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891 results on '"Middleton, L"'

151. Cortical Lewy bodies and Aβ burden are associated with prevalence and timing of dementia in Lewy body diseases

Author

Ruffmann, C., primary, Calboli, F. C. F., additional, Bravi, I., additional, Gveric, D., additional, Curry, L. K., additional, de Smith, A., additional, Pavlou, S., additional, Buxton, J. L., additional, Blakemore, A. I. F., additional, Takousis, P., additional, Molloy, S., additional, Piccini, P., additional, Dexter, D. T., additional, Roncaroli, F., additional, Gentleman, S. M., additional, and Middleton, L. T., additional

Published
2015
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157. Silent embolic infarcts on computed tomography brain scans and risk of ipsilateral hemispheric events in patients with asymptomatic internal carotid artery stenosis

Author

Kakkos, Sk, Sabetai, M, Tegos, T, Stevens, J, Thomas, D, Griffin, M, Geroulakos, G, Nicolaides AN Adovasio, B, Ziani, B, Alò, Fp, Cicilioni, Cg, Ambrosio, G, Andreev, A, Andreozzi, Gm, Verlato, F, Camporese, G, Arosio, E, Barkauskas, E, Barros D'Sa AA, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, Gp, Simoni, G, Bell, P, Biasi, Gm, Mingazzini, P, Bornstein, Nm, Bouchier Hayes, D, Fitzgerald, P, Cairols, Ma, Cao, Pg, Derango, P, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopoulos, E, Andreadis, Ea, Dimakakos, Pb, Kotsis, T, Eikelboom, B, Entz, L, Aloi Ferrari Bardile, T, Salerno, M, Fernandes J, Fernandes e., Pedro, L, Fitzgerald, De, O'Shaunnersy, A, Fletcher, J, Forconi, S, Cappeli, R, Bicchi, M, Arrigucci, S, Gallai, V, Cardaiolli, G, Kakkos, S, Gomez Isaza LF, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Giannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, Bb, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, Tyllis, T, Minar, E, Willfort, A, Moggi, L, Nenci, G, Radicchia, S, Nicolaides, A, Norgren, L, Ribbe, E, Novo, S, Tantillo, R, Olinic, D, Paaske, W, Pagnan, A, Pauletto, P, Pagliara, V, Pettina, G, Pratesi, C, Matticari, S, Polivka, J, Sevcik, P, Poredos, P, Blinc, A, Pujia, A, Raso, A, Rispoli, Pietro, Conforti, M, Robinson, T, Dennis, Ms, Rosfors, S, Rudofsky, G, Schroeder, T, Gronholdt, Ml, Finocchi, C, Rodriguez, G, Spartera, C, Ventura, M, Scarpelli, P, Sprynger, M, Sadzot, B, Hottermans, C, Taylor, Pr, Tovar Pardo, A, Negreira, J, Vayssairat, M, Faintuch, Jm, Valaikiené, J, Walker, Mg, Wilkinson, Ar, Barnett, Hj, Bernstein, Ef, Jones, Am, Moore, W, Myers, K, Strandness, De, Toole, J, Tsapogas, M, and van Gijn, J.

Published
2009

158. Smoking and risk for amyotrophic lateral sclerosis: analysis of the EPIC cohort

Author

Gallo, V., Bueno de Mesquita, H.B., Vermeulen, R.C.H., Andersen, P.M., Kyrozis, A., Linseisen, J., Kaaks, R., Allen, N.E., Roddam, A.W., Boshuizen, H.C., Peeters, P.H.M., Palli, D., Mattiello, A., Sieri, S., Tumino, R., Jimenez-Martin, J.M., Diaz, M.J., Suarez, L.R., Trichopoulou, A., Agudo, A., Arriola, L., Barricante-Gurrea, A., Bingham, S., Khaw, K.T., Manjer, J., Lindkvist, B., Overvad, K., Bach, F.W., Tjonneland, A., Olsen, A., Bergmann, M.M., Boeing, H., Clavel-Chapelon, F., Lund, E., Hallmans, G., Middleton, L., Vineis, P., Riboli, E., Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Risk Assessment of Toxic and Immunomodulatory Agents, and Dep IRAS

Subjects
Adult, Male, Questionnaires, Risk, medicine.medical_specialty, International Cooperation, Cohort Studies, Sex Factors, Internal medicine, medicine, Humans, ddc:610, Amyotrophic lateral sclerosis, Risk factor, Aged, Proportional Hazards Models, business.industry, Proportional hazards model, Mortality rate, Amyotrophic Lateral Sclerosis, Smoking, Age Factors, Middle Aged, Former Smoker, medicine.disease, European Prospective Investigation into Cancer and Nutrition, Europe, Neurology, Cohort, Physical therapy, Female, Neurology (clinical), business, Cohort study
Abstract

Udgivelsesdato: 2009-Apr OBJECTIVE: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. METHODS: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. RESULTS: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrollment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2.32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. INTERPRETATION: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure.

Published
2009
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161. A randomised controlled trial of self-help interventions in patients with a primary care diagnosis of irritable bowel syndrome

Author

Andrew C Robinson, Middleton L, David G. Thompson, Anne Rogers, Anne Kennedy, David Reeves, and Lee

Subjects
Adult, Male, medicine.medical_specialty, Office Visits, Health Status, MEDLINE, Psychological intervention, law.invention, Irritable Bowel Syndrome, Quality of life (healthcare), Randomized controlled trial, Patient Education as Topic, law, Intervention (counseling), Outpatients, medicine, Humans, Psychiatry, Irritable bowel syndrome, business.industry, Gastroenterology, Primary care physician, medicine.disease, Self Care, Self-Help Groups, Treatment Outcome, Physical therapy, Quality of Life, Regression Analysis, Female, Pamphlets, business, Patient education, Follow-Up Studies
Abstract

Functional abdominal symptoms are very common and account for nearly two million primary care consultations in Britain every year and produce significant morbidity. The aims of this study were to evaluate the impact of two self-help interventions on consultation rates and symptom severity in patients with a primary care diagnosis of irritable bowel syndrome.A total of 420 patients from 54 primary care centres were randomised either to receive self-help information in the form of a guidebook or the guidebook plus a "self-help" group meeting or to be in a control group receiving neither intervention. Data were collected using questionnaires and primary care records.At one year, patients in the guidebook group had a 60% reduction in primary care consultations (p0.001) and a reduction in perceived symptom severity (p0.001) compared with controls. Allocation to the self-help group conferred no additional benefit. Actual symptom scores did not change significantly in any group. Costs per patient were reduced by Pounds 73 (confidence interval Pounds 43, Pounds 103) or 40% per year.Introduction of a self-help guidebook results in a reduction in primary care consultations, a perceived reduction in symptoms, and significant health service savings. This suggests that patients attending their primary care physician with functional abdominal symptoms should be offered self-help information as part of their management.

Published
2005

163. Severity of asymptomatic carotid stenosis and risk of ipsilateral hemispheric ischaemic events: results from the ACSRS study

Author

Adovasio, R, Ziani, B, Alò, Fp, Cicilioni, Cg, Ambrosio, G, Andreev, A, Andreozzi, Gm, Verlato, F, Camporese, G, Arosio, E, Barkauskas, E, Barros D'Sa AA, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, Gp, Simoni, G, Bell, P, Biasi, Gm, Mingazzini, P, Bornstein, Nm, Bouchier Hayes, D, Fitzgerald, P, Cairols, Ma, Cao, Pg, Derango, P, Carboni, Gp, Geoffredo, C, Catalono, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopoulos, E, Andreadis, Ea, Middleton, L, Pantziaris, M, Tyllis, T, Minar, E, Willfort, A, Moggi, L, Nenci, G, Radicchia, S, Nicolaides, A, Kakkos, S, Thomas, D, Norgren, L, Ribbe, E, Novo, S, Tantillo, R, Olinic, D, Paaske, W, Pagnan, A, Pauletto, P, Pagliara, V, Pettina, G, Pratesi, C, Matticari, S, Polivka, J, Sevcik, P, Poredos, P, Blinc, A, Videcnik, V, Pujia, A, Raso, A, Rispoli, Pietro, Conforti, M, Robinson, T, Dennis, Ms, Rosfos, S, Rudofsky, G, Schroeder, T, Gronholdt, Ml, Finocchi, C, Rodriguez, G, Dimakakos, Pb, Kotsis, T, Eikelboom, B, Entz, L, Ferrari, Bardile, Aloi, T, Salerno, M, Fernandes J, Fernandes e., Pedro, L, Fitzgerald, De, O'Shaunnersy, A, Fletcher, F, Forconi, S, Cappeli, R, Bicchi, M, Arrigucci, S, Gallai, V, Cardaiolli, G, Geroulakos, G, Gomez Isaza LF, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Giannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, Bb, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Barnett, Hj, Bernstein, Ef, Jones, Am, Moore, W, Myers, K, Strandness, De, Toole, J, Tsapogas, M, van Gijn, J, Spartera, C, Ventura, M, Scarpelli, P, Sprynger, M, Sadzot, B, Hottermans, C, Moonen, Taylor, Pr, Tovar Pardo, A, Negreira, J, Vayssairat, M, Faintuch, Jm, Valaikiené, J, Walker, Mg, and Wilkinson, A. R.

Published
2005

167. A common biological basis of obesity and nicotine addiction

Author

Thorgeirsson, T.E. (Thorgeir), Gudbjartsson, D.F. (Daniel), Sulem, P. (Patrick), Besenbacher, S. (Søren), Styrkarsdottir, U. (Unnur), Thorleifsson, G. (Gudmar), Walters, G.B. (Bragi), Furberg, H. (Helena), Sullivan, P. (Patrick), Marchini, J. (Jonathan), McCarthy, M.I. (M.), Steinthorsdottir, V. (Valgerdur), Thorsteinsdottir, U. (Unnur), Zwart, J-A. (John-Anker), Surakka, I. (Ida), Vink, J.M. (Jacqueline), Amin, N. (Najaf), Geller, F. (Frank), Rafnar, T. (Thorunn), Esko, T. (Tõnu), Walter, S. (Stefan), Gieger, C. (Christian), Rawal, R. (Rajesh), Mangino, M. (Massimo), Prokopenko, I. (Inga), Mägi, R. (Reedik), Keskitalo, K. (Kaisu), Gudjonsdottir, I.H. (Iris), Gretarsdottir, S. (Solveig), Stefansson, H. (Hreinn), Aulchenko, Y.S. (Yurii), Nelis, M. (Mari), Aben, K.K.H. (Katja), Heijer, M. (Martin) den, Soranzo, N. (Nicole), Valdes, A.M. (Ana Maria), Steves, C.J. (Claire), Uitterlinden, A.G. (André), Hofman, A. (Albert), Tönjes, A. (Anke), Kovacs, P. (Peter), Hottenga, J.J. (Jouke Jan), Willemsen, G.A.H.M. (Gonneke), Vogelzangs, N. (Nicole), Döring, A. (Angela), Dahmen, N. (N.), Nitz, B. (Barbara), Ripatti, S. (Samuli), Perola, M. (Markus), Kettunen, J. (Johannes), Hartikainen, A.L., Pouta, A. (Anneli), Laitinen, J. (Jaana), Isohanni, M.K. (Matti), Huei-Yi, S. (Shen), Allen, M. (Maxine), Krestyaninova, M. (Maria), Hall, A. (Anne), Thompson, J.R. (John), Oskarsson, H. (Hogni), Tyrfingsson, T. (Thorarinn), Kiemeney, L.A.L.M. (Bart), Jarvelin, M.-R. (Marjo-Riitta), Salomaa, V. (Veikko), Stumvoll, M. (Michael), Spector, T.D. (Timothy), Wichmann, H.E. (Heinz Erich), Metspalu, A. (Andres), Samani, N.J. (Nilesh), Penninx, B.W.J.H. (Brenda), Oostra, B.A. (Ben), Boomsma, D.I. (Dorret), Tiemeier, H.W. (Henning), Duijn, C.M. (Cornelia) van, Kaprio, J. (Jaakko), Gulcher, J.R. (Jeffrey), Kim, Y. (Yunjung), Dackor, J. (Jennifer), Boerwinkle, E.A. (Eric), Franceschini, N. (Nora), Ardissino, D. (Diego), Bernardinelli, L. (Luisa), Mannucci, P.M. (Pier), Mauri, F. (Francesco), Merlini, P.A. (Piera), Absher, D. (Devin), Assimes, T.L. (Themistocles), Fortmann, S.P. (Stephen), Iribarren, C. (Carlos), Knowles, J.W. (Joshua), Quertermous, T. (Thomas), Ferrucci, L. (Luigi), Tanaka, T. (Toshiko), Bis, J.C. (Joshua), Haritunians, T. (Talin), McKnight, B. (Barbara), Psaty, B.M. (Bruce), Taylor, K.D. (Kent), Thacker, E.L. (Evan), Almgren, P. (Peter), Groop, L. (Leif), Ladenvall, C. (Claes), Boehnke, M. (Michael), Jackson, A.U. (Anne), Mohlke, K.L. (Karen), Stringham, H.M. (Heather), Tuomilehto, J. (Jaakko), Benjamin, E.J. (Emelia), Hwang, S.J., Levy, D. (Daniel), Preis, S.R., Vasan, R.S. (Ramachandran Srini), Duan, J. (Jubao), Gejman, P.V. (Pablo), Levinson, D.F. (Douglas), Sanders, A.R. (Alan), Shi, J. (Jianxin), Lips, E.H. (Esther), McKay, J.D. (James), Agudo, A. (Antonio), Barzan, L. (Luigi), Bencko, V. (Vladimir), Benhamou, S. (Simone), Castellsagué, X. (Xavier), Canova, C. (Cristina), Conway, D.I. (David), Fabianova, E. (Eleonora), Foretova, L. (Lenka), Janout, V. (Vladimir), Healy, C.M. (Claire), Holcátová, I. (Ivana), Kjaerheim, K. (Kristina), Lagiou, P., Lissowska, J. (Jolanta), Lowry, R. (Ray), MacFarlane, T.V. (Tatiana), Mates, D. (Dana), Richiardi, L. (Lorenzo), Rudnai, P. (Peter), Szeszenia-Dabrowska, N. (Neonilia), Zaridze, D., Znaor, A. (Ariana), Lathrop, M. (Mark), Brennan, P. (Paul), Bandinelli, S. (Stefania), Frayling, T.M. (Timothy), Guralnik, J.M. (Jack), Milaneschi, Y. (Yuri), Perry, J.R.B. (John), Altshuler, D. (David), Elosua, R. (Roberto), Kathiresan, S. (Sekar), Lucas, G. (Gavin), Melander, O. (Olle), O'Donnell, C.J. (Christopher), Schwartz, S.M. (Stephen), Voight, B.F. (Benjamin), Smith, A.V. (Davey), Geus, E.J.C. (Eco) de, Chanock, S.J. (Stephen), Gu, F. (Fangyi), Hankinson, S.E. (Susan), Hunter, D. (David), Chasman, D.I. (Daniel), Everett, B.M. (Brendan), Paré, G. (Guillaume), Ridker, P.M. (Paul), Li, M.D. (Ming), Maes, H.H. (Hermine), Audrain-Mcgovern, J. (Janet), Posthuma, D. (Danielle), Thornton, L.M. (Laura), Lerman, C. (Caryn), Rose, J.E. (Jed), Ioannidis, J.P.A. (John), Kraft, P. (Peter), Lin, D.Y. (Dan), Liu, J. (Jason), Muglia, P. (Pierandrea), Waterworth, D. (Dawn), Pillai, A.D. (Ajay), Middleton, L. (Lefkos), Berrettini, W. (Wade), Knouff, C.W. (Christopher), Yuan, X. (Xin), Waeber, G. (Gérard), Vollenweider, P. (Peter), Preisig, M. (Martin), Wareham, N.J. (Nick), Zhao, J.H. (Jing Hua), Loos, R.J.F. (Ruth), Barroso, I.E. (Inês), Khaw, K-T. (Kay-Tee), Grundy, S.M. (Scott), Barter, P. (Phil), Mahley, R. (Robert), Kesaniemi, Y.A. (Antero), McPherson, R. (Ruth), Vincent, J. (John), Strauss, J.S. (John S), Kennedy, J. (James), Farmer, A.E. (Anne E), Mcguffin, P. (Peter), Day, R.N. (Richard), Matthews, K. (Keith), Bakke, A.B. (Arnold B.), Gulsvik, A. (Amund), Lucae, S. (Susanne), Ising, M. (Marcus), Brueckl, T. (Tanja), Horstmann, S. (Sonja), Heinrich, J. (Joachim), Lamina, C. (Claudia), Polasek, O. (Ozren), Zgaga, L. (Lina), Huffman, J.E. (Jennifer), Campbell, S. (Susan), Kooner, J.S. (Jaspal), Chambers, J.C. (John), Burnett, M.S., Devaney, J. (Joseph), Pichard, A.D., Kent, K.M. (Kenneth), Satler, L.F., Lindsay, J.M. (Joseph), Waksman, R. (Ron), Epstein, S.E. (Stephen), Wilson, J.F. (James), Wild, S.H. (Sarah), Campbell, H. (Harry), Vitart, V. (Veronique), Reilly, M.P. (Muredach), Li, M. (Mingyao), Qu, L. (Liming), Wilensky, A. (Asaf), Matthai, W. (William), Hakonarson, H. (Hakon), Rader, D.J. (Daniel), Franke, A. (Andre), Wittig, M. (Michael), Schäfer, A. (Arne), Uda, M. (Manuela), Terracciano, A., Xiao, X. (Xiangjun), Busonero, F., Scheet, P. (Paul), Schlessinger, D., Clair, D.S., Rujescu, D. (Dan), Abecasis, G.R. (Gonçalo), Grabe, H.J. (Hans Jörgen), Teumer, A. (Alexander), Völzke, H. (Henry), Petersmann, A. (Astrid), John, U. (Ulrich), Rudan, I. (Igor), Hayward, C. (Caroline), Wright, A.F. (Alan), Kolcic, I. (Ivana), Wright, B.J. (Benjamin), Balmforth, A.J. (Anthony), Anderson, C. (Carl), Ahmed, T. (Tariq), Mathew, J. (Joseph), Parkes, M. (Miles), Satsangi, J. (Jack), Caulfield, M. (Mark), Munroe, P. (Patricia), Farrall, M. (Martin), Dominiczak, A. (Anna), Worthington, H. (Helen), Thomson, W. (Wendy), Eyre, D.S. (Dylan Samuel), Barton, A. (Anne), Mooser, V. (Vincent), Francks, C. (Clyde), Thorgeirsson, T.E. (Thorgeir), Gudbjartsson, D.F. (Daniel), Sulem, P. (Patrick), Besenbacher, S. (Søren), Styrkarsdottir, U. (Unnur), Thorleifsson, G. (Gudmar), Walters, G.B. (Bragi), Furberg, H. (Helena), Sullivan, P. (Patrick), Marchini, J. (Jonathan), McCarthy, M.I. (M.), Steinthorsdottir, V. (Valgerdur), Thorsteinsdottir, U. (Unnur), Zwart, J-A. (John-Anker), Surakka, I. (Ida), Vink, J.M. (Jacqueline), Amin, N. (Najaf), Geller, F. (Frank), Rafnar, T. (Thorunn), Esko, T. (Tõnu), Walter, S. (Stefan), Gieger, C. (Christian), Rawal, R. (Rajesh), Mangino, M. (Massimo), Prokopenko, I. (Inga), Mägi, R. (Reedik), Keskitalo, K. (Kaisu), Gudjonsdottir, I.H. (Iris), Gretarsdottir, S. (Solveig), Stefansson, H. (Hreinn), Aulchenko, Y.S. (Yurii), Nelis, M. (Mari), Aben, K.K.H. (Katja), Heijer, M. (Martin) den, Soranzo, N. (Nicole), Valdes, A.M. (Ana Maria), Steves, C.J. (Claire), Uitterlinden, A.G. (André), Hofman, A. (Albert), Tönjes, A. (Anke), Kovacs, P. (Peter), Hottenga, J.J. (Jouke Jan), Willemsen, G.A.H.M. (Gonneke), Vogelzangs, N. (Nicole), Döring, A. (Angela), Dahmen, N. (N.), Nitz, B. (Barbara), Ripatti, S. (Samuli), Perola, M. (Markus), Kettunen, J. (Johannes), Hartikainen, A.L., Pouta, A. (Anneli), Laitinen, J. (Jaana), Isohanni, M.K. (Matti), Huei-Yi, S. (Shen), Allen, M. (Maxine), Krestyaninova, M. (Maria), Hall, A. (Anne), Thompson, J.R. (John), Oskarsson, H. (Hogni), Tyrfingsson, T. (Thorarinn), Kiemeney, L.A.L.M. (Bart), Jarvelin, M.-R. (Marjo-Riitta), Salomaa, V. (Veikko), Stumvoll, M. (Michael), Spector, T.D. (Timothy), Wichmann, H.E. (Heinz Erich), Metspalu, A. (Andres), Samani, N.J. (Nilesh), Penninx, B.W.J.H. (Brenda), Oostra, B.A. (Ben), Boomsma, D.I. (Dorret), Tiemeier, H.W. (Henning), Duijn, C.M. (Cornelia) van, Kaprio, J. (Jaakko), Gulcher, J.R. (Jeffrey), Kim, Y. (Yunjung), Dackor, J. (Jennifer), Boerwinkle, E.A. (Eric), Franceschini, N. (Nora), Ardissino, D. (Diego), Bernardinelli, L. (Luisa), Mannucci, P.M. (Pier), Mauri, F. (Francesco), Merlini, P.A. (Piera), Absher, D. (Devin), Assimes, T.L. (Themistocles), Fortmann, S.P. (Stephen), Iribarren, C. (Carlos), Knowles, J.W. (Joshua), Quertermous, T. (Thomas), Ferrucci, L. (Luigi), Tanaka, T. (Toshiko), Bis, J.C. (Joshua), Haritunians, T. (Talin), McKnight, B. (Barbara), Psaty, B.M. (Bruce), Taylor, K.D. (Kent), Thacker, E.L. (Evan), Almgren, P. (Peter), Groop, L. (Leif), Ladenvall, C. (Claes), Boehnke, M. (Michael), Jackson, A.U. (Anne), Mohlke, K.L. (Karen), Stringham, H.M. (Heather), Tuomilehto, J. (Jaakko), Benjamin, E.J. (Emelia), Hwang, S.J., Levy, D. (Daniel), Preis, S.R., Vasan, R.S. (Ramachandran Srini), Duan, J. (Jubao), Gejman, P.V. (Pablo), Levinson, D.F. (Douglas), Sanders, A.R. (Alan), Shi, J. (Jianxin), Lips, E.H. (Esther), McKay, J.D. (James), Agudo, A. (Antonio), Barzan, L. (Luigi), Bencko, V. (Vladimir), Benhamou, S. (Simone), Castellsagué, X. (Xavier), Canova, C. (Cristina), Conway, D.I. (David), Fabianova, E. (Eleonora), Foretova, L. (Lenka), Janout, V. (Vladimir), Healy, C.M. (Claire), Holcátová, I. (Ivana), Kjaerheim, K. (Kristina), Lagiou, P., Lissowska, J. (Jolanta), Lowry, R. (Ray), MacFarlane, T.V. (Tatiana), Mates, D. (Dana), Richiardi, L. (Lorenzo), Rudnai, P. (Peter), Szeszenia-Dabrowska, N. (Neonilia), Zaridze, D., Znaor, A. (Ariana), Lathrop, M. (Mark), Brennan, P. (Paul), Bandinelli, S. (Stefania), Frayling, T.M. (Timothy), Guralnik, J.M. (Jack), Milaneschi, Y. (Yuri), Perry, J.R.B. (John), Altshuler, D. (David), Elosua, R. (Roberto), Kathiresan, S. (Sekar), Lucas, G. (Gavin), Melander, O. (Olle), O'Donnell, C.J. (Christopher), Schwartz, S.M. (Stephen), Voight, B.F. (Benjamin), Smith, A.V. (Davey), Geus, E.J.C. (Eco) de, Chanock, S.J. (Stephen), Gu, F. (Fangyi), Hankinson, S.E. (Susan), Hunter, D. (David), Chasman, D.I. (Daniel), Everett, B.M. (Brendan), Paré, G. (Guillaume), Ridker, P.M. (Paul), Li, M.D. (Ming), Maes, H.H. (Hermine), Audrain-Mcgovern, J. (Janet), Posthuma, D. (Danielle), Thornton, L.M. (Laura), Lerman, C. (Caryn), Rose, J.E. (Jed), Ioannidis, J.P.A. (John), Kraft, P. (Peter), Lin, D.Y. (Dan), Liu, J. (Jason), Muglia, P. (Pierandrea), Waterworth, D. (Dawn), Pillai, A.D. (Ajay), Middleton, L. (Lefkos), Berrettini, W. (Wade), Knouff, C.W. (Christopher), Yuan, X. (Xin), Waeber, G. (Gérard), Vollenweider, P. (Peter), Preisig, M. (Martin), Wareham, N.J. (Nick), Zhao, J.H. (Jing Hua), Loos, R.J.F. (Ruth), Barroso, I.E. (Inês), Khaw, K-T. (Kay-Tee), Grundy, S.M. (Scott), Barter, P. (Phil), Mahley, R. (Robert), Kesaniemi, Y.A. (Antero), McPherson, R. (Ruth), Vincent, J. (John), Strauss, J.S. (John S), Kennedy, J. (James), Farmer, A.E. (Anne E), Mcguffin, P. (Peter), Day, R.N. (Richard), Matthews, K. (Keith), Bakke, A.B. (Arnold B.), Gulsvik, A. (Amund), Lucae, S. (Susanne), Ising, M. (Marcus), Brueckl, T. (Tanja), Horstmann, S. (Sonja), Heinrich, J. (Joachim), Lamina, C. (Claudia), Polasek, O. (Ozren), Zgaga, L. (Lina), Huffman, J.E. (Jennifer), Campbell, S. (Susan), Kooner, J.S. (Jaspal), Chambers, J.C. (John), Burnett, M.S., Devaney, J. (Joseph), Pichard, A.D., Kent, K.M. (Kenneth), Satler, L.F., Lindsay, J.M. (Joseph), Waksman, R. (Ron), Epstein, S.E. (Stephen), Wilson, J.F. (James), Wild, S.H. (Sarah), Campbell, H. (Harry), Vitart, V. (Veronique), Reilly, M.P. (Muredach), Li, M. (Mingyao), Qu, L. (Liming), Wilensky, A. (Asaf), Matthai, W. (William), Hakonarson, H. (Hakon), Rader, D.J. (Daniel), Franke, A. (Andre), Wittig, M. (Michael), Schäfer, A. (Arne), Uda, M. (Manuela), Terracciano, A., Xiao, X. (Xiangjun), Busonero, F., Scheet, P. (Paul), Schlessinger, D., Clair, D.S., Rujescu, D. (Dan), Abecasis, G.R. (Gonçalo), Grabe, H.J. (Hans Jörgen), Teumer, A. (Alexander), Völzke, H. (Henry), Petersmann, A. (Astrid), John, U. (Ulrich), Rudan, I. (Igor), Hayward, C. (Caroline), Wright, A.F. (Alan), Kolcic, I. (Ivana), Wright, B.J. (Benjamin), Balmforth, A.J. (Anthony), Anderson, C. (Carl), Ahmed, T. (Tariq), Mathew, J. (Joseph), Parkes, M. (Miles), Satsangi, J. (Jack), Caulfield, M. (Mark), Munroe, P. (Patricia), Farrall, M. (Martin), Dominiczak, A. (Anna), Worthington, H. (Helen), Thomson, W. (Wendy), Eyre, D.S. (Dylan Samuel), Barton, A. (Anne), Mooser, V. (Vincent), and Francks, C. (Clyde)

Abstract

Smoking influences body weight such that smokers weigh less than non-smokers and smoking cessation often leads to weight increase. The relationship between body weight and smoking is partly explained by the effect of nicotine on appetite and metabolism. However, the brain reward system is involved in the control of the intake of both food and tobacco. We evaluated the effect of single-nucleotide polymorphisms (SNPs) affecting body mass index (BMI) on smoking behavior, and tested the 32 SNPs identified in a meta-analysis for association with two smoking phenotypes, smoking initiation (SI) and the number of cigarettes smoked per day (CPD) in an Icelandic sample (N=34 216 smokers). Combined according to their effect on BMI, the SNPs correlate with both SI (r=0.019, P=0.00054) and CPD (r=0.032, P=8.0 × 10-7). These findings replicate in a second large data set (N=127 274, thereof 76 242 smokers) for both SI (P=1.2 × 10-5) and CPD (P=9.3 × 10-5). Notably, the variant most strongly associated with BMI (rs1558902-A in FTO) did not associate with smoking behavior. The association with smoking behavior is not due to the effect of the SNPs on BMI. Our results strongly point to a common biological basis of the regulation of our appetite for tobacco and food, and thus the vulnerability to nicotine addiction and obesity.

Published
2013
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168. Comparing Morphological Evolution during Tensile Deformation of Two Precise Polyethylenes via 2D Fitting of in SituX-ray Scattering

Author

Trigg, Edward B., Middleton, L. Robert, Yan, Lu, and Winey, Karen I.

Abstract

Some types of precise polyethylenes, or linear polyethylenes containing precisely periodic functional groups, exhibit significant strain hardening under tensile deformation. Here we perform in situX-ray scattering during tensile deformation of two precise polyethylenes: one with pendant carboxylic acid groups every 21st carbon (p21AA) and another with pendant imidazolium bromide groups every 15th carbon (p15ImBr). p21AA exhibits significant strain hardening and its layered structure orients with the layer normal along the tensile axis, while p15ImBr does notexhibit strain hardening and its layer normal orients perpendicularto the tensile axis. Quantitative evaluation of the 2D fiber patterns shows that p21AA undergoes a morphological transition, from a semicrystalline structure to a nanofibrillar structure, while the morphology of p15ImBr reorients and the chain folding structure is preserved. This suggests that fibrillization plays an important role in the strain hardening mechanism.

Published
2018
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169. Classification Performance of Motor Unit Action Potential Features

Author

Constantinos Pattichis, Elia, A., Schizas, C. N., and Middleton, L. T.

Abstract

The objective of this study is to examine the classification performance of the following motor unit action potential (MUAP) feature sets: i) time domain measures, ii) frequency measures, iii) autoregressive coefficients AR, and iv) cepstral coefficients. Two different feature selection methods were used: i) univariate analysis, and ii) multiple covariance analysis. Both methods showed that: i) the duration measure is the best discriminator, ii) the median frequency, FMED is the best discriminator among the frequency measures, and iii) the cepstral coefficients are better discriminators than the AR coefficients. Furthermore, the recognition rate of the above feature sets was investigated using the K-means nearest neighbour clustering algorithm. Time domain measures and cepstral coefficients gave the highest recognition score.

Published
2002

172. Asymptomatic internal carotid artery stenosis and cerebrovascular risk stratification

Author

Nicolaides, A, Kakkos, S, Kyriacou, E, Griffin, M, Sabetai, M, Thomas, D, Tegos, T, Geroulakos, G, Labropoulos, N, Dor, C, Morris, T, Naylor, R, Abbott, A, Adovasio, R, Ziani, B, Alò, F, Cicilioni, C, Ambrosio, G, Andreev, A, Andreozzi, G, Verlato, F, Camporese, G, Arosio, E, Barkauskas, E, Barros D'Sa, A, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, G, Simoni, G, Bell, P, Biasi, G, Mingazzini, P, Bornstein, N, Bouchier Hayes, D, Fitzgerald, P, Cairols, M, Cao, P, Derango, P, Carboni, G, Geoffredo, C, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopoulos, E, Andreadis, E, Dimakakos, P, Kotsis, T, Eikelboom, B, Entz, L, Ferrari Bardileah, N, Aloi, T, Salerno, M, Fernandes, J, Pedro, L, Fitzgerald, D, O'Shaunnersy, A, Fletcher, J, Forconi, S, Cappeli, R, Bicchi, M, Arrigucci, S, Gallai, V, Cardaiolli, G, Gomez Isaza, L, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Giannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, B, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, Tyllis, T, Minar, E, Willfort, A, Moggi, L, Nenci, G, Radicchia, S, Norgren, L, Ribbe, E, Novo, S, Tantillo, R, Olinic, D, Paaske, W, Pagnan, A, Pauletto, P, Pagliara, V, Pettina, G, Pratesi, C, Matticari, S, Polivka, J, Sevcik, P, Poredos, P, Blinc, A, Videcnik, V, Pujia, A, Raso, A, Rispoli, P, Conforti, M, Robinson, T, Dennis, M, Rosfors, S, Rudofsky, G, Schroeder, T, Gronholdt, M, Finocchi, C, Rodriguez, G, Spartera, C, Ventura, M, Scarpelli, P, Sprynger, M, Sadzot, B, Hottermans, C, Moonenbp, N, Taylor, P, Tovar Pardo, A, Negreira, J, Vayssairat, M, Faintuch, J, Valaikiené, J, Walker, M, Wilkinson, A, BIASI, GIORGIO MARIA, MINGAZZINI, PAOLO, DeRango, P, Ferrari Bardileah, n, McCollum, P, Moonenbp, n, Wilkinson, A., Nicolaides, A, Kakkos, S, Kyriacou, E, Griffin, M, Sabetai, M, Thomas, D, Tegos, T, Geroulakos, G, Labropoulos, N, Dor, C, Morris, T, Naylor, R, Abbott, A, Adovasio, R, Ziani, B, Alò, F, Cicilioni, C, Ambrosio, G, Andreev, A, Andreozzi, G, Verlato, F, Camporese, G, Arosio, E, Barkauskas, E, Barros D'Sa, A, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, G, Simoni, G, Bell, P, Biasi, G, Mingazzini, P, Bornstein, N, Bouchier Hayes, D, Fitzgerald, P, Cairols, M, Cao, P, Derango, P, Carboni, G, Geoffredo, C, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopoulos, E, Andreadis, E, Dimakakos, P, Kotsis, T, Eikelboom, B, Entz, L, Ferrari Bardileah, N, Aloi, T, Salerno, M, Fernandes, J, Pedro, L, Fitzgerald, D, O'Shaunnersy, A, Fletcher, J, Forconi, S, Cappeli, R, Bicchi, M, Arrigucci, S, Gallai, V, Cardaiolli, G, Gomez Isaza, L, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Giannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, B, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, Tyllis, T, Minar, E, Willfort, A, Moggi, L, Nenci, G, Radicchia, S, Norgren, L, Ribbe, E, Novo, S, Tantillo, R, Olinic, D, Paaske, W, Pagnan, A, Pauletto, P, Pagliara, V, Pettina, G, Pratesi, C, Matticari, S, Polivka, J, Sevcik, P, Poredos, P, Blinc, A, Videcnik, V, Pujia, A, Raso, A, Rispoli, P, Conforti, M, Robinson, T, Dennis, M, Rosfors, S, Rudofsky, G, Schroeder, T, Gronholdt, M, Finocchi, C, Rodriguez, G, Spartera, C, Ventura, M, Scarpelli, P, Sprynger, M, Sadzot, B, Hottermans, C, Moonenbp, N, Taylor, P, Tovar Pardo, A, Negreira, J, Vayssairat, M, Faintuch, J, Valaikiené, J, Walker, M, Wilkinson, A, BIASI, GIORGIO MARIA, MINGAZZINI, PAOLO, DeRango, P, Ferrari Bardileah, n, McCollum, P, Moonenbp, n, and Wilkinson, A.

Abstract

Background: The purpose of this study was to determine the cerebrovascular risk stratification potential of baseline degree of stenosis, clinical features, and ultrasonic plaque characteristics in patients with asymptomatic internal carotid artery (ICA) stenosis. Methods: This was a prospective, multicenter, cohort study of patients undergoing medical intervention for vascular disease. Hazard ratios for ICA stenosis, clinical features, and plaque texture features associated with ipsilateral cerebrovascular or retinal ischemic (CORI) events were calculated using proportional hazards models. Results: A total of 1121 patients with 50% to 99% asymptomatic ICA stenosis in relation to the bulb (European Carotid Surgery Trial [ECST] method) were followed-up for 6 to 96 months (mean, 48). A total of 130 ipsilateral CORI events occurred. Severity of stenosis, age, systolic blood pressure, increased serum creatinine, smoking history of more than 10 pack-years, history of contralateral transient ischemic attacks (TIAs) or stroke, low grayscale median (GSM), increased plaque area, plaque types 1, 2, and 3, and the presence of discrete white areas (DWAs) without acoustic shadowing were associated with increased risk. Receiver operating characteristic (ROC) curves were constructed for predicted risk versus observed CORI events as a measure of model validity. The areas under the ROC curves for a model of stenosis alone, a model of stenosis combined with clinical features and a model of stenosis combined with clinical, and plaque features were 0.59 (95% confidence interval [CI] 0.54-0.64), 0.66 (0.62-0.72), and 0.82 (0.78-0.86), respectively. In the last model, stenosis, history of contralateral TIAs or stroke, GSM, plaque area, and DWAs were independent predictors of ipsilateral CORI events. Combinations of these could stratify patients into different levels of risk for ipsilateral CORI and stroke, with predicted risk close to observed risk. Of the 923 patients with <70% stenos

Published
2010

173. Common genetic variation and susceptibility to partial epilepsies: a genome-wide association study

Author

Kasperaviciūte, D, Catarino, C B, Heinzen, E L, Depondt, C, Cavalleri, G L, Caboclo, L O, Tate, S K, Jamnadas-Khoda, J, Chinthapalli, K, Clayton, L M S, Shianna, K V, Radtke, R A, Mikati, M A, Gallentine, W B, Husain, A M, Alhusaini, S, Leppert, D, Middleton, L T, Gibson, R A, Johnson, M R, Matthews, P M, Hosford, D, Heuser, K, Amos, L, Ortega, M, Zumsteg, D, Wieser, H G, Steinhoff, B J, Krämer, G, Hansen, J, Dorn, T, Kantanen, A M, Gjerstad, L, Peuralinna, T, Hernandez, D G, Eriksson, K J, Kälviäinen, R K, Doherty, C P, Wood, N W, Pandolfo, M, Duncan, J S, Sander, J W, Delanty, N, Goldstein, D B, Sisodiya, S M, Kasperaviciūte, D, Catarino, C B, Heinzen, E L, Depondt, C, Cavalleri, G L, Caboclo, L O, Tate, S K, Jamnadas-Khoda, J, Chinthapalli, K, Clayton, L M S, Shianna, K V, Radtke, R A, Mikati, M A, Gallentine, W B, Husain, A M, Alhusaini, S, Leppert, D, Middleton, L T, Gibson, R A, Johnson, M R, Matthews, P M, Hosford, D, Heuser, K, Amos, L, Ortega, M, Zumsteg, D, Wieser, H G, Steinhoff, B J, Krämer, G, Hansen, J, Dorn, T, Kantanen, A M, Gjerstad, L, Peuralinna, T, Hernandez, D G, Eriksson, K J, Kälviäinen, R K, Doherty, C P, Wood, N W, Pandolfo, M, Duncan, J S, Sander, J W, Delanty, N, Goldstein, D B, and Sisodiya, S M

Abstract

Partial epilepsies have a substantial heritability. However, the actual genetic causes are largely unknown. In contrast to many other common diseases for which genetic association-studies have successfully revealed common variants associated with disease risk, the role of common variation in partial epilepsies has not yet been explored in a well-powered study. We undertook a genome-wide association-study to identify common variants which influence risk for epilepsy shared amongst partial epilepsy syndromes, in 3445 patients and 6935 controls of European ancestry. We did not identify any genome-wide significant association. A few single nucleotide polymorphisms may warrant further investigation. We exclude common genetic variants with effect sizes above a modest 1.3 odds ratio for a single variant as contributors to genetic susceptibility shared across the partial epilepsies. We show that, at best, common genetic variation can only have a modest role in predisposition to the partial epilepsies when considered across syndromes in Europeans. The genetic architecture of the partial epilepsies is likely to be very complex, reflecting genotypic and phenotypic heterogeneity. Larger meta-analyses are required to identify variants of smaller effect sizes (odds ratio<1.3) or syndrome-specific variants. Further, our results suggest research efforts should also be directed towards identifying the multiple rare variants likely to account for at least part of the heritability of the partial epilepsies. Data emerging from genome-wide association-studies will be valuable during the next serious challenge of interpreting all the genetic variation emerging from whole-genome sequencing studies.

Published
2010

174. Silent embolic infarcts on computed tomography brain scans and risk of ipsilateral hemispheric events in patients with asymptomatic internal carotid artery stenosis

Author

Kakkos, S, Sabetai, M, Tegos, T, Stevens, J, Thomas, D, Griffin, M, Geroulakos, G, Nicolaides, A, Adovasio, R, Ziani, B, Alò, F, Cicilioni, C, Ambrosio, G, Andreev, A, Andreozzi, G, Verlato, F, Camporese, G, Arosio, E, Barkaukas, E, Barros D'Sa, A, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, G, Simoni, G, Bell, P, Biasi, G, Mingazzini, P, Bornstein, N, Bouchier Hayes, D, Fitzgerald, P, Cairols, M, Cao, P, Derango, P, Carboni, G, Geoffredo, C, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopoulos, E, Andreadis, A, Dimakakos, P, Kotsis, T, Eikelboom, B, Entz, L, Ferrari Bardile, T, Salerno, M, Fernandes, J, Pedro, L, Fitzgerald, D, O'Shaunnersy, A, Fletcher, J, Forconi, S, Capelli, R, Bicchi, M, Arrigucci, S, Gallai, V, Cardaiolli, G, Gomez Isaza, L, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Giannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, B, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, Tyllis, T, Minar, E, Willfort, A, Moggi, L, Nenci, G, Radicchia, S, Norgren, L, Ribbe, E, Novo, S, Tantillo, R, Olinic, D, Paaske, W, Pagnan, A, Pauletto, P, Pagliara, V, Pettina, G, Pratesi, C, Matticari, S, Polivka, J, Sevcik, P, Poredos, P, Blinc, A, Videcnik, V, Pujia, A, Raso, A, Rispoli, P, Conforti, M, Robinson, T, Dennis, M, Rosfors, S, Rudofsky, G, Finocchi, C, Rodriguez, G, Spartera, C, Ventura, M, Scarpelli, P, Sprynger, M, Sadzot, B, Hottermans, C, Moonenbj, N, Taylor, P, Tovar Pardo, A, Negreira, J, Vayssairat, M, Faintuch, J, Valaikiene, J, Walker, M, Wilkinson, A, BIASI, GIORGIO MARIA, MINGAZZINI, PAOLO, DeRango, P, McCollum, P, Moonenbj, n, Wilkinson, A., Kakkos, S, Sabetai, M, Tegos, T, Stevens, J, Thomas, D, Griffin, M, Geroulakos, G, Nicolaides, A, Adovasio, R, Ziani, B, Alò, F, Cicilioni, C, Ambrosio, G, Andreev, A, Andreozzi, G, Verlato, F, Camporese, G, Arosio, E, Barkaukas, E, Barros D'Sa, A, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, G, Simoni, G, Bell, P, Biasi, G, Mingazzini, P, Bornstein, N, Bouchier Hayes, D, Fitzgerald, P, Cairols, M, Cao, P, Derango, P, Carboni, G, Geoffredo, C, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopoulos, E, Andreadis, A, Dimakakos, P, Kotsis, T, Eikelboom, B, Entz, L, Ferrari Bardile, T, Salerno, M, Fernandes, J, Pedro, L, Fitzgerald, D, O'Shaunnersy, A, Fletcher, J, Forconi, S, Capelli, R, Bicchi, M, Arrigucci, S, Gallai, V, Cardaiolli, G, Gomez Isaza, L, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Giannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, B, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, Tyllis, T, Minar, E, Willfort, A, Moggi, L, Nenci, G, Radicchia, S, Norgren, L, Ribbe, E, Novo, S, Tantillo, R, Olinic, D, Paaske, W, Pagnan, A, Pauletto, P, Pagliara, V, Pettina, G, Pratesi, C, Matticari, S, Polivka, J, Sevcik, P, Poredos, P, Blinc, A, Videcnik, V, Pujia, A, Raso, A, Rispoli, P, Conforti, M, Robinson, T, Dennis, M, Rosfors, S, Rudofsky, G, Finocchi, C, Rodriguez, G, Spartera, C, Ventura, M, Scarpelli, P, Sprynger, M, Sadzot, B, Hottermans, C, Moonenbj, N, Taylor, P, Tovar Pardo, A, Negreira, J, Vayssairat, M, Faintuch, J, Valaikiene, J, Walker, M, Wilkinson, A, BIASI, GIORGIO MARIA, MINGAZZINI, PAOLO, DeRango, P, McCollum, P, Moonenbj, n, and Wilkinson, A.

Abstract

Objectives: This study tested the hypothesis that silerit embolic infarcts on computed tomography (CT) brain scans can predict ipsilateral neurologic hemispheric events and stroke in patients with asymptomatic internal carotid artery stenosis. Methods: In a prospective multicenter natural history study, 821 patients with asymptomatic carotid stenosis graded with duplex scanning who had CT brain scans were monitored every 6 months for a maximum of 8 years. Duplex scans were reported centrally, and stenosis was expressed as a percentage in relation to the normal distal internal carotid criteria used by the North American Symptomatic Carotid Endarterectomy Trialists. CT brain scans were reported centrally by a neuroradiologist. In 146 patients (17.8%), 8 large cortical, 15 small cortical, 72 discrete subcortical, and 51 basal ganglia ipsilateral infarcts were present; these were considered likely to be embolic and were classified as such. Other infarct types, lacunes (n = 15), watershed (n = 9), and the presence of diffuse white matter changes (n = 95) were not considered to be embolic. Results: During a mean follow-up of 44.6 months (range, 6 months-8 years), 102 ipsilateral hemispheric neurologic events (amaurosis fugax in 16, 38 transient ischemic attacks [TIAs], and 47 strokes) occurred, 138 patients died, and 24 were lost to follow-up. In 462 patients with 60% to 99% stenosis, the cumulative event-free rate at 8 years was 0.81 (2.4% annual event rate) when embolic infarcts were absent and 0.63 (4.6% annual event rate) when present (log-rank P = .032). In 359 patients with <60% stenosis, embolic infarcts were not associated with increased risk (log-rank P = .65). In patients with 60% to 99% stenosis, the cumulative stroke-free rate was 0.92 (1.0% annual stroke rate) when embolic infarcts were absent and 0.71 (3.6% annual stroke rate) when present (log-rank P = .002). In the subgroup of 216 with moderate 60% to 79% stenosis, the cumulative TIA or stroke-free rate

Published
2009

175. Smoking and risk for amyotrophic lateral sclerosis: analysis of the EPIC cohort.

Author

Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Gallo, V., Bueno de Mesquita, H.B., Vermeulen, R.C.H., Andersen, P.M., Kyrozis, A., Linseisen, J., Kaaks, R., Allen, N.E., Roddam, A.W., Boshuizen, H.C., Peeters, P.H.M., Palli, D., Mattiello, A., Sieri, S., Tumino, R., Jimenez-Martin, J.M., Diaz, M.J., Suarez, L.R., Trichopoulou, A., Agudo, A., Arriola, L., Barricante-Gurrea, A., Bingham, S., Khaw, K.T., Manjer, J., Lindkvist, B., Overvad, K., Bach, F.W., Tjonneland, A., Olsen, A., Bergmann, M.M., Boeing, H., Clavel-Chapelon, F., Lund, E., Hallmans, G., Middleton, L., Vineis, P., Riboli, E., Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Gallo, V., Bueno de Mesquita, H.B., Vermeulen, R.C.H., Andersen, P.M., Kyrozis, A., Linseisen, J., Kaaks, R., Allen, N.E., Roddam, A.W., Boshuizen, H.C., Peeters, P.H.M., Palli, D., Mattiello, A., Sieri, S., Tumino, R., Jimenez-Martin, J.M., Diaz, M.J., Suarez, L.R., Trichopoulou, A., Agudo, A., Arriola, L., Barricante-Gurrea, A., Bingham, S., Khaw, K.T., Manjer, J., Lindkvist, B., Overvad, K., Bach, F.W., Tjonneland, A., Olsen, A., Bergmann, M.M., Boeing, H., Clavel-Chapelon, F., Lund, E., Hallmans, G., Middleton, L., Vineis, P., and Riboli, E.

Published
2009

177. Prediagnostic body fat and risk of death from amyotrophic lateral sclerosis: The EPIC cohort

Author

Gallo, V., primary, Wark, P. A., additional, Jenab, M., additional, Pearce, N., additional, Brayne, C., additional, Vermeulen, R., additional, Andersen, P. M., additional, Hallmans, G., additional, Kyrozis, A., additional, Vanacore, N., additional, Vahdaninia, M., additional, Grote, V., additional, Kaaks, R., additional, Mattiello, A., additional, Bueno-de-Mesquita, H. B., additional, Peeters, P. H., additional, Travis, R. C., additional, Petersson, J., additional, Hansson, O., additional, Arriola, L., additional, Jimenez-Martin, J.-M., additional, Tjonneland, A., additional, Halkjaer, J., additional, Agnoli, C., additional, Sacerdote, C., additional, Bonet, C., additional, Trichopoulou, A., additional, Gavrila, D., additional, Overvad, K., additional, Weiderpass, E., additional, Palli, D., additional, Quiros, J. R., additional, Tumino, R., additional, Khaw, K.-T., additional, Wareham, N., additional, Barricante-Gurrea, A., additional, Fedirko, V., additional, Ferrari, P., additional, Clavel-Chapelon, F., additional, Boutron-Ruault, M.-C., additional, Boeing, H., additional, Vigl, M., additional, Middleton, L., additional, Riboli, E., additional, and Vineis, P., additional

Published
2013
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178. Quantitative linkage genome scan for atopy in a large collection of Caucasian families

Author

Webb, B.T., Oord, E., Akkari, A., Wilton, S., Ly, T., Duff, R., Barnes, K.C., Carlsen, K., Gerritsen, J., Lenney, W., Silverman, M., Sly, P., Sundy, J., Tsanakas, J., Berg, A., Whyte, M., Blumenthal, M., Vestbo, J., Middleton, L., Helms, P.J., Anderson, W.H., Pillai, S.G., Webb, B.T., Oord, E., Akkari, A., Wilton, S., Ly, T., Duff, R., Barnes, K.C., Carlsen, K., Gerritsen, J., Lenney, W., Silverman, M., Sly, P., Sundy, J., Tsanakas, J., Berg, A., Whyte, M., Blumenthal, M., Vestbo, J., Middleton, L., Helms, P.J., Anderson, W.H., and Pillai, S.G.

Abstract

Quantitative phenotypes correlated with a complex disorder offer increased power to detect linkage in comparison to affected-unaffected classifications. Asthma is a complex disorder characterized by periods of bronchial obstruction and increased bronchial hyper reactivity. In childhood and early adulthood, asthma is frequently associated also with quantitative measures of atopy. Genome wide quantitative multipoint linkage analysis was conducted for serum IgE levels and percentage of positive skin prick test (SPT(per)) using three large groups of families originally ascertained for asthma. In this report, 438 and 429 asthma families were informative for linkage using IgE and SPT(per) which represents 690 independent families. Suggestive linkage (LOD > or = 2) was found on chromosomes 1, 3, and 8q with maximum LODs of 2.34 (IgE), 2.03 (SPT(per)), and 2.25 (IgE) near markers D1S1653, D3S2322-D3S1764, and D8S2324, respectively. The results from chromosomes 1 and 3 replicate previous reports of linkage. We also replicate linkage to 5q with peak LODs of 1.96 (SPT(per)) and 1.77 (IgE) at or near marker D5S1480. Our results provide further evidence implicating chromosomes 1, 3, and 5q. The current report represents one of the biggest genome scans so far reported for asthma related phenotypes. This study also demonstrates the utility of increased sample sizes and quantitative phenotypes in linkage analysis of complex disorders.

Published
2007

179. Quantitative linkage genome scan for atopy in a large collection of Caucasian families.

Author

Webb, BT, van den Oord, E, Akkari, A, Wilton, S, Ly, T, Duff, R, Barnes, KC, Carlsen, K, Gerritsen, J, Lenney, W, Silverman, M, Sly, P, Sundy, J, Tsanakas, J, von Berg, A, Whyte, M, Blumenthal, M, Vestbo, Jørgen, Middleton, L, Helms, PJ, Anderson, WH, Pillai, SG, Webb, BT, van den Oord, E, Akkari, A, Wilton, S, Ly, T, Duff, R, Barnes, KC, Carlsen, K, Gerritsen, J, Lenney, W, Silverman, M, Sly, P, Sundy, J, Tsanakas, J, von Berg, A, Whyte, M, Blumenthal, M, Vestbo, Jørgen, Middleton, L, Helms, PJ, Anderson, WH, and Pillai, SG

Abstract

Quantitative phenotypes correlated with a complex disorder offer increased power to detect linkage in comparison to affected-unaffected classifications. Asthma is a complex disorder characterized by periods of bronchial obstruction and increased bronchial hyper reactivity. In childhood and early adulthood, asthma is frequently associated also with quantitative measures of atopy. Genome wide quantitative multipoint linkage analysis was conducted for serum IgE levels and percentage of positive skin prick test (SPT(per)) using three large groups of families originally ascertained for asthma. In this report, 438 and 429 asthma families were informative for linkage using IgE and SPT(per) which represents 690 independent families. Suggestive linkage (LOD >/= 2) was found on chromosomes 1, 3, and 8q with maximum LODs of 2.34 (IgE), 2.03 (SPT(per)), and 2.25 (IgE) near markers D1S1653, D3S2322-D3S1764, and D8S2324, respectively. The results from chromosomes 1 and 3 replicate previous reports of linkage. We also replicate linkage to 5q with peak LODs of 1.96 (SPT(per)) and 1.77 (IgE) at or near marker D5S1480. Our results provide further evidence implicating chromosomes 1, 3, and 5q. The current report represents one of the biggest genome scans so far reported for asthma related phenotypes. This study also demonstrates the utility of increased sample sizes and quantitative phenotypes in linkage analysis of complex disorders., Quantitative phenotypes correlated with a complex disorder offer increased power to detect linkage in comparison to affected-unaffected classifications. Asthma is a complex disorder characterized by periods of bronchial obstruction and increased bronchial hyper reactivity. In childhood and early adulthood, asthma is frequently associated also with quantitative measures of atopy. Genome wide quantitative multipoint linkage analysis was conducted for serum IgE levels and percentage of positive skin prick test (SPT(per)) using three large groups of families originally ascertained for asthma. In this report, 438 and 429 asthma families were informative for linkage using IgE and SPT(per) which represents 690 independent families. Suggestive linkage (LOD >/= 2) was found on chromosomes 1, 3, and 8q with maximum LODs of 2.34 (IgE), 2.03 (SPT(per)), and 2.25 (IgE) near markers D1S1653, D3S2322-D3S1764, and D8S2324, respectively. The results from chromosomes 1 and 3 replicate previous reports of linkage. We also replicate linkage to 5q with peak LODs of 1.96 (SPT(per)) and 1.77 (IgE) at or near marker D5S1480. Our results provide further evidence implicating chromosomes 1, 3, and 5q. The current report represents one of the biggest genome scans so far reported for asthma related phenotypes. This study also demonstrates the utility of increased sample sizes and quantitative phenotypes in linkage analysis of complex disorders.

Published
2007

180. Usual medical treatments or levonorgestrel-IUS for women with heavy menstrual bleeding: long-term randomised pragmatic trial in primary care.

Author

Kai, J., Middleton, L., Daniels, J., Tryposkiadis, K., Pattison, H., Gupta, J., Kai, Joe, Middleton, Lee, Daniels, Jane, Pattison, Helen, Tryposkiadis, Konstantinos, Gupta, Janesh, and ECLIPSE trial collaborative group

Subjects
MENSTRUATION, WOMEN'S health, PRIMARY care, LEVONORGESTREL, FAMILY medicine, PROGESTATIONAL hormones, HYSTERECTOMY, COMPARATIVE studies, CONTRACEPTIVE drugs, INTRAUTERINE contraceptives, LONGITUDINAL method, RESEARCH methodology, MEDICAL cooperation, MENORRHAGIA, QUALITY of life, RESEARCH, EVALUATION research, RANDOMIZED controlled trials, TREATMENT effectiveness, THERAPEUTICS
Abstract

Background: Heavy menstrual bleeding (HMB) is a common, chronic problem affecting women and health services. However, long-term evidence on treatment in primary care is lacking.Aim: To assess the effectiveness of commencing the levonorgestrel-releasing intrauterine system (LNG-IUS) or usual medical treatments for women presenting with HMB in general practice.Design and Setting: A pragmatic, multicentre, parallel, open-label, long term, randomised controlled trial in 63 primary care practices across the English Midlands.Method: In total, 571 women aged 25-50 years, with HMB were randomised to LNG-IUS or usual medical treatment (tranexamic/mefenamic acid, combined oestrogen-progestogen, or progesterone alone). The primary outcome was the patient reported Menorrhagia Multi-Attribute Scale (MMAS, measuring effect of HMB on practical difficulties, social life, psychological and physical health, and work and family life; scores from 0 to 100). Secondary outcomes included surgical intervention (endometrial ablation/hysterectomy), general quality of life, sexual activity, and safety.Results: At 5 years post-randomisation, 424 (74%) women provided data. While the difference between LNG-IUS and usual treatment groups was not significant (3.9 points; 95% confidence interval = -0.6 to 8.3; P = 0.09), MMAS scores improved significantly in both groups from baseline (mean increase, 44.9 and 43.4 points, respectively; P<0.001 for both comparisons). Rates of surgical intervention were low in both groups (surgery-free survival was 80% and 77%; hazard ratio 0.90; 95% CI = 0.62 to 1.31; P = 0.6). There was no difference in generic quality of life, sexual activity scores, or serious adverse events.Conclusion: Large improvements in symptom relief across both groups show treatment for HMB can be successfully initiated with long-term benefit and with only modest need for surgery. [ABSTRACT FROM AUTHOR]

Published
2016
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181. Cortical Lewy bodies and Aβ burden are associated with prevalence and timing of dementia in Lewy body diseases.

Author

Ruffmann, C., Calboli, F. C. F., Bravi, I., Gveric, D., Curry, L. K., Smith, A., Pavlou, S., Buxton, J. L., Blakemore, A. I. F., Takousis, P., Molloy, S., Piccini, P., Dexter, D. T., Roncaroli, F., Gentleman, S. M., and Middleton, L. T.

Subjects
LEWY body dementia, PARKINSON'S disease, DEMENTIA, NEUROLOGICAL disorders, AMYLOID beta-protein, APOLIPOPROTEIN E
Abstract

Aims Our main objective was to determine the neuropathological correlates of dementia in patients with Lewy body disease (LBD). Furthermore, we used data derived from clinical, neuropathological and genetic studies to investigate boundary issues between Dementia with Lewy bodies (DLB) and Parkinson's disease with (PDD) and without (PDND) dementia. Methods One hundred and twenty-one cases with a neuropathological diagnosis of LBD and clinical information on dementia status were included in the analysis (55 PDD, 17 DLB and 49 PDND). We carried out topographical and semi-quantitative assessment of Lewy bodies (LB), Aβ plaques and tau-positive neuropil threads (NT). The APOE genotype and MAPT haplotype status were also determined. Results The cortical LB (CLB) burden was the only independent predictor of dementia (OR: 4.12, P < 0.001). The total cortical Aβ plaque burden was an independent predictor of a shorter latency to dementia from onset of motor signs ( P = 0.001). DLB cases had a higher LB burden in the parietal and temporal cortex, compared to PDD. Carrying at least one APOE ϵ4 allele was associated with a higher cortical LB burden ( P = 0.02), particularly in the neocortical frontal, parietal and temporal regions. Conclusions High CLB burden is a key neuropathological substrate of dementia in LBD. Elevated cortical LB pathology and Aβ plaque deposition are both correlated with a faster progression to dementia. The higher CLB load in the temporal and parietal regions, which seems to be a distinguishing feature of DLB, may account for the shorter latency to dementia and could be mediated by the APOE ϵ4 allele. [ABSTRACT FROM AUTHOR]

Published
2016
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182. Factors associated with mortality in patients with asymptomatic carotid stenosis: Results from the ACSRS study

Author

Kakkos, S, Nicolaides, A, Griffin, M, Sabetai, M, Dhanjil, S, Thomas, D, Sonecha, T, Salmasi, A, Geroulakos, G, Georgiou, N, Francis, S, Ioannidou, E, Dore, C, Adovasio, R, Ziani, B, Alò, F, Cicilioni, C, Ambrosio, G, Andreev, A, Andreozzi, G, Verlato, F, Camporese, G, Arosio, E, Barkauskas, E, Barros D'Sa, A, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, G, Simoni, G, Bell, P, Biasi, G, Mingazzini, P, Bornstein, N, Bouchier Hayes, D, Fitzgerald, P, Cairols, M, Cao, P, Derango, P, Carboni, G, Geoffredo, C, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopolous, E, Andreadis, E, Dimakakos, P, Kotsis, T, Eikelboom, B, Entz, L, Ferrari Bardilead, N, Aloi, T, Salerno, M, Fernandez, J, Pedro, L, Fitzgerald, D, O'Shaunnersy, A, Fletcher, J, Forconi, S, Cappeli, R, Bicchi, M, Arigucci, S, Gallai, V, Cardaiolli, G, Gomez Isaza, L, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Glannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, B, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, DeRango, P, Ferrari Bardilead, n, McCollum, P, Pantziaris, M., BIASI, GIORGIO MARIA, MINGAZZINI, PAOLO, Kakkos, S, Nicolaides, A, Griffin, M, Sabetai, M, Dhanjil, S, Thomas, D, Sonecha, T, Salmasi, A, Geroulakos, G, Georgiou, N, Francis, S, Ioannidou, E, Dore, C, Adovasio, R, Ziani, B, Alò, F, Cicilioni, C, Ambrosio, G, Andreev, A, Andreozzi, G, Verlato, F, Camporese, G, Arosio, E, Barkauskas, E, Barros D'Sa, A, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, G, Simoni, G, Bell, P, Biasi, G, Mingazzini, P, Bornstein, N, Bouchier Hayes, D, Fitzgerald, P, Cairols, M, Cao, P, Derango, P, Carboni, G, Geoffredo, C, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopolous, E, Andreadis, E, Dimakakos, P, Kotsis, T, Eikelboom, B, Entz, L, Ferrari Bardilead, N, Aloi, T, Salerno, M, Fernandez, J, Pedro, L, Fitzgerald, D, O'Shaunnersy, A, Fletcher, J, Forconi, S, Cappeli, R, Bicchi, M, Arigucci, S, Gallai, V, Cardaiolli, G, Gomez Isaza, L, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Glannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, B, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, DeRango, P, Ferrari Bardilead, n, McCollum, P, Pantziaris, M., BIASI, GIORGIO MARIA, and MINGAZZINI, PAOLO

Abstract

Aim. This study determines the factors associated with mortality in patients with asymptomatic carotid stenosis. Methods. Patients (n=1 101) with asymptomatic internal carotid artery stenosis greater than 50% in relation to the bulb diameter were followed up for a period of 6 to 84 (median 38) months. Stenosis was graded using duplex scanning and expressed as a percentage of the carotid bulb diameter. Clinical and biochemical risk factors were recorded. The end-points were ipsilateral ischemic stroke, cardiovascular death and all cause mortality. Results. In a Cox multivariate analysis 6 factors emerged as independent predictors of risk. Age, male gender, cardiac failure, left ventricular hypertrophy on electrocardiogram (ECG) and myocardial ischemia on ECG were associated with increased risk. Antiplatelet therapy was associated with decreased risk. Based on these risk factors a high-risk group consisting of one third of the population with a 40% cumulative cardiovascular death rate and a 66% all cause death rate at 7 years could be identified. The remaining 2/3 consisted of a low-risk group with a 10% cumulative cardiovascular death rate and a 21% all cause death rate at 7 years (P<0.0001 compared to the high risk group). There was not any significant difference in the cumulative ipsilateral stroke rate, which was 12% in the low and 13% in the high cardiovascular risk group (Log Rank P>0.05). Conclusion. The methodology and findings from the ACSRS natural history study need to be applied to randomized controlled trials on the value of carotid endarterectomy or stenting in patients with asymptomatic carotid stenosis. They may help refine the indications for intervention in patients with carotid endarterectomy.

Published
2005

183. Effect of image normalization on carotid plaque classification and the risk of ipsilateral hemispheric ischemic events: Results from the Asymptomatic Carotid Stenosis and Risk of Stroke study

Author

Nicolaides, A, Kakkos, S, Griffin, M, Sabetai, M, Dhanjil, S, Thomas, D, Geroulakos, G, Georgiou, N, Francis, S, Ioannidou, E, Doré, C, Asymptomatic Carotid, S, Risk of Stroke Study Group: Adovasio, R, Ziani, B, Alò, F, Cicilioni, C, Ambrosio, G, Andreev, A, Andreozzi, G, Verlato, F, Camporese, G, Arosio, E, Barkauskas, E, Barros, D, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, G, Simoni, G, Bell, P, Biasi, G, Mingazzini, P, Bornstein, N, Bouchier Hayes, D, Fitzgerald, P, Cairols, M, Cao, P, Derango, P, Carboni, G, Geoffredo, C, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopoulos, E, Andreadis, E, Dimakakos, P, Kotsis, T, Eikelboom, B, Entz, L, Ferrari, B, Aloi, T, Salerno, M, Fernandes e. Fernandes, J, Pedro, L, Fitzgerald, D, O'Shaunnersy, A, Fletcher, J, Forconi, S, Cappeli, R, Bicchi, M, Arrigucci, S, Gallai, V, Cardaiolli, G, Gomez Isaza, L, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Giannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, B, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, Tyllis, T, Minar, E, Willfort, A, Moggi, L, Nenci, G, Radicchia, S, Norgren, L, Ribbe, E, Novo, S, Tantillo, R, Olinic, D, Paaske, W, Pagnan, A, Pauletto, P, Pagliara, V, Pettina, G, Pratesi, C, Matticari, S, Polivka, J, Sevcik, P, Poredos, P, Blinc, A, Videcnik, V, Pujia, A, Raso, A, Rispoli, P, Conforti, M, Robinson, T, Dennis, M, Rosfors, S, Rudofsky, G, Schroeder, T, Gronholdt, M, Finocchi, C, Rodriguez, G, Spartera, C, Ventura, M, Scarpelli, P, Sprynger, M, Sadzot, B, Hottermans, C, Moonen, Taylor, P, Tovar Pardo, A, Negreira, J, Vayssairat, M, Faintuch, J, Valaikiené, J, Walker, M, Wilkinson, A, Nicolaides, AN, Kakkos, SK, Thomas, DJ, Doré, CJ, Asymptomatic Carotid Stenosis, Alò, FP, Cicilioni, CG, Andreozzi, GM, Barros, D'Sa AA, Novelli, GP, Bornstein, NM, Cairols, MA, Cao, PG, DeRango, P, Carboni, GP, Andreadis, EA, Dimakakos, PB, Ferrari Bardile, Fitzgerald, DE, Gomez Isaza, LF, Lee, BB, McCollum, P, Dennis, MS, Gronholdt, ML, Taylor, PR, Faintuch, JM, Walker, MG, Wilkinson, AR, BIASI, GIORGIO MARIA, MINGAZZINI, PAOLO, Nicolaides, A, Kakkos, S, Griffin, M, Sabetai, M, Dhanjil, S, Thomas, D, Geroulakos, G, Georgiou, N, Francis, S, Ioannidou, E, Doré, C, Asymptomatic Carotid, S, Risk of Stroke Study Group: Adovasio, R, Ziani, B, Alò, F, Cicilioni, C, Ambrosio, G, Andreev, A, Andreozzi, G, Verlato, F, Camporese, G, Arosio, E, Barkauskas, E, Barros, D, Brannigan, P, Batchvarova, V, Dramov, A, Belardi, P, Novelli, G, Simoni, G, Bell, P, Biasi, G, Mingazzini, P, Bornstein, N, Bouchier Hayes, D, Fitzgerald, P, Cairols, M, Cao, P, Derango, P, Carboni, G, Geoffredo, C, Catalano, M, Chambers, B, Goetzmann, M, Dickinson, A, Clement, D, Bobelyn, M, Coccheri, S, Conti, E, Diamantopoulos, E, Andreadis, E, Dimakakos, P, Kotsis, T, Eikelboom, B, Entz, L, Ferrari, B, Aloi, T, Salerno, M, Fernandes e. Fernandes, J, Pedro, L, Fitzgerald, D, O'Shaunnersy, A, Fletcher, J, Forconi, S, Cappeli, R, Bicchi, M, Arrigucci, S, Gallai, V, Cardaiolli, G, Gomez Isaza, L, Gorgoyannis, G, Liasis, N, Graf, M, Guarini, P, Hardy, S, Harris, P, Aston, S, Iosa, G, Katsamouris, A, Giannoukas, A, Krzanowski, M, Ladurner, G, Leal Monedero, J, Lee, B, Liapis, C, Galanis, P, Liboni, W, Pavanelli, E, Mannarino, E, Vaudo, G, Mccollum, P, Levison, R, Micieli, G, Bosone, D, Middleton, L, Pantziaris, M, Tyllis, T, Minar, E, Willfort, A, Moggi, L, Nenci, G, Radicchia, S, Norgren, L, Ribbe, E, Novo, S, Tantillo, R, Olinic, D, Paaske, W, Pagnan, A, Pauletto, P, Pagliara, V, Pettina, G, Pratesi, C, Matticari, S, Polivka, J, Sevcik, P, Poredos, P, Blinc, A, Videcnik, V, Pujia, A, Raso, A, Rispoli, P, Conforti, M, Robinson, T, Dennis, M, Rosfors, S, Rudofsky, G, Schroeder, T, Gronholdt, M, Finocchi, C, Rodriguez, G, Spartera, C, Ventura, M, Scarpelli, P, Sprynger, M, Sadzot, B, Hottermans, C, Moonen, Taylor, P, Tovar Pardo, A, Negreira, J, Vayssairat, M, Faintuch, J, Valaikiené, J, Walker, M, Wilkinson, A, Nicolaides, AN, Kakkos, SK, Thomas, DJ, Doré, CJ, Asymptomatic Carotid Stenosis, Alò, FP, Cicilioni, CG, Andreozzi, GM, Barros, D'Sa AA, Novelli, GP, Bornstein, NM, Cairols, MA, Cao, PG, DeRango, P, Carboni, GP, Andreadis, EA, Dimakakos, PB, Ferrari Bardile, Fitzgerald, DE, Gomez Isaza, LF, Lee, BB, McCollum, P, Dennis, MS, Gronholdt, ML, Taylor, PR, Faintuch, JM, Walker, MG, Wilkinson, AR, BIASI, GIORGIO MARIA, and MINGAZZINI, PAOLO

Abstract

The aim of this study was to determine the effect of image normalization on plaque classification and the risk of ipsilateral ischemic neurologic events in patients with asymptomatic carotid stenosis. The first 1,115 patients recruited to the Asymptomatic Carotid Stenosis and Risk of Stroke (ACSRS) study with a follow-up of 6 to 84 months (mean 37.1 months) were included in this study. Duplex ultrasonography was used for grading the degree of internal carotid artery stenosis and for plaque characterization (types 1-5), which was performed before and after image normalization. One hundred sixteen ipsilateral ischemic hemispheric events occurred. Image normalization resulted in 60% of plaques being reclassified. Before image normalization, a high event rate was associated with all types of plaque. After image normalization, 109 (94%) of the events occurred in patients with plaque types 1 to 3. For patients with European Carotid Stenosis Trial (ECST) 70 to 99% diameter stenosis (equivalent to North American Symptomatic Carotid Endarterectomy Trial [NASCET] 50-99%) with plaque types 1 to 3, the cumulative stroke rate was 14% at 7 years (2% per year), and for patients with plaque types 4 and 5, the cumulative stroke rate was 0.9% at 7 years (0.14% per year). The results suggest that asymptomatic patients with plaque types 4 and 5 classified as such after image normalization are at low risk irrespective of the degree of stenosis.

Published
2005

184. BMJ

Author

Davies, L., primary, Saing, C. W., additional, Power, S., additional, Middleton, L., additional, and Yoganathan, K., additional

Published
2011
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195. A comparative study of LRRK2, PINK1 and genetically undefined familial Parkinson's disease

Author

Nishioka, K., primary, Kefi, M., additional, Jasinska-Myga, B., additional, Wider, C., additional, Vilarino-Guell, C., additional, Ross, O. A, additional, Heckman, M. G, additional, Middleton, L. T, additional, Ishihara-Paul, L., additional, Gibson, R. A, additional, Amouri, R., additional, Ben Yahmed, S., additional, Ben Sassi, S., additional, Zouari, M., additional, El Euch, G., additional, Farrer, M. J, additional, and Hentati, F., additional

Published
2009
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196. Genome-wide association study of recurrent major depressive disorder in two European case–control cohorts

Author

Muglia, P, primary, Tozzi, F, additional, Galwey, N W, additional, Francks, C, additional, Upmanyu, R, additional, Kong, X Q, additional, Antoniades, A, additional, Domenici, E, additional, Perry, J, additional, Rothen, S, additional, Vandeleur, C L, additional, Mooser, V, additional, Waeber, G, additional, Vollenweider, P, additional, Preisig, M, additional, Lucae, S, additional, Müller-Myhsok, B, additional, Holsboer, F, additional, Middleton, L T, additional, and Roses, A D, additional

Published
2008
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197. Study of large inbred Friedreich ataxia families reveals a recombination between D9S15 and the disease locus

Author

Belal, S., Panayides, K., Sirugo, G., Hamida, C. B., Ioannou, P., Hentati, F., Jacques S Beckmann, Koenig, M., Mandel, J. -L, Hamida, M. B., and Middleton, L. T.

Subjects
Adult, Male, Recombination, Genetic, congenital, hereditary, and neonatal diseases and abnormalities, Adolescent, Genetic Linkage, Chromosome Mapping, Original Articles, Pedigree, Consanguinity, Haplotypes, Friedreich Ataxia, Humans, Female, Lod Score, Chromosomes, Human, Pair 9
Abstract

Friedreich ataxia is a neurodegenerative disorder with autosomal recessive inheritance. Precise linkage mapping of the Friedreich ataxia locus (FRDA) in 9q13-q21 should lead to the isolation of the defective gene by positional cloning. The two closest DNA markers, D9S5 and D9S15, show very tight linkage to FRDA, making difficult the ordering of the three loci. We present a linkage study of three large Friedreich ataxia families of Tunisian origin, with several multiallelic markers around D9S5 and D9S15. Haplotype data were used to investigate genetic homogeneity of the disease in these geographically related families. A meiotic recombination was found in a nonaffected individual, which excludes a 150-kb segment, including D9S15, as a possible location for the Friedreich ataxia gene and which should orient the search in the D9S5 region.

Published
1992

198. PINK1 mutations and parkinsonism

Author

Ishihara-Paul, L., primary, Hulihan, M. M., additional, Kachergus, J., additional, Upmanyu, R., additional, Warren, L., additional, Amouri, R., additional, Elango, R., additional, Prinjha, R. K., additional, Soto, A., additional, Kefi, M., additional, Zouari, M., additional, Sassi, S. B., additional, Yahmed, S. B., additional, El Euch-Fayeche, G., additional, Matthews, P. M., additional, Middleton, L. T., additional, Gibson, R. A., additional, Hentati, F., additional, and Farrer, M. J., additional

Published
2008
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200. Outcome in fetal lower urinary tract obstruction: a prospective registry study.

Author

Morris, R. K., Middleton, L. J., Malin, G. L., Quinlan‐Jones, E., Daniels, J., Khan, K. S., Deeks, J., and Kilby, M. D.

Subjects
*COMPARATIVE studies, *FETAL diseases, *GESTATIONAL age, *LONGITUDINAL method, *RESEARCH methodology, *EVALUATION of medical care, *MEDICAL cooperation, *PREGNANCY, *PROGNOSIS, *RESEARCH, *URINARY organs, *LOGISTIC regression analysis, *EVALUATION research, *ACQUISITION of data, *THERAPEUTICS, URETHRAL obstruction
Abstract

Objective: To describe influences on decision-making and prognostic variables in the prenatal management of fetal lower urinary tract obstruction (LUTO).Methods: This was a prospective registry study of pregnant women with a male fetus with LUTO from centers within the British Isles and The Netherlands. Women and/or their clinicians were given the treatment option of either conservative management or vesicoamniotic shunting (VAS). Baseline characteristics of women in the registry, reasons for entry to the registry and pregnancy outcomes were assessed. The main study outcomes were survival to 28 days after delivery, further survival to 2 years and renal function. Logistic regression analysis was used to examine prognostic variables that affected outcome. Results were compared with those of women in a randomized controlled trial (RCT) who were allocated randomly to a treatment option.Results: Forty-five women were registered, of whom 78% (35/45) underwent conservative management. Twenty-seven women entered the registry owing to their clinician's preference for management and 18 because of their own preference. Compared to the conservative-management group of the RCT, a higher proportion of women in the registry opting for conservative management had a normal amniotic fluid volume at diagnosis (P = 0.05) and a diagnosis of LUTO ≥ 24 weeks' gestation (P = 0.003). On multivariable logistic regression analysis, these variables showed a significant association with perinatal survival (P < 0.001). Survival to 28 days after delivery was higher in the conservative-management group, at 69% (24/35), compared to 40% (4/10) in the VAS group (P = 0.02) but this difference had limited statistical significance owing to small study size (relative risk, 0.58 (95% CI, 0.26-1.29); P = 0.14).Conclusion: In our prospective registry, the majority of fetuses with LUTO received conservative management, which was associated with better short- and long-term outcomes. A significant proportion of these pregnancies had normal amniotic fluid volume and a gestational age at diagnosis of ≥ 24 weeks, characteristics shown to be associated with improved survival. [ABSTRACT FROM AUTHOR]

Published
2015
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