1,355,171 research outputs found
Interview with Khaled Beydoun
No full textThe following is a transcription of an interview with Professor Khaled Beydoun, conducted at the University of Michigan Law School on March 15, 2019. The transcript has been lightly edited for clarity
Oxcarbazepine in neuropathic pain
No full textNeuropathic pain is a frequent condition that can result from a variety of underlying conditions and is frequently chronic and difficult to treat. A number of drugs are used to treat neuropathic pain, including anticonvulsants and antidepressants. Oxcarbazepine, a recently introduced antiepileptic drug, was found to possess antineuralgic properties in animal models of neuropathic pain. Several double-blind, placebo-controlled trials have evaluated oxcarbazepine in painful diabetic neuropathy and trigeminal neuralgia. There is good evidence that oxcarbazepine is effective in relieving the pain associated with trigeminal neuralgia. Its efficacy in treating painful diabetic neuropathy is less clear; however, it seems to be useful when tolerated at doses of 1800 mg-day. © 2007 Informa UK Ltd.ALTMAN DG, 1995, BRIT MED J, V311, P485; Backonja M, 1998, JAMA-J AM MED ASSOC, V280, P1831, DOI 10.1001-jama.280.21.1831; Berger A, 2004, J PAIN, V5, P143, DOI 10.1016-j.jpain.2003.12.004; Beydoun A, 2000, NEUROLOGY, V54, P2245; Beydoun A, 2003, J PAIN SYMPTOM MANAG, V25, pS18, DOI 10.1016-S0885-3924(03)00066-6; Beydoun A, 2002, 21 AM PAIN SOC ANN M; Beydoun A, 2006, ACTA NEUROL SCAND, V113, P395, DOI 10.1111-j.1600-0404.2006.00631.x; Bialer M., 2002, ANTIEPILEPTIC DRUGS, P459; Bridges D, 2001, BRIT J ANAESTH, V87, P12, DOI 10.1093-bja-87.1.12; CALABRESI P, 1995, EPILEPSIA, V36, P990, DOI 10.1111-j.1528-1157.1995.tb00957.x; Campbell JN, 2006, NEURON, V52, P77, DOI 10.1016-j.neuron.2006.09.021; Carey TS, 1996, SPINE, V21, P339, DOI 10.1097-00007632-199602010-00018; Clark MR, 2000, J PSYCHOSOM RES, V48, P51, DOI 10.1016-S0022-3999(99)00076-8; Crawford P, 2002, CNS DRUGS, V16, P263, DOI 10.2165-00023210-200216040-00005; DAM M, 1989, EPILEPSY RES, V3, P70; DAVIES HTO, 1993, PAIN, V54, P341, DOI 10.1016-0304-3959(93)90035-N; DEVOR M, 1993, J NEUROSCI, V13, P1976; DEVOR M, 1991, BRIT MED BULL, V47, P619; Dogra S, 2005, EUR J PAIN, V9, P543, DOI 10.1016-j.ejpain.2004.11.006; DOUGHERTY PM, 1992, BRAIN RES, V570, P109, DOI 10.1016-0006-8993(92)90570-Y; Eisenberg E, 2001, NEUROLOGY, V57, P505; FARAGO F, 1987, EUR NEUROL, V26, P73, DOI 10.1159-000116315; Farrar JT, 2003, J PAIN SYMPTOM MANAG, V25, P406, DOI 10.1016-S0885-3924(03)00162-3; Flesch G, 2004, CLIN DRUG INVEST, V24, P185, DOI 10.2165-00044011-200424040-00001; Fox A, 2003, PAIN, V105, P355, DOI 10.1016-S0304-3959(03)00253-7; Galer BS, 2000, DIABETES RES CLIN PR, V47, P123, DOI 10.1016-S0168-8227(99)00112-6; Grosskopf J, 2006, ACTA NEUROL SCAND, V114, P177, DOI 10.1111-j.1600-0404.2005.00559.x; Harati Y, 1998, NEUROLOGY, V50, P1842; Ichikawa K, 2001, EUR J PHARMACOL, V420, P119, DOI 10.1016-S0014-2999(01)01007-X; Jang Y, 2005, ANESTH ANALG, V101, P800, DOI 10.1213-01.ane.0000167283.80463.d7; Karceski S, 2005, EPILEPSY BEHAV, V7, pS1, DOI 10.1016-j.yebeh.2005.06.001; KRAMER L, CLIN EXP REP CLIN DO; Kutluay E, 2003, EPILEPSY BEHAV, V4, P175, DOI 10.1016-S1525-5050(03)00037-4; Lesser H, 2004, NEUROLOGY, V63, P2104; LINDSTROM P, 1987, PAIN, V30, pS85, DOI 10.1016-0304-3959(87)91248-6; Loney PL, 1999, PHYS THER, V79, P384; Magenta P, 2005, NEUROL SCI, V26, P218, DOI 10.1007-s10072-005-0464-z; May TW, 2003, CLIN PHARMACOKINET, V42, P1023, DOI 10.2165-00003088-200342120-00002; MCLEAN MJ, 1994, EPILEPSIA, V35, pS5, DOI 10.1111-j.1528-1157.1994.tb05949.x; Meyer-Rosberg K, 2001, EUR J PAIN-LONDON, V5, P391, DOI 10.1053-eujp.2001.0260; *NOV PHARM CORP, 2000, TRIL PROD MON; PORTENOY RK, 1990, PAIN, V43, P273, DOI 10.1016-0304-3959(90)90025-9; Raskin J, 2005, PAIN MED, V6, P346, DOI 10.1111-j.1526-4637.2005.00061.x; REMILLARD G, 1994, EPILEPSIA, V35, pS28, DOI 10.1111-j.1528-1157.1994.tb05946.x; Rowbotham M, 1998, JAMA-J AM MED ASSOC, V280, P1837, DOI 10.1001-jama.280.21.1837; Rowbotham MC, 2004, PAIN, V110, P697, DOI 10.1016-j.pain.2004.05.010; Sachdeo RC, 2002, ANN NEUROL, V51, P613, DOI 10.1002-ana.10190; SATO J, 1991, SCIENCE, V251, P1608, DOI 10.1126-science.2011742; Schmidt D, 2004, EPILEPSY BEHAV, V5, P627, DOI 10.1016-j.yebeh.2004.07.004; SCHMUTZ M, 1994, EPILEPSIA, V35, pS47, DOI 10.1111-j.1528-1157.1994.tb05967.x; Smith TE, 2000, HOSP MED, V61, P760; STEFANI A, 1995, EPILEPSIA, V36, P997, DOI 10.1111-j.1528-1157.1995.tb00958.x; TAYLOR S, 2006, PAIN PRACT, V6, P22; Vaillancourt PD, 1999, MED CLIN N AM, V83, P627, DOI 10.1016-S0025-7125(05)70127-9; WAMIL A W, 1991, Epilepsia, V32, P65; Wernicke JF, 2006, NEUROLOGY, V67, P1411, DOI 10.1212-01.wnl.0000240225.04000.1a; WHITE HS, 1999, EPILIPSIA, V40, pS1; XIE YK, 1993, SCI CHINA SER B, V36, P68; ZAKRZEWSKA JM, 1989, J NEUROL NEUROSUR PS, V52, P472, DOI 10.1136-jnnp.52.4.472; Ziegler D, 1992, J Diabetes Complications, V6, P49, DOI 10.1016-1056-8727(92)90049-Q128
Oxcarbazepine in painful diabetic neuropathy: Results of a dose-ranging study
No full textObjectives - To evaluate the efficacy and safety of oxcarbazepine in patients with diabetic neuropathy in a multicenter, double-blind, placebo-controlled, dose-ranging 16-week study. Methods - A total of 347 patients were randomized to oxcarbazepine 600 mg-day (n = 83), 1,200 mg-day (n = 87), 1,800 mg-day (n = 88), or placebo (n = 89). The primary efficacy variable was change in mean visual analog scale (VAS) score from baseline to the last week of the study. Results - No difference between any oxcarbazepine group and the placebo group was noted for the primary efficacy variable. Both the 1,200- and 1,800-mg-day groups showed a trend toward statistical significance (P = 0.101, P = 0.096, respectively). Statistically significant differences were found between the oxcarbazepine 1,200-mg-day (P = 0.038) and 1,800-mg-day (P = 0.005) groups and placebo in the overall mean weekly VAS scores for the entire double-blind treatment phase. Conclusions - Although the primary efficacy variable did not reach statistical significance, patients taking oxcarbazepine 1,200 and 1,800 mg-day showed improvements in VAS scores compared with placebo. Oxcarbazepine may provide clinically meaningful pain relief in patients with painful diabetic neuropathy. © 2006 The Authors.Backonja M, 2003, CLIN THER, V25, P81, DOI 10.1016-S0149-2918(03)90011-7; Backonja M, 1998, JAMA-J AM MED ASSOC, V280, P1831, DOI 10.1001-jama.280.21.1831; Bang Lynne, 2003, Paediatr Drugs, V5, P557, DOI 10.2165-00148581-200305080-00006; Barcs G, 2000, EPILEPSIA, V41, P1597; Beydoun A, 2000, NEUROLOGY, V54, P2245; Beydoun A, 2001, EPILEPSY BEHAV, V2, P187, DOI 10.1006-ebeh.2001.0198; BEYDOUN A, 2002, J PAIN S1, V3, P38; Beydoun A, 2004, CLIN J PAIN, V20, P174, DOI 10.1097-00002508-200405000-00007; Bill PA, 1997, EPILEPSY RES, V27, P195, DOI 10.1016-S0920-1211(97)00024-7; Christe W, 1997, EPILEPSY RES, V26, P451, DOI 10.1016-S0920-1211(96)01013-3; Collins SL, 2000, J PAIN SYMPTOM MANAG, V20, P449, DOI 10.1016-S0885-3924(00)00218-9; DAM M, 1989, EPILEPSY RES, V3, P70; Dogra S, 2005, EUR J PAIN, V9, P543, DOI 10.1016-j.ejpain.2004.11.006; Duby JJ, 2004, AM J HEALTH-SYST PH, V61, P160; Dworkin RH, 2003, ARCH NEUROL-CHICAGO, V60, P1524, DOI 10.1001-archneur.60.11.1524; Farrar JT, 2003, J PAIN SYMPTOM MANAG, V25, P406, DOI 10.1016-S0885-3924(03)00162-3; Glauser TA, 2000, NEUROLOGY, V54, P2237; GROSSKOPF J, IN PRESS ACTA NEUROL; Guerreiro MM, 1997, EPILEPSY RES, V27, P205, DOI 10.1016-S0920-1211(97)00025-9; Ichikawa K, 2001, EUR J PHARMACOL, V420, P119, DOI 10.1016-S0014-2999(01)01007-X; Lindstrom P., 1987, PAIN S, V30, pS85; MCQUAY H, 1995, BRIT MED J, V311, P1047; Raskin P, 2004, NEUROLOGY, V63, P865; Rosenstock J, 2004, PAIN, V110, P628, DOI 10.1016-j.pain.2004.05.001; Sachdeo R, 2001, NEUROLOGY, V57, P864; Schachtar SC, 1999, NEUROLOGY, V53, P2211; Schmader KE, 2002, CLIN J PAIN, V18, P350, DOI 10.1097-00002508-200211000-00002; STEFANI A, 1995, EPILEPSIA, V36, P997, DOI 10.1111-j.1528-1157.1995.tb00958.x; Thienel U, 2004, ACTA NEUROL SCAND, V110, P221, DOI 10.1111-j.1600-0404.2004.00338.x; WAMIL A W, 1991, Epilepsia, V32, P65; Wellington K, 2001, CNS DRUGS, V15, P137, DOI 10.2165-00023210-200115020-0000559535
Valproate-induced thrombocytopenia: A prospective monotherapy study
No full textPurpose: The frequency of valproate (VPA)-induced thrombocytopenia varied widely in previous studies, due to methodological differences. Our objective was to evaluate the relationship between trough VPA plasma levels and platelet counts and assess risk factors for the development of thrombocytopenia. Methods: Patients with refractory partial epilepsy were enrolled in this double-blind, multicenter, concentration-response trial that evaluated the efficacy and safety of high versus low trough plasma VPA concentrations following administration of divalproex sodium as monotherapy. Trough VPA concentrations and concomitant platelet counts were drawn at baseline and intermittently throughout the 24-week trial. Bivariate correlations and multivariate stepwise regression analysis were performed between platelet counts and multiple variables. A logistic regression analysis was done to determine the probability of developing thrombocytopenia at various VPA levels. Results: A total of 851 VPA levels and concomitant platelet counts were analyzed in 265 patients. Of these, 17.7percent of patients experienced at least one episode of thrombocytopenia (platelet count ≤ 100,000-μl) after exposure to divalproex sodium. A significant negative correlation was found between VPA levels and platelet counts. Women were significantly more likely to develop thrombocytopenia. The probability of developing thrombocytopenia substantially increased at trough VPA levels above 100 μg-ml in women and above 130 μg-ml in men. Discussion: Our data strongly support a causal relationship between rising plasma VPA levels and reduced platelet counts, with additional risk factors including female gender and lower baseline platelet counts. © 2008 International League Against Epilepsy.Allarakhia IN, 1996, PEDIATR NEUROL, V14, P303, DOI 10.1016-0887-8994(96)00052-5; Anderson GD, 1997, J NEUROSURG, V87, P252, DOI 10.3171-jns.1997.87.2.0252; BARR RD, 1982, ARCH DIS CHILD, V57, P681; Beydoun A, 1997, NEUROLOGY, V48, P182; Conley EL, 2001, PHARMACOTHERAPY, V21, P1325, DOI 10.1592-phco.21.17.1325.34418; COULTER DL, 1980, JAMA-J AM MED ASSOC, V244, P785; DELGADO MR, 1994, J CHILD NEUROL, V9, P311; GANICK DJ, 1990, AM J PEDIAT HEMATOL, V12, P80; GIDAL B, 1994, NEUROLOGY, V44, P1418; Hauser E, 1996, BRAIN DEV-JPN, V18, P105, DOI 10.1016-0387-7604(95)00139-5; HOFFMAN LM, 1982, CAN MED ASSOC J, V126, P358; KISHI T, 1994, ARCH DIS CHILD, V71, P153; LEVY RH, 1984, EPILEPSIA, V25, pS10, DOI 10.1111-j.1528-1157.1984.tb05631.x; LOISEAU P, 1975, EPILEPSIA, V16, P609, DOI 10.1111-j.1528-1157.1975.tb04743.x; LOISEAU P, 1981, EPILEPSIA, V22, P141, DOI 10.1111-j.1528-1157.1981.tb04094.x; MAY RB, 1993, EPILEPSIA, V34, P1098, DOI 10.1111-j.1528-1157.1993.tb02139.x; MORRIS N, 1981, CAN MED ASSOC J, V125, P63; NEOPHYTIDES AN, 1979, ANN NEUROL, V5, P389, DOI 10.1002-ana.410050414; Oluboka OJ, 2000, J AM GERIATR SOC, V48, P349; RAWORTH RE, 1978, LANCET, V1, P670; RICHARDSON SGN, 1976, BRIT MED J, V1, P221; ROBINSON D, 1995, J AM GERIATR SOC, V43, P198; SANDLER RM, 1978, BRIT MED J, V2, P1683; SCHOBBEN F, 1974, PHARM WEEKBLAD, V109, P30; TOHEN M, 1995, AM J PSYCHIAT, V152, P413; Trannel TJ, 2001, AM J PSYCHIAT, V158, P128, DOI 10.1176-appi.ajp.158.1.128; TURNBULL DM, 1983, ANN NEUROL, V14, P38, DOI 10.1002-ana.410140107; VAJDA F, 1976, TREATMENT EPILEPSY, P91; Verrotti A, 1999, PEDIATR NEUROL, V21, P611, DOI 10.1016-S0887-8994(99)00060-0; von Voss H, 1976, Br Med J, V2, P179; Warkentin TE, 2006, BLOOD, V108, P2937, DOI 10.1182-blood-2005-11-012450; WINFIELD DA, 1976, BRIT MED J, V2, P981; WULFF K, 1977, EPILEPSIA, V18, P149, DOI 10.1111-j.1528-1157.1977.tb04463.x; Wyngaarden J. B., 1992, CECIL TXB MED27272
Treatment of idiopathic generalized epilepsy - A review of the evidence
No full textIntroduction: Epilepsy is stratified into idiopathic partial, symptomatic partial, idiopathic generalized (IGE) and symptomatic generalized epilepsies. Areas covered: The epidemiology and clinical characteristics of IGE are reviewed in this paper. Clinically, IGE is characterized by the occurrence of any of the following three seizure types: absence seizures, myoclonic seizures and primarily generalized tonic-clonic seizures. To assess the presence of evidence-based data on the treatment of IGE, the literature was extensively reviewed for studies evaluating the treatment of IGE with various antiepileptic drugs. These studies were stratified into four classes based on recently described criteria. Class I studies were considered as providing evidence of the efficacy of the drug in patients with IGE. Finally, suggestions to evaluate the efficacy of a study drug in patients with IGE are presented. Expert opinion: Based on the reviewed data, there is strong evidence-based data to support the use of valproate and ethosuximide for the treatment of childhood absence seizures; for the use of topiramate as monotherapy or adjunctive therapy for patients with primarily generalized tonic-clonic seizures; for the use of adjunctive therapy with lamotrigine for the treatment of primarily generalized tonic-clonic seizures; and for the use of levetiracetam as adjunctive therapy for the treatment of myoclonic or primarily generalized tonic-clonic seizures. To evaluate a new drug as a potential treatment for patients with IGE requires a rational methodology, discussed in this review. © 2012 Informa UK, Ltd.Adab N, 2004, J NEUROL NEUROSUR PS, V75, P1575, DOI 10.1136-jnnp.2003.029132; Adie W J, 1924, Proc R Soc Med, V17, P19; Arroyo S, 2005, ACTA NEUROL SCAND, V112, P214, DOI 10.1111-j.1600-0404.2005.00485.x; Atakli D, 1998, SEIZURE-EUR J EPILEP, V7, P63, DOI 10.1016-S1059-1311(98)90010-3; Bauer J, 2008, ACTA NEUROL SCAND, V117, P55, DOI 10.1111-j.1600-0404.2007.00940.x; Benbadis SR, 2003, NEUROLOGY, V61, P1793; Beran RG, 1998, EPILEPSIA, V39, P1329, DOI 10.1111-j.1528-1157.1998.tb01332.x; Berg AT, 1999, EPILEPSIA, V40, P439, DOI 10.1111-j.1528-1157.1999.tb00738.x; Berg AT, 2010, EPILEPSIA, V51, P676, DOI 10.1111-j.1528-1167.2010.02522.x; Berkovic SF, 2007, NEUROLOGY, V69, P1751, DOI 10.1212-01.wnl.0000268699.34614.d3; Beydoun A, 2001, EPILEPSY BEHAV, V2, P187, DOI 10.1006-ebeh.2001.0198; Biton V, 2005, NEUROLOGY, V65, P1737, DOI 10.1212-01.wnl.0000187118.19221.e4; Biton V, 1999, NEUROLOGY, V52, P1330; Biton V, 2010, EPILEPSY BEHAV, V19, P352, DOI 10.1016-j.yebeh.2010.07.022; BOURGEOIS B, 1987, EPILEPSIA, V28, pS8, DOI 10.1111-j.1528-1157.1987.tb05769.x; BRODIE MJ, 1995, LANCET, V345, P476, DOI 10.1016-S0140-6736(95)90581-2; Brodie MJ, 2002, EPILEPSIA, V43, P993, DOI 10.1046-j.1528-1157.2002.45401.x; CALLAGHAN N, 1982, DEV MED CHILD NEUROL, V24, P830; Callenbach PMC, 1998, EPILEPSIA, V39, P331, DOI 10.1111-j.1528-1157.1998.tb01382.x; Canger R, 2000, CLIN DRUG INVEST, V20, P215, DOI 10.2165-00044011-200020040-00002; Commission on Classification and Terminology of the International League Against Epilepsy, 1989, EPILEPSIA, V30, P389; BANCAUD J, 1981, EPILEPSIA, V22, P489; Dulac O, 1997, EPILEPSIA, V38, P1251; COVANIS A, 1982, EPILEPSIA, V23, P693, DOI 10.1111-j.1528-1157.1982.tb05085.x; DULAC O, 1982, ARCH FR PEDIATR, V39, P347; Engel J, 2001, EPILEPSIA, V42, P316, DOI 10.1046-j.1528-1157.2001.t01-1-36500.x; Engel Jr J, 1989, CONT NEUROLOGY SERIE, V31; Fattore C, 2011, EPILEPSIA, V52, P802, DOI 10.1111-j.1528-1167.2010.02976.x; Fisher RS, 2008, EPILEPSIA, V49, P7, DOI 10.1111-j.1528-1167.2008.01921.x; Fisher RS, 2005, EPILEPSIA, V46, P470, DOI 10.1111-j.0013-9580.2005.66104.x; Frank LM, 1999, EPILEPSIA, V40, P973, DOI 10.1111-j.1528-1157.1999.tb00805.x; GASTAUT H, 1975, EPILEPSIA, V16, P457, DOI 10.1111-j.1528-1157.1975.tb06073.x; Gelisse P, 2004, EPILEPSIA, V45, P1282, DOI 10.1111-j.0013-9580.2004.19704.x; Genton P, 2000, NEUROLOGY, V55, P1106; Glauser T, 2006, EPILEPSIA, V47, P10941; Glauser TA, 2010, NEW ENGL J MED, V362, P790, DOI 10.1056-NEJMoa0902014; GOLLA FL, 1957, J MENT SCI, V103, P214; Guerrini R, 2005, SEIZURE-EUR J EPILEP, V14, P371, DOI 10.1016-j.seizure.2005.05.001; Guerrini Renzo, 2005, Adv Neurol, V95, P273; HEATHFIELD K G, 1961, BRIT MED J, V2, P565; Hitiris N, 2005, EPILEPSIA, V46, P149, DOI 10.1111-j.1528-1167.2005.00327.x; Holland KD, 2010, ACTA NEUROL SCAND, V121, P149, DOI 10.1111-j.1600-0404.2009.01308.x; Jallon P, 2005, EPILEPSIA, V46, P10, DOI 10.1111-j.1528-1167.2005.00309.x; Koutroumanidis M, 2005, EPILEPSIA, V46, P96, DOI 10.1111-j.1528-1167.2005.00320.x; Loiseau J, 2000, CHILDHOOD ABSENCE EP; LOMBROSO CT, 1960, EPILEPSIA, V1, P493; MANFORD M, 1992, ARCH NEUROL-CHICAGO, V49, P801; Marson AG, 2007, LANCET, V369, P1016, DOI 10.1016-S0140-6736(07)60461-9; Mattson RH, 2003, EPILEPSIA, V44, P2, DOI 10.1046-j.1528-1157.44.s.2.3.x; MIKKELSEN B, 1976, ARCH NEUROL-CHICAGO, V33, P322; Mohanraj R, 2005, EPILEPSY BEHAV, V6, P382, DOI 10.1016-j.yebeh.2005.01.008; Morrow J, 2006, J NEUROL NEUROSUR PS, V77, P193, DOI 10.1136-jnnp.2005.074203; Nejad SEM, 2009, INT J PHARMACOL, V5, P313; Nicolson A, 2004, J NEUROL NEUROSUR PS, V75, P75; Noachtar S, 2008, NEUROLOGY, V70, P607, DOI 10.1212-01.wnl.0000297512.18364.40; Nordli DR, 2005, EPILEPSIA, V46, P48, DOI 10.1111-j.1528-1167.2005.00313.x; Panayiotopoulos CP, 2005, EPILEPSIA, V46, P1, DOI 10.1111-j.1528-1167.2005.00330.x; PANAYIOTOPOULOS CP, 1989, BRAIN, V112, P1039, DOI 10.1093-brain-112.4.1039; Panayiotopoulos CP, 2007, CLIN GUIDE EPILEPTIC; Panayiotopoulos CP, 2011, EPILEPSIA, V52, P2155, DOI 10.1111-j.1528-1167.2011.03288.x; Panayiotopoulos CP, 2005, EPILEPSIA, V46, P57, DOI 10.1111-j.1528-1167.2005.00314.x; Posner EB, 2005, COCHRANE DB SYST REV, V4; RESOR SR, 1990, NEUROLOGY, V40, P1677; Sadleir LG, 2009, EPILEPSIA, V50, P1572, DOI 10.1111-j.1528-1167.2008.02001.x; SATO S, 1982, NEUROLOGY, V32, P157; Steinhoff BJ, 2005, SEIZURE-EUR J EPILEP, V14, P597, DOI 10.1016-j.seizure.2005.09.011; Striano P, 2005, ACTA NEUROL SCAND, V111, P211, DOI 10.1111-j.1600-0404.2005.00385.x; Trevathan E, 2006, PEDIATRICS, V118, pE371, DOI 10.1542-peds.2006.0148; VILLARREAL HJ, 1978, NEUROLOGY, V28, P886; Wilfong A, 2005, EPILEPSY RES, V64, P31, DOI 10.1016-j.eplepsyres.2005.02.006; ZIMMERMAN FT, 1958, NEUROLOGY, V8, P76975
A dimensional tolerancing knowledge management system using Nested Ripple Down Rules (NRDR)
No full textThis paper proposes to use a knowledge acquisition (KA) approach based on Nested Ripple Down Rules (NRDR) to assist in mechanical design focusing on dimensional tolerancing. A knowledge approach to incrementally model expert design processes is implemented. The knowledge is acquired in the context of its use, which substantially supports the KA process. The knowledge is captured which human designers utilize in order to specify dimensional tolerances on shafts and mating holes in order to meet desired classes of fit as set by relevant engineering standards in order to demonstrate the presented approach. The developed dimensional tolerancing knowledge management system would help mechanical designers become more effective in the time-consuming tolerancing process of their designs in the future. © 2009 Elsevier Ltd. All rights reserved.*AM NAT STAND I, 1994, MATH DEF DIM TOL; *AM NAT STAND I, 1994, DIM TOL; [Anonymous], 1997, 1030347 ISO; Beydoun C, 2005, INT J COOP INF SYST, V14, P45; Beydoun G, 2001, INT J HUM-COMPUT ST, V54, P407, DOI 10.1006-ijhc.2000.0445; Beydoun G, 2000, INT J HUM-COMPUT ST, V52, P493, DOI 10.1006-ijhc.1999.0338; BEYDOUN G, 1997, ADV TOPICS ARTIFICIA, V1342, P177, DOI 10.1007-3-540-63797-4_70; Chapman CB, 1999, KNOWL-BASED SYST, V12, P257, DOI 10.1016-S0950-7051(99)00013-1; Chiesi F., 2003, J COMPUTING INFORM S, V3, P100, DOI 10.1115-1.1574064; Compton P., 1990, Knowledge Acquisition, V2, DOI 10.1016-S1042-8143(05)80017-2; Compton P., 1994, EUR KNOWL ACQ WORKSH; Desrochers A, 2003, J MECH DESIGN, V125, P14, DOI 10.1115-1.153974; FINGER S, 2000, IFIP TC5 WG5 2 3 WOR; Gaines B.R., 1991, 6 BANFF KNOWL ACQ KN; Hoffmann A., 1991, 12 INT C ART INT IJC; Hu J, 2007, P I MECH ENG C-J MEC, V221, P455, DOI [10.1243-0954406JMES438, 10.1243-0954406jmes438]; HU X, 2000, P DETC 00 2000 ASME; *ISO, 1999, 1030342 ISO; Kang B., 1998, 9 AAAI SPONS BANFF K; KING DA, 1994, J MECH DESIGN, V116, P480, DOI 10.1115-1.2919404; Linster M., 1993, 2 GENERATION EXPERT, P477; Meadows J., 1995, GEOMETRIC DIMENSIONI; Menzies T., 1995, P 9 BANFF KNOWL ACQ; Radack G.M., 1994, ASME SERIES INT ADV; Rezayat M., 2000, COMPUT AIDED DESIGN, V32, P94; ROY U, 1994, CYBERNET SYST, V25, P611, DOI 10.1080-01969729408902345; Shen Z, 2005, J COMPUT INF SCI ENG, V5, P247, DOI 10.1115-1.1979509; Shen Z, 2004, J COMPUT INF SCI ENG, V3, P95, DOI 10.1115-1.1573236; Shigley J.E., 1986, STANDARD HDB MACHINE; WANG N, 1993, J MECH DESIGN, V115, P757, DOI 10.1115-1.2919265; Wu WD, 2004, J MECH DESIGN, V126, P581, DOI 10.1115-1.176077521
Oxcarbazepine
No full textA review of the chemistry, pharmacology, clinical pharmacology, and clinical use of the antiepileptic drug oxcarbazepine
Hadia Beydoun-Mawlawi Thesis
No full textThis study explores the Museum of Fine Arts Houstonâs (MFAH) relationship with Houstonâs growing Latino population and asks how MFAH adapts its programs for this community in order to serve, as its motto states, as âa place for all people.â This study is based on interviews, focus groups, and surveys both at MFAH and in Houstonâs Latino communities. Several efforts are underway to broaden the museumâs Latino audience base, including the commitment to an expanded Latin American art department and the inclusion of bilingual wall-texts and brochures for select exhibitions. Surveys of Latino community members and Latino visitors to the MFAH indicate that they are satisfied by how the MFAH reflects Houstonâs diverse cultures but 47% of community members donât feel that the MFAH is a place for all people. Interviews conducted with museum staff reveal that there is no institutional attempt to appeal specifically to the Latino community, whether marketing public programs or outreach. This study puts forth recommendations to help the MFAH increase its Latino audience, including providing improved information about discounts and free admission, offering Spanish programs that integrate visual and performing arts, providing interactive programs for children, offering a selection of Latino-themed exhibitions curated by local artists that promote local Latino talent, and developing close relationships with Latino cultural and community centers.M.S., Arts Administration -- Drexel University, 201
Emerging drugs for partial onset seizures
No full textImportance of the field: Patients with epilepsy have recurrent unproved seizures. Epilepsy is common, with a prevalence range that centers at around 1percent. Patients with epilepsy can have a poor quality of life and suffer significant social stigma. Despite the availability of a large number of antiepileptic drugs (AEDs) including standard and newer ones, a significant percentage of patients with epilepsy remain poorly controlled. Areas covered in this review: In this review, we briefly summarize data on the available AEDs, then present current information on the emerging AEDs, including their chemical structure, pharmacology, mechanism of action, and efficacy and adverse event profile in clinical trials. The AEDs included are rufinamide, lacosamide, eslicarbazepine, retigabine, brivaracetam, ganaxolone, stiripentol and carisbamate. Most of the literature related to these AEDs was published in the past 5 years. What the reader will gain: The reader will become familiar with the pharmacology of emerging AEDs and the results of clinical trials with these AEDs. The reader will also be able to assess the advantages of AEDs and their potential respective places in the treatment of epilepsy. Take home message: The emerging AEDs offer predominantly improved pharmacokinetics and tolerability and occasionally new mechanisms of action. 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