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396 results on '"Ford, C. E."'

18. Matern Child Health J

Author

FORD, C. E., COETZEE, D., WINSTON, J., CHIBWESHA, C. J., EKOUEVI, Didier K, WELTY, T. K., TIH, P. M., MAMAN, S., STRINGER, E. M., STRINGER, J. S. A., and CHI, B. H.

Published
2019

22. Nanochannel Array Glass

Author

Tonucci, R. J., Justus, B. L., Campillo, A. J., and Ford, C. E.

Published
1992

24. Nondisjunction

Author

Ford, C. E., Burgio, G. Roberto, editor, Fraccaro, Marco, editor, Tiepolo, Luciano, editor, and Wolf, Ulrich, editor

Published
1981
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26. Chromosomes Of Man

Author

Polani, Paul E., Briggs, J. H., and Ford, C. E.

Published
1959

32. Structure-assisted design of mechanism-based irreversible inhibitors of human rhinovirus 3C protease with potent antiviral activity against multiple rhinovirus serotypes

Author

MATTHEWS, D. A., DRAGOVICH, P. S., WEBBER, S. E., FUHRMAN, S. A., PATICK, A. K., ZALMAN, L. S., HENDRICKSON, T. F., LOVE, R. A., PRINS, T. J., MARAKOVITS, J. T., ZHOU, R., TIKHE, J., FORD, C. E., MEADOR, J. W., FERRE, R. A., BROWN, E. L., BINFORD, S. L., BROTHERS, M. A., DELISLE, D. M., and WORLAND, S. T.

Subjects
Rhinoviruses -- Research, Proteases -- Research, Viral vaccines -- Research, Influenza vaccines -- Research, Science and technology
Abstract

Human rhinoviruses, the most important etiologic agents of the common cold, are messenger-active single-stranded monocistronic RNA viruses that have evolved a highly complex cascade of proteolytic processing events to control viral gene expression and replication. Most maturation cleavages within the precursor polyprotein are mediated by rhinovirus 3C protease (or its immediate precursor, 3CD), a cysteine protease with a trypsin-like polypeptide fold. High-resolution crystal structures of the enzyme from three viral serotypes have been used for the design and elaboration of 3C protease inhibitors representing different structural and chemical classes. Inhibitors having [Alpha],[Beta]-unsaturated carbonyl groups combined with peptidyl-binding elements specific for 3C protease undergo a Michael reaction mediated by nucleophilic addition of the enzyme's catalytic Cys-147, resulting in covalent-bond formation and irreversible inactivation of the viral protease. Direct inhibition of 3C proteolytic activity in virally infected cells treated with these compounds can be inferred from dose-dependent accumulations of viral precursor polyproteins as determined by SDS/PAGE analysis of radiolabeled proteins. Cocrystal-structure-assisted optimization of 3C-protease-directed Michael acceptors has yielded molecules having extremely rapid in vitro inactivation of the viral protease, potent antiviral activity against multiple rhinovirus serotypes and low cellular toxicity. Recently, one compound in this series, AG7088, has entered clinical trials.

Published
1999

33. The 11q;22q translocation: A European collaborative analysis of 43 cases

Author

Fraccaro, M., Lindsten, J., Ford, C. E., Iselius, L., Antonelli, A., Aula, P., Aurias, A., Bain, A. D., Bartsch-Sandhoff, M., Bernardi, F., Boyd, E., Buchanan, L. F., Cameron, A. H., de la Chapelle, A., Ciuffa, G., Cuoco, C., Dutrillaux, B., Dutton, G., Ferguson-Smith, M. A., Francesconi, D., Geraedts, J. P. M., Gimelli, G., Gueguen, J., Gärsner, E., Hagemeijer, A., Hansen, F. J., Hollings, P. E., Hustinx, T. W. J., Kaakinen, A., van de Kamp, J. J. P., von Koskull, H., Lejeune, J., Lindenbaum, R. H., McCreanor, H. H., Mikkelsen, M., Mitelman, F., Nicoletti, B., Nilsby, J., Nilsson, B., Noel, B., Padovani, E., Pasquali, F., de Pater, J., Pedersen, C., Petersen, F., Robson, E. B., Rotman, J., Ryynänen, M., Sachs, E., Salat, J., Smythe, R. H., Stabell, I., Šubrt, I., Vampirelli, P., Wessner, G., Zergollern, L., and Zuffardi, O.

Published
1980
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37. A framework for quantifying net benefits of alternative prognostic models

Author

Rapsomaniki, E., White, I. R., Wood, A. M., Thompson, S. G., Tipping, R. W., Ford, C. E., Simpson, L. M., Folsom, A. R., Chambless, L. E., Panagiotakos, D. B., Pitsavos, C., Chrysohoou, C., Stefanadis, C., Knuiman, M., Whincup, P. H., Wannamethee, S. G., Morris, R. W., Kiechl, S., Willeit, J., Oberhollenzer, F., Mayr, A., Wald, N., Lawlor, D. A., Yarnell, J. W., Gallacher, J., Casiglia, E., Tikhonoff, V., Nietert, P. J., Sutherland, S. E., Bachman, D. L., Keil, J. E., Cushman, M., Tracy, R., Tybjaerg-Hansen, A., Nordestgaard, B. G., Frikke-Schmidt, R., Giampaoli, S., Palmieri, L., Panico, S., Vanuzzo, D., Pilotto, L., Gomez de la Camara, A., Gomez Gerique, J. A., Simons, L., Mccallum, J., Friedlander, Y., Lee, A. J., Taylor, J., Guralnik, J. M., Wallace, R., Blazer, D. G., Khaw, K. -T., Schottker, B., Muller, H., Rothenbacher, D., Jansson, J. -H., Wennberg, P., Nissinen, A., Donfrancesco, C., Salomaa, V., Harald, K., Jousilahti, P., Vartiainen, E., Woodward, M., D'Agostino Sr, R. B., Wolf, P. A., Vasan, R. S., Pencina, M. J., Bladbjerg, E. -M., Jorgensen, T., Moller, L., Jespersen, J., Dankner, R., Chetrit, A., Lubin, F., Rosengren, A., Lappas, G., Eriksson, H., Bjorkelund, C., Lissner, L., Bengtsson, C., Nagel, D., Kiyohara, Y., Arima, H., Doi, Y., Ninomiya, T., Rodriguez, B., Dekker, J. M., Nijpels, G., Stehouwer, C. D. A., Iso, H., Kitamura, A., Yamagishi, K., Noda, H., Goldbourt, U., Kauhanen, J., Salonen, J. T., Cooper, J. A., Verschuren, W. M. M., Blokstra, A., Shea, S., Doring, A., Meisinger, C., Bueno-de-Mesquita, H. B., Kuller, L. H., Grandits, G., Gillum, R. F., Mussolino, M., Bauer, K. A., Kirkland, S., Shaffer, J., Korin, M. R., Sato, S., Amouyel, P., Arveiler, D., Evans, A., Ferrieres, J., Schulte, H., Assmann, G., Westendorp, R. G., Buckley, B. M., Packard, C. J., Sattar, N., Cantin, B., Despres, J. -P., Dagenais, G. R., Barrett-Connor, E., Wingard, D. L., Bettencourt, R., Gudnason, V., Aspelund, T., Sigurdsson, G., Thorsson, B., Witteman, J., Kardys, I., Tiemeier, H., Hofman, A., Tunstall-Pedoe, H., Tavendale, R., Lowe, G. D. O., Howard, B. V., Zhang, Y., Best, L., Umans, J., Ben-Shlomo, Y., Davey-Smith, G., Njolstad, I., Wilsgaard, T., Ingelsson, E., Lind, L., Giedraitis, V., Lannfelt, L., Gaziano, J. M., Stampfer, M., Ridker, P., Wassertheil-Smoller, S., Manson, J. E., Marmot, M., Clarke, R., Fletcher, A., Brunner, E., Shipley, M., Buring, J., Shepherd, J., Cobbe, S. M., Ford, I., Robertson, M., Marin Ibanez, A., Feskens, E. J. M., Kromhout, D., Interne Geneeskunde, and RS: CARIM School for Cardiovascular Diseases

Subjects
Nutrition and Disease, Epidemiology, Cost effectiveness, Cost-Benefit Analysis, cardiovascular-disease, Kaplan-Meier Estimate, 01 natural sciences, Health informatics, 010104 statistics & probability, 0302 clinical medicine, cardiovascular disease, Voeding en Ziekte, Econometrics, Medicine, 030212 general & internal medicine, Research Articles, competing risks, validation, Framingham Risk Score, Cost–benefit analysis, coronary heart-disease, Discriminant Analysis, cohort, Prognosis, 3. Good health, Cardiovascular Diseases, Meta-analysis, Risk assessment, metaanalysis, Statistics and Probability, reclassification, Context (language use), risk score, Risk Assessment, screening strategies, statins, 03 medical and health sciences, Meta-Analysis as Topic, Humans, 0101 mathematics, cost-effectiveness, Proportional Hazards Models, VLAG, business.industry, Proportional hazards model, Cardiovascular disease, Competing risks, Cost-effectiveness, Net benefit, Screening strategies, Epidemiologic Research Design, predictive ability, R1, meta-analysis, roc curve, business, net benefit
Abstract

New prognostic models are traditionally evaluated using measures of discrimination and risk reclassification, but these do not take full account of the clinical and health economic context. We propose a framework for comparing prognostic models by quantifying the public health impact (net benefit) of the treatment decisions they support, assuming a set of predetermined clinical treatment guidelines. The change in net benefit is more clinically interpretable than changes in traditional measures and can be used in full health economic evaluations of prognostic models used for screening and allocating risk reduction interventions. We extend previous work in this area by quantifying net benefits in life years, thus linking prognostic performance to health economic measures; by taking full account of the occurrence of events over time; and by considering estimation and cross-validation in a multiple-study setting. The method is illustrated in the context of cardiovascular disease risk prediction using an individual participant data meta-analysis. We estimate the number of cardiovascular-disease-free life years gained when statin treatment is allocated based on a risk prediction model with five established risk factors instead of a model with just age, gender and region. We explore methodological issues associated with the multistudy design and show that cost-effectiveness comparisons based on the proposed methodology are robust against a range of modelling assumptions, including adjusting for competing risks. Copyright © 2011 John Wiley & Sons, Ltd.

Published
2012

50. The non-canonical Wnt ligand, Wnt5a, is upregulated and associated with epithelial to mesenchymal transition in epithelial ovarian cancer.

Author

Ford, C. E., Punnia-Moorthy, G., Henry, C. E., Llamosas, E., Nixdorf, S., Olivier, J., Caduff, R., Ward, R. L., and Heinzelmann-Schwarz, V.

Subjects
*WNT proteins, *LIGANDS (Biochemistry), *EPITHELIAL cells, *MESENCHYMAL stem cells, *OVARIAN cancer treatment, *CELLULAR signal transduction
Abstract

Objective Aberrant Wnt signalling has previously been associated with gynaecological cancers, and the aim of this study was to investigate the expression of Wnt5a in epithelial ovarian cancer, and clarify its role in activating or inhibiting β-catenin dependent and independent Wnt signalling pathways. Method Wnt5a expression was investigated in a large cohort of epithelial ovarian cancer patient samples using immunohistochemistry and correlated with clinicopathological variables. Wnt5a function was investigated in vitro in ovarian cell lines. Results Wnt5a expression was found to be upregulated in all major subtypes (serous, endometrioid, clear cell and mucinous) of epithelial ovarian cancer compared to borderline tumours and benign controls. Treatment of ovarian surface epithelial cells with recombinant Wnt5a decreased cell adhesion and was associated with increased epithelial to mesenchymal transition (EMT). In addition, downstream targets of β-catenin dependent Wnt signalling were inhibited, and β-catenin independent targets increased following Wnt5a upregulation. Knockdown of Wnt5a in ovarian cancer cells was associated with a mesenchymal to epithelial transition (MET), but had no significant effect on cell migration or proliferation. Conclusion This study adds to the increasing evidence that Wnt signalling may play an important role in ovarian cancer development. Utilising an unparalleled large cohort of 623 patients, Wnt5a protein expression was shown to be significantly higher in ovarian cancer patients when compared to benign and borderline ovarian tumours and healthy control patients. In addition, we have utilised in vitro models to show for the first time in ovarian cancer that Wnt5a driven non-canonical pathways can alter epithelial to mesenchymal transition (EMT). [ABSTRACT FROM AUTHOR]

Published
2014
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