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757 results on '"Mattson, M. P."'

210. Expression and function of the leucine zipper protein Par-4 in apoptosis

Author

Sells, S F, primary, Han, S S, additional, Muthukkumar, S, additional, Maddiwar, N, additional, Johnstone, R, additional, Boghaert, E, additional, Gillis, D, additional, Liu, G, additional, Nair, P, additional, Monnig, S, additional, Collini, P, additional, Mattson, M P, additional, Sukhatme, V P, additional, Zimmer, S G, additional, Wood, D P, additional, McRoberts, J W, additional, Shi, Y, additional, and Rangnekar, V M, additional

Published
1997
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212. Reactive Oxygen Species as Causal Agents in the Neurotoxicity of the Alzheimer's Disease-Associated Amyloid Beta Peptide

Author

HENSLEY, K., primary, BUTTERFIELDLD, D. A., additional, HALL, N., additional, COLE, P., additional, SUBRAMANIAM, R., additional, MARK, R., additional, MATTSON, M. P., additional, MARKESBERY, W. R., additional, HARRIS, M. E., additional, AKSENOV, M., additional, AKSENOVA, M., additional, WU, J. F., additional, and CARNEY, J. M., additional

Published
1996
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229. Synthesis and Evaluation of Neuroprotective α,β-Unsaturated Aldehyde Scavenger Histidyl-Containing Analogues of Carnosine

Author

Guiotto, A., Calderan, A., Ruzza, P., Osler, A., Rubini, C., Jo, D.-G., Mattson, M. P., and Borin, G.

Abstract

The synthesis, scavenging activity, and cytoprotective profiles of histidyl-containing carnosine analogues bearing hydrazide or 1,2-diol moieties is reported. Some compounds have demonstrated higher aldehyde-sequestering efficiency than carnosine and were also efficient in protecting SH-SY5Y neuroblastoma cells and rat hippocampal neurons from 4-hydroxy-trans-2,3-nonenal (HNE)-mediated death. The cytoprotective efficacy of these compounds suggests their potential use as therapeutic agents for disorders that involve excessive membrane lipids peroxidation and HNE-mediated neuronal toxicity.

Published
2005

232. Novel p53 Inactivators with Neuroprotective Action:  Syntheses and Pharmacological Evaluation of 2-Imino-2,3,4,5,6,7-hexahydrobenzothiazole and 2-Imino-2,3,4,5,6,7-hexahydrobenzoxazole Derivatives

Author

Zhu, X., Yu, Q.-s., Cutler, R. G., Culmsee, C. W., Holloway, H. W., Lahiri, D. K., Mattson, M. P., and Greig, N. H.

Abstract

Tumor suppressor protein, p53, is an intracellular protein that is critical within the biochemical cascade that leads to cell death via apoptosis. Recent studies identified the tetrahydrobenzothiazole analogue, pifithrin-α (2), as a p53 inhibitor that was effective in protecting neuronal cells against a variety of lethal insults and reducing the side effects of anticancer drugs. As up-regulation of p53 has been described as a common feature of several neurodegenerative disorders, including Alzheimer's disease, 2 and novel analogues (3−16) were synthesized to (i) assess the value of tetrahydrobenzothiazole analogues as neuroprotective agents and (ii) define the structural requirements for p53 inactivation. Not only did 2 exhibit neuroprotective activity in both tissue culture and in vivo stroke models but also compounds 6, 7, 10, 13, 15, and 16 proved to be highly potent in protecting PC12 cells and compounds 3, 4, and 6 were highly potent in protecting primary hippocampal cells against death induced by the DNA-damaging agent, camptothecin.

Published
2002
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233. Measurement of the Ds±lifetime

Author

Iori, M, Alkhazov, G, Atamantchouk, A.G, Balatz, M.Y, Bondar, N.F, Cooper, P.S, Dauwe, L.J, Davidenko, G.V, Dersch, U, Dolgolenko, A.G, Dzyubenko, G.B, Edelstein, R, Emediato, L, Endler, A.M.F, Engelfried, J, Eschrich, I, Escobar, C.O, Evdokimov, A.V, Filimonov, I.S, Garcia, F.G, Gaspero, M, Giller, I, Golovtsov, V.L, Gouffon, P, Gülmez, E, Kangling, He, Jun, S.Y, Kaya, M, Kilmer, J, Kim, V.T, Kochenda, L.M, Konorov, I, Kozhevnikov, A.P, Krivshich, A.G, Krüger, H, Kubantsev, M.A, Kubarovsky, V.P, Kulyavtsev, A.I, Kuropatkin, N.P, Kurshetsov, V.F, Kushnirenko, A, Kwan, S, Lach, J, Lamberto, A, Landsberg, L.G, Larin, I, Leikin, E.M, Li, Y, Luksys, M, Lungov, T, Maleev, V.P, Mao, D, Mao, C, Mao, Z, Mathew, P, Mattson, M, Matveev, V, McCliment, E, Moinester, M.A, Molchanov, V.V, Morelos, A, Nelson, K.D, Nemitkin, A.V, Neoustroev, P.V, Newsom, C, Nilov, A.P, Nurushev, S.B, Ocherashvili, A, Onel, Y, Ozel, E, Ozkorucuklu, S, Penzo, A, Petrenko, S.V, Pogodin, P, Procario, M, Prutskoi, V.A, Ramberg, E, Rappazzo, G.F, Razmyslovich, B.V, Rud, V.I, Russ, J, Schiavon, P, Simon, J, Sitnikov, A.I, Skow, D, Smith, V.J, Srivastava, M, Steiner, V, Stepanov, V, Stutte, L, Svoiski, M, Terentyev, N.K, Thomas, G.P, Uvarov, L.N, Vasiliev, A.N, Vavilov, D.V, Verebryusov, V.S, Victorov, V.A, Vishnyakov, V.E, Vorobyov, A.A, Vorwalter, K, You, J, Zhaog, W, Zheng, S, and Zukanovich-Funchal, R

Abstract

We report a precise measurement of the D±smeson lifetime. The data were taken by the SELEX experiment (E781) spectrometer using 600 GeV/cΣ−, π−and pbeams. The measurement has been done using 918 reconstructed D±s. The lifetime of the D±sis measured to be 472.5±17.2±6.6 fs, using K∗(892)0K±and φπ±decay modes. The lifetime ratio of Ds±to D0is 1.145±0.049.

Published
2001
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234. Measurement of the Σ−charge radius by Σ−–electron elastic scattering

Author

Eschrich, I, Krüger, H, Simon, J, Vorwalter, K, Alkhazov, G, Atamantchouk, A.G, Balatz, M.Y, Bondar, N.F, Cooper, P.S, Dauwe, L.J, Davidenko, G.V, Dersch, U, Dirkes, G, Dolgolenko, A.G, Dzyubenko, G.B, Edelstein, R, Emediato, L, Endler, A.M.F, Engelfried, J, Escobar, C.O, Evdokimov, A.V, Filimonov, I.S, Garcia, F.G, Gaspero, M, Giller, I, Golovtsov, V.L, Gouffon, P, Gülmez, E, He, Kangling, Iori, M, Jun, S.Y, Kaya, M, Kilmer, J, Kim, V.T, Kochenda, L.M, Königsmann, K, Konorov, I, Kozhevnikov, A.P, Krivshich, A.G, Kubantsev, M.A, Kubarovsky, V.P, Kulyavtsev, A.I, Kuropatkin, N.P, Kurshetsov, V.F, Kushnirenko, A, Kwan, S, Lach, J, Lamberto, A, Landsberg, L.G, Larin, I, Leikin, E.M, Li, Yunshan, Luksys, M, Lungov, T, Maleev, V.P, Mao, D, Mao, Chensheng, Mao, Zhenlin, Masciocchi, S, Mathew, P, Mattson, M, Matveev, V, McCliment, E, Moinester, M.A, Molchanov, V.V, Morelos, A, Nelson, K.D, Nemitkin, A.V, Neoustroev, P.V, Newsom, C, Nilov, A.P, Nurushev, S.B, Ocherashvili, A, Onel, Y, Ozel, E, Ozkorucuklu, S, Penzo, A, Petrenko, S.V, Pogodin, P, Povh, B, Procario, M, Prutskoi, V.A, Ramberg, E, Rappazzo, G.F, Razmyslovich, B.V, Rud, V.I, Russ, J, Scheglov, Y, Schiavon, P, Sitnikov, A.I, Skow, D, Smith, V.J, Srivastava, M, Steiner, V, Stepanov, V, Stutte, L, Svoiski, M, Terentyev, N.K, Thomas, G.P, Uvarov, L.N, Vasiliev, A.N, Vavilov, D.V, Verebryusov, V.S, Victorov, V.A, Vishnyakov, V.E, Vorobyov, A.A, You, J, Zhao, Wenheng, Zheng, Shuchen, and Zukanovich-Funchal, R

Abstract

The Σ−mean squared charge radius has been measured in the space-like Q2range 0.035–0.105 GeV2/c2by elastic scattering of a Σ− beam off atomic electrons. The measurement was performed with the SELEX (E781) spectrometer using the Fermilab hyperon beam at a mean energy of 610 GeV/c.

Published
2001
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235. Radiative decay width of the a2(1320)−meson

Author

Molchanov, V.V., Alkhazov, G., Atamantchouk, A.G., Balatz, M.Y., Bondar, N.F., Casey, D., Cooper, P.S., Dauwe, L.J., Davidenko, G.V., Dersch, U., Dolgolenko, A.G., Dzyubenko, G.B., Edelstein, R., Emediato, L., Endler, A.M.F., Engelfried, J., Eschrich, I., Escobar, C.O., Evdokimov, A.V., Ferbel, T., Filimonov, I.S., Garcia, F.G., Gaspero, M., Giller, I., Golovtsov, V.L., Gouffon, P., G, E., Hammer, C., He, Kangling, Iori, M., Jun, S.Y., Kaya, M., Kilmer, J., Kim, V.T., Kochenda, L.M., Konorov, I., Kozhevnikov, A.P., Krivshich, A.G., Kr, H., Kubantsev, M.A., Kubarovsky, V.P., Kulyavtsev, A.I., Kuropatkin, N.P., Kurshetsov, V.F., Kushnirenko, A., Kwan, S., Lach, J., Lamberto, A., Landsberg, L.G., Larin, I., Leikin, E.M., Li, Yunshan, Luksys, M., Lungov, T., Maleev, V.P., Mao, D., Mao, Chensheng, Mao, Zhenlin, Mathew, P., Mattson, M., Matveev, V., McCliment, E., Moinester, M.A., Morelos, A., Mukhin, V.A., Nelson, K.D., Nemitkin, A.V., Neoustroev, P.V., Newsom, C., Nilov, A.P., Nurushev, S.B., Ocherashvili, A., Onel, Y., Ozel, E., Ozkorucuklu, S., Penzo, A., Petrenko, S.V., Pogodin, P., Procario, M., Prutskoi, V.A., Ramberg, E., Rappazzo, G.F., Razmyslovich, B.V., Rud, V.I., Russ, J., Schiavon, P., Simon, J., Sitnikov, A.I., Skow, D., Slattery, P., Smith, V.J., Srivastava, M., Steiner, V., Stepanov, V., Stutte, L., Svoiski, M., Terentyev, N.K., Thomas, G.P., Uvarov, L.N., Vasiliev, A.N., Vavilov, D.V., Verebryusov, V.S., Victorov, V.A., Vishnyakov, V.E., Vorobyov, A.A., Vorwalter, K., You, J., Zhao, Wenheng, Zheng, Shuchen, Zhu, Z.H., Zielinski, M., and Zukanovich, R.

Abstract

Coherent π+π−π−production in the interactions of a beam of 600GeVπ−mesons with C, Cu and Pb nuclei has been studied with the SELEX facility (Experiment E781 at Fermilab). The a2(1320) meson signal has been detected in the Coulomb (low q2) region. The Primakoff formalism used to extract radiative decay width of this meson yields Γ=284±25±25keV, which is the most precise measurement to date.

Published
2001
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236. p38 MAP kinase mediates nitric oxide-induced apoptosis of neural progenitor cells.

Author

Cheng, A, Chan, S L, Milhavet, O, Wang, S, and Mattson, M P

Abstract

Neural progenitor cells (NPC) can proliferate, differentiate into neurons or glial cells, or undergo a form of programmed cell death called apoptosis. Although death of NPC occurs during development of the nervous system and in the adult, the underlying mechanisms are unknown. Here we show that nitric oxide (NO) can induce death of C17.2 NPC by a mechanism requiring activation of p38 MAP kinase, poly(ADP-ribose) polymerase, and caspase-3. Nitric oxide causes release of cytochrome c from mitochondria, and Bcl-2 protects the neural progenitor cells against nitric oxide-induced death, consistent with a pivotal role for mitochondrial changes in controlling the cell death process. Inhibition of p38 MAP kinase by SB203580 abolished NO-induced cell death, cytochrome c release, and activation of caspase-3, indicating that p38 activation serves as an upstream mediator in the cell death process. The anti-apoptotic protein Bcl-2 protected NPC against nitric oxide-induced apoptosis and suppressed activation of p38 MAP kinase. The ability of nitric oxide to trigger death of NPC by a mechanism involving p38 MAP kinase suggests that this diffusible gas may regulate NPC fate in physiological and pathological settings in which NO is produced.

Published
2001
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244. Synthesis and in Vitro and in Vivo Activity of (−)-(1R,5R,9R)- and (+)-(1S,5S,9S)-N-Alkenyl-, -N-Alkynyl-, and -N-Cyanoalkyl-5,9-dimethyl-2‘-hydroxy-6,7-benzomorphan Homologues

Author

May, E. L., Jacobson, A. E., Mattson, M. V., Traynor, J. R., Woods, J. H., Harris, L. S., Bowman, E. R., and Aceto, M. D.

Abstract

Two of the synthesized (−)-(1R,5R,9R)-N-homologues (N-but-3-enyl- and N-but-3-ynyl-5,9-dimethyl-2‘-hydroxy-6,7-benzomorphan (9, 13)) were found to be about 20 times more potent than morphine in the mouse tail-flick assay (ED50 = 0.05 mg/kg), and (−)-(1R,5R,9R)-N-but-2-ynyl-5,9-dimethyl-2‘-hydroxy-6,7-benzomorphan ((−)-(1R,5R,9R)-N-but-2-ynylnormetazocine, 12) was about as potent as the opioid antagonist N-allylnormetazocine (AD50 in the tail-flick vs morphine assay = 0.3 mg/kg). All of the homologues examined had higher affinity for the κ-opioid receptor than the μ-receptor except (−)-N-but-2-ynyl-normetazocine (12), which had a κ/μ ratio = 7.8 and a δ/μ ratio = 118. The (−)-N-2-cyanoethyl (3), -allyl (8), and -but-3-ynyl (13) analogues had good affinity (<10 nM) for δ-opioid receptors. Two homologues in the (+)-(1S,5S,9S)-normetazocine series, N-pent-4-enyl (24) and N-hex-5-enyl (25), were high-affinity and selective σ1-ligands (Ki = 2 nM, σ2/σ1 = 1250, and 1 nM, σ2/σ1 = 750, respectively); in contrast, N-allylnormetazocine (22) had relatively poor affinity at σ1, and its σ1/σ2 ratio was <100.

Published
2000

249. Hepatic cytochrome P-450 expression in tumor necrosis factor-alpha receptor (p55/p75) knockout mice after endotoxin administration.

Author

W, Warren G, M, Poloyac S, S, Gary D, P, Mattson M, and A, Blouin R

Abstract

Hepatic cytochromes P-450 (CYP) are well characterized drug and xenobiotic metabolizing enzymes that are extensively regulated by genetic and environmental factors. Inflammatory mediators, including interleukins (ILs), interferons (IFNs), and tumor necrosis factor-alpha (TNF-alpha), have been shown to down-regulate several CYP isoforms; however, elucidation of the inflammatory mediators that are responsible for specific CYP down-regulation is difficult. The purpose of this experiment was to evaluate the role endogenous TNF-alpha plays in the regulation of liver CYP expression after endotoxin administration. Mice deficient in the p55 and p75 TNF receptors and wild-type mice were given Gram-negative bacterial lipopolysaccharide (LPS) and killed 24 h after administration. CYP analysis indicates that LPS decreases CYP1A, CYP2B, CYP3A, and CYP4A independently of TNF-alpha. CYP2D9 and CYP2E1 activities show differential responses to LPS between wild-type and TNF p55/p75 receptor knockout mice, indicating the down-regulation of CYP2D9 and CYP2E1 is differentially modulated by TNF-alpha expression. Furthermore, TNF-alpha appears to affect the constitutive expression of CYP2D9 and CYP2E1. To date, this is the first evidence suggesting that a proinflammatory cytokine is involved in the constitutive regulation of drug-metabolizing enzymes.

Published
1999

250. Anti-apoptotic role of telomerase in pheochromocytoma cells.

Author

Fu, W, Begley, J G, Killen, M W, and Mattson, M P

Abstract

Telomerase is a protein-RNA enzyme complex that adds a six-base DNA sequence (TTAGGG) to the ends of chromosomes and thereby prevents their shortening. Reduced telomerase activity is associated with cell differentiation and accelerated cellular senescence, whereas increased telomerase activity is associated with cell transformation and immortalization. Because many types of cancer have been associated with reduced apoptosis, whereas cell differentiation and senescence have been associated with increased apoptosis, we tested the hypothesis that telomerase activity is mechanistically involved in the regulation of apoptosis. Levels of telomerase activity in cultured pheochromocytoma cells decreased prior to cell death in cells undergoing apoptosis. Treatment of cells with the oligodeoxynucleotide TTAGGG or with 3,3'-diethyloxadicarbocyanine, agents that inhibit telomerase activity in a concentration-dependent manner, significantly enhanced mitochondrial dysfunction and apoptosis induced by staurosporine, Fe2+ (an oxidative insult), and amyloid beta-peptide (a cytotoxic peptide linked to neuronal apoptosis in Alzheimer's disease). Overexpression of Bcl-2 and the caspase inhibitor zVAD-fmk protected cells against apoptosis in the presence of telomerase inhibitors, suggesting a site of action of telomerase prior to caspase activation and mitochondrial dysfunction. Telomerase activity decreased in cells during the process of nerve growth factor-induced differentiation, and such differentiated cells exhibited increased sensitivity to apoptosis. Our data establish a role for telomerase in suppressing apoptotic signaling cascades and suggest a mechanism whereby telomerase may suppress cellular senescence and promote tumor formation.

Published
1999

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