108 results on '"Al Moutaery K"'
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2. Surgical Management of Spinal Tuberculosis
- Author
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Al Sebai, M. Wasef, Madkour, M. Monir, Al Moutaery, K. R., and Madkour, M. Monir, editor
- Published
- 2004
- Full Text
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3. Bioterrorism and Brucellosis
- Author
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Madkour, M. Monir, Al-Moutaery, K. R., Al-Otaibi, K. E., and Madkour, M. Monir
- Published
- 2001
- Full Text
- View/download PDF
4. Neurobrucellosis
- Author
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Madkour, M. Monir, Al-Moutaery, K. R., Al-Deeb, S., Al-Swailem, R., Al-Okaily, F., and Madkour, M. Monir
- Published
- 2001
- Full Text
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5. Operation for delayed symptomatic brain oedema after treatment of an arteriovenous malformation by embolization and radiosurgery
- Author
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Schaller, C., Liefner, M., Ansari, S., and Al Moutaery, K.
- Published
- 2005
- Full Text
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6. Effect of Acrylamide on Neurological Recovery Following Spinal Cord Injury in Rats
- Author
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Al Moutaery, K., Morais, C., Biary, N., Al Deeb, S., and Tariq, M.
- Published
- 1999
- Full Text
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7. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain: Abstracts of Symposia and free communications
- Author
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Harms, L., Bock, A., JÄnisch, W., Valdueza, J., Weber, J., Link, I., De Keyser, J., Goossens, A., Wilczak, N., Vedeler, C., Bjorge, L., Uvestad, E., Conti, G., Williams, K., Ginsberg, L., Rafique, S., Rapoport, S. I., Gershfeld, N. L., De La Meilleure, G., Crevits, L., Faiss, J. H., Heye, N., Blanke, J., Sackmann, A., Kastrup, O., Doornbos, R., van der Worp, H. B., Kappelle, L. J., Bar, P. R., Davie, C. A., Barker, G. J., Brenton, D., Miller, D. H., Thompson, A. J., Block, F., Schwarz, M., Delodovici, L., Baruzzi, F., Bonaldi, G., Dario, A., Marra, A., Mercuri, A., Dworzak, F., Cavallari, P., Confalonieri, P., Zuffi, M., Antozzi, C., Cornelio, F., Baldissera, F., Chassande, B., Ameri, A., Eymard, B., Poisson, M., Vérier, A., Brunet, P., Congia, S., Murgia, P. L., Cannas, A., Borghero, G., Uselli, S., Mellino, G., Ferrai, R., Lampis, R., Massa, R., Muzzetto, B., Giannini, F., Rossi, S., Cioni, R., d'Aniello, C., Guarneri, A., Battistini, N., Ceriani, F., Del Santo, A., Poloni, M., Campo, J. F., Iglesias, F., Guitera, M. V., Farinas, C., Pascual, J., Leno, C., Berciano, J., Thorpe, I. W., Kendall, B. E., McDonald, W. I., Moulignier, A., Dromer, F., Baudrimont, M., Dupont, B., Gozlan, J., El Amrani, M., Petit, J. C., Roullet, E., Sterzi, R., Causaran, R., Protti, A., Riva, M., Erminio, F., Arena, O., Villa, F., Maccagnano, E., Miletta, M., Spinelli, F., Ben-Hur, T., Weidenfeldl, J., Rao, N. S., Chari, C. C., Laforet, P., Matheron, S., Adams, D., Chemouilli, Ph., Desi, M., Said, G., Davous, P., Lionnet, F., Pulik, M., Genet, P., Rozenberg, F., Cartier, L. M., Castillo, J. L., Cea, J. G., Villagra, R., de Saint Martin, L., Mahieux, F., Manifacier, M. J., Mattos, K., Queiros, C., Publio, L., Vinhas, V., PeÇanha-Martins, A. C., Melo, A., Liska, U., Zifko, U., Budka, H., Drlicek, M., Grisold, W., Kaufmann, R., Kaiser, R., Czygan, M., Gomes, I., Jones, N., Cunha, S., EmbiruÇu, E. Katiane, Vieira, V., Araujo, I., Alexandra, M., Ferreira, A., Goes, J., Chemouilli, P., Israel-Biet, Masson, H., Lacroix, C., Gasnault, J., Hildebrandt-Müller, B., Oschmann, P., Krack, P., Willems, W. R., Dorndorf, W., Freitas, V., Bittencourt, A., Fernandes, D., Nascimento, M. H., Severo, M., Moraes, D., Muller, M., Hasert, K., Merkelbach, S., Schimrigk, K., van Oosten, B. W., Lai, M., Polman, C. H., Bertelsmann, F. W., Hodgkinson, S., Cabre, P. H., Volpe, L., Smadja, D., Vernant, J. P., Villaroya, H., Violleau, K., Younes-Chennoufi, A. Ben, Baumann, N., Villanueva-Hemandez, P., Ballabriga, J., Basart, E., Arbizu, T. X., Perez-Serra, J., Vinuels, F., Giron, J. M., Castilla, J. M., Redondo, L., Izquierdo, G., Lauer, K., Henneberg, A., Bittmann, N., Link, D., Wollinsky, K. H., Mobner, R., Fassbender, K., Kuhnen, J., Schwartz, A., Hennerici, M., Miller, A., Lider, O., Abramsky, O., Weiner, H. L., Offner, H., Vanderbark, A. A., Paoino, E., Fainardi, E., Addonizio, M. C., Ruppi, P., Tola, M. R., Granieri, E., Carreras, M., Sazdovitch, V., Joutel, A., Verdier-taillefer, M. H., Heinzlef, O., Radder, C., Tournier-Lasserve, E., Brenner, R. E., Munro, P. M. G., Williams, S. C. R., Bell, J. D., Hawkins, C. P., Filippi, M., Campi, A., Dousset, V., Canal, N., Comi, G., Zhu, J., Weber, F., Retska, R., List, J., Zhang, L., Brock, M., Taphoorn, M. J. B., Heimans, J. J., van der Veen, E. A., Karim, A. B. M. F., Sarazin, M., Argentino, N., Delattre, J. Y., Derkinderen, P., Buchwald, B., Schroter, G., Serve, G., Franke, C. H., Conrad, B., Kitchen, N. D., Thomas, D. G. T., Forman, A. D., Ang, Kie- Kian, Price, R., Stephens, C., Salmaggi, A., Nermni, R., Silvani, A., Forno, M. G., Luksch, R., Boiardi, A., Grzelec, H., Fryze, C., Nowacki, P., Zdziarska, B., Sanson, M., Merel, P., Richard, S., Rouleau, G., Thomas, G., Olsen, N. K., Pfeiffer, P., Egund, N., Bentzen, S. M., Johannesen, L., Mondrup, K., Rose, C., Zyluk, B., Wondrusch, E., Berger, O., Fast, N., Jellinger, K., Lindner, K., Urman, A., Thibault, J. L., Duyckaerts, Ch., Strik, H., Muller, B., Richter, E., Krauseneck, P., Steinbrecher, A., Schabet, M., Hess, C., Bamberg, M., Dichgans, J., Counsell, C. E., McLeod, M., Grant, R., Creel, G. B., Claus, D., Sieber, E., Engelhardt, A., Rechlin, T., Thierauf, P., Neubauer, U., Peresson, M., Di Giovacchino, G., Romani, G. L., Di Silverio, F., Danek, A., Kuffner, M., Hoermann, R., Schopohl, J., Laska, M., Heye, B., Zangaladze, A. T., Valls-SoIè, J., Cammarota, A., Alvarez, R., Tolosa, E., Hallett, M., Ulbricht, D., Ganslandt, O., Kober, H., Vieth, J., Grummich, P., Pongratz, H., Brigel, C., Fahlbusch, R., Serra, F. P., Palma, V., Nolfe, G., Buscaino, G. A., Rothstein, T. L., Gibson J. M., Morrison P. M., Collins A. D., Eiselt, M., Wagnur, H., Zwiener, U., Schindler, T., Efendi, H., Ertekin, C., Erfas, M., Larsson, L. E., Sirin, H., AraÇ, N., Toygar, A., Demir, Y., Seddigh, S., Vogt, T. H., Hundemer, H., Visbeck, A., Pastena, L., Faralli, F., Mainardi, G., Gagliardi, R., Linden, D., Berlit, P., Lopez, O. L., Becker, J. T., Jungreis, C., Brenner, R., Rezek, D., Dekesky, S. T., Estol, C., Boller, F., Fernandez, J. M., Mederer, S., Batlle, J., Turon, A., Codina, A., Hitzenberger, P., Vila, N., Valls-SolÇ, J., Chamorro, A., Pouget, J., Schmied, A., Morin, D., Azulay, J. Ph., Vedel, J. P., Montalt, J., Escudero, J., Barona, R., Campos, A., Varli, K., Ertem, E., Uludag, B., Yagiz, A., Privorkin, Z., Steinvil, Y., Kott, E., Combarros, O., Sanchez-Pernaute, R., Orizaola, P., Mokrusch, Th., Kutluaye, E., Selcuki, D., Ertikin, C., Zettl, U., Gold, R., Harvey, G. K., Hartung, H. P., Toyka, K. V., Wokke, J. H. J., Oey, P. L., Ippel, P. F., Jansen, G. H., Franssen, H., Toyooka, K., Fujimura, H., Ueno, S., Yoshikawa, H., Yorifuji, S., Yanagihara, T., Talamon, C., Tzourio, C., Kiefer, R., Jung, S., Toyka, K., Ruolt, I., Tranchant, C., Mohr, M., Warter, J. M., Younger, D. S., Rosoklija, G., Hays, A. P., Kurita, R., Hasegawa, O., Matsumto, M., Komiyama, A., Nara, Y., Oueslati, S., Belal, S., Turki, I., Ben Hamida, C., Hentati, F., Ben Hamida, M., Kwiecinski, H., Krolicki, L., Domzal-Stryga, A., Dellemijn, P. L. I., van Deventer, P., van Moll, B., Drogendijk, T., Vecht, Ch. J., Nemni S., Amadio, Fazio, R., Galardin, G., Delodovici, M. L., Peghi, E., Monticelli, M. L., Sessa, A., Viguera, M. L., Palomar, M., Gamez, J., Cervera, C., Navarro, C., Serena, J., Duran, I., Fernandez, A. L., Comabella, M., Nos, C., Rio, J., Montalban, J., Navarro, X., Verdu, E., Darbra, S., Buti, M., Mrabet, A., Fredj, M., Gouider, R., Tounsi, H., Khalfallah, N., Haddad, A., Dbaiss, T., Ghnassia, R., Rouillet, E., Chedru, F., Porsche, H., Strenge, H., Li, S. W., Young, Y. P., Garcia, A. A., Baron, P., Scarpini, E., Bianchi, R., Conti, A., Livraghi, S., Rees, J. H., Gregson, N. A., Hughes, R. A. C., Sedano, M. J., Calleja, J., Canga, E., Bahou, Y., Biary, N., Al Deeb, S. M., Guern, E. L. E., Gugenheim, M., Tardieu, S., Aisonobe, T. M., Agid, Y., Bouche, P., Brice, A., Rautenstrauss, B., Nelis, E., Grehl, H., Van Broeckhoven, C., Pfeiffer, R. A., Liehr, T., Ganzmann, E., Gehring, C., Neundörfer, B., Geremia, L., Doronzo, R., Sacilotto, G., Sergi, P., Pastorino, G. C., Scarlato, G., Planté-Bordeneuve, V., Mantel, A., Baas, F., Moser, H., Antonini, A., Psylla, M., Günther, I., Vontobell, P., Beer, H. F., Leenders, K. L., Chaudhuri, K. Ray, Parker, J., Pye, I. F., Millac, P. A. H., Abbott, R. J., Sutter, M., Albani, C., de Rijk, M. C., Breteler, M. M. B., Graveland, G. A., van der Mechè, F. G. A., Hofman, A., Keipes, M., Hilger, Ch., Diederich, N., Metz, H., Hentges, F., Pollak, P., Benabid, A. L., Limousin, P., Hoffmann, D., Benazzouz, A., Perret, J., Laihinen, A., Rinne, J. O., Ruottinen, H., Nagren, K., Lehikoinen, P., Oikonen, V., Ruotsalainen, U., Rinne, U. K., Cocozza, S., Pizzuti, A., Cavalcanti, F., Monticelli, A., Pianese, L., Redolfi, E., Paiau, F., Di Donato, S., Pandolfo, M., Palau, F., Monros, E., De Michele, G., Smeyers, P., Lopez-ArLandis, J., Uilchez, J., Filla, A., Genis, D., Matilla, T., Volpini, V., Blanchs, M. I., Davalos, A., Molins, A., Rosell, J., Estivill, X., De Jonghe, P., Smeyers, G., Krols, L., Mercelis, R., Hazan, J., Weissenbach, J., Martin, J. J., Warner, T. A. T., Williams, L., Orb, A. S., Harding, A. E., Giunti, P., Sweeney, M. G., Spadaro, M., Jodice, C., Novelletto, A., Malaspina, P., Frontali, M., Salmon, E., Gregoire, Del Fiore, Comar, Franck, G., Scheltens, P. H., Siegfried, K., Dartigues, E., De Deyn, P., Horn, R., Nelson, I., Hanna, M. G., Morgan-Hughes, J. A., Collinge, J., Palmer, M. S., Campbell, T., Mahal, S., Sidle, K., Humphreys, C., Tavitian, B., Pappata, S., Jobert, A., Crouzel, A. M., DiGiamberardino, L., Steimetz, G., Barbanti, P., Fabbrini, G., Salvatore, M., Buzzi, M. G., Di Piero, V., Petraroli, R., Sbriccoli, A., Pocchiari, M., Macchi, G., Lenzi, G. L., Spiegel, R., Maguire, P., Schmid, W., Ott, A., Bots, M. L., Grobbe, D. E., Hofman, A., Howard, R. S., Russell, S., Losseff, N., Hirsch, N. P., Couderc, R., Bailleul, S., Nargeot, M. C., Touchon, J., Picot, M. C., Rizzo, M., Watson, G., McGehee, D., Dingus, T., Kappos, L., Radü, E. W., Haas, J., Hartard, C. H., Spuler, S., Yousry, T., Voltz, R., Scheller, A., Holler, E., Hohlfeld, R., Scolding, N. J., Sussman, J., Kolar, O. J., Farlow, M. R., Rice, P. H., Zipp, F., Sotgiu, S., Weiss, E. H., Wekerle, H., Chalmers, R., Robertson, N., Compston, D. A. S., Martino, G., Clementi, E., Brambilla, E., Moiola, L., Martinelli, V., Colombo, B., Poggi, A., Rovaris, M., Grimaldi, L. M. E., Roth, M. P., Descoins, P., Ballivet, S., Ruidavets, J. B., Waubant, E., Nogueira, L., Cambon-Thomsen, A., Clanet, M., Leppert, D., Hauser, S., Lugaresi, A., Tartaro, A., D'aurelio, P., Befalo, L. L. O., Thomas, A., Malatesta, G., Gambi, D., Benedikz, J. E. G., Magnusson, H., Poser, C. M., Guomundsson, G., Bates, T. E., Davies, S. E. C., Clark, J. B., Landon, D. N., ùther, J. R., Rautenberg, W., Overgaard, K., Sereghy, T., Pedersen, H., Boysen, G., Diez-Tejedor, E., Carceller, F., Gutierrez, M., Lopez-Pajares, R., Roda, J. M., Chandra, B., Ricart, W., Gonzalez-Huix, F., Molina, A., Rundek, T., Demarin, V., De Reuck, J., Boon, P., Decoq, D., Strijckmans, K., Goethals, P., Lemahieu, I., Nibbio, A., Chabriat, H., Vahedi, K., Nagy, T., Verin, M., Mas, J. L., Julien, J., Ducrocq, X., Iba-Zizen, M. T., Cabanis, E. A., Bousser, M. G., Rolland, Y., Landgraf, F., Bompais, B., Lemaitre, M. H., Edan, G., Vorstrup, S., Knudsen, L., Olsen, K. Skovgaard, Videbaek, C., Schroeder, T., van Gijn, J., Jansen, H. M. L., Pruim, J., Paans, A. M. J., Willemsen, A. T. M., Hew, J. M., vd Vliet, A. M., Haaxma, R., Vaalburg, W., Minderhoud, J. M., Korf, J., Soudain, S. E., Ho, T. W., Mishu, B., Li, C. Y., Nachainkin, I., Gao, C. Y., Cornblath, D. R., Griffin, J. W., Asbury, A. K., Blaser, M. J., McKhann, G. M., Ho, T., Macko, C., Xue, P., Stadlan, E. M., Ramos-Alvarez, M., Valenciano, L., Visser, L. H., van der Meché, F. G. A., van Darn, P. A., Meulstee, J., Schmitz, P. I. M., Jacobs, B., Oomes, P. G., Kleyweg, R. P., Jacobs, B. C., Endtz, H. P., van Doorn, P. A., van der Mech, F. G. A., Van den Berg, L. H., Mollee, I., Logtenberg, T., Thomas, P. K., Plant, G., Baxter, P. J., Luis, R. Santiago, Matsumoto, M., Notermans, N. C., Wokke, J. H. J., Lokhorst, H. M., van der Graaf, Y., Jennekens, F. G. I., Azulay, J. P., Bille-Turg, F., Valentin, P., Farnarier, G. G., Pellissier, J. F., Serratrice, G., Quasthoff, S., Schneider, U., Grafe, P., Hilkens, P. H. E., Moll, J. W. B., van der Burg, M. E. L., Planting, A. S. T., van Putten, W. L. J., van den Bent, M. J., Birklein, F., Spitzer, A., Lang, E., Neundorfer, B., Diehl, R. R., Lücke, D., Smith, G. D. P., Mathias, C. J., Serra, J., Campera, M., Ochoa, J. L., Ray Chaudhuri, K., Pavitt, D., Alam, M., Handwerker, H. O., Bleasdale-Barr, K., Smith, G., Murray, N. M. F., Hawkins, P., Pepys, M., Gellera, C., DiDonato, S., Taroni, F., Uncini, A., Di Muzio, A., Servidei, S., Silvestri, G., Lodi, R., Iotti, S., Barbiroli, B., Morrissey, S. P., Borruat, F. X., Francis, D., Mosely, I., Hansen, H. C., Helmke, K., Kunze, K., Sadzot, B., Maquet, P., Lemaire, Plenevaux, Damhaut, Sommer, C., Myers, R. R., Berta, E., Mantegazza, R., Argov, Z., Shapira, Y., Wirguin, I., Beuuer, J., Franke, C., Roberts, M., Willison, H., Vincent, A., Newsom-Davis, J., Morrison, K. E., Damels, R., Francis, M., Campbell, L., Davies, K. E., Kohler, W., Bucka, C., Hertel, G., Kanovsky, P., Auer, D., Ackermann, H., Klose, U., Naegele, Th., Bien, S., Voigt, K., Fink, G. R., Stephan, K. M., Wise, R. J. S., Mullatti, N., Hewer, L., Frackowiak, R. S. J., Weiller, C. S., Rijnites, M., Jueptner, M., Bauermann, T., Krams, M., Diener, H. C., van Walderveen, M. A. A., Barkhof, F., Hommes, O. R., Valk, J., Willmer, J. P., Guzman, D. A., Passingham, R. E., Silbersweig, D., Ceballos-Baumann, A., Frith, C. D., Frackowiak, R., Lucas, C. H., Goullard, L., Marchau, M. J., Godefroy, O., Rondepierre, P. H., Chamas, E., Mounier-Vehier, F., Leys, D., Renato, J., Verdugo, M. S. C., Campero, M., Jose, L., Ochoa, D. S. C., Vivancos, F., Tejedor, E. Diez, Martinez, N., Roda, J., Frank, A., Barreiro, P., Satoh, Y., Nagata, K., Maeda, T., Hirata, Y., YalÇinerner, B., Ozkara, C., Ozer, F., Ozer, S., Hanoglu, L., Zunker, P., Pozo, J. L., Oberwittler, C., Schick, A., Buschmann, H. -Ch., Ringelstein, E. Bernd, Lara, M., Anzola, G. P., Magoni, M., Volta, G. Dalla, Tarasov, A., Feigin, V., Beaudry, M. G., Carrier, S., Chicoutimi, Henriques, I. L., Bogoussslavsky, J., van Melle, G., Mathieu, J., Perusse, L., Allard, P., Prevost, C., Cantin, L., Bouchard, J. M., De Braekeleer, M., Agbo, C., Neau, J. P., Tantot, A. M., Dary-Auriol, M., Ingrand, P., Gil, R., Baltadjiev, D., Zekin, D., Sabey, K., Gennaula, C. P., Pope, B. A., Caparros-Lefebvre, D., Girard-Buttaz, I., Pruvo, J. P., Petit, H., Hipola, D., Martin, M., Giménez-Roldan, S., Ivanez, V., Japaridze, G., Carrasco, J. L., Picomell, I., Herranz, J. L., Macias, J. A., Nieto, M., Noya, M., Oller, L., Kiteva-Trencevska, G., Delgado, M. R., Liu, H., Luengo, A., Parra, J., Colas, J., Fernandez, M. J., Manzanares, R., Kornhuber, M. E., Malashkhia, V., Orkodashili, G., Martinez, M., Bonaventura, I., Porta, G., Martinez, I., Fernandez, A., Aguilar, M., Masnou, P., Drouet, A., Dreyfus, M., Cartron, J., Morel-Kopp, M. C., Tchernia, G., Kaplan, C., Lammers, M. W., Hekster, Y. A., Keyser, A., Meinardi, H., Renier, W. O., Boon, P. A. J. M., Have, M. D., Kint, B., Cruz, P., Cadilha, A., Almeida, R., Goncalves, M., Pimenta, M., Ramos, L. M. P., Polder, T. W., Broere, C. A., Polman, L., Rother, I., Rother, M., Schlaug, G., Arnold, S., Holthausen, H., Wunderlich, G., Ebner, A., Luders, H., Witte, O. W., Seitz, R. J., Serra, L. L., Gallicchio, B., Rotondi, F., Wieshmann, U., Meierkord, H., Sabev, K., Di Carlo, V., Gueguen, B., Derouesné, Ch., Ancri, D., Bourdel, M. C., Guillou, S., Aliaga, R., Chornet, M. A., Rodrigo, A., Pascual, A. Pascual -Leone, Catala, M. D., Pascual-Leone, A., Benbadis, S. R., Dinner, D. S., Chelune, G. J., Lüders, H. O., Piedmonte, M. R., Blanco, T., Lopez, M. P., Romero, B., Deltoro, A., Pascual, A., Pascual, Leone, Bolgert, F., Josse, M. O., Tassan, P., Touze, E., Laplane, D., Godenberg, F., Brizioli, E., Del Gobbo, M., Pelliccioni, G., Scarpino, O., Durak, H., Damlacik, G., Tunca, Z., Fidaner, H., Yurekli, Y., Yemez, B., Kaygisiz, A., Anllo, E. A., Esperet, E., Giovagnoli, A. R., Casazza, M., Spreafico, R., Avanzini, G., Mascheroni, S., Vecchio, I., Tornali, C., Antonuzzo, A., Grasso, A. A., Bella, R., Pennisi, G., Raffaele, R., Broeckx, J., Schildermans, F., Hospers, W., Deberdt, W., Carney, J. M., Aksenova, M., Chen, M. S., Juncadella, M., Busquets, N., De la Fuente, I., Rodriguez, A., Rubio, F., Soler, R., Khati, C., Pillon, B., Deweer, B., Malapani, C., Malichard, N., Dubois, B., Rancurel, G., Lopez, D. L., Jungreia, G., DeKosky, S. T., Boiler, F., Weiller, C., Rijntjes, M., Mueller, S. P., Maguire, E. A., Burke, E. T., Staunton, H., Phillips, J., Rousseaux, M., Pena, J., Bertran, I., Santacruz, P., Lopez, R., Catafau, A., Lomena, F., Blesa, R., Rampello, L., Nicoletti, A., Cabaret, M., Lesoin, F., Steinling, M., Tournev, I., Maier-Hauff, K., Schroeder, M., Wolf, A., Cochin, J. P., Noel, I., Augustin, P., Auzou, P., Hannequin, D., Maria, V., Lopez-Bresnahan, Danielle, D. M., Antin-Ozerkis B. A., Bartels, E., Rodiek, S. O., Flugel, K. A., Campos, D. M., Salas-Puig, J., Del Rio, J. Sanhez, Vidal, J. A., Lahoz, C. H., Eraksoy, M., Barlas, O., Barlas, M., Bayindir, C., Ozcan, H., Birbamer, G., Gerstenbrand, F., Felber, S., Luz, G., Aichner, F., Seidel, G., Kaps, M., Hutzelmann, A., Gerriets, T., Kruggel, F., Martin, P. J., Gaunt, M. E., Abbot, R. J., Naylor, A. R., Meary, E., Dilouya, A., Meder, J. F., De Recondo, J., Lebtahi, R., Neff, K. W., Meairs, S., Viola, S., Matta, E., Aquilone, L., Rise, I. R., Authier, F. J., Kondo, H., Ghnassia, R. T., Degos, J. D., Gherardi, R. 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O., Joussen, K., Sonka, K., Chave, B., Confort-Gouny, S., Houallah, T., Neundoerfer, B., Tex, S., Seeber, C., Mokrusch, T., Urdiain, T. X. Arbizu, Yelamos, S. M., Villanueva, P., Serra, J. Peres, Braghi, S., Bonifacio, E., Natali-Sora, M. G., Debbink, Y. N., Marra, T. R., Mossman, S., Timmings, P., Seitz-Dertinger, S., Solbach, W., Mainz, A., Manfredini, E., Calabrese, E., Allaria, S., Mariani, C., Sinaki, M., Lynn, S., Westerlind, K., Ossege, L. M., Voss, B., Wiethege, Th., Sindern, E., Malin, J. p., Le Doze, F., Chapon, F., de la Sayette, V., Schaeffer, S., Dary, M., Lechevalier, B., Viader, F., de Pommery, J., Weill-Fulazza, J., Menetrey, M., Lazzarino, L. G., Nicolai, A., Nappo, A., Blin, J., Mazetti, P., Mazoyer, B., Ayed, S. Ben, Rivaud, S., Vidailhet, M., Pierrot-Deseilligny, C., Chase, T., Jordan, K. G., Gergaud, J. M., Breux, J. P., Roblot, P., Grollier, G., Giraudon, B. Becq, Dobato, J. L., Gilabert, Y. Perez, Blanco, J. L. 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L., Constantin, C., Cassatella, M. A., Langdon, D. W., Webb, S., Gasparini, P., Zeviani, A., Kidd, D., Mammi, S., Cahalon, L., Hershkoviz, R., Lahat, N., Wallach, D., Annunziata, P., Martino, T., Maimone, D., Guazzi, G. C., Porrini, A. M., Dell'Arciprete, L., Rothwell, P. M., Stewart, R. R. C., Cull, R. E., Willmes, K., Poeck, K., Russell, D., Braekken, S. K., Brucher, R., Svennevig, J., Hermesl, M., Bruckmann, H., Biraben, A., Sliwka, U., Meyer, B., Schondube, F., Noth, J., Lavenu, I., Lammers, C., Waldecker, B., Haberbosch, W., Stam, J., Schneider, R., Gautier, J. C., Berlit, T. P., Fauser, B., Kuhne, D., Geraud, G., Danielli, A., Larrue, V., Bes, A., Timmerman, E., Bono, F., Bruni, A. C., Valalentino, P., Montesi, M. P., Talerico, G., Zappia, M., Sabatelli, M., Quattrone, A., Pareyson, D., Lorenzetti, D., Sghirlanzoni, A., Castellotti, B., Lupski, J. R., Archidiacono, N., Antonacci, R., Marzella, R., Rocchi, M., Samuel, D., Goulon-Goeau, C., Costa, P. 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M., Pleiffer, G., Kunre, K., Dieterich, M., Brandt, Th., Guarino, M., Stracciari, A., Pazzaglia, P., D'Alessandro, R., Santilli, I., Donato, M., The European Velnacrine Study Group, The Dutch Guillain-Barré study group, The COP-1 Multicenter Clinical and Research Group Study, and European Study Group
- Published
- 1994
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- View/download PDF
8. Penetrating craniocerebral shrapnel injuries during “Operation Desert Storm”: Early results of a conservative surgical treatment
- Author
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Chaudhri, K. A., Choudhury, A. R., Al Moutaery, K. R., and Cybulski, G. R.
- Published
- 1994
- Full Text
- View/download PDF
9. Cervical cord compression and severe hydrocephalus in a child with Saudi variant of multiple sulfatase deficiency: Report of case
- Author
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Al-Moutaery, K. R., Choudhury, A. R., and Hassanen, M. O.
- Published
- 1994
- Full Text
- View/download PDF
10. Sodium benzoate attenuates iminodipropionitrile-induced behavioral syndrome in rats
- Author
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Tariq, M., Khan, H. A., Al Moutaery, K., and Al Deeb, S.
- Published
- 2004
11. Enhanced catheter propagation with hypercapnia during superselective cerebral catherisation
- Author
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Djurberg, H. G., Tjan, G. T., and Al Moutaery, K. R.
- Published
- 1998
- Full Text
- View/download PDF
12. Effect of Lidocaine on Harmaline-Induced Tremors in the Rat
- Author
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Biary, N, Arshaduddin, M, Al Deeb, S, Al Moutaery, K, and Tariq, M
- Published
- 2000
- Full Text
- View/download PDF
13. Internal Carotid Artery Injury and Occlusion from Camel Collision
- Author
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Ansari, S. A., Al Shbrien, I., and Al Moutaery, K.
- Published
- 1998
- Full Text
- View/download PDF
14. Saudi normative data for the Wisconsin Card Sorting Test, Stroop Test, Test of Non-verbal Intelligence-3, Picture Completion and Vocabulary (subtest of the Wechsler Adult Intelligence Scale-Revised)
- Author
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Al-Ghatani, A. M., Marc Obonsawin, Binshaig, B. A., and Al-Moutaery, K. R.
- Subjects
RC0321 - Abstract
There are 2 aims for this study: first, to collect normative data for the Wisconsin Card Sorting Test (WCST), Stroop test, Test of Non-verbal Intelligence (TONI-3), Picture Completion (PC) and Vocabulary (VOC) sub-test of the Wechsler Adult Intelligence Scale-Revised for use in a Saudi Arabian culture, and second, to use the normative data provided to generate the regression equations. To collect the normative data and generate the regression equations, 198 healthy individuals were selected to provide a representative distribution for age, gender, years of education, and socioeconomic class. The WCST, Stroop test, TONI-3, PC, and VOC were administrated to the healthy individuals. This study was carried out at the Department of Clinical Neurosciences, Riyadh Military Hospital, Riyadh, Kingdom of Saudi Arabia from January 2000 to July 2002. Normative data were obtained for all tests, and tables were constructed to interpret scores for different age groups. Regression equations to predict performance on the 3 tests of frontal function from scores on tests of fluid (TONI-3) and premorbid intelligence were generated from the data from the healthy individuals. The data collected in this study provide normative tables for 3 tests of frontal lobe function and for tests of general intellectual ability for use in Saudi Arabia. The data also provide a method to estimate preinjury ability without the use of verbally based tests.
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- 2011
15. Cerebral palsy: Incidence and clinical features in Saudi Arabia
- Author
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Al-Asmari, A., primary, Al Moutaery, K., additional, Akhdar, F., additional, and Al Jadid, M., additional
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- 2006
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16. Vagus nerve stimulation: indications and limitations.
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Steiger, H. -J., Sakas, Damianos E., Simpson, Brian A., Ansari, Sohail, Chaudhri, K., and Al Moutaery, K.
- Abstract
Vagus nerve stimulation (VNS) is an established treatment for selected patients with medically refractory seizures. Recent studies suggest that VNS could be potentially useful in the treatment of resistant depressive disorder. Although a surgical procedure is required in order to implant the VNS device, the possibility of a long-term benefit largely free of severe side effects could give VNS a privileged place in the management of resistant depression. In addition, VNS appears to affect pain perception in depressed adults; a possible role of VNS in the treatment of severe refractory headache, intractable chronic migraine and cluster headache has also been suggested. VNS is currently investigated in clinical studies, as a potential treatment for essential tremor, cognitive deficits in Alzheimer's disease, anxiety disorders, and bulimia. Finally, other studies explore the potential use of VNS in the treatment of resistant obesity, addictions, sleep disorders, narcolepsy, coma and memory and learning deficits. [ABSTRACT FROM AUTHOR]
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- 2007
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17. A Patient with Meningioma Showing Multiple Cytogenetic Abnormalities and a Constitutional Translocation (3;9)(q13.3;q22)
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Niazi, M., primary, van Dijken, P.J., additional, and Al Moutaery, K., additional
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- 1998
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18. Role of nitric oxide (NO) in IDPN-induced neuro-behavioral and vestibular toxicity
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Tariq, M., primary, Khan, H.A., additional, Al Moutaery, K., additional, and Al Deeb, S., additional
- Published
- 1998
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19. 3-42-08 Effect of diethyldithiocarbamate on iminodipropionitrile induced movement disorders in rats
- Author
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Tariq, M., primary, Al Deeb, S., additional, and Al Moutaery, K., additional
- Published
- 1997
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20. Effect of fenfluramine, a 5HT releaser/uptake inhibitor on neurological recovery following spinal cord injury in rats
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Tariq, M., primary, Morais, C., additional, and Al Moutaery, K., additional
- Published
- 1997
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21. Intractable hiccup induced by brainstem lesion
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Al Deeb, Saleh M., primary, Sharif, H., additional, Al Moutaery, K., additional, and Biary, N., additional
- Published
- 1991
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22. Granulomatous spinal infections: MR imaging.
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Sharif, H S, primary, Clark, D C, additional, Aabed, M Y, additional, Haddad, M C, additional, al Deeb, S M, additional, Yaqub, B, additional, and al Moutaery, K R, additional
- Published
- 1990
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23. Dipyridamole attenuates the development of iminodipropionitrile-induced dyskinetic abnormalities in rats
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Tariq, M., Al-Deeb, S., Al-Moutaery, K., and Bruyn, G. W.
- Published
- 1995
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24. P2C84 - Role of nitric oxide (NO) in IDPN-induced neuro-behavioral and vestibular toxicity
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Tariq, M., Khan, H.A., Al Moutaery, K., and Al Deeb, S.
- Published
- 1998
- Full Text
- View/download PDF
25. P-3-314 - Effect of fenfluramine, a 5HT releaser/uptake inhibitor on neurological recovery following spinal cord injury in rats
- Author
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Tariq, M., Morais, C., and Al Moutaery, K.
- Published
- 1997
- Full Text
- View/download PDF
26. Establishment of the Military Neurosurgeons Committee within the World Federation of Neurosurgical Societies.
- Author
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Mauer UM, Ecklund JM, Al Moutaery K, and Brotchi J
- Subjects
- Humans, International Cooperation, Advisory Committees organization & administration, Congresses as Topic organization & administration, Military Medicine organization & administration, Neurosurgery organization & administration, Societies, Medical organization & administration
- Abstract
In 2009, during the World Congress of Neurological Surgery in Boston, Massachusetts, the World Federation of Neurosurgical Societies (WFNS) Executive Committee decided to establish a Military Neurosurgeons Committee. A separate scientific session on military neurosurgery was held at the next WFNS Interim Meeting in September 2011 in Brazil. A further separate session on military neurosurgery will take place at the next WFNS Meeting in Seoul, South Korea., (Copyright © 2013 Elsevier Inc. All rights reserved.)
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- 2013
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27. Arab Islamic medical revelations.
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Al Moutaery K
- Subjects
- Arabs, History, Medieval, Humans, Islam, Language, Medicine, Arabic history, Neurosurgery history
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- 2010
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28. Trolox ameliorates 3-nitropropionic acid-induced neurotoxicity in rats.
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Al Mutairy A, Al Kadasah S, Elfaki I, Arshaduddin M, Malik D, Al Moutaery K, and Tariq M
- Subjects
- Animals, Antioxidants therapeutic use, Chromans therapeutic use, Corpus Striatum metabolism, Corpus Striatum physiopathology, Disease Models, Animal, Dopamine metabolism, Dose-Response Relationship, Drug, Drug Administration Schedule, Female, Glutathione metabolism, Nerve Degeneration chemically induced, Nerve Degeneration drug therapy, Nerve Degeneration physiopathology, Neurons drug effects, Neurons metabolism, Neurons pathology, Neurotoxicity Syndromes metabolism, Neurotoxicity Syndromes physiopathology, Neurotoxins toxicity, Nitric Oxide metabolism, Nitro Compounds toxicity, Oxidative Stress drug effects, Oxidative Stress physiology, Propionates toxicity, Rats, Rats, Wistar, Thiobarbituric Acid Reactive Substances metabolism, Treatment Outcome, Tyrosine 3-Monooxygenase drug effects, Tyrosine 3-Monooxygenase metabolism, Antioxidants pharmacology, Chromans pharmacology, Corpus Striatum drug effects, Neurotoxicity Syndromes drug therapy, Neurotoxins antagonists & inhibitors, Nitro Compounds antagonists & inhibitors, Propionates antagonists & inhibitors
- Abstract
3-nitropropionic acid (3-NPA) is a naturally occurring neurotoxin produced by legumes of the genus Astragalus and Arthrium fungi. Acute exposure to 3-NPA results in striatal astrocytic death and variety of behavior dysfunction in rats. Oxidative stress has been reported to play an important role in 3-NPA-induced neurotoxicity. Trolox is a potent free radical chain breaking antioxidant which has been shown to restore structure and function of the nervous system following oxidative stress. This rapid and efficient antioxidant property of trolox was attributed to its enhanced water solubility as compared with alpha-tocopherol. This investigation was aimed to study the effect of trolox against 3-NPA-induced neurotoxicity in female Wistar rats. The animals received trolox (0, 40 mg, 80 mg and 160 mg/kg, orally) daily for 7 days. 3-NPA (25mg/kg, i.p.) was administered daily 30 min after trolox for the same duration. One additional group of rats served as control (vehicle only). On day 8, the animals were observed for neurobehavioral performance. Immediately after behavioral studies, the animal's brains were dissected out for histological studies. Lesions in the striatal dopaminergic neurons were assessed by immunohistochemical method using tyrosine hydroxylase immunostaining. Administration of 3-NPA alone caused significant depletion of striatal dopamine and glutathione, whereas, the levels of thiobarbituric acid reactive substance (TBARS) and nitric oxide (NO) were significantly increased suggesting an elevated level of oxidative stress. Trolox significantly and dose-dependently protected animals against 3-NPA-induced neurobehavioral, neurochemical and structural abnormalities. These results clearly suggest that protective effect of trolox against 3-NPA-induced neurotoxicity is mediated through its free radical scavenging activity., (Copyright (c) 2009 Elsevier Inc. All rights reserved.)
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- 2010
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29. Pentoxifylline attenuates iminodipropionitrile-induced behavioral abnormalities in rats.
- Author
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Al Kadasah S, Al Mutairy A, Siddiquei M, Khan HA, Abdulwahid Arif I, Al Moutaery K, and Tariq M
- Subjects
- Animals, Brain metabolism, Dose-Response Relationship, Drug, Dyskinesia, Drug-Induced drug therapy, Dyskinesia, Drug-Induced etiology, Dyskinesia, Drug-Induced psychology, Glutathione metabolism, Male, Motor Activity drug effects, Neurotoxicity Syndromes etiology, Neurotoxicity Syndromes psychology, Oxidative Stress drug effects, Rats, Rats, Sprague-Dawley, Reflex drug effects, Vitamin E metabolism, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Antioxidants pharmacology, Behavior, Animal drug effects, Neurotoxicity Syndromes drug therapy, Nitriles antagonists & inhibitors, Nitriles toxicity, Pentoxifylline pharmacology
- Abstract
This investigation was undertaken to study the effect of pentoxifylline (PTX) on iminodipropionitrile (IDPN)-induced behavioral abnormalities [excitation with choreiform and circling movements (ECC) syndrome] in rats. The animals were intraperitoneally injected with IDPN (100 mg/kg) daily for 7 days. PTX was administered daily 30 min before IDPN in the doses of 25, 50, and 100 mg/kg for 9 days. The animals were observed for neurobehavioral abnormalities including dyskinetic head movements, circling, tail hanging, air righting reflex, and contact inhibition of the righting reflex. The onset of ECC syndrome was observed on day 8 in the group treated with IDPN alone; all animals in this group became dyskinetic on day 10. Co-treatment with PTX dose dependently delayed the onset time and significantly reduced the incidence and severity of IDPN-induced ECC syndrome; high dose of PTX completely inhibited the abnormal behavioral signs in IDPN-treated rats. Administration of IDPN caused significant depletions in cerebral glutathione and vitamin E levels. Treatment with PTX dose dependently attenuated IDPN-induced oxidative stress in rats. The beneficial effects of PTX against IDPN toxicity may be attributed to its antioxidant and anti-inflammatory properties.
- Published
- 2009
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30. Protective effect of hydrocortisone on iminodipropionitrile-induced neurotoxicity in rats.
- Author
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Tariq M, Khan HA, Siddiquei MM, Al Moutaery K, and Al Deeb S
- Subjects
- Animals, Corpus Striatum drug effects, Corpus Striatum metabolism, Dose-Response Relationship, Drug, Dyskinesia, Drug-Induced pathology, Female, Glutathione drug effects, Glutathione metabolism, Hair Cells, Vestibular drug effects, Hair Cells, Vestibular metabolism, Hippocampus drug effects, Hippocampus metabolism, Neurotoxins toxicity, Nitriles toxicity, Olfactory Bulb drug effects, Olfactory Bulb metabolism, Rats, Rats, Wistar, Anti-Inflammatory Agents pharmacology, Dyskinesia, Drug-Induced drug therapy, Hydrocortisone pharmacology, Motor Activity drug effects
- Abstract
Occupational and environmental exposure of synthetic nitriles is of potential relevance to human health. Iminodipropionitrile (IDPN), a prototype nitrile toxin, has been shown to produce dyskinetic syndrome in rodents. This study reports the effect of concomitant exposure of rats to hydrocortisone and IDPN on behavioural abnormalities namely excitation, circling and chorea (ECC) syndrome. Four groups of female Wistar rats were given hydrocortisone (0, 10, 30 and 60 mg/kg, gavage, for 10 days) 30 min. before IDPN (100 mg/kg, intraperitoneally for 8 days). Two additional groups of rats were treated with either saline (control group) or 60 mg/kg of hydrocortisone (drug alone group). The animals were observed for neurobehavioural abnormalities including dyskinetic head movement, circling, tail hanging, air righting reflex and contact inhibition of righting reflex. After behavioural studies, the animals were killed, and the discrete brain regions and temporal bones were collected for biochemistry and inner ear histopathology, respectively. Hydrocortisone significantly and dose dependently attenuated the incidence and severity of IDPN-induced behavioural syndrome. Administration of hydrocortisone (60 mg/kg) alone significantly increased glutathione (GSH) levels in olfactory bulb and striatum, whereas IDPN alone significantly reduced GSH levels in olfactory bulb, striatum and hippocampus. Hydrocortisone (60 mg/kg) significantly compensated IDPN-induced depletions of GSH in different brain regions. Hydrocortisone also protected the animals against IDPN-induced vestibular hair cell degeneration. The protective effect of hydrocortisone may be attributed to its anti-inflammatory and antioxidant properties.
- Published
- 2007
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31. Time-course of lipid peroxidation in different organs of mice treated with Echis pyramidum snake venom.
- Author
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Al Asmari A, Al Moutaery K, Manthari RA, and Khan HA
- Subjects
- Animals, Kinetics, Male, Malondialdehyde analysis, Mice, Organ Specificity, Viperidae, Brain drug effects, Heart drug effects, Kidney drug effects, Lipid Peroxidation drug effects, Liver drug effects, Lung drug effects, Snake Venoms pharmacology
- Abstract
This study examined the effect of Echis pyramidum (EP) venom on time-course of lipid peroxidation in different vital organs of mice. Adult male Swiss albino mice were injected with EP venom (2 mg/kg, i.p.); control mice received vehicle alone (normal saline). Mice were killed at 1, 3, 6, 12, and 24 h post-envenomation. The liver, lung, kidney, heart, and brain (cerebrum and cerebellum) were collected for the estimation of malondialdehyde (MDA), an index of lipid peroxidation. The results of this study showed that a single injection of EP venom caused a significant lipid peroxidation in all the organs studied. The onset of lipid peroxidation was as early as 1 h and persisted for several hours, suggesting an important role of oxidative stress in the cytotoxicity of EP venom., ((c) 2006 Wiley Periodicals, Inc.)
- Published
- 2006
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32. Neuroprotective effect of nicotine against 3-nitropropionic acid (3-NP)-induced experimental Huntington's disease in rats.
- Author
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Tariq M, Khan HA, Elfaki I, Al Deeb S, and Al Moutaery K
- Subjects
- Animals, Corpus Striatum drug effects, Corpus Striatum metabolism, Corpus Striatum physiopathology, Disease Models, Animal, Dopamine metabolism, Dose-Response Relationship, Drug, Down-Regulation drug effects, Down-Regulation physiology, Drug Interactions, Female, Glutathione metabolism, Huntington Disease chemically induced, Huntington Disease physiopathology, Injections, Subcutaneous, Motor Activity drug effects, Motor Activity physiology, Nerve Degeneration physiopathology, Nerve Degeneration prevention & control, Neuroprotective Agents therapeutic use, Nicotine therapeutic use, Nicotinic Agonists pharmacology, Nicotinic Agonists therapeutic use, Nitro Compounds, Oxidative Stress drug effects, Oxidative Stress physiology, Propionates, Rats, Rats, Wistar, Receptors, Nicotinic drug effects, Receptors, Nicotinic metabolism, Tyrosine 3-Monooxygenase metabolism, Huntington Disease drug therapy, Nerve Degeneration drug therapy, Neuroprotective Agents pharmacology, Nicotine pharmacology
- Abstract
Nicotinic acetylcholine receptors (nAChRs) are regarded as potential therapeutic targets to control various neurodegenerative diseases. Owing to the relevance of cholinergic neurotransmission in the pathogenesis of Huntington's disease (HD) this investigation was aimed to study the effect of nicotine, a nAChR agonist, on 3-nitropropionic acid (3-NP)-induced neurodegeneration in female Wistar rats. Systemic administration of 3-NP in rats serves as an important model of HD. The animals received subcutaneous injections of nicotine (0, 0.25, 0.50 and 1.00 mg/kg) daily for 7 days. 3-NP (25 mg/kg, i.p.) was administered daily 30 min after nicotine for the same duration. One additional group of rats served as control (vehicle only). On day 8, the animals were observed for neurobehavioral performance (motor activity, inclined plane test, grip strength test, paw test and beam balance). Immediately after behavioral studies, the animals were transcardially perfused with neutral buffered formalin (10%) and brains were fixed for histological studies. Lesions in the striatal dopaminergic neurons were assessed by immunohistochemical method using tyrosine hydroxylase (TH) immunostaining. Treatment of rats with nicotine significantly and dose-dependently attenuated 3-NP-induced behavioral deficits. Administration of 3-NP alone caused significant depletion of striatal dopamine (DA) and glutathione (GSH), which was significantly and dose-dependently attenuated by nicotine. Preservation of striatal dopaminergic neurons by nicotine was also confirmed by immunohistochemical studies. These results clearly showed neuroprotective effect of nicotine in experimental model of HD. The clinical relevance of these findings in HD patients remains unclear and warrants further studies.
- Published
- 2005
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33. Exacerbation of harmaline-induced tremor by imipramine.
- Author
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Arshaduddin M, Kadasah S, Al Deeb S, Al Moutaery K, and Tariq M
- Subjects
- Animals, Drug Synergism, Male, Rats, Rats, Sprague-Dawley, Tremor physiopathology, Harmaline toxicity, Imipramine toxicity, Tremor chemically induced
- Abstract
Imipramine is a well-established tricyclic antidepressant which was first approved for the treatment of depression in the late fifties. Antidepressant effect of imipramine is attributed to inhibition of serotonin (5HT) and noradrenaline (NA) reuptake in brain. These monoamines have been implicated in a variety of neurological disorders including tremor. In the present investigation attempt was made to study the effect of imipramine on harmaline-induced tremor in rats. Male Sprague Dawley rats weighing 115+/-2.5 g were given harmaline (10 mg/kg, i.p.) alone or along with imipramine (30 min before harmaline) in doses of 60 and 90 mg/kg respectively. The latency of onset, intensity and duration of tremor and EMG were recorded. To substantiate the role of 5HT in aetiopathology of tremor the above experiment was repeated in the rats pretreated with P-chlorophenylalanine (PCPA), a potent 5HT depleter. The levels of 5HT and 5-hydroxyindole acetic acid (5HIAA) in the brain stem were measured using high performance liquid chromatography. Imipramine dose-dependently exacerbated the duration, intensity and amplitude of EMG following harmaline-induced tremor. Imipramine treatment further decreased harmaline-induced 5HT turnover in the brain stem. However, this was statistically insignificant. Depletion of 5HT produced a significant reduction in the intensity and duration of harmaline-induced tremor. In conclusion, this study suggests that imipramine exacerbates harmaline-induced tremor. Clinical use of imipramine for the treatment of depression in patients who also suffer from tremors may require a close monitoring.
- Published
- 2005
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- View/download PDF
34. Metoclopramide attenuates iminodipropionitrile-induced oxidative stress and neurobehavioral toxicity in rats.
- Author
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Ahmad Khan H, Al Deeb S, Al Moutaery K, and Tariq M
- Subjects
- Animals, Female, Metoclopramide therapeutic use, Motor Activity drug effects, Motor Activity physiology, Oxidative Stress physiology, Rats, Rats, Wistar, Metoclopramide pharmacology, Movement Disorders drug therapy, Movement Disorders metabolism, Nitriles toxicity, Oxidative Stress drug effects
- Abstract
Metoclopramide (MET) has long been used as a neuroleptic and antiemetic drug in clinical practice. Motor impairment and dyskinesia have been reported in some patients following chronic treatment with MET. Occasionally, the adverse symptoms may appear even after acute exposure to MET in more susceptible population (such as elderly individual) or due to concomitant exposure to MET and certain neurotoxins. Iminodipropionitrile (IDPN), a prototype nitrile toxin, has been shown to produce dyskinetic syndrome in rodents. This study reports the effect of concomitant exposure of rats to MET and IDPN on behavioral abnormalities in rats namely excitation, circling and chorea (ECC) syndrome. Four groups of female Wistar rats (aged 3 months) were given MET (0, 10, 40 and 80 mg/kg, i.p., for 11 days) 30 min before IDPN (100 mg/kg, i.p. for 8 days). Two additional groups of rats were treated with either saline (control group) or 80 mg/kg of MET (drug alone group). The animals were observed for neurobehavioral abnormalities including dyskinetic head movement, circling, tail hanging, air righting reflex and contact inhibition of righting reflex. Horizontal and vertical locomotor activities and fore limbs grip strength were also measured. On day 12, the animals were sacrificed and brains were collected for biochemical analysis. MET significantly and dose-dependently protected the animals against IDPN-induced ECC syndrome, motor impairment and deficiency in grip strength. MET also protected the animals against IDPN-induced oxidative stress.
- Published
- 2004
- Full Text
- View/download PDF
35. Citalopram, a selective serotonin reuptake inhibitor augments harmaline-induced tremor in rats.
- Author
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Arshaduddin M, Al Kadasah S, Biary N, Al Deeb S, Al Moutaery K, and Tariq M
- Subjects
- Analysis of Variance, Animals, Behavior, Animal, Brain Chemistry drug effects, Central Nervous System Stimulants toxicity, Dose-Response Relationship, Drug, Drug Synergism, Electromyography methods, Female, Hydroxyindoleacetic Acid metabolism, Muscle, Skeletal drug effects, Rats, Rats, Sprague-Dawley, Serotonin metabolism, Time Factors, Citalopram pharmacology, Harmaline toxicity, Selective Serotonin Reuptake Inhibitors pharmacology, Tremor chemically induced
- Abstract
Citalopram, a serotonin reuptake inhibitor (SSRI) is one of the widely used antidepressants. Apart from its antidepressant activity citalopram is also used for anxiety, panic disorders, obsessive-compulsive disorder and behavioral disturbances of dementia. Tremor is the second most common neurological adverse effect in patients receiving treatment with SSRIs. Use of these agents in depressed patients with essential tremor has not been studied. The present study was undertaken to investigate the effect of chronic citalopram treatment on harmaline-induced tremors in rats. Female Sprague-Dawley rats weighing 70+/-2 g were given citalopram in doses of 0, 10, 20 and 40 mg/kg by gavage for 2 weeks. On the 15th day, the rats were given harmaline (10 mg/kg, i.p.) 30 min after the last dose of citalopram. The latency of onset, intensity and duration of tremor and EMG were recorded. Serotonin (5HT) and 5-hydroxy indole acetic acid (5HIAA) were measured in brain stem. Citalopram dose dependently exacerbated the duration, intensity and amplitude of EMG of harmaline-induced tremor. A significant decrease in 5HT turnover (5HIAA/5HT ratio) in the brain stem was observed suggesting a possible role of serotoninergic impairment in citalopram-induced augmentation of harmaline-induced tremor. Clinical implications of these observations warrant further investigation.
- Published
- 2004
- Full Text
- View/download PDF
36. Influence of age on iminodipropionitrile-induced vestibular and neurobehavioral toxicities in rats.
- Author
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Khan HA, Al Deeb S, Al Moutaery K, and Tariq M
- Subjects
- Animals, Disease Models, Animal, Dose-Response Relationship, Drug, Dyskinesia, Drug-Induced blood, Dyskinesia, Drug-Induced pathology, Ear, Inner drug effects, Ear, Inner pathology, Glutathione blood, Injections, Intraperitoneal, Male, Motor Activity drug effects, Neurotoxins administration & dosage, Nitriles administration & dosage, Oxidative Stress drug effects, Rats, Rats, Wistar, Aging, Behavior, Animal drug effects, Dyskinesia, Drug-Induced etiology, Neurotoxins toxicity, Nitriles toxicity
- Abstract
A direct association between aging and drug-induced dyskinesia has been reported by several investigators. Iminiodipropionitrile (IDPN), a prototype nitrile compound produces a motor syndrome in rodents, which resembles neuroleptic drug induced dyskinesia. In this investigation attempt has been made to study the effect of age on IDPN induced vestibular hair cell degeneration and resulting dyskinetic syndrome. Male Wistar rats aged 3, 6 and 12 weeks received IDPN in the doses of 0, 200 and 400 mg/kg, intraperitoneally for 3 consecutive days. IDPN-induced dyskinesia was assessed using a behavioral testing battery on days 3, 4, 5, 6, 7, 14, 21 and 28. The rats were sacrificed on day 28; temporal bones were excised for vestibular histopathology and sera were collected for measuring the indices of oxidative stress (glutathione and conjugated dienes). IDPN in the dose of 200 mg/kg produced dyskinesia in 12 weeks old rats, but failed to do so in 3 and 6 weeks old rats. The high dose of IDPN (400 mg/kg) caused dyskinesia in all age groups, however, its onset and severity were age-dependent. Older rats showed an early onset and significantly high incidence of dyskinesia as compared to younger rats. The susceptibility of rats to IDPN-induced behavioral deficits was proportional to oxidative stress and degeneration of sensory hair cells in the crista ampullaris.
- Published
- 2003
- Full Text
- View/download PDF
37. Caffeine impairs short-term neurological outcome after concussive head injury in rats.
- Author
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Al Moutaery K, Al Deeb S, Ahmad Khan H, and Tariq M
- Subjects
- Animals, Blood-Brain Barrier drug effects, Brain Concussion pathology, Caffeine administration & dosage, Caffeine pharmacokinetics, Central Nervous System Stimulants administration & dosage, Central Nervous System Stimulants pharmacokinetics, Disease Models, Animal, Dose-Response Relationship, Drug, Female, Nervous System Diseases pathology, Rats, Rats, Wistar, Severity of Illness Index, Time Factors, Brain Concussion complications, Caffeine adverse effects, Central Nervous System Stimulants adverse effects, Nervous System Diseases etiology, Outcome Assessment, Health Care
- Abstract
Objective: Adenosine is an endogenous neuroprotective agent that is released during ischemia, hypoxia, epilepsy, and ischemic brain injury. Caffeine is a receptor antagonist for adenosine that might interfere with the neuroprotective effect of adenosine in ischemic-hypoxic conditions. An investigation was undertaken to study the effect of caffeine on neurological function, edema formation, and blood-brain barrier permeability after experimental head injury in rats., Methods: Adult female Wistar rats classified into different groups received caffeine intraperitoneally at doses of 0, 50, 100, and 150 mg/kg body weight. Thirty minutes after the caffeine treatment, the animals were subjected to concussive head injury (CHI) administered by a controlled cortical impact device. Neurological severity score was recorded in each rat at 2 hours after CHI. Specific gravity, water content (as an indicator of edema), and blood-brain barrier impairment were analyzed in the cortical tissue surrounding the injury site. The levels of myeloperoxidase and malondialdehyde in the cortical region were measured as indicators of neutrophil infiltration and lipid peroxidation, respectively., Results: A significant increase in righting latency and neurological deficiency after CHI was observed in caffeine-treated rats as compared with untreated animals. Although no deaths occurred in the rats exposed to CHI after pretreatment with saline, pretreatment with caffeine caused significant mortality of animals after trauma in a dose-dependent manner. Caffeine also exacerbated neutrophil infiltration, edema, and disruption of blood-brain barrier in the traumatic cortex. Light microscopy of brain revealed more severe hemorrhage and neuronal degeneration in the injured hemisphere of caffeine-treated rats as compared with rats in the injury-alone group. A significant increase in malondialdehyde in the brain of injured rats treated with caffeine before CHI clearly indicated the role of oxidative stress., Conclusion: Caffeine adversely affects outcome after CHI, possibly as a result of blockade of adenosine receptors. The findings also point toward the involvement of free radical-mediated neuronal damage in caffeine-induced exacerbation of neurotrauma.
- Published
- 2003
- Full Text
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38. Attenuation of iminodipropionitrile induced behavioral syndrome by sodium salicylate in rats.
- Author
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Tariq M, Khan HA, Al Moutaery K, and Al Deeb S
- Subjects
- Animals, Brain Chemistry drug effects, Dose-Response Relationship, Drug, Dyskinesia, Drug-Induced psychology, Ear, Inner drug effects, Ear, Inner pathology, Female, Glutathione metabolism, Hand Strength physiology, Motor Activity drug effects, Neurotoxicity Syndromes pathology, Postural Balance drug effects, Rats, Rats, Sprague-Dawley, Behavior, Animal drug effects, Cyclooxygenase Inhibitors pharmacology, Neurotoxicity Syndromes drug therapy, Neurotoxicity Syndromes psychology, Nitriles antagonists & inhibitors, Nitriles toxicity, Sodium Salicylate pharmacology
- Abstract
Iminodipropionitrile (IDPN) produces irreversible behavioral abnormalities characterized by excitation with choreiform and circling movements (ECC) syndrome in rodents. Concomitant exposure to drugs or environmental chemicals has been shown to alter IDPN-induced neurobehavioral toxicity. This investigation was undertaken to study the effect of sodium salicylate (SS) on IDPN-induced behavioral abnormalities in rats. The animals were exposed to IDPN (100 mg/kg ip) daily for 8 days. SS was administered daily 30 min before IDPN in the doses of 50, 100 and 200 mg/kg ip for 12 days. The animals were observed for neurobehavioral abnormalities including dyskinetic head movements, circling, tail hanging, air righting reflex and contact inhibition of the righting reflex. Horizontal and vertical locomotor activities and forelimbs grip strength were also measured. After behavioral studies, the animals were sacrificed, and the cerebrum and temporal bones were collected for glutathione analysis and inner ear histopathology, respectively. The onset of ECC syndrome was observed on Day 9 in the IDPN-alone group with 100% incidence on Day 12. Cotreatment with salicylate dose-dependently delayed the onset time and significantly attenuated the incidence and severity of IDPN-induced neurobehavioral signs. IDPN alone significantly increased horizontal motor activity and reduced vertical motor activity and forelimbs grip strength; these effect were significantly reversed by salicylate treatment. Treatment with salicylate also attenuated IDPN-induced depletion of GSH in the cerebrum, suggesting its free radical scavenging property.
- Published
- 2002
- Full Text
- View/download PDF
39. 2-deoxy-D-glucose attenuates harmaline induced tremors in rats.
- Author
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Tariq M, Arshaduddin M, Biary N, Al Moutaery K, and Al Deeb S
- Subjects
- Animals, Dose-Response Relationship, Drug, Electromyography, Female, Hand Strength, Harmaline toxicity, Male, Motor Activity drug effects, Postural Balance drug effects, Psychomotor Performance drug effects, Rats, Rats, Wistar, Reflex drug effects, Tremor chemically induced, Antimetabolites pharmacology, Deoxyglucose pharmacology, Harmaline antagonists & inhibitors, Tremor prevention & control
- Abstract
Neuronal hyperactivity in essential tremor is accompanied by high energy demand in cerebellum, medulla and the thalamus. It has been suggested that brain regions that have increased metabolic demands are highly vulnerable to interruptions in glucose metabolism. In the present investigation attempt was made to study the effect of 2-deoxyglucose (2DG) a glycolytic pathway inhibitor on harmaline induced tremor in rats. Wistar rats of either sex weighing 100+/-3 g were given harmaline (10 mg/kg, i.p.) alone or along with 2DG (15 min before harmaline) in doses of 300, 600 and 900 mg/kg, respectively. The latency of onset, intensity and duration of tremor following harmaline administration were recorded. Neurobehavioral responses, electromyography (EMG) and levels of blood glucose and cerebellar serotonin (5HT) were determined after 40 min of harmaline administration. 2DG significantly and dose dependently attenuated severity of harmaline induced tremors and amplitude of EMG. Treatment of rats with 2DG alone reduced the locomotor activity, however, no significant change was observed in grip strength, landing foot splay, air righting reflex and response to tactile stimuli. Harmaline alone and along with 2DG had no effect on behavioral parameters except a decrease in landing foot splay. 2DG produced a dose-dependent hyperglycemia and attenuated harmaline induced increase in cerebellar 5HT levels. Our results clearly suggest the protective effect of 2DG in harmaline induced tremor. Further studies are warranted to assess the role of glucoprivation in the suppression of neuronal excitability in tremors.
- Published
- 2002
- Full Text
- View/download PDF
40. Effect of acute caffeine on severity of harmaline induced tremor in rats.
- Author
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Al-Deeb S, Al-Moutaery K, Arshaduddin M, Biary N, and Tariq M
- Subjects
- Animals, Disease Models, Animal, Electromyography, Harmaline, Injections, Intraperitoneal, Male, Monoamine Oxidase Inhibitors, Rats, Rats, Sprague-Dawley, Severity of Illness Index, Tremor chemically induced, Caffeine adverse effects, Central Nervous System Stimulants adverse effects, Tremor physiopathology
- Abstract
Recent studies suggest an association between caffeine consumption and tremor. However, the available literature is scanty and inconclusive. The present study was undertaken to investigate the effect of acute caffeine treatment on harmaline induced tremors in the rat. Four groups of male Sprague-Dawley rats (six animals in each group) weighing 88+/-2 g were administered harmaline (10 mg/kg, intraperitoneally (i.p.)) for inducing experimental tremors. The rats in group 1 served as controls and received normal saline, whereas the animals in groups 2, 3 and 4 were given caffeine (i.p.) at doses of 50, 100 and 150 mg/kg, respectively 60 min after harmaline administration. The latency of onset, intensity and duration of tremor and electromyographic (EMG) responses were recorded. Treatment of rats with caffeine resulted in a significant increase in the intensity and duration of harmaline induced tremors. Caffeine also enhanced the EMG amplitude in harmaline treated animals. In conclusion, the results of this study suggest that acute treatment with caffeine significantly potentiates the severity of harmaline induced tremors in rats.
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- 2002
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41. Baclofen attenuates harmaline induced tremors in rats.
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Tariq M, Arshaduddin M, Biary N, Al Moutaery K, and Al Deeb S
- Subjects
- Animals, Brain drug effects, Brain metabolism, Brain physiopathology, Dose-Response Relationship, Drug, Drug Interactions physiology, Electromyography, Essential Tremor metabolism, Essential Tremor physiopathology, Female, Muscle Contraction drug effects, Muscle Contraction physiology, Olivary Nucleus drug effects, Olivary Nucleus physiopathology, Rats, Rats, Wistar, Reaction Time drug effects, Reaction Time physiology, Receptors, GABA-B metabolism, Synaptic Transmission drug effects, Synaptic Transmission physiology, Tremor chemically induced, Tremor metabolism, Baclofen pharmacology, Essential Tremor drug therapy, GABA Agonists pharmacology, Harmaline antagonists & inhibitors, Receptors, GABA-B drug effects, Tremor drug therapy, gamma-Aminobutyric Acid deficiency
- Abstract
Recent experimental and clinical studies clearly suggest the role of gamma-aminobutyric acid (GABA) in the pathogenesis of tremors. The present study was undertaken to investigate the effect of baclofen, a GABA B receptor agonist on harmaline induced tremors. Four groups of female Wistar rats weighing 100+/-15 g were injected with harmaline (10 mg/kg, intraperitoneally) for inducing experimental tremors. The animals in groups 2, 3 and 4 were given baclofen by gavage at doses of 2.5, 5 and 10 mg/kg, respectively, half an hour before harmaline administration, whereas, the rats in group 1 served as control and received water. The latency of onset, intensity and duration of tremor and electromyographic (EMG) responses were recorded. Treatment with baclofen resulted in a dose dependent decrease in the intensity of tremor. Our EMG study also revealed a significant decrease in the amplitude of tremors in baclofen treated rats. A highly significant increase in latency of onset of tremor was observed in the rats treated with high dose (10 mg/kg) of baclofen only. This study clearly suggests beneficial effects of baclofen in harmaline induced tremors.
- Published
- 2001
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42. Dorsal spine injuries in Saudi Arabia--an unusual cause.
- Author
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Ansari SA, Mandoorah M, Abdalrahim M, and Al Moutaery KR
- Subjects
- Accidents, Traffic, Adult, Animals, Camelus, Female, Humans, Male, Middle Aged, Radiography, Saudi Arabia, Spinal Injuries diagnostic imaging, Spinal Injuries etiology
- Abstract
Background: Motor vehicle accidents are the most common cause of spinal injuries in Saudi Arabia. Camel collisions usually result in cervical spine injuries. Although extremely rare, dorsal spine injuries have also resulted from these accidents., Method: Retrospective analysis of the type of accident of all the patients with dorsal spine injuries was conducted at the supra-regional spinal injuries rehabilitation unit in Riyadh., Results: Of all the patients' records reviewed, three patients' injuries to the dorsal spine had resulted from car accidents involving a camel. These patients, during further interviews, described in detail the exact mechanism of their injuries. Protective lateral bending to avoid the direct impact of the animal resulted in their injuries., Conclusion: Camel collisions remain a significant cause of mortality and morbidity although they affect the cervical spine most often. Dorsal spine injuries can result from protective lateral bending in unrestrained drivers and passengers.
- Published
- 2001
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43. Protective effect of quinacrine on striatal dopamine levels in 6-OHDA and MPTP models of Parkinsonism in rodents.
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Tariq M, Khan HA, Al Moutaery K, and Al Deeb S
- Subjects
- 3,4-Dihydroxyphenylacetic Acid metabolism, Animals, Glutathione metabolism, Homovanillic Acid metabolism, Male, Mice, Mice, Inbred C57BL, Neuroprotective Agents pharmacology, Oxidative Stress physiology, Oxidopamine, Parkinsonian Disorders metabolism, Phospholipases metabolism, Rats, Rats, Wistar, Sympatholytics, Brain Chemistry drug effects, Dopamine metabolism, Enzyme Inhibitors pharmacology, Parkinsonian Disorders drug therapy, Quinacrine pharmacology
- Abstract
Recent studies provide evidence that phospholipase A2 (PLA2) may play a role in the development of experimental parkinsonism. In this investigation an attempt was made to determine a possible protective effect of quinacrine (QNC), a PLA2 inhibitor on MPTP as well as 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in rodents. For MPTP studies, adult male mice (C57 BL) were treated with MPTP (30 mg/kg, i.p.) daily for 5 days. QNC was injected i.p. in the doses of 0, 10, 30 and 60 mg/kg daily 30 min before MPTP in four different groups. Two other groups of mice received either vehicle (control) or a high dose of QNC (60 mg/kg). Two hours after the last injection of MPTP, striata were collected for the analysis of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and glutathione (GSH). For the 6-OHDA study, male Wistar rats were infused with 6-OHDA (60 microg) in the right striatum under chloral hydrate anesthesia. The rats in different groups were treated with 0, 5, 15 and 30 mg/kg QNC (i.p.) for 4 days, while first injection was given 30 min before 6-OHDA. On day 5, rats were sacrificed and striata were stored at -80 degrees C. Administration of MPTP or 6-OHDA significantly reduced striatal DA, which was significantly attenuated by QNC. Concomitant treatment with QNC also protected animals against MPTP or 6-OHDA-induced depletion of striatal GSH. Our findings clearly suggest the role of PLA2 in MPTP and 6-OHDA induced neurotoxicity and oxidative stress. However, further studies are warranted to explore the therapeutic potential of PLA2 inhibitors for the treatment of Parkinson's disease.
- Published
- 2001
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44. Vitamin E decreases valproic acid induced neural tube defects in mice.
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Al Deeb S, Al Moutaery K, Arshaduddin M, and Tariq M
- Subjects
- Administration, Oral, Animals, Crown-Rump Length, Dose-Response Relationship, Drug, Female, Fetal Weight drug effects, Fetus abnormalities, Fetus drug effects, Fetus pathology, Mice, Mice, Inbred BALB C, Neural Tube Defects chemically induced, Neural Tube Defects embryology, Pregnancy, Teratogens, Valproic Acid, Neural Tube Defects prevention & control, Vitamin E administration & dosage
- Abstract
The present study was undertaken to investigate the effect of vitamin E on valproic acid (VPA) induced teratogenesis. Pregnant Balb mice were divided into six groups of 10-11 animals each. The mice in group 1 served as control and were injected with saline subcutaneously on day 8 of gestation, whereas, animals in group 2 received a single injection of VPA (700 mg/kg (s.c.)). Groups 3 and 4 received an oral administration of vitamin E in the doses of 250 and 500 mg/kg, respectively, 1 h before VPA injection. Group 5 and 6 were given vitamin E only, in the same doses as group 3 and 4. On day 18 of gestation, the mice were killed by cervical dislocation. Embryotoxicity was assessed by counting the number of implants, live and dead fetuses, resorptions, crown rump length and fetal body weight. The fetuses were observed for malformations including neural tube defects (excencephaly), open eye lid and micrognathae. VPA administration resulted in a significant reduction of the average live fetuses/litter, fetal weight and crown rump length and a significant increase in malformations (excencephaly, open eye lid and micrognathae). Concomitant administration of vitamin E significantly attenuated VPA induced decrease in the fetal weight, crown rump length and malformations.
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- 2000
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45. Effect of aluminum on neurological recovery in rats following spinal cord injury.
- Author
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Al Moutaery K, Al Deeb S, Biary N, Morais C, Ahmad Khan H, and Tariq M
- Subjects
- Animals, Electrophysiology, Male, Motor Activity, Pain physiopathology, Pain Measurement, Rats, Rats, Sprague-Dawley, Sensation, Spinal Cord metabolism, Spinal Cord pathology, Spinal Cord Injuries pathology, Vitamin E metabolism, Vocalization, Animal, Aluminum poisoning, Nervous System drug effects, Nervous System physiopathology, Spinal Cord Injuries physiopathology
- Abstract
Object: This investigation was undertaken to study the effect of aluminum on neurobehavioral, electrophysiological, structural, and biochemical changes in rats following spinal cord injury (SCI)., Methods: Adult male Sprague-Dawley rats classified into different groups were given aluminum sulfate-dosed drinking water in the concentrations of 0%, 0.25%, 0.5% and 1%, respectively. After 30 days of aluminum treatment, the animals were subjected to spinal cord trauma. Laminectomy was performed at T7-8 in anesthetized rats, followed by placement of a compression plate (2.2 x 5 mm) loaded with a 35-g weight over the exposed spinal cord for 5 minutes. Control animals underwent the same surgical procedure, but the compression injury was not induced (sham). Postoperative neurological function was assessed using the inclined-plane test and by obtaining a modified Tarlov score and vocal/sensory score daily for 10 days. Electrophysiological changes were assessed using corticomotor evoked potentials, whereas pathological changes were assessed by light microscopy. The level of vitamin E in the spinal cord was measured as an index of antioxidant defense. The behavioral, biochemical, and histological analyses were performed in a blinded fashion., Conclusions: Analysis of results obtained in the behavioral studies revealed that the compression of spinal cord produced transient paraparesis in which a maximum motor deficit occurred at Day 1 following SCI and resolved over a period of 10 days. Administration of aluminum significantly impaired the recovery following SCI. Analysis of the results of the biochemical, electrophysiological, and histopathological studies also confirmed the deleterious effects of aluminum on recovery from SCI in rats.
- Published
- 2000
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46. Attenuation of acrylamide-induced neurotoxicity in diabetic rats.
- Author
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Al Deeb S, Al Moutaery K, Arshaduddin M, Biary N, and Tariq M
- Subjects
- Analysis of Variance, Animals, Electromyography, Gait drug effects, Hindlimb, Lipid Peroxides metabolism, Male, Muscle, Skeletal drug effects, Muscle, Skeletal physiology, Muscle, Skeletal physiopathology, Rats, Rats, Sprague-Dawley, Sciatic Nerve metabolism, Acrylamide toxicity, Diabetes Mellitus, Experimental physiopathology, Locomotion drug effects, Motor Activity drug effects, Neurotoxins toxicity
- Abstract
In recent years, an increasing number of cases of neuropathy have been reported as a result of accidental or occupational exposure to chemicals. Acrylamide (Acr), a widely used industrial chemical, is known to produce peripheral neuropathy that resembles diabetic neuropathy in many ways. However, the interaction between diabetes and Acr has not been studied. The present study was undertaken to examine the effect of streptozotocin (STZ)-induced diabetes on Acr-induced neurotoxicity in rats. Male Sprague-Dawley rats weighing 300 +/- 10 g were divided into four groups of 10 animals each. The rats in group 1 served as control, and received normal saline. The animals in group 2 were given Acr dissolved in physiological saline (50 mg/kg IP 3 days/week) for 2 weeks. The rats in group 3 and 4 were made diabetic by administering a single IP injection of STZ (50 mg/kg). The animals in group 3 served as diabetic control, whereas the rats in group 4 received Acr in the same dose regimen as in group 2, a week after induction of diabetes. Neurobehavioral responses including foot print length, hind limb function, landing foot splay, and the ability to stay on an inclined plane were assessed 48 h after the last dose of Acr followed by electrophysiological measurements. The animals were then sacrificed, and sciatic nerves were collected for biochemical analysis. The results of this study clearly showed a significant deterioration of neurobehavioral and electrophysiological responses in Acr-treated rats. Although no significant change in these parameters was observed in the diabetic (only) group, Acr-induced functional deficiency was significantly reduced in diabetic animals. However, the difference in electrophysiological response in Acr-treated diabetic and nondiabetic rats was not found to be statistically significant (p 0.05). The precise mechanism by which Acr induced neurobehavioral toxicity is reduced in diabetic animals warrants further investigations.
- Published
- 2000
- Full Text
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47. Exacerbation of iminodipropionitrile-induced behavioral toxicity, oxidative stress, and vestibular hair cell degeneration by gentamicin in rats.
- Author
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Al Deeb S, Al Moutaery K, Khan HA, and Tariq M
- Subjects
- Animals, Body Weight drug effects, Brain drug effects, Brain metabolism, Drug Synergism, Female, Hair Cells, Vestibular pathology, Lipid Peroxides metabolism, Malondialdehyde metabolism, Posture, Rats, Rats, Sprague-Dawley, Reflex drug effects, Stereotyped Behavior drug effects, Gentamicins toxicity, Hair Cells, Vestibular drug effects, Motor Activity drug effects, Neurotoxins toxicity, Nitriles toxicity, Oxidative Stress drug effects
- Abstract
This study describes the effect of gentamicin, an aminoglycoside antibiotic on iminodipropionitrile (IDPN)-induced abnormal neurobehavioral syndrome in female Sprague-Dawley rats. The animals were exposed to IDPN in the dose of 100 mg/kg/day intraperitoneally for 7 days. Gentamicin (GM) was administered intraperitoneally daily 1 h before IDPN in the doses of 10, 40, and 80 mg/kg body weight in three different groups of rats. One more group of animals received gentamicin alone (80 mg/kg) and served as the gentamicin-alone group. The intensity of IDPN induced characteristic excitation with choreiform, and the circling movement (ECC) syndrome was examined using an observational test battery including dyskinetic head movements, circling, tail hanging, air righting reflex, and contact inhibition of the righting reflex on days 6, 8, 10, 12, 19, 26, and 33. The animals for histopathological observation were sacrificed on day 10, whereas the remaining animals that were used for long-term behavioral studies were sacrificed on day 35 for biochemical observations. The blood and brain samples were collected for the analysis of blood urea nitrogen (BUN), serum creatinine, cerebral malondialdehyde (MDA), conjugated dienes, and lipid hydroperoxides, whereas temporal bones were collected for inner ear histopathology. Our results showed that gentamicin significantly and dose dependently exacerbated the incidence and the severity of the IDPN-induced behavioral syndrome. The histopathology of the inner ear demonstrated more severe loss of sensory hair cells in the crista ampullaris of the rats treated with IDPN plus gentamicin compared to the IDPN-alone treated animals. Concomitant treatment with gentamicin also potentiated IDPN-induced increase in free radical indices, suggesting a possible role of oxidative stress in gentamicin-induced aggravation of IDPN toxicity. Further studies are warranted to determine the role of aminoglycosides in nitrile toxicity and drug-induced movement disorders.
- Published
- 2000
- Full Text
- View/download PDF
48. Diethyldithiocarbamate (DEDC) impairs neuronal recovery following sciatic nerve injury in rats.
- Author
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Tariq M, Arshaduddin M, Biary N, Al Deeb S, and Al Moutaery K
- Abstract
Purpose: Diethyldithiocarbamate (DEDC) is a substituted dithiocarbamate that is metabolically interconvertible with disulfiram (Ant-abuse). In recent years DEDC has received considerable attention because of its clinical applications and potential role in mediating both the toxic and therapeutic actions of disulfiram which is frequently used for alcohol aversion therapy. DEDC is known for its multiplicity of action that exerts both pro- and antioxidant effects. In rodents DEDC has been shown to produce neuroprotective as well as neurotoxic effects. The purpose of this study was to examine the effect of DEDC on neurological recovery following sciatic nerve crush injury (SNCI) in rats. Methods: Adult female Wistar rats were subjected to SNCI with a haemostat under deep anaesthesia. The animals were orally treated with DEDC at the doses of 250 mg/kg, 500 mg/kg and 750 mg/kg body weight 1 hr before SNCI and then once daily for 60 days. The animals were observed for sciatic functional index (walking deficit), electrophysiological and histological changes. Vitamin E level was measured to deter-mine antioxidant status of sciatic nerve. Results: Crush injury to the sciatic nerve resulted in a significant impairment of functional response which gradually recovered over a period of 22 days. Treatment of animals with DEDC caused a significant delay in functional recovery which was accompanied by poor histo-logical and electrophysiological outcome. Prooxidant effect of DEDC is quite evident from a significant decrease in vitamin E levels in both injured and uninjured sciatic nerves. Conclusions: Our results demonstrate that exposure to DEDC adversely affects recovery from peripheral nerve injury. The delay may to some extent be attributed to DEDC induced oxidative stress.
- Published
- 2000
49. An unusual cause of depressed skull fracture: case report.
- Author
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Ansari S and Al Moutaery K
- Subjects
- Animals, Camelus, Child, Preschool, Frontal Lobe diagnostic imaging, Frontal Lobe surgery, Humans, Magnetic Resonance Imaging, Male, Parietal Lobe diagnostic imaging, Parietal Lobe surgery, Saudi Arabia, Skull Fracture, Depressed diagnosis, Skull Fracture, Depressed surgery, Tomography, X-Ray Computed, Accidents, Traffic, Frontal Lobe injuries, Parietal Lobe injuries, Skull Fracture, Depressed etiology
- Abstract
Background: Camel collision accidents are a common occurrence in Saudi Arabia, with a high rate of mortality and morbidity. Isolated injuries are rare because of the nature of impact sustained by the person., Case Description: A 4-year-old child with an isolated depressed skull fracture resulting from a camel collision is described. The other occupants of the car were crushed to death. The child sustained only an impact to his head, causing a compound depressed skull fracture with localized cortical damage., Conclusions: Camel collision accidents are a common cause of mortality and morbidity in Saudi Arabia. Isolated skull injuries are rare and result from a localized impact. This is the first report of a compound depressed skull fracture from such an incident. The extent of the problem and efforts toward prevention are described.
- Published
- 1999
- Full Text
- View/download PDF
50. Nitric oxide synthase inhibitor aminoguanidine potentiates iminodipropionitrile-induced neurotoxicity in rats.
- Author
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Tariq M, Khan HA, Al Deeb S, and Al Moutaery K
- Subjects
- Administration, Oral, Animals, Dose-Response Relationship, Drug, Drug Synergism, Dyskinesia, Drug-Induced, Dyskinesias epidemiology, Dyskinesias physiopathology, Hair Cells, Auditory drug effects, Hair Cells, Auditory pathology, Head physiopathology, Incidence, Male, Movement drug effects, Rats, Rats, Wistar, Reflex drug effects, Enzyme Inhibitors pharmacology, Guanidines pharmacology, Neurotoxins pharmacology, Nitric Oxide Synthase antagonists & inhibitors, Nitriles pharmacology
- Abstract
This investigation was undertaken to study the effect of nitric oxide synthase inhibitor, aminoguanidine on iminodipropionitrile (IDPN)-induced neurobehavioral and vestibular toxicity in rats. The dyskinetic syndrome was produced in male Wistar rats by i.p. injections of IDPN (100 mg/kg) for 6 days. Aminoguanidine was administered orally in the doses of 50, 150 and 300 mg/kg, 60 min before IDPN in three different groups. Control rats received vehicle only, whereas another group was treated with 300 mg/kg of aminoguanidine alone (without IDPN). Our results showed that aminoguanidine significantly and dose dependently exacerbated the incidence and intensity of IDPN-induced dyskinetic head movements. Aminoguanidine potentiated IDPN-induced loss of air righting reflex. The histopathological examination of inner ear showed aggravation of IDPN-induced degeneration of sensory hair cells in the crista ampullaris by aminoguanidine. These results suggest the role of nitric oxide in IDPN-induced neurobehavioral and vestibular toxicity.
- Published
- 1999
- Full Text
- View/download PDF
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