Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The release of 14C-containing compounds from rat cortical slices prelabeled with 14C-adenine consisted largely of adenosine (6-7%), inosine (13-18%), and hypoxanthine (70-74%), with small amounts of nucleotides including cyclic AMP and adenine. This efflux was increased by both ouabain (0.1 mM) and veratridine (0.05 mM), the increment in released radioactivity consisting almost entirely of these three compounds. However, relatively more inosine than adenosine output was evoked by ouabain while the reverse was true with veratridine. Phenytoin partially reversed the effect of both depolarizing agents. After prelabeling, the efflux from astrocytoma cell cultures contained predominantly inosine (74%) and hypoxanthine (23%) with little adenosine. Ouabain increased the release of 14C-adenine derivatives, and this increase was diminished by phenytoin. Preliminary studies with neuroblastoma cell cultures have shown considerable variability in the composition of the effluent, with hypoxanthine the prevalent compound and almost no adenosine. Ouabain enhanced the efflux from these cells, and this effect was apparently reversed by phenytoin.
Epilepsia 1977 Sep
PMID:Effects of phenytoin on the release of 14C-adenine derivatives. 89 89

A method is described for determining selenium in fish tissues, meat, cereals, milk powder, and other materials by flameless atomic absorption spectrophotometry. Samples are solubilized in HNO3 and atomized in a graphite furnace in the presence of nickel nitrate. Recoveries of 0.500 and 1.000 microgram selenium added to several fish samples averaged 99.0 and 98.3%, respectively, with standard deviations of 5.3 and 4.0. Results agreed with those obtained for samples previously analyzed by fluorometry, and with results for NBS Standard Reference Material. The detection limit was 3 ng/ml solution and 50 ng/g sample.
J Assoc Off Anal Chem 1977 Sep
PMID:Flameless atomic absorption spectrophotometry of selenium in fish and food products. 89 19

A modification of a flow olfactometer with a new application appartus, with which "quasi-free" nasal respiration allows the elimination of adaptation without a special testing room, subsequent results using this device to examine olfactory thresholds before and after septum operations, as well as reference to threshold increases in 57 post-operative cases of cheilognathopalatoschisis are reported. An esthesio-neuroblastoma as well as the deformity syndrome with cheilognathopalatoschisis and encephalodystrophy are used as examples for combined olfactory transmission and perception disorders. Studies of 55 smokers with primary neurosensory disorders demonstrated a threefold increase in the olfactory threshold and an up to 50% decrease "fatique-time". A mean acetone deviation factor of 1.93 was seen in 100 students from 20-27 years of age before and after eating. Correspondingly, after a substantial breakfast and lunch, the olfactory threshold attained its maximum daily value within 90 minutes, much more pronounced than after intake of 80 grams of glucose solution. In contrast to the literature, the olfactory threshold was seen to continuously increase, dependent on age. Studies of the perceptive and recognition threshold on 100 normal individuals and 28 patients with hyposmia exhibited with 3 sigma, a significant difference. In patients with hyposmia, the absolute values for the two threshold types vary greatly, however not their deviation factors. More importance should be attached to the sense of smell as the so-called lesser senses give us the greatest pleasures.
Rhinology 1976 Sep
PMID:Results of clinical olfactometric studies. 97 91

Out of 17 enzymes studied, only 9 were detectable by starch gel electrophoresis in mouse neuroblastoma cells in culture. Prostaglandin E1 (PGE1) and 4(-3-butoxy-4-methoxybenzyl)-2-imidazolidinone (R020-1724), a specific inhibitor of cAMP phosphodiesterase, were used to induce "differentiation". Lactate and 6-phosphogluconate dehydrogenases and adenylate kinase were expressed as single bands in untreated neuroblastoma and induced "differentiated" cells, but the electrophoretic mobility of these enzymes in PGE1-treated cells was slower than that in malignant and R020-1724-treated cells. Three bands of glucose 6-phosphate dehydrogenase were detectable in PGE1-treated cells, whereas the R020-1724-treated cells had two bands and the untreated neuroblastoma cells had only one band. Aldolase was also expressed as a single band; however, the activity of this enzyme was much higher in PGE1-treated cells, whereas the activity was bately detectable for R020-1724-treated and untreated neuroblastoma cells. Some of the enzymes which are present in vivo are absent in vitro. Alkaline phosphatase is present in brain but is absent in neuroblastoma cells in vivo and in vitro. Two bands each of triose phsophate isomerase, fumarase and aldolase are present in brain, but only one band of these enzymes is present in neuroblastoma cells. Although PGE1 and R020-1724 induce many differentiated functions in neuroblastoma cells in a similar manner, PGE1 appears to change characteristically the expression of several enzymes.
Br J Cancer 1976 Sep
PMID:Altered enzyme expression in "differentiated" murine neuroblastoma cells. 97 99

Total serum LDH activity and isoenzyme distribution were studied in children with neuroblastoma at the time of hospital admission. The total LDH was determined in 26 cases, and 20 (77%) of them showed elevation of its activity. On the other hand, in 9 of these 26 cases, the isoenzyme distribution was determined along with the total LDH. All 9 cases, 4 of them with normal total LDH activity, showed an abnormal isoenzyme pattern with a percentage increase in the intermediate fractions (malignant pattern). The results suggest the usefulness of the determination of serum LDH isoenzymes as a screening procedure in children with malignant tumors including neuroblastoma.
Eur J Pediatr 1976 Sep 01
PMID:Serum lactate dehydrogenase isoenzyme pattern in neuroblastoma. 97 80

Three neuroblastoma systems were used to define fucose-containing glycopeptides on the cell surface and to relate them to the phenotypic expressions of neuronal functions. These systems were a) clonal lines of mouse neuroblastoma C-1300, b) cell hybrids of mouse neuroblastoma and rat glioma, and c) human neuroblastomas, primary cells from the tumor, and cell lines. The results suggest that similarities exist in the membrane glycopeptides available at the surface of the mouse and human cells. It is proposed that these similarities correspond to the ability of the cells to perform the differentiated functions of neuronal cells or to exist as tumors. Based on analogy with other cell membranes, a schema is given for the structure of the membrane glycopeptides on the neuroblastoma cell.
J Natl Cancer Inst 1976 Sep
PMID:Glycoproteins on the surface of neuroblastoma cells. 97 72

The proliferative behavior of neuroblastoma cells in bone marrow was evaluated before and after perturbation by chemotherapy. The data presented indicated that the proliferating fraction of the tumor cells before therapy was small. In most of the patients, initial therapy with a non-cell-cycle specific agent increased the mitotic and labeling indices. If initial therapy was followed by a cell cycle-specific agent, variable kinetic responses were observed. Although the number of patients was small and the follow-up was short, there was a correlation between the clinical response and the kinetic changes induced by the chemotherapy. Evaluation of cell kinetic changes during the initial course of chemotherapy might identify early those patients who are unlikely to have a good clinical response. Similar studies in the evaluation of new drugs to aid in identifying agents that favorably change cell kinetics and thus therapy for children with neuroblastoma was urged.
J Natl Cancer Inst 1976 Sep
PMID:Cell kinetics and chemotherapy in neuroblastoma. 97 73

To determine the relationship of cell-mediated immunity (CMI) to survival, I studied 67 children with the histologically confirmed diagnosis of neuroblastoma. CMI was measured by testing the ability of patients to develop sensitization to dinitrochlorobenzene (DNCB) and to respond to challenge. Reactions at the challenge sites were considered positive only when induration and swelling were present. Ninety percent of the patients with localized neuroblastoma and 27% of those with disseminated neuroblastoma were DNCB reactive. This suggested that patients with DNCB-positive reactions have a better chance of survival than those who are DNCB negative. Some patients with disseminated disease were evaluated in longitudinal studies, and alterations in reactivity did occur with changes in disease status and/or chemotherapy. The suggestion was made that this test systme is potentially useful in estimating survival in children with neuroblastoma.
J Natl Cancer Inst 1976 Sep
PMID:Reactions to dinitrochlorobenzene in patients with neuroblastoma and survival. 97 76

Plasma carcinoembryonic antigen (CEA) was assayed with a radioimmune procedure in 27 healthy control children. The upper limit of plasma CEA (mean +2 SD) was derived from healthy controls and was 3.35 ng/ml. This value was compared with those obtained from 15 children with active neuroblastoma, 7 with active embryonal rhabdomyosarcoma, 16 with treated neuroblastoma and without evidence of disease, 14 disease-free patients with embryonal rhabdomyosarcoma, and 17 patients still on therapy. The neuroblastoma and embryonal rhabdomyosarcoma patients with active disease had higher CEA values than did the successfully treated neuroblastoma and embryonal rhabdomyosarcoma patients. CEA plasma values greater than 3.35 ng/ml were found in 35% and 24% of patiens with neuroblastoma and embryonal rhabdomyosarcoma, respectively.
J Natl Cancer Inst 1976 Sep
PMID:Carcinoembryonic antigen in children with neuroblastoma. 97 77

Many years after apparent cure recrudescence of neuroblastoma was reported in 2 patients. In 1 patient, two recurrences occurred 5 and 10 years after apparent disappearance of tumor. Factors contributing to the extraordinary clinical course are unknown. Speculation rests on tumor characteristics, environmental influences, immunity, or the development of a second primary tumor.
J Natl Cancer Inst 1976 Sep
PMID:Recrudescence of neuroblastoma after apparent cure. 97 78


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