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)

Serum proteins as constituents of vasogenic brain edema were visualized both macroscopically and microscopically applying a double layer immunofluorescence technique to paraffin embedded material derived from three experimental series: peritumorous edema following xeno-transplantation of glioma cells, edema after cerebral embolization with micropheres, and edema after unilateral MCA occlusion. Exclusively cats were used as experimental animals. The staining procedures resulted in selective green fluorescence of vessel contents as well as edema protein, which was demonstrable even macroscopically at times, where edema formation reaches a maximum in each experimental series. Microscopically, serum protein could be traced up to the end of observation time ranging from 1 to 4 weeks, where the specific fluorescence was related to cellular structures. As compared to other techniques employed in brain edema localization, immunostaining mainly offers the following advantages: avoidance of in vivo tracing, better structural resolution in paraffin than in freeze sections, high specificity and sensitivity in antigen localization.
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PMID:A specific immunofluorescence technique for the demonstration of vasogenic brain edema in paraffin embedded material. 36 45

The leukocyte reactions of 106 neurosurgical cases, including 63 brain tumors, 10 intracerebral hematomas, 10 cerebral infarctions, 10 subarachnoidal hemorrhages, 8 cerebral injuries and 5 chronic subdural hematomas, against the extracts of gliomas and normal brain tissues were tested by capillary migration (LMI) and adherence inhibition (LAI) assays. Both tests showed specific responses with autochthonous and allogeneic glioma extracts in glioma patients. The sensitivity of LAI was superior to that of LMI, although LAI also showed adherence enhancement in the presence of weakly sensitized leukocytes or weak antigenic stimuli. Leukocytes from glioma patients showed positive inhibition with normal brain tissues from patients with glioma and intracerebral hematoma. Positive leukocyte reactions with normal brain tissues were also confirmed in patients with intracerebral hematomas, cerebral infarctions and severe cerebral lacerations, but not in those with subarachnoidal hemorrhages, minor cerebral contusions and chronic subdural hematomas. These results suggest that the leukocytes of patients with destructive brain lesions were autosensitized by normal brain antigens. The autosensitization has some advantages in that destroyed brain tissues are eliminated, but the hyperimmune state might cause postictal brain edema and should be properly controlled by steroids.
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PMID:[Autosensitization of neurosurgical cases by normal brain tissue antigens (author's transl)]. 39 28

The clinical status of patients with glioma is influenced by 1) the histological malignancy of the tumor, 2) the tumor volume, 3) secondary status such as brain edema or intracranial hypertension due to the tumor, and 4) the host immunity. Due to some improvement in at least 2) and 3) by the initial treatment, most low grade glioma cases pass through a clinically silent postsurgical period. However, at a certain point, transition to a high grade tumor malignant transformation may occur with exacerbation of the symptoms. Twenty-two cases of histologically established low grade glioma experienced over the past 7 years, in which immunological status was evaluated, were analyzed. Nine cases (41%) showed malignant transformation. Characteristic pictures of the clinical symptoms, computed tomography (CT) scan findings, immunological status, and morphological findings (mainly immunohistochemical examination) in nine cases were delineated. The findings at the time of exacerbation of the symptoms were as follows. In all cases CT scan demonstrated the change in the main lesion from low density to mixed density and were compatible with a high grade glioma. Reduction in host immunity was verified. Morphological increase in the tumor volume, increase in histological malignancy and deterioration in the secondary status due to the tumor were confirmed. Necrosis of the tumor cells as well as increase in giant cells and gemistocytes were observed. Immunohistochemical analysis revealed a decrease and irregularity in glial fibrillary acidic protein positive cells and positive processes as well as increase in vimentin intensity. These findings demonstrate change in the biological characteristics of the tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinicopathological study on low grade glioma. In relation to malignant transformation]. 170 58

To investigate whether brain tumors secrete a factor(s) responsible for peritumoral brain edema, we studied the effect of conditioned medium from cultured C6 glioma cells on rat brain capillary permeability. Three different fractions of conditioned medium were obtained. SUP-N was a culture supernatant incubated 4 hours in serum-free medium. SUP-C was the 60-100 fold concentrated fraction obtained by dialysis-concentration of SUP-N; it contained 950 micrograms/ml of protein greater than 10 k-daltons from 3 x 10(8) cells. SUP-L was a water-dispersible lipid fraction from SUP-N; the major components of SUP-L were neutral lipids and free fatty acids. The supernatant fractions and their corresponding control solutions were infused into normal rat brain, and capillary permeability was determined using quantitative autoradiography by measuring the unidirectional entry constant, K (micrograms l/g.min), of 14C-alpha-aminoisobutyric acid (14C-AIB) into brain tissue. SUP-C and SUP-L significantly increased capillary permeability of normal brain; the effect of SUP-C was more intense and extensive than that of SUP-L. The highest mean K value (Kmax) of SUP-C was 10.83 +/- 0.99 and that of the control was 2.53 +/- 0.22 (p less than 0.001). The Kmax of SUP-L was 5.61 +/- 0.23 and that of the control was 2.67 +/- 0.36 (p less than 0.01). A time-course study after infusion of SUP-C demonstrated that more than 1.5 hours is required for the supernatant fraction to open the barrier and that the effect of SUP-C was reversible. The increase of capillary permeability induced by SUP-C was significantly inhibited by pretreatment of rats with dexamethasone (10 mg/kg, ip) 1 hour before intracerebral infusion of SUP-C (Kmax (untreated): 8.30 +/- 0.82, Kmax (treated): 1.33 +/- 0.64, p less than 0.001). These results indicate that experimental brain tumors secrete at least two different diffusible factors responsible for capillary endothelial leakage in normal brain. One is a protein of molecular weight greater than 10 k-daltons, whose effect is inhibited by glucocorticoids, and the other is a waterdispersible lipid.
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PMID:Increased capillary permeability in rat brain induced by factors secreted by cultured C6 glioma cells: role in peritumoral brain edema. 202 71

In this study we investigated the ultrastructure of human glioma capillaries in operated sample of low grade astrocytomas and malignant gliomas. Electronmicrographs of a total of 58 vessels were analyzed with computer assisted morphometry for ultrastructural evidence of permeability routes. All of these vessels were present in the marginal area of tumors devoid of necrosis, less than 10 micron in diameter and containing one nucleus at least on axial section. We found that: (1) The number of pinocytic vesicles was significantly higher in capillaries from malignant glioma (an average of 8.1 per 1 micron (2) cytoplasm) than those from low grade astrocytoma (an average of 4.0 per 1 micron (2) cytoplasm). In capillaries from malignant glioma, most of the pinocytic vesicles were arranged in the abluminal side of endothelium and some of them were fused each other. (2) Abnormal endothelial intercellular junctions which were defined as short tight junctions (less than or equal to 0.25 microns) were equally but infrequently seen in low grade astrocytomas and malignant gliomas. (3) Fenestrations in the endothelium were not seen. Therefore we suggest that the high vascular permeability and resultant brain edema in malignant gliomas is likely to increased pinocytic vesicles and rare but abnormal inter endothelial junctions.
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PMID:[Ultrastructure of glioma vessel--morphometric study for vascular permeability]. 205 22

Using in vitro techniques, we have shown that astrocytes do not increase the ouabain-sensitive Na(+)-K(+)-ATPase activity in cerebral endothelial cells. However, malignant astrocytoma cells when co-cultured with cerebral endothelial cells significantly enhance ouabain-sensitive Na(+)-K(+)-ATPase activity in cerebral endothelial cells. Also, Na(+)-K(+)-ATPase activity in cerebral endothelial cells co-cultured with malignant astrocytoma cells is inhibited by corticosteroids to the same degree as ouabain. These results suggest that brain edema associated with malignant glioma may in part be due to an increase in ouabain-sensitive Na(+)-K(+)-ATPase activity at the blood-brain barrier and that the antiedema effects of corticosteroids may be due to a reduction in the activity of this enzyme.
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PMID:Glioma cell influence on cerebral endothelial cell Na(+)-K(+)-ATPase. 216 68

Small animal models such as the rat have serious limitations for multiple human scale instrumentation, surgical manipulations, and computerized tomographic (CT) evaluations, so that large animal models are required for the study using them. Although brain tumors induced with Rous sarcoma virus in neonatal beagle or adult monkey had been reported, these animals are very expensive ones for tumor research. A major drawback of virally induced brain tumor model is, moreover, the need for specialized viral facilities and safety precautions for laboratory personnel. In this paper, a cat glioma model implanted with C6 glioma cells derived from rats injected with N-nitrosomethylurea is reported. For an implantation dose of 5 x 10(5) cells/50 microliters, C6 glioma cells were suspended in modified Eagle medium supplemented with 10% fetal bovine serum and 0.5% agar. Twenty adult mongrel cats were injected with 5 x 10(5) C6 glioma cells intracerebrally. Implanted cats had brain tumors of about 10 mm in diameter with a yield of 80%. The mean survival was about 3 weeks after implantation. Tumors developed as spheroidal, hemorrhagic masses with central areas of necrosis and peripheral edema. They were located within the parenchyma of the implanted region. This tumor possessed many of the histological and radiological characteristics of human glioblastoma such as the following: Areas of hemorrhage and necrosis surrounded by pseudopallisading were observed within the tumor consisting of spindle-shaped cells with pleomorphic nuclei. A mass lesion with ring or garland-like enhancement surrounded by brain edema was shown on the CT scans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental brain tumor in adult mongrel cat]. 239 Mar 66

Cat brain tumors were produced by stereotactical xenotransplantation of rat glioma clone F98 into the internal capsule of the left hemisphere. Two to four weeks after implantation, the tissue content of water, sodium, potassium, calcium, magnesium, serum albumin, serum immunoglobulin, and hemoglobin was measured in samples taken from the tumor, from peritumoral white and gray matter, and from homotopic regions of the opposite hemisphere. Extravasated serum protein content was determined by subtracting intravascular from total tissue protein, using the hemoglobin content as a marker of blood volume. The development of brain tumors was accompanied by severe vasogenic brain edema, which was clearly confined to the ipsilateral white matter. The increase of water was paralleled by an increase of sodium, calcium, and serum proteins. Potassium and magnesium content remained constant. The calculated sodium and calcium content of edema fluid approximated that of blood serum. The content of blood proteins was about 50% lower, but the ratio of albumin/immunoglobulin was the same as in blood. It is concluded that peritumoral edema is a combination of plasma ultrafiltrate and whole plasma extravasation with different modes of formation. Implications for the pathophysiology and therapy of peritumoral edema are discussed.
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PMID:Quantitative analysis of experimental peritumoral edema in cats. 239 38

Vasogenic brain edema was produced by transplantation of rat glioma C6 cells into rat brain. Using this model, we measured neurotransmitter concentrations and water content of regional brain tissue. In the tumor-implanted controls, monoamine neurotransmitters in the hypothalamus, cortex, and striatum significantly decreased. When treated with DEX, these monoamines tended to return to the levels of the sham-operated controls. Additionally, DEX markedly lowered tumoral monoamines. In the nonsurgical animals, DEX significantly increased norepinephrine but not DA. Regardless of treating with DEX or not, water content showed no changes in the hypothalamus and striatum in the tumor-implanted animals. However, the increase in water content in the cortex was significant, and this increase could be reduced by DEX to the levels of controls. Water content of tumor tissue could also be markedly reduced by DEX. In the nonsurgical animals, there were no changes in water content between DEX-treated and nontreated animals. In conclusion, brain edema produced by the brain tumor may reduce noradrenergic and dopaminergic activities. This is more likely due to compression anoxia caused by the tumor mass, glial hydrops, and edema fluid. It is presumed that the effect of DEX is due to reduction of water content of the tumor and peritumoral white matter as well as by increasing noradrenergic activity.
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PMID:Effect of dexamethasone on neurotransmitter amines in a rat glioma model. 239 42

Neurological improvement in brain-tumor patients treated with dexamethasone (DEX) precedes a reduction in peritumor brain edema. In the study reported here, levels of noradrenaline (NA), dopamine (DA) and 5-hydroxytryptamine (5-HT), homovanillic acid (HVA) and 5-hydroxyindole-3-acetic acid (5-HIAA) and tissue water content were measured in grey and white matter adjacent to a 9L glioma in the cat to study DEX-neurotransmitter interactions as possible mechanisms for the acute neurological effects of DEX. Tumor-bearing and control cats were treated or not treated with DEX (0.25 mg/kg IV, 0.25 mg/kg IM) with 0.25 mg/kg IM repeated once (DEX 1) or 3 times (DEX 2) 6 hr apart. In control animals DEX 1 treatment led to significant decreases in concentration of DOPAC; DEX 2 treatment led to increases in HVA and 5-HIAA. Peritumor grey matter from untreated tumor-bearing animals had decreased levels of NA and DA and the metabolite DOPAC with no changes in 5-HT and 5-HIAA. DEX 2 but not DEX 1 resulted in a normalization (increase) in peritumor levels of DA and DOPAC. Neither dose of DEX reduced white matter edema. These findings suggest that the acute beneficial effect of DEX on neurological status may be due to alleviation of neurotransmitter amine and metabolite depletion.
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PMID:Effect of dexamethasone on monoamine and metabolite levels in a brain-tumor model. 246 98


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