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)

Endogenous opioid systems participate in carcinogenic events. To understand further the action of opioids on growth, S20Y neuroblastoma cells in tissue culture were exposed to i) [Met5]-enkephalin, a naturally occurring opioid pentapeptide, at a concentration (10(-6) M) that inhibits cell replication by 66% of control levels, ii) [Met5]-enkephalin (10(-6) M) and the opioid antagonist naloxone (10(-6) M) which blocks opioid agonist action, or iii) naltrexone (10(-6) M), a potent antagonist that disrupts endogenous opioid-opioid receptor interaction and increased cell number 76% above control values. The morphology of cells exposed to these agents for 2-4 days were similar to controls (i.e., exposed to sterile water) as determined by scanning and transmission electron microscopy. These results support the hypothesis that endogenous opioid systems act as trophic factors as they regulate growth; their effects on cell growth and survival, however, do not alter the basic ultrastructural morphology of the cells. Moreover, these data strengthen the validity of paradigms and therapeutic regimens that utilize opioid agonists and antagonists to modulate the relationship of endogenous opioid-opioid receptor interactions in neural cancer.
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PMID:Endogenous opioid systems and neural cancer: transmission and scanning electron microscopic studies of murine neuroblastoma in tissue culture. 321 9

The catabolism of phosphatidylcholine (PtdCho) has been studied in cultured murine neuroblastoma (N1E-115), C6 glioma, rat brain primary glia, and human fibroblast cells. Cells were pulse labelled for 96 h with [methyl-3H]choline followed by a chase for up to 24 h in medium containing 4 mM choline. Measurement of the radioactivity and mass of choline-containing compounds in these cells indicated that the major degradative pathway is PtdCho----lysophosphatidylcholine (lysoPtdCho)----glycerophosphocholine (GroPCho)----choline. At all times during the chase, PtdCho, sphingomyelin and lysoPtdCho comprised 72-92% of the cell-associated radioactivity; the remaining 10-30% was water-soluble and was chiefly GroPCho (30-80%) in all cell lines. In fibroblasts, however, phosphocholine (PCho) was also a major labelled water-soluble component (33-54%). The specific activity of GroPCho closely parallelled that of PtdCho in fibroblasts, but decreased faster than PtdCho in C6 and N1E-115 cells. We postulate that this may be due to distinct pools of PtdCho in the cell with differing rates of turnover. The changes in specific activity of PCho suggest that the major portion is formed by synthesis rather than as a degradative product. However, the inability to reduce the specific activity of this fraction to that of the intracellular choline suggests that a portion may be derived from either PtdCho or GroPCho.
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PMID:Phosphatidylcholine metabolism in cultured cells: catabolism via glycerophosphocholine. 339 Apr 56

Cholinergic neurons are unique among cells since they alone utilize choline not only as a component of major membrane phospholipids, such as phosphatidylcholine (Ptd-Cho), but also as a precursor of their neurotransmitter acetylcholine (AcCho). It has been hypothesized that choline-phospholipids might serve as a storage pool of choline for AcCho synthesis. The selective vulnerability of cholinergic neurons in certain neurodegenerative diseases (e.g., Alzheimer disease, motor neuron disorders) might result from the abnormally accelerated liberation of choline (to be used as precursor of AcCho) from membrane phospholipids, resulting in altered membrane composition and function and compromised neuronal viability. However, the proposed metabolic link between membrane turnover and AcCho synthesis has been difficult to demonstrate because of the heterogeneity of the preparations used. Here we used a population of purely cholinergic cells (human neuroblastoma, LA-N-2), incubated in the presence of [methyl-3H]methionine to selectively label PtdCho synthesized by methylation of phosphatidylethanolamine, the only pathway of de novo choline synthesis. PtdCho, purified by thin-layer chromatography, contained 90% of the label incorporated into lipids, demonstrating that LA-N-2 cells contained phosphatidylethanolamine N-methyltransferase. Three peaks of radioactive material that cochromatographed with authentic Ac-Cho, choline, and phosphocholine were observed when the water-soluble metabolites of the [3H]PtdCho were purified by high-performance liquid chromatography. Their identities were ascertained by subjecting them to enzymatic modifications with acetylcholinesterase, choline oxidase, and alkaline phosphatase, respectively. The results demonstrate that AcCho can be synthesized from choline derived from the degradation of endogenous PtdCho formed de novo by methylation of phosphatidylethanolamine.
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PMID:Synthesis of acetylcholine from choline derived from phosphatidylcholine in a human neuronal cell line. 347 63

The effects of the potent tumour-promoting phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) on phosphatidylcholine (PtdCho) metabolism were investigated in the neuroblastoma X glioma hybrid cell line NG108-15. TPA (100 nM) stimulated by 150-200% the release into the medium of 3H radioactivity from cells that had been pre-labelled with [3H]choline. H.p.l.c. analysis of the medium revealed that TPA stimulated the release of only free [3H]choline (212 +/- 11% of control), without affecting such other labelled metabolites as [3H]phosphocholine and [3H]glycerophosphocholine. This effect was concentration-dependent, with a half-maximal effect obtained at 27.5 +/- 6.8 nM, and was observable as early as 5-10 min after exposure to TPA. The TPA-induced release of [3H]choline into the medium was accompanied by a small and variable decrease in cellular [3H]PtdCho (to 93 +/- 4% of control). However, the radioactivity associated with water-soluble cellular choline metabolites (mainly [3H]phosphocholine and [3H]glycerophosphocholine) remained unchanged. TPA also stimulated the release of [3H]choline derived from [3H]PtdCho that had been produced via the methylation pathway from [3H]methionine. These data suggest that phosphatidylcholine may serve as the source of free choline released from the cells in response to TPA. The possible enzymic mechanisms underlying this response are discussed.
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PMID:Stimulation of choline release from NG108-15 cells by 12-O-tetradecanoylphorbol 13-acetate. 356 13

We have examined the effects of phorbol esters on phosphatidylcholine (PtdCho) metabolism in the neuroblastoma-glioma hybrid cell line NG108-15. 12-O-Tetradecanoylphorbol-13-acetate (TPA), 100 nM, stimulated twofold the incorporation of [3H]choline into PtdCho during 2 h of incubation at 37 degrees C. This effect of TPA was concentration dependent, exhibiting an EC50 of 24.5 +/- 4.4 nM. The effect of TPA was also time dependent and became apparent only after a lag period of 15-30 min. TPA also decreased the incorporation of [3H]choline into water-soluble cellular constituents in a manner whose concentration and time-dependence paralleled the changes observed in PtdCho content. HPLC analysis of this pool revealed that the levels of its major (85-95%) constituent, [3H]phosphocholine, were decreased by 29 +/- 5%, whereas those of [3H]glycerophosphocholine (0.5-2% of the pool) were increased by 84 +/- 4%. PtdCho labeling was also stimulated when cells were pulse labeled with [3H]choline and chased in the presence of TPA. The incorporation of [3H]inositol, [14C]ethanolamine, or [14C]serine into phospholipids was not affected by TPA. The non-tumor-promoting compounds phorbol and 4 alpha-phorbol-12,13-didecanoate (at 100 nM) were completely ineffective in modulating choline incorporation, whereas the biologically active analogs 4 beta-phorbol-12,13-didecanoate and 4 beta-phorbol-12,13-dibutyrate were as effective as TPA. We conclude that tumor-promoting phorbol esters can modulate PtdCho metabolism in neural-derived cells. The mechanisms mediating this effect and the possible involvement of PtdCho metabolism in normal signal transduction events and in the biological actions of tumor promoters are discussed.
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PMID:Phosphatidylcholine biosynthesis in the neuroblastoma-glioma hybrid cell line NG108-15: stimulation by phorbol esters. 377 85

The conditions (e.g. pH, resin, particle size, foreign ions) affecting the uptake of Cd(II), Cr(III), Cu(II) and Pb(II) from aqueous solution by the SM-7 (also called XAD-7) resin, were studied. Based on these studies, a two-column method was developed to overcome the effect of complexation by humic substances. The method was successfully tested with the NBS multielement water standard, SRM 1643a, and was subsequently applied to enrich Cd(II), Cr(III), Cu(II) and Pb(II) in 15 drinking water samples from Hamilton, Ontario. The metals were determined using graphite furnace atomic absorption spectrometry. The results for the drinking water samples showed that leaching of copper and lead occurred from the distribution system.
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PMID:Preconcentration of cadmium, chromium, copper and lead in drinking water on the polyacrylic ester resin, XAD-7. 400 60

Mercury in water samples, at levels below parts per billion, was collected by dithizone flotation. The statistical detection limit of Hg in seawater was 4 times better than that with a hydrous iron oxide--APDC flotation system in neutron activation determination. The same floated dithizone precipitate can be used repeatedly for collection from several volumes of the water sample. The Hg content in seawater was 0.017 micrograms/L. Average recovery from waters containing 0.025 micrograms/L, 0.05 micrograms/L and 0.1 micrograms/L was 98%. The method was applied successfully to the determination of Hg in NBS 1641b. Methyl mercury is also collected by the procedure described.
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PMID:Neutron activation determination of mercury in waters after preconcentration by flotation of dithizone-mercury complexes. 400 61

The factor(s) present in extracts prepared from the brains of newborn A/J or C57B1/6 mice, which inhibits S20Y neuroblastoma cell growth in vitro, was partially characterized. Twice as much inhibitory activity was extracted per gram wet weight of brain than torso, and inhibitor recovery was greatest in extracts prepared from brains of mice 1 week or less in age. The inhibitory factor(s) was water-soluble and was stable to heating at 100 degrees C, to freezing, and to lyophilization. It was susceptible to the action of pronase. The factor(s) behaved like a molecule of molecular weight approximately 700 upon passage through ultrafiltration membranes. Growth of rat hepatoma (H4), murine melanoma (B16), and transformed murine fibroblasts (WT19 and B6-HCMV) was not significantly inhibited by brain extract. Growth of rat glioma cells (C6) was significantly reduced but to a lesser degree than that of murine neuroblastoma cells (S20Y and N115) and glioma cells (G26-20). These results suggest that the inhibitor expresses a cell specificity.
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PMID:Partial characterization of a brain extract factor(s) inhibitory to transformed neural cells. 405 87

Incubation of neuroblastoma NIE 115 cells with veratrine leads to an apparent reduction in the number of muscarinic acetylcholine receptors assayed by [3H]scopolamine methyl chloride binding. No true down-regulation of the receptors occurs but a component of veratrine with muscarinic receptor affinity, which is not veratridine, enters the intracellular water space during the incubation period and competes with [3H]scopolamine methyl chloride for the muscarinic binding sites in subsequent ligand binding assays unless it is carefully washed away. Treatment of cells with the agonist carbamoylcholine does, however, lead to a true downregulation of muscarinic receptors.
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PMID:The effect of sodium channel activators on muscarinic receptors of neuroblastoma cells. 629 75

The therapeutic effects of cefmenoxime (CMX), a new synthetic cephalosporin antibiotic, were examined in the treatment of various pediatric infections. Patients treated were infants and children ranging from one-month-old to 13-year-old suffering from pharyngitis in 2 cases, bronchopneumonia in 3 cases, cervical lymphadenitis in 2 cases, urinary tract infections in 7 cases, tympanitis in 2 cases, suppurative meningitis, sepsis, subcutaneous apostem, acute enteritis, chest wall apostem, phlegmon, staphylococcal scalded skin syndrome in 1 case each, a total of 23 cases. As regards method of administration, CMX from a vial was dissolved in physiological saline or distilled water for injection, and the solution was administered by 3 to 5 minutes one short intravenous injection (14 cases), or CMX was diluted with large volume parenteral product and administered by 30 to 60 minutes drip infusion (9 cases). The dosage of the drug was 30 to 200 mg/kg/day; 103 mg/kg/day and under in 21 cases, 150 mg/kg/day and 200 mg/kg/day in 1 case each. The administration was continued for 3 to 27 days. As regards clinical efficacy, "good" or "excellent" results were obtained in all the cases except 2 cases, one was alpha-Streptococcus acute tympanitis supervening neuroblastoma, and the other was Pseudomonas urinary tract infection. The efficacy rate was 91.3% with excellent in 11 cases, good in 10 cases. As regards bacteriological effects, of 13 strains of Gram-positive bacteria, 10 strains were eliminated and 3 strains were not changed, while of 10 strains of Gram-negative bacteria, 8 strains were eliminated and 2 strains were reduced; thus CMX showed better results against Gram-negative bacteria rather than against Gram-positive ones. The antimicrobial activity of CMX against Gram-positive bacteria was inferior to those of CTM and CEZ, but CMX showed the highest antimicrobial activity against Gram-negative bacteria. No clinical side effects nor abnormal laboratory findings obviously attributable to CMX were observed.
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PMID:[Therapeutic effects of cefmenoxime in the treatment of various infections on infants and children]. 630 39


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