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

The determination of protein nitrogen in feeds and wheat by microcomputer controlled titration is described. The method involves direct titration of ammonia with standard hypochlorite titrant in the presence of bromide. The titrant is delivered by an automatic buret, and the microcomputer controlled, automatically computed potentiometric end points are precise to 0.1% over a 5-fold concentration range of nitrogen. Digestions performed with both mercury and copper catalysts show comparable results. Samples are weighed before digestion by an electronic balance interfaced to the computer which records sample number and weight. An automatic pipet aliquots, dilutes, and buffers samples directly from the digestion tubes; the samples can be immediately titrated with the automatic titrator. The results for protein in NBS standards and check feed samples from an offical testing program compare closely with average values reported for these standards. Results show that feed and wheat samples contained 10-100% protein. Precision for successive aliquots of the same digests is 0.1-0.4%relative standard deviation; precision for multiple digestions of the same sample is 0.1-0.8%.
 ...
PMID:Microcomputer controlled titration for determination of protein nitrogen in feeds and wheat. 39 95

We have used the polymerase chain reaction (PCR) to detect amplification of the MYCN oncogene in neuroblastoma cell lines and to distinguish primary tumors with a single copy from those with MYCN amplification using DNA extracted from frozen sections. Two primer pairs were used to co-amplify a 428-bp fragment of the MYCN oncogene along with a 268-bp fragment of the beta-globin gene (a single-copy reference standard). After 30 cycles of PCR, the products were resolved by agarose gel electrophoresis. MYCN gene amplification was identified by visual comparison of the relative intensities of MYCN and beta-globin PCR product bands on the ethidium bromide-stained gel. This semiquantitative approach, while inadequate for precise determination of copy number, provided a simple, rapid, nonisotopic method for differentiating tumors with MYCN amplification from those with a single copy. Seventy-four primary tumors were classified as amplified or nonamplified by semiquantitative PCR. Twenty-two of 23 tumors known to carry MYCN gene amplification by Southern analysis were correctly identified by PCR. The single false-negative result was due to a sampling error: DNA was extracted from a block of tissue containing small foci of tumor surrounded by normal tissue. Fifty-one of 51 tumors with a single copy of MYCN were also correctly identified by PCR. We conclude that semiquantitative PCR is a reliable, non-isotopic alternative to Southern blotting for detection of MYCN gene amplification that can be performed rapidly on DNA extracted from frozen sections.
 ...
PMID:Rapid detection of MYCN gene amplification in neuroblastomas using the polymerase chain reaction. 134 70

The activation of protein kinase C was investigated in digitonin-permeabilized human neuroblastoma SH-SY5Y cells by measuring the phosphorylation of the specific protein kinase C substrate myelin basic protein4-14. The phosphorylation was inhibited by the protein kinase C inhibitory peptide PKC19-36 and was associated to a translocation of the enzyme to the membrane fractions of the SH-SY5Y cells. 1,2-Dioctanoyl-sn-glycerol had no effect on protein kinase C activity unless the calcium concentration was raised to concentrations found in stimulated cells (above 100 nM). Calcium in the absence of other activators did not stimulate protein kinase C. Phorbol 12-myristate 13-acetate was not dependent on calcium for the activation or the translocation of protein kinase C. The induced activation was sustained for 10 min, and thereafter only a small net phosphorylation of the substrate could be detected. Calcium or dioctanoylglycerol, when applied alone, only caused a minor translocation, whereas in combination a marked translocation was observed. Arachidonic acid (10 microM) enhanced protein kinase C activity in the presence of submaximal concentrations of calcium and dioctanoylglycerol. Quinacrine and p-bromophenacyl bromide did not inhibit calcium- and dioctanoylglycerol-induced protein kinase C activity at concentrations which are considered to be sufficient for phospholipase A2 inhibition.
 ...
PMID:Activation of protein kinase C in permeabilized human neuroblastoma SH-SY5Y cells. 137 89

Deletion of the short arm of chromosome 1 is among the most recurrent cytogenetic alterations found in neuroblastoma and has been associated with short survival. However, this prognostic information, which relies on time-consuming techniques, is not yet routinely exploited. In order to set up a reliable and simple routine test to determine 1p deletion in neuroblastoma, we have used the polymerase chain reaction to genotype neuroblastoma DNA at 2 loci containing a variable number of tandem repeats and located on the distal part of the short arm of chromosome 1. Agarose gel electrophoresis and ethidium bromide staining of the amplification products enable a simple determination of constitutional and tumor genotypes at these loci to be made. A total of 37 samples from 29 patients were studied with this technique. Loss of heterozygosity (LOH) could be identified in 8 cases. In each case the results obtained were in agreement with those achieved by the Southern procedure. This technique will be of particular interest in the pretherapeutic analysis of 1p deletions in small tumor samples obtained by fine-needle aspirates of the primary tumor. It should also enable retrospective studies from paraffin-embedded tumor fragments to be made and provide information for the analysis of tumor heterogeneity in neuroblastoma and in other tumors with 1p deletions.
 ...
PMID:PCR assay for chromosome 1p deletion in small neuroblastoma samples. 139 34

The biomolecular mechanisms that mediate signal transduction by type II (gamma) interferon (IFN) are poorly understood. IFN-gamma is a potent growth inhibitory cytokine also endowed with antiviral, immunomodulatory, and differentiating activities on various cell targets, including neural cells. IFN-gamma induced a rapid and transient activation of phospholipase A2 in LAN-5, a human neuroblastoma cell line. A consequence of phospholipase A2 activation was the release of arachidonic acid and the generation of lysophospholipids from membrane phospholipids. Treatment of pre-labeled LAN-5 cells with a receptor-saturating concentration of IFN-gamma led to a time-dependent release of [3H]arachidonic acid into the culture media and generation of [32P]lysophosphatidylcholine. Pretreatment of cultures with the phospholipase A2 inhibitor, bromophenacyl bromide, markedly inhibited both [3H]arachidonic acid release and lysophosphatidylcholine production induced by IFN-gamma treatment. Pretreatment of LAN-5 cells with nordihydroguaiaretic acid, a lipoxygenase inhibitor, or with indomethacin, a cyclooxygenase inhibitor, amplified the release of [3H]arachidonic acid and production of lysophosphatidylcholine induced by non-saturating concentrations of IFN-gamma. In parallel, and with the same time-dependent effect, a significant decrease in phosphatidylcholine labeling was observed in IFN-gamma-treated cells, further indicating that a potential signal transduction mechanism of IFN-gamma is the hydrolysis of membrane phosphatidylcholine by phospholipase A2.
 ...
PMID:Stimulation of receptor-coupled phospholipase A2 by interferon-gamma. 152 78

The lead-associated nuclear protein, p32/6.3, increases significantly in the postnatally developing rat cerebral cortex (Egle and Shelton, J. Biol. Chem., 261 (1986) 2294-2298). In the present study, this increase has been identified with late development of the cerebral cortex or forebrain because p32/6.3 reached adult levels 10 to 14 days after birth in guinea pig (a precocial animal) and after hatching in chicken. Comparison with other developmental processes indicates that p32/6.3 reaches adult levels just before or during the period of synapse maturation. Thus p32/6.3 may prove useful as a biochemical indicator of nuclear maturation in this period. The developmental regulation of p32/6.3 was further studied in mouse neuroblastoma 2a (Nb2a) cells. In vitro induction of differentiation of Nb2a cells by serum withdrawal from the culture medium increased p32/6.3, implicating p32/6.3 with differentiating neurons. This association was further strengthened when treatment of the Nb2a cells for 24 h with dibutyryl cAMP (1-5 mM), papaverine (5-12.5 micrograms/ml) or 3-isobutyl-1-methylxanthine (IBMX; 50-250 microM) increased the abundance of p32/6.3 1.5- to 3-fold more than serum withdrawal alone. 8-Bromo-cAMP (2-4 mM), N6-benzoyl cAMP (4 mM) and forskolin (10 microM) also increased the abundance of p32/6.3 in Nb2a cells, arguing that cAMP is involved in p32/6.3 regulation. These results, in conjunction with the postnatal increase of p32/6.3 in cerebral cortex, suggest a relationship between p32/6.3 levels and neuronal maturation.
 ...
PMID:A lead-associated nuclear protein which increases in maturing brain and in differentiating neuroblastoma 2A cells exposed to cyclic AMP-elevating agents. 170 8

Neuroblastoma cells were used to examine the effect of high concentrations of glucose or galactose and accumulation of polyols on the resting membrane potential. Polyol levels are increased and myo-inositol content decreased when neuroblastoma cells are chronically exposed to media containing 30 mM glucose or 30 mM galactose compared to cells grown in media containing 30 mM fructose. Furthermore, the 6 h accumulation and incorporation into phospholipid of extracellular myo-inositol is decreased in cells exposed to media containing 30 mM glucose or 30 mM galactose compared to cells grown in media containing 30 mM fructose. The resting membrane potential was determined by examining the steady-state accumulation of the lipophilic cation tetra[3H]phenylphosphonium bromide (TPP+). The resting membrane potential of cells grown in media containing 30 mM fructose is about -70 mV which is very similar to the resting membrane potential of cells grown in unsupplemented media. The resting membrane potential is significantly decreased in cells grown in media containing 30 mM glucose or 30 mM galactose. myo-Inositol metabolism and content and polyol levels are maintained at near normal values and the resting membrane potential is improved when media containing 30 mM glucose or 30 mM galactose are supplemented with 0.4 mM sorbinil. Acute exposure of neuroblastoma cells to 2 mM ouabain had no significant effect on [3H]TPP+ accumulation. This suggests that acute inhibition of Na+/K+ pump activity does not decrease the resting membrane potential of neuroblastoma cells. The decrease in resting membrane potential may be induced by the metabolic abnormalities and/or chronic decrease in Na+/K+ pump activity which occur when neuroblastoma cells are chronically exposed to increased glucose or galactose concentrations.
 ...
PMID:Resting membrane potential in 41A3 mouse neuroblastoma cells. Effect of increased glucose and galactose concentrations. 184 97

The venoms of the Naja species are known to be cytotoxic. This toxicity has been attributed to the presence of small nonenzymatic polypeptides of 60 amino acid residues, designated as cardiotoxins or cytotoxins. We investigated the cytotoxic potency of Naja nigricollis venom fractions and isolated another type of cytotoxic component which is even more potent than cardiotoxins. This cytotoxic compound, which was designated as nigexine, was purified to homogeneity and its amino acid sequence was determined. Nigexine is a basic phospholipase A2 consisting of a single chain of 118 amino acids. A detailed investigation of the cytotoxic effects on epithelial FL cells, C-13T neuroblastoma cells, and promyelocytic leukemia HL 60 cells revealed that nigexine not only altered cell viability but also prevented cell proliferation. This is a property that was specific to nigexine since other phospholipases A2 from various sources had no detectable cytotoxic activity. The cytotoxic activity of nigexine was not dependent on the presence of divalent cations, unlike its enzymatic activity. In particular, the cytotoxic activity of nigexine was identical in the presence or absence of either 2 mM Ca2+ or Sr2+, or 6 mM EDTA. We also present evidence based on chemical modifications that cytotoxic activity was not correlated with enzymatic activity. Thus, modification with parabromophenacyl bromide totally abolished the enzymatic activity of nigexine, which nevertheless retained 6-20% of the cytotoxicity of native nigexine. Conversely, treatment with cyanogen bromide gave a compound that retained 7% of the enzymatic activity of the parent molecule but was devoid of detectable cytotoxicity.
 ...
PMID:Nigexine, a phospholipase A2 from cobra venom with cytotoxic properties not related to esterase activity. Purification, amino acid sequence, and biological properties. 275 14

Differentiation in the mouse neuroblastoma cells is induced by cAMP and is characterized by neurite extension and increased acetylcholinesterase, cAMP-phosphodiesterase, and RI cAMP-binding activities. To gain a better understanding of the regulation of expression and the possible function of the RI cAMP-binding protein in neuroblastoma cell differentiation, we evaluate the specificity of action of cAMP analogues and agents that increased intracellular cAMP concentration in the induction of the 47,000-dalton RI protein. The amount of RI in cell extracts was quantitated by the photoactivated incorporation of 8-N3-[32P]cAMP into the 47,000-dalton RI and by ELISA and Western blot techniques. Our results showed that dibutyryl cAMP, forskolin, prostaglandin E1, 3-isobutyl-1-methyl xanthine, and papavarine gave a 2- to 4-fold increase in the RI cAMP-binding protein coincident with the expression of various morphological and biochemical differentiation phenotypes in the mouse neuroblastoma cells. However, the effects of 8-bromo-cAMP were different. 8-Bromo-cAMP effectively promoted neurite extension and increased acetylcholinesterase and cAMP-phosphodiesterase activities; however, there was no concomitant increase in the RI cAMP-binding protein. The result raises interesting questions concerning the coupling of expression of the various differentiation phenotypes in the mouse neuroblastoma cells.
 ...
PMID:Specificity of the action of cAMP agonists in the induction of RI cAMP-binding protein in mouse neuroblastoma cells. 283 19

Inhibitors of arachidonate metabolism and perturbants of the oxidation-reduction state of the cell were employed to develop a pharmacologic profile for muscarinic receptor-mediated cyclic GMP formation in murine neuroblastoma cells (clone N1E-115). Several lipoxygenase inhibitors [eicosatetraynoic acid (ETYA), nordihydroguaiaretic acid (NDGA), FPL 57231, FPL 55712, BW755c, propylgallate, and AA861] blocked the elevation of [3H]cyclic GMP induced by muscarinic receptor activation. The cyclooxygenase inhibitors indomethacin and ibuprofen were two orders of magnitude less potent in blocking the muscarinic receptor-mediated [3H]cyclic GMP response than in blocking cyclooxygenase in other systems. ETYA and NDGA did not affect the muscarinic inhibition of the prostaglandin E1-mediated increases in [3H]cyclic AMP levels in N1E-115 cells. ETYA did not have a reproducible effect on the muscarinic receptor-induced release of inositol phosphates. Thus, these lipoxygenase inhibitors appeared to be selective for the effector system coupled to the low-affinity muscarinic agonist-receptor conformation, i.e. that which induces cyclic GMP formation. Other effective inhibitors of the cyclic GMP response were methylene blue, catalase, bromphenacyl bromide, retinal, dithiothreitol, quinacrine, and oxidized glutathione. The antioxidant alpha-tocopherol in the concentration range of 100 microM to 1 mM potentiated the receptor response. Arachidonic acid itself was an inhibitor of the muscarinic receptor-mediated cyclic GMP response (IC50 = 45 microM). Linoleic acid and oleic acid were less potent (IC50 = 130 and 190 microM, respectively), and stearic acid was ineffective. When arachidonic acid was air-oxidized, its inhibitory potency was increased 10-fold. Most but not all of the spontaneously-produced oxidative metabolites, separable by reverse-phase high pressure liquid chromatography, were inhibitory to the receptor response. Enzymatically synthesized 12-hydroxyeicosatetraenoic acid and 15-hydroxyeicosatetraenoic acid inhibited the muscarinic receptor [3H]cyclic GMP response, with IC50 values of 17 and 8 microM respectively. Catalase was effective in blocking the muscarinic cyclic GMP response (IC50 = 5 microM) while having no effect on either the muscarinic receptor-induced inositol phosphate release or the reduction of cyclic AMP levels. Thus, the effector system for increasing cyclic GMP in these cells displays may of the expected characteristics for the involvement of a lipoxygenase or a related enzyme that oxidatively metabolizes arachidonate in order to activate the guanylate cyclase.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Blockade of N1E-115 murine neuroblastoma muscarinic receptor function by agents that affect the metabolism of arachidonic acid. 301 48


1 2 3 4 5 6 7 8 9 10 Next >>