraction, and histological diagnosis of brain tumor.
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PMID:Clinical application of diffusion-weighted magnetic resonance imaging to intracranial disorders. 756 97

A lifetime oncogenicity study in Fischer 344 rats was conducted to accurately characterize the carcinogenic potency of acrylamide. Acrylamide was administered in drinking water throughout the 106-week study at concentrations required to provide a dose of 0, 0.1, 0.5, or 2.0 mg/kg/day to males or 0, 1.0, or 3.0 mg/kg/day to females. Complete necropsy and gross pathology examinations were performed on all study animals. Histopathology examinations were conducted on selected tissues of all high-dose and control animals. Selected tissues from intermediate and low-dose groups were subjected to histopathological examinations as required to clarify high- and control-dose group observations. There was no visual observation of neurotoxicity in any study animal but sciatic nerve degeneration was observed in the male and female high-dose groups. Increased mortality related to acrylamide was observed in the high-dose male group from Month 17 to the end of the study and in the high-dose females during Month 24. Mesotheliomas of the testicular tunic were significantly increased in the high-dose male group. The combined incidence of mammary gland adenocarcinomas and fibroadenomas was significantly increased in both acrylamide-dosed female groups. Males and females in the high-dose groups as well as females of the low-dose group had significantly (p < 0.001) increased thyroid follicular cell adenomas and adenocarcinomas. A variety of other tumor types observed with increased incidence in a previous acrylamide oncogenicity study (i.e., combined CNS glial neoplasms, papillomas of the oral cavity, adenomas of the clitoral gland, and uterine adenocarcinomas) were not observed to be present at increased incidence in this study. This study confirms previously described acrylamide induction of benign tumors of the thyroid and mammary glands as well as mesotheliomas of the testis. By using a larger number of animals with an unbalanced study design, this study showed that acrylamide did not induce glial tumors and demonstrated that the no-observable-effect level for scrotal mesotheliomas is 0.5 mg/kg. It also demonstrated that the increased incidence of mammary tumors was again within historical control ranges.
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PMID:A lifetime oncogenicity study in rats with acrylamide. 758 34


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