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)

Increasing evidence suggests that alcohols act within specific binding pockets of selective neural proteins; however, antagonists at these sites have not been identified. 1-Alcohols from methanol through 1-butanol inhibit with increasing potency the cell-cell adhesion mediated by the immunoglobulin cell adhesion molecule L1. An abrupt cutoff exists after 1-butanol, with 1-pentanol and higher 1-alcohols showing no effect. Here, we demonstrate surprisingly strict structural requirements for alcohol inhibition of cell-cell adhesion in L1-transfected NIH 3T3 fibroblasts and in NG108-15 neuroblastoma x glioma hybrid cells treated with BMP-7, an inducer of L1 and neural cell adhesion molecule. The target site discriminates the tertiary structure of straight-chain and branched-chain alcohols and appears to comprise both a hydrophobic binding site and an adjacent hydrophilic allosteric site. Modifications to the 2- and 3-carbon positions of 1-butanol increased potency, whereas modifications that restrict movement about the 4-carbon abolished activity. The effects of ethanol and 1-butanol on cell-cell adhesion were antagonized by 1-pentanol (IC(50) = 715 microM) and 1-octanol (IC(50) = 3.6 microM). Antagonism by 1-octanol was complete, reversible, and noncompetitive. 1-Octanol also antagonized ethanol inhibition of BMP-7 morphogenesis in NG108-15 cells. 1-Octanol and related compounds may prove useful in dissecting the role of altered cell adhesion in ethanol-induced injury of the nervous system.
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PMID:Antagonists of alcohol inhibition of cell adhesion. 1072 68

Extension of dendrites and axons in neurons may compensate for and repair damaged neuronal circuits in the dementia brain. Our aim in the present study was to explore drugs activating neurite outgrowth and regenerating the neuronal network. We found that the methanol extract of Ashwagandha (roots of Withania somnifera; 5 microg/ml) significantly increased the percentage of cells with neurites in human neuroblastoma SK-N-SH cells. The effect of the extract was dose- and time-dependent mRNA levels of the dendritic markers MAP2 and PSD-95 by RT-PCR were found to be markedly increased by treatment with the extract, whereas those of the axonal marker Tau were not. Immunocytochemistry demonstrated the specific expression of MAP2 in neurites extended by the extract. These results suggest that the methanol extract of Ashwagandha promotes the formation of dendrites.
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PMID:Dendrite extension by methanol extract of Ashwagandha (roots of Withania somnifera) in SK-N-SH cells. 1088 56

We previously reported that the methanol extract of Ashwagandha (roots of Dunal) induced dendrite extension in a human neuroblastoma cell line. In this study, we found that six of the 18 compounds isolated from the methanol extract enhanced neurite outgrowth in human neuroblastoma SH-SY5Y cells. Double immunostaining was performed in rat cortical neurons using antibodies to phosphorylated NF-H as an axonal marker, and to MAP2 as a dendritic marker. In withanolide A-treated cells, the length of NF-H-positive processes was significantly increased compared with vehicle-treated cells, whereas, the length of MAP2-positive processes was increased by withanosides IV and VI. These results suggest that axons are predominantly extended by withanolide A, and dendrites by withanosides IV and VI.
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PMID:Axon- or dendrite-predominant outgrowth induced by constituents from Ashwagandha. 1239 10

Clinical reports and descriptions of chronic fatigue syndrome (CFS) and chronic ciguatera fish poisoning (CCFP) show great similarities in clinical symptomology. These similarities in the literature suggested the exploration of lipids in sera of CFS, CCFP, and other diseases with the membrane immunobead assay (MIA), which is typically used for screening ciguateric ocean fish. Sera from patients with other diseases, including hepatitis B, cancer, and diabetes, were included to assess the degree of specificity involved. Sera were treated with acetone in a ratio of 1 part serum to 4 parts acetone. The suspension was centrifuged, and the acetone layer was evaporated. The residue was weighed and redissolved in 1.0 mL methanol and tested by the MIA, undiluted and titered to 1:160. The undiluted acetone fraction of the 37 normal showed +/- activity to +activity with 16 no titer, 15 with 1:5 titer and two with 1:10 titer, and four with > or =1:40 titers. One hundred fifteen CFS sera showed 1 with 1+ and 114 with 2+ activity in the undiluted samples, 1 with 1:10 titer, 3 with 1:20 titer, 31 with 1:40 titer, 50 with 1:80 titer, and 30 with 160 titer. Thus 95.6% of the samples had > or =1:40 titer. Eight hepatitis B sera samples had > or =1:40 titers. Four CCFP samples had > or =1:40 titers. Three of 16 cancer samples had 1:40 titer. These data are summarized in Fig. 1. As shown in Table 1, a significant increase (P<0.001) in the chronic phase lipids (CPLs) was shown relative to the normal group. A preliminary chemical study in C18 octadecylsilyl columns showed all fractions (100% chloroform, 9:1 chloroform : methanol, 1:1 chloroform : methanol, and 100% methanol) to contain lipids reactive to MAb-CTX with different intensities. Prostaglandins were shown in 100% methanol fraction. Competitive MIA with crude fish ciguatoxin and CFS with synthetic JKLM ciguatoxin epitope suggested similarities in structure with ciguatoxin. This was compatible with the neuroblastoma assay demonstrated in the C(18) column fractions 9:1 and 1:1, chloroform : methanol solvents.
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PMID:Chronic phase lipids in sera of chronic fatigue syndrome (CFS), chronic ciguatera fish poisoning (CCFP), hepatitis B, and cancer with antigenic epitope resembling ciguatoxin, as assessed with MAb-CTX. 1278 62

Methanol extracts of domestic plants of Korea were evaluated as a potential inhibitor of neutral pH optimum and membrane-associated 60 kDa sphingomyelinase (N-SMase) activity. In this study, we partially purified N-SMase from bovine brain membranes using ammonium sulfate. It was purified approximately 163-fold by the sequential use of DE52, Butyl-Toyopearl, DEAE-Cellulose, and Phenyl-5PW column chromatographies. The purified N-SMase activity was assayed in the presence of the plant extracts of three hundreds species. Based on the in vitro assay, three plant extracts significantly inhibited the N-SMase activity in a time- and concentration-dependent manner. To further examine the inhibitory pattern, a Dixon plot was constructed for each of the plant extracts. The extracts of Abies nephrolepis, Acer tegmentosum, and Ginkgo biloba revealed a competitive inhibition with the inhibition constant (Ki) of 11.9 microg/ mL, 9.4 microg/mL, and 12.9 microg/mL, respectively. These extracts also inhibited in a dose-dependent manner the production of ceramide induced by serum deprivation in human neuroblastoma cell line SH-SY5Y.
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PMID:Identification of three competitive inhibitors for membrane-associated, Mg2+-dependent and neutral 60 kDa sphingomyelinase activity. 1617 18

The methanol extract from Morinda citrifolia fruits was tested for cytotoxicity activity on the MTT assay. The appearance of cytotoxic changes after exposure to the extract was in a concentration dependent manner. The median lethal concentrations (LC(50)) of the extract in baby hamster kidney (BHK) cells, African green monkey kidney (Vero) cells and human laryngeal carcinoma (Hep2) cells were found to be 2.5, 3 and 5 mg/mL, respectively. A concentration of 0.1 mg/mL of crude extract exhibited cytotoxic activity against breast cancer (MCF7) and neuroblastoma (LAN5) cell lines at 29% and 36%, respectively. The same concentration of extract showed no toxicity to Vero and very little toxicity to BHK (6%) and Hep2 (13%) cells.
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PMID:Tumor cell-selective antiproliferative effect of the extract from Morinda citrifolia fruits. 1661 39

A simple and sensitive liquid chromatography/tandem mass spectrometry (LC-MS/MS) method using an atmospheric pressure chemical ionization source (APCI) for the quantification of fenretinide (4-HPR) in mouse plasma was developed and validated. After a simple protein precipitation of plasma sample by acetonitrile, 4-HPR was analyzed by LC-APCI-MS/MS. High-performance liquid chromatography (HPLC) separation was conducted on a Hypurity C18 column (50mmx2.1mm, 5microm) with a flow rate 0.60mL/min using a gradient mobile phase comprised of 0.05% formic acid in water (A) and methanol (B), and a run time of 4.5min. The elimination of a tedious sample preparation process and a shorter run time substantially reduced total analysis time. The method was linear over the range 0.5-100ng/mL, with r>0.998. The intra- and inter-assay precisions were 1.4-9.2% and 5.1-8.2%, respectively, and the intra- and inter-assay accuracies were 93.9-98.6% and 92.7-95.3%, respectively. The absolute recoveries were 90.3% (1.5ng/mL), 97.0% (7.5ng/mL) and 92.1% (75.0ng/mL) for 4-HPR, and 99.1% for the internal standard (150ng/mL). The analytical method had excellent sensitivity using a small sample volume (30microL) with the lower limit of quantification (LLOQ) 0.5ng/mL. This method is robust and has been successfully employed in a pharmacokinetic study of 4-HPR in a mouse xenograft model of neuroblastoma.
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PMID:A rapid, sensitive and selective liquid chromatography/atmospheric pressure chemical ionization tandem mass spectrometry method for determination of fenretinide (4-HPR) in plasma. 1803 19

Newborn screening programs use whole blood dried on filter paper as the standard specimen. Metabolites are reasonably stable and can easily be sent to screening laboratories by regular mail. The recommended sample collection procedure is to spot native blood without anticoagulants onto the filter paper, because anticoagulants can interfere with the different laboratory methods. However, visual examination of the blood spots cannot always detect contamination. In this study, whole blood was drawn by venous puncture from a healthy volunteer, spiked with the corresponding metabolites and EDTA, and spotted onto filter paper. TSH and 17alpha-hydroxyprogesterone were determined by time resolved fluoroimmunoassays with the AutoDelfia system. Total galactose, biotinidase activity, and galactose-1-phosphate uridyltransferase activity were measured photometrically or fluorometrically. Succinyl acetone was estimated indirectly through the inhibition of porphobilinogen synthase activity (PBGS assay). EDTA, amino acids, and acylcarnitines were converted to the corresponding butyl esters, after extraction with methanol, and analysed by LC-MS/MS. EDTA contamination gives falsely elevated 17-OHP values and falsely reduced TSH and PBGS values. The inclusion of an EDTA determination in routine screening revealed that at least 0.06% of newborn screening samples were contaminated with EDTA. In conclusion, non-conformity during the pre-analytical phase is a source of false positive and false negative screening results. Determination of EDTA from NBS blood spots can reliably identify these samples and prevent screening errors.
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PMID:Determination of EDTA in dried blood samples by tandem mass spectrometry avoids serious errors in newborn screening. 1865 Nov 77

Cadmium, lead and copper were determined in synthetic sea-water, drinking water and the NBS 1643b Trace Elements in Water standard reference material at mug/l. levels by flame atomic-absorption spectrometry after on-line preconcentration by sorbent extraction with a flow-injection system. Bonded silica with octadecyl functional groups packed in a micro column of 100 mul capacity was used to collect diethylammonium diethyldithiocarbamate complexes of the heavy metals in the aqueous samples. The sample loading time was 20 sec at a flow-rate of 3.3 ml/min. Ethanol or methanol was used to elute the adsorbed analytes into the spectrometer. The sample loading rate, elution rate and pH were optimized. Enrichment factors of 19-25 for Cd, Pb and Cu were achieved at sampling frequencies of 120/hr with precisions of 1.4, 1.0 and 1.3% rsd (n = 11), respectively. The detection limits (3sigma) for Cd, Pb and Cu were 0.3, 3 and 0.2 mug/l., respectively. Determination of Cd, Pb and Cu in NBS SRM 1643b showed good agreement with the certified values. Recoveries of Cd and Pb added to sea-water were 95 and 102%, respectively.
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PMID:Determination of cadmium, lead and copper in water samples by flame atomic-absorption spectrometry with preconcentration by flow-injection on-line sorbent extraction. 1896 93

In Traditional Chinese Medicine a number of herbs are used to alleviate age-related diseases including memory impairment and dementia, among them stems of Cynomorium songaricum, Cynomoriaceae. In this study, we evaluated the protective effect of different extracts of aerial parts of C. songaricum on amyloid-beta peptide (Abeta) and hypoxanthine/xanthine oxidase induced cell death in SK-N-SH neuroblastoma cells. Abeta (20 microM) as well as superoxide anions generated by the hypoxanthine/xanthine oxidase system both reduced cell viability to about 60%. The methanolic extract of C. songaricum attenuated Abeta induced cell death at concentrations of 100 and 10 microg/ml, an even stronger effect was observed for the ethyl acetate fraction obtained from the crude methanolic extract. On the other hand, the dichloromethane as well as water fractions showed no protective effects. In order to further analyze the protective mode of action, the ability of extracts to protect against superoxide anions induced cell death was also evaluated. In this system, cell viability could again be restored by methanol and ethyl acetate extracts, the latter showingsignificant protective effects even at concentrations as low as 0.1 microg/ml.
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PMID:Extracts of Cynomorium songaricum protect human neuroblastoma cells from beta-amyloid25-35 and superoxide anion induced injury. 1982 6


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