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716 results on '"Darby, C"'

52. Human islet expression levels of Prostaglandin E2 synthetic enzymes, but not prostaglandin EP3 receptor, are positively correlated with markers of β-cell function and mass in non-diabetic obesity

Author

Truchan, Nathan A., primary, Fenske, Rachel J., additional, Sandhu, Harpreet K., additional, Weeks, Alicia M., additional, Patibandla, Chinmai, additional, Wancewicz, Benjamin, additional, Pabich, Samantha, additional, Reuter, Austin, additional, Harrington, Jeffrey M., additional, Brill, Allison L., additional, Peter, Darby C., additional, Nall, Randall, additional, Daniels, Michael, additional, Punt, Margaret, additional, Kaiser, Cecilia E., additional, Cox, Elizabeth D., additional, Ge, Ying, additional, Davis, Dawn B., additional, and Kimple, Michelle E., additional

Published
2021
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53. Agonist-independent Gαz activity negatively regulates beta-cell compensation in a diet-induced obesity model of type 2 diabetes

Author

Schaid, Michael D., primary, Green, Cara L., additional, Peter, Darby C., additional, Gallagher, Shannon J., additional, Guthery, Erin, additional, Carbajal, Kathryn A., additional, Harrington, Jeffrey M., additional, Kelly, Grant M., additional, Reuter, Austin, additional, Wehner, Molly L., additional, Brill, Allison L., additional, Neuman, Joshua C., additional, Lamming, Dudley W., additional, and Kimple, Michelle E., additional

Published
2021
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54. Development and application of high-throughput screens for the discovery of compounds that disrupt ErbB4 signaling: Candidate cancer therapeutics

Author

Cullum, Richard L., primary, Lucas, Lauren M., additional, Senfeld, Jared I., additional, Piazza, John T., additional, Neel, Logan T., additional, Whig, Kanupriya, additional, Zhai, Ling, additional, Harris, Mackenzie H., additional, Rael, Cristina C., additional, Taylor, Darby C., additional, Cook, Laura J., additional, Kaufmann, David P., additional, Mill, Christopher P., additional, Jacobi, Megan A., additional, Smith, Forrest T., additional, Suto, Mark, additional, Bostwick, Robert, additional, Gupta, Ram B., additional, David, Allan E., additional, and Riese, II, David J., additional

Published
2020
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55. Abstract A19: Discovery and characterization of selective and nonselective inhibitors of ErbB4 signaling: Putative targeted melanoma therapeutics

Author

Lucas, Lauren M., primary, Cullum, Richard L., additional, Senfeld, Jared I., additional, Cook, Laura J., additional, Harris, Mackenzie H., additional, Kaufmann, David Z., additional, Rael, Cristina C., additional, Taylor, Darby C., additional, Piazza, John T., additional, Neel, Logan T., additional, Gupta, Ram B., additional, David, Allan E., additional, and Riese, David J., additional

Published
2020
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57. The dynamics of buried seed banks beneath woodlands, with particular reference to Hypericum pulchrum

Author

Darby, C. D.

Subjects
577, Tree seed germination factors
Abstract

This study has examined the rate at which the seeds of certain species disappear from woodland soils, and whether the composition of the seed banks beneath stands of known age can be used to reveal management history. Associated with this is an investigation of the spatial distribution of the stored propagules. A question arises as to whether species with long lived seeds can survive as buried seed long enough to take advantage of the opening of the canopy and soil disturbance resulting from the falling of old trees. Given the great life span of most trees, this is a strategy open only to species with exceptionally long lived seed banks. One such species is Hypericum pulchrum, which, as the seed bank surveys carried out in this study show, can exist as viable seeds beneath woodlands of great age in the Tavistock Woodland Estate in Devon. Is this germination and reproduction on tree falls sufficient to maintain Hypericum in the seed bank indefinitely ? To answer this question, a computer model was developed to examine the effect of various parameters on the survival time of a Hypericum seed bank beneath a simulated woodland. The model allowed prediction of both the mean density of buried seeds in a unit area, and the development of pattern within the seed bank. Analysis of the simulation results established that the dispersal of Hypericum was insufficient to maintain a seed bank by a "chain reaction" of windthrown reinforcement. The implications of this are discussed with respect to pioneer species within both temperate and tropical forests.

Published
1987

58. Irish endocrine society: Proceedings of meeting held 7th/8th November, 1997

Author

Gleeson, A., Owens, D., Collins, P., Johnson, A., Tomkin, G. H., Sexton, D. M., Creedon, G., Ledwith, M., Griffin, M., O’Meara, N., Collins, P. B., Kilbane, M. T., Tuite, A. M., Shering, S. G., Smith, D. F., McDermott, F. W. M., O’Higgins, N. J., Smyth, P. P. A., McKenna, K., Thompson, C. J., Kohler, W. M., O’Shea, D., Alaghband-Zadeh, J., Latham, K., Carter, G., Smyth, P. P. A., Shering, S. G., Kilbane, M. T., McDermott, E. W. M., Smith, D. F., O’Higgins, N. J., Lovell, S. L., Leslie, H., Doherty, C., Hadden, D. R., McGeown, Mary G., Kinsley, B. T., McKenna, T. J., Byrne, P. M., Gallagher, C., McKennal, M. J., Li Voon Chong, S. W., Darby, C., Freyne, P., Cullen, M. J., McKone, E., Heffernan, A., Darko, D. A., Kyrialcides, E., O’Shea, D., Burr, R., Carter, G., Armstrong, V. L., Ennis, C. N., Hunter, S. J., Sheridan, B., Atkinson, A. B., Bell, P. M., Giblin, L., Griffin, M. E., Otridge, B., O’Meara, N. M., Kinsley, B. T., Weinger, K., Bajaj, M., Levy, C. J., Waters, M., Simonson, D. C., Cox, D. J., Jacobson, A. M., Armstrong, V. L., Ennis, C. N., Sheridan, B., Atkinson, A. B., Bell, P. M., Traub, A. I., Creedon, G., Sexton, D., Griffin, M., O’Meara, N., Collins, P., Wiggam, M. I., Bell, P. M., Sheridan, B., Walmsley, A. E., Atkinson, A. B., Leary, A. C., Grealy, G., Higgins, T. M., Buckley, N., Barry, D. G., Murphy, D., Ferriss, J. B., McConnell, E. M., Bell, P. M., Hadden, D. R., McCance, R., Atkinson, A. B., Nikookam, K., Suliman, M. E., Carroll, M., Webster, J., Wilson, R. M., Cullen, D. R., McAllister, A. S., McCance, D. R., Hadden, D. R., Bell, P. M., Leslie, H., Sheridan, B., Atkinson, A. B., Alavi, Z., O’Hare, J. A., McAllister, A. S., Atkinson, A. B., McCance, D. R., Johnston, G. D., McKenna, M. J., and Freaney, R.

Published
1998
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59. Coronary Computed Tomography Angiography–Derived Plaque Quantification in Patients With Acute Coronary Syndrome

Author

Ellen Hoffmann, Jess D. Rames, Richard R. Bayer, Damiano Caruso, Sheldon E. Litwin, David Jochheim, Ullrich Ebersberger, Moritz H. Albrecht, Darby C Shuler, Carlo N. De Cecco, Moritz Baquet, Salvatore A. Chiaramida, Christian Tesche, Taylor M. Duguay, U. Joseph Schoepf, and Akos Varga-Szemes

Subjects
Male, medicine.medical_specialty, Acute coronary syndrome, Coronary Artery Disease, 030204 cardiovascular system & hematology, acute coronary syndrome, 030218 nuclear medicine & medical imaging, angina, Angina, Coronary artery disease, Lesion, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Humans, Angina, Stable, Vascular Calcification, Retrospective Studies, Computed tomography angiography, stable, Framingham Risk Score, medicine.diagnostic_test, business.industry, Coronary Stenosis, Retrospective cohort study, Middle Aged, aged, angina, stable, computed tomography angiography, coronary angiography, medicine.disease, Plaque, Atherosclerotic, Stenosis, ROC Curve, Cardiology, Female, Radiology, medicine.symptom, Cardiology and Cardiovascular Medicine, business
Abstract

This study investigated the discriminatory value of quantitative atherosclerotic plaque markers derived from coronary computed tomography angiography (cCTA) in patients with first acute coronary syndrome (ACS) compared with patients with stable coronary artery disease (CAD). Forty patients (56.9 ± 9.3 years, 55% men) admitted with their first ACS and Framingham risk score-matched controls with stable CAD were retrospectively analyzed. All patients had undergone cCTA followed by invasive coronary angiography. Total plaque volume, calcified and noncalcified plaque volumes, plaque burden (in %), remodeling index, lesion length, presence of napkin-ring sign, segment involvement score, and segment stenosis score were derived from cCTA and compared between both groups on a per-lesion and per-patient level. Patients with ACS showed a significant higher number of obstructive CAD and higher values for segment stenosis score, segment involvement score, noncalcified plaque volume, lesion length, and remodeling index than the stable angina group (all p0.05). On a per-lesion level, culprit lesions had significantly higher values for plaque burden, total plaque volume, noncalcified plaque volume, remodeling index, lesion length, and prevalence of napkin-ring sign in comparison to nonculprit lesions (all p0.05). On receiver-operating characteristics (ROC) analysis, a stepwise model demonstrated incremental discriminatory power for identifying ACS both per-patient (area under the curve 0.92, p0.0001) as well as per-lesion (area under the curve 0.88, p0.0001). cCTA-derived culprit plaque markers show discriminatory value both on a per-patient and per-lesion level. A combination of markers added to the Framingham risk score yields the greatest discriminatory ability.

Published
2017
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62. Prostaglandin EP3 Receptor signaling is required to prevent insulin hypersecretion and metabolic dysfunction in a non-obese mouse model of insulin resistance

Author

Darby C. Peter, Rachel J. Fenske, Michelle E. Kimple, Michael D. Schaid, Austin Reuter, and Jaclyn A. Wisinski

Subjects
0301 basic medicine, Blood Glucose, Male, medicine.medical_specialty, Physiology, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Prostaglandin, 030209 endocrinology & metabolism, Biology, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Insulin resistance, In vivo, Physiology (medical), Insulin-Secreting Cells, Internal medicine, Diabetes mellitus, Insulin Secretion, medicine, Animals, Insulin, Promoter Regions, Genetic, 030304 developmental biology, Mice, Knockout, 2. Zero hunger, Mice, Inbred BALB C, 0303 health sciences, geography, geography.geographical_feature_category, medicine.disease, Islet, Phenotype, Rats, Mice, Inbred C57BL, 030104 developmental biology, Endocrinology, chemistry, Receptors, Prostaglandin E, EP3 Subtype, Female, lipids (amino acids, peptides, and proteins), Beta cell, Insulin Resistance, Ex vivo, Research Article
Abstract

When homozygous for the LeptinOb mutation (Ob), Black-and-Tan Brachyury (BTBR) mice become morbidly obese and severely insulin resistant, and by 10 weeks of age, frankly diabetic. Previous work has shown Prostaglandin EP3 Receptor (EP3) expression and activity is up-regulated in islets from BTBR-Ob mice as compared to lean controls, actively contributing to their beta-cell dysfunction. In this work, we aimed to test the impact of beta-cell-specific EP3 loss on the BTBR-Ob phenotype by crossing Ptger3 floxed mice with the Rat insulin promoter (RIP)-CreHerr driver strain. Instead, germline recombination of the floxed allele in the founder mouse – an event whose prevalence we identified as directly associated with underlying insulin resistance of the background strain – generated a full-body knockout. Full-body EP3 loss provided no diabetes protection to BTBR-Ob mice, but, unexpectedly, significantly worsened BTBR-lean insulin resistance and glucose tolerance. This in vivo phenotype was not associated with changes in beta-cell fractional area or markers of beta-cell replication ex vivo. Instead, EP3-null BTBR-lean islets had essentially uncontrolled insulin hypersecretion. The selective up-regulation of constitutively-active EP3 splice variants in islets from young, lean BTBR mice as compared to C57BL/6J, where no phenotype of EP3 loss has been observed, provides a potential explanation for the hypersecretion phenotype. In support of this, high islet EP3 expression in Balb/c females vs. Balb/c males was fully consistent with their sexually-dimorphic metabolic phenotype after loss of EP3-coupled Gαz protein. Taken together, our findings provide a new dimension to the understanding of EP3 as a critical brake on insulin secretion.New and NoteworthyIslet Prostaglandin EP3 receptor (EP3) signaling is well-known as up-regulated in the pathophysiological conditions of type 2 diabetes, contributing to beta-cell dysfunction. Unexpected findings in mouse models of non-obese insulin sensitivity and resistance provide a new dimension to our understanding of EP3 as a key modulator of insulin secretion. A previously-unknown relationship between mouse insulin resistance and the penetrance of Rat insulin promoter-driven germline floxed allele recombination is critical to consider when creating beta-cell-specific knockouts.For Table of Contents Use Only

Published
2019
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63. Beta‐cell‐specific loss of the inhibitory G protein, Gα z , alters development and pathophysiology of Type 1 Diabetes

Author

Kathryn A. Carbajal, Darby C. Peter, Michelle E. Kimple, Rachel J. Fenske, Austin Reuter, and Haley Wienkes

Subjects
medicine.medical_specialty, Type 1 diabetes, Chemistry, medicine.disease, Biochemistry, Pathophysiology, Endocrinology, Internal medicine, Genetics, medicine, Beta cell, Inhibitory G-protein, Molecular Biology, Biotechnology
Published
2019
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64. Increasing the dietary ratio of omega 3:omega 6 polyunsaturated fatty acids positively impacts inflammation and islet outcomes in Type 1 Diabetes

Author

Michelle E. Kimple, Rachel J. Fenske, Darby C. Peter, and Haley Wienkes

Subjects
chemistry.chemical_classification, Type 1 diabetes, geography, medicine.medical_specialty, geography.geographical_feature_category, business.industry, Inflammation, medicine.disease, Islet, Biochemistry, Omega, Endocrinology, chemistry, Internal medicine, Genetics, medicine, medicine.symptom, business, Molecular Biology, Biotechnology, Polyunsaturated fatty acid
Published
2019
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66. Safety of a Restrictive versus Liberal Approach to Red Blood Cell Transfusion on the Outcome of AKI in Patients Undergoing Cardiac Surgery: A Randomized Clinical Trial

Author

Garg A, Badner N, Bagshaw S, Cuerden M, Fergusson D, Gregory A, Hall J, Hare G, Khanykin B, McGuinness S, Parikh C, Roshanov P, Shehata N, Sontrop J, Syed S, Tagarakis G, Thorpe K, Verma S, Wald R, Whitlock R, Mazer C, de Medicis E, Masse M, Marchand J, MacAdams C, Seal D, Ferland A, Ali I, Maier K, Creary T, Tittley L, Spence J, Jaffer I, Brodutch S, Lellouche F, Bussieres J, Dagenais F, Lizotte P, Gagne N, Tremblay H, Breton C, Bouchard P, Bainbridge D, Bentall T, Beique F, Ramachandran S, Rochon A, Vervais M, Grenier S, Grocott H, Kashani H, Ambrose E, McVagh J, Mazer, Hare, Verma, Crescini C, Yagnik S, Slabiak A, Han K, Fremes S, Karkhanis R, Baig N, Sidhu S, MacArthur R, Reid K, Boehnke S, Hudson C, Rubens F, Winch D, Klein R, Grey R, Teoh K, Wiley W, Darby C, Ho A, Saha T, Shore D, Shelley J, Lamarche Y, Sirois C, Brown C, Dube C, Holden K, Roy L, Rolfe B, Brown S, Saczkowski R, Senner W, Carrier F, Noiseux N, Hebert P, Benettaib F, Ghamraoui A, Lebrasseur M, Beattie W, Carroll J, Poonawala H, Zbitnew G, Howells S, Mawhinney R, Sampson S, Yegappan C, Schroeder R, Perfect S, Jones M, Leff J, Nair S, Moncada K, Joco C, Harrison M, Greilich P, Landgraf K, Kramer R, Gallant B, Fontes M, Stavris K, Rosengart T, Debakey M, Omer S, Coffey K, Broussard E, Tseng E, London M, Stanley K, Casson L, Julien M, Myles P, Wallace S, Galagher W, Ditoro A, Royse A, Royse C, Williams Z, Tivendale L, Dong N, Judelman S, Leyden J, Yarad E, Doane M, Player C, Scott D, Slater B, Corcoran P, Hu R, Sidiropoulos S, Baulch S, Brewster D, Simpson S, Smith J, Hulley A, Painter T, de Prinse L, Bannon P, Turner L, Beattie L, Eslick A, Cope L, Sanderson B, Baker R, Pesudovs B, Bennetts J, Dimovski D, Duggan N, Ives K, Yap C, Byrne K, Mans G, Termaat J, Young P, Ridgeon E, Reddy S, Hurford S, Mackle D, Baker T, Hunt A, Cruz R, Henderson S, Mehrtens J, Parke R, Gilder E, Cowdrey K, Dalton J, Butler M, Long S, Lammert A, Blakemore A, Walker C, France D, Hutchison R, Xue S, Gu J, Chen X, Fan A, Suraya S, Raja N, Yusnida I, Azura T, Saibon T, Bing M, Hwang N, Tan R, Ang F, Chin T, Mehta C, Jain A, Sharma P, Shah R, Shaikh P, Kanchi M, Sigamani A, Anusha K, Johansson P, Anderson T, Olesen L, Lilleor N, Rasmussen S, Fenger A, Treskatsch S, Mezger V, Falk E, Habicher M, Sander M, Edinger F, Koch C, Boening A, Oswald I, Bulat-Genc S, Seeberger D, Fassl J, Seeberger E, Eberle B, Takala J, Stucki M, Mateo E, Moreno J, Gabaldon T, Cobo I, Pena J, Ferrer C, Carmona P, Lopez Cantero M, Pajares A, Zarragoikoetxea I, Galan J, Urrutia G, Martinez-Zapata M, Rivilla M, Cegarra V, Acosta-Isaac R, Gajate-Martin L, Candela-Toha A, Simopoulos V, Karangelis D, Filipescu D, Paunescu A, Fawzy H, Mawlana W, Preisman S, Raanani E, Kogan D, Matot I, Cattan A, Artsi H, Galhardo C, Olival S, Toledo R, Villar J, Hernandez E, Montes F, Vaquiro E, Garavito C, Abello M, Manrique E, Vasquez S, Aguilar L, Coral M, Rodriguez H, Tellez J, Martinez C, Biccard B, Alphonsus C, Spiess B, Hall R, Kent B, Denault A, Deschamps A, TRICS Investigators, and Perioperative Anesthesia Clinical

Abstract

Background Safely reducing red blood cell transfusions can prevent transfusion-related adverse effects, conserve the blood supply, and reduce health care costs. Both anemia and red blood cell transfusion are independently associated with AKI, but observational data are insufficient to determine whether a restrictive approach to transfusion can be used without increasing AKI risk. Methods In a prespecified kidney substudy of a randomized noninferiority trial, we compared a restrictive threshold for red blood cell transfusion (transfuse if hemoglobin= 0.3 mg/dl within 48 hours of surgery, or >= 50% within 7 days of surgery. Results Patients in the restrictive-threshold group received significantly fewer transfusions than patients in the liberal-threshold group (1.8 versus 2.9 on average, or 38% fewer transfusions in the restricted threshold group compared with the liberal-threshold group; P

Published
2019

69. Irish Society of Gastroenterology: Proceedings of Winter Meeting held November, 1994 in Dublin

Author

Neelamakam, P. K., Brazil, E., Attwood, S., Traynor, O., Yaqoob, J., Khan, M. I., O’Toole, D., Noonan, N., Carey, C., Kelleher, D., Weir, D. G., Keeling, P. W. N., Monahan, D., Cogan, L., Willoughby, R., Jackson, J., Whelan, A., Weir, D. G., Feighery, C., Kaminski, G. Z., Conroy, A., Dooley, S., Parfrey, N. A., McEneaney, P., O’Morain, C., McGrath, J. P., Stuart, R. C., Hill, J., Byrne, P. J., Timon, C., Chung, S. C. S., VanHasselt, A., Hennessy, T. P. J., Hamilton, D., Mulcahy, D., Walsh, D., Farrely, C., Tormey, W., Fielding, J., Watson, G., Conroy, A., Kaminski, G. Z., Dooley, S., Parfrey, N. A., Khan, M. I., Yaqoob, J., Cherukuri, A., Maloney, M., Toole, D. O., Corcoran, M., Noonan, N., Weir, D. G., Keeling, P. W. N., Coffey, J., Butt, F., McAvinchey, D., Delaney, P. V., Burke, G. J., Feighery, C., Youngprapakorn, S., Srinivasan, U., Willoughby, R., Leonard, N., O’Farrelly, C., Morain, C. O., Weir, D. G., Whelan, C. A., Barry, E., Collins, C., Costello, P., Willoughby, R., Feighery, C., O’Herlihy, C., O’Donoghue, D. P., O’Farrelly, C., Yaqoob, J., Khan, M. I., Corcoran, M., Clabby, C., Toole, D. O., Noonan, N., Kelleher, D., Weir, D. G., Keeling, P. W. N., McCarthy, J., Kenny-Walsh, E., Whelton, M. J., Morrin, M., Khan, F., Delaney, P., O’Keeffe, J., Mills, K., Willoughby, R., Feighery, C., Bennett, M. A., Kay, E. W., Mulcahy, H., O’Donoghue, D. P., Leader, M., Croke, D. T., Yaqoob, J., Fan, X. G., Khan, I., Toole, D. O., Noonan, N., Carey, C., Kelleher, D., Weir, D. G., Keeling, P. W. N., Keating, S., Morrison, C., Buckley, M., O’Morain, C., O’Reilly, F. M., Darby, C., Courtney, M. G., Murphy, G. M., Fielding, J. F., O’Boyle, C. J., Boyle, T. J., Costello, P., Mulhall, K., Kerin, M. J., Courtney, D., Quill, D. S., Given, H. F., Kehoe, S., Boyle, T. J., Quirke, R., Stephens, R. B., Norris, S., Costello, P., Collins, C., Traynor, O., McEntee, G., Hegarty, J., Farrelly, C., Thottaparambil, D., Thomas, R., Houghton, G., Sachithanandan, S., Geoghegan, A., Leader, M., Doyle, S., McGrath, J. P., McCaul, C., Byrne, P. J., Walsh, T. N., Hennessy, T. P. J., Khan, M. I., Yaqoob, J., Farrell, R., Gusau, B., Toole, D. O., Carey, C., Noonan, N., Kelleher, D., Keeling, P. W. N., Courtney, M. G., O’Mahoney, M. S., AlBloushi, S., Sachithanandan, J., Walshe, J., Carmody, M., Donohoe, J., Shattock, A. G., Parfrey, N., Fielding, J. F., Collins, C., Lynch, S., Madrigal, L., Norris, S., McEntee, J., Traynor, O., Hegarty, J., O’Farrelly, C., Khan, M. I., Yaqoob, J., Murphy, R., Ahmed, Z., Ryan, M., Montwill, C., Morgan, A., Smith, P., Walker, F., Murphy, A., Moloney, M., McGrath, S., Kelleher, D., Taraneweh, E., Bhatia, A. K., O’Keeffe, D., McCarthy, P., Rajan, E., Albloushi, S., Farrell, B. O’, Shattock, A., Courtney, M. G., Fielding, J. F., Buckley, M., Kearney, D., Lee, J., Gleeson, F., Khan, M. I., Yaqoob, J., Murphy, R., Ahmed, Z., Montwill, C., Ryan, M., Morgan, A., Smith, P., Walker, F., McNamara, B., Cuffe, J., O’Sullivan, G. C., Harvey, B. J., Curran, B., Bennett, M. A., Croke, D. T., Mulcahy, H., Kay, E., Leader, M., O’Donoghue, D. P., Yaqoob, J., Khan, M. I., Corcoran, M., Clabby, C., O’Toole, D., Noonan, N., Weir, D. G., Keeling, P. W. N., Lawler, L., Attwood, S. E. A., Bourke, G., Hyland, J., Owens, W. A., Loughrey, C. M., McAleer, J. A., McManus, K. G., Dillon, J. F., Wong, F. C., Lo, T. C. N., Chan, K. H., Plevris, J. N., Finlayson, N. D. C., Miller, J. D., Bouchier, I. A. D., Hayes, P. C., Walsh, S. V., Egan, L. J., Connolly, C. E., Stevens, F. M., Egan, E. L., McCarthy, C. F., Ma, Q. Y., Magee, G. D., Ardill, J. E., Buchanan, K. D., Rowlands, B. J., McGettigan, P., Chan, R., Shea, B. O’, McManus, J., Feely, J., Donoghue, J., Fanning, N., Mathias, J., Gillen, P., Tanner, W. A., Keane, F. B. V., Campbell, D. M., Donnelly, V., O’Connell, D., Behan, M., O’Herlihy, C., O’Connell, P. R., Ko, C. S., Mealy, K., Walsh, T. N., Hennessy, T. P. J., Gusau, B. M., O’Toole, D., Farrell, R., Noonan, N., Maloney, M., Goggins, M., Yakoub, J., Keeling, P. W. N., Farrell, R. J., Goggins, M., Kelleher, D., Weir, D. G., Keeling, P. W. N., Mahmud, N., Weir, D. G., and Kelleher, D.

Published
1995
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70. National Scientific Medical Meeting 1994 Abstracts

Author

Carson, K. D., Grimes, S. B., McGinley, J. M., Thornton, M. T., Mulhall, J., Bourke, A. M., McCrory, C., Marsh, B., Hone, R., Phelan, D., White, M., Fabry, J., Hughes, D., Carson, K., Donnelly, M., Shanahan, E., Fitzpatrick, G. J., Bourke, M., Warde, D., Buggy, D., Hughes, N., Taylor, A., Dowd, N., Markham, T., Blunnie, W., Nicholson, G., O’Leary, E., Cunningham, A. J., Dwyer, R., McMechan, S., Cullen, C., Dempsey, G., Wright, G., MacKenzie, G., Anderson, J., Adgey, J., Walsh, M., O’Callaghan, P., Graham, I., O’Hare, J. A., Geoghegan, M., Iman, N., Shah, P., Chander, R., Lavin, F., Daly, K., Johnston, P. W., Imam, Z., Adgey, A. A. J., Rusk, R. A., Richardson, S. G., Hale, A., Kinsella, B. M., FitzGerald, G. A., King, G., Crean, P., Gearty, G., Cawley, T., Docherty, J. R., Geraghty, J., Osborne, H., Upton, J., D’Arcy, G., Stinson, J., Cooke, T., Colgan, M. P., Hall, M., Tyrrell, J., Gaffney, K., Grouden, M., Moore, D. J., Shanik, G., Feely, J., Delanty, N., Reilly, M., Lawson, J. A., Fitzgerald, D. J., Reilly, M. P., McAdam, B. F., Bergin, C., Walshe, M. J., Herity, N. A., Allen, J. D., Silke, B., Singh, H. P., O’Neill, S., Hargrove, M., Coleman, E., Shorten, E., Aherne, T., Kelly, B. E., Hill, D. H., McIlrath, E., Morrow, B. C., Lavery, G. G., Blackwood, B., Fee, J. P. H., Kevin, L., Doran, M., Tansey, D., Boylan, I., McShane, A. J., O’Reilly, G., Tuohy, B., Grainger, P., Larkin, T., Mahady, J., Malone, J., Condon, C., Donoghue, T., O’Leary, J., Lyons, J. F., Tay, Y. K., Tham, S. N., Khoo Tan, H. S., Gibson, G., O’Grady, A., Leader, M., Walshe, J., Carmody, M., Donohoe, J., Murphy, G. M., O’Connor, W., Barnes, L., Watson, R., Darby, C., O’Moore, R., Mulcahy, F., O’Toole, E., O’Briain, D. S., Young, M. M., Buckley, D., Healy, E., Rogers, S., Ni Scannlain, N., McKenna, M. J., McBrinn, Y., Murray, B., Freaney, R., Barrett, E., Razza, Q., Abuaisha, F., Powell, D., Murray, T. M., Powell, A. M., O’Mongain, E., O’Neill, J., Kernan, R. 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F., Lynch, S., McManus, R., O’Farrelly, C., Madrigal, L., Feighery, C., O’Donoghue, D., Whelan, C. A., Rea, I. M., Stewart, M., Campbell, P., Alexander, H. D., Crockard, A. D., Morris, T. C. M., Maguire, H., Davidson, F., Kaminski, G. Z., Butler, K., Hillary, I. B., Parfrey, N. A., Crowley, B., McCreary, C., Keane, C., O’Reilly, M., Goh, J., Kennedy, M., Fitzgerald, M., Scott, T., Murphy, S., Hildebrand, J., Holliman, R., Smith, C., Kengasu, K., Riain, U. Ni, Cormican, M., Flynn, J., Glennon, M., Smith, T., Whyte, D., Keane, C. T., Barry, T., Noone, D., Maher, M., Dawson, M., Gilmartin, J. J., Gannon, F., Eljamel, M. S., Allcut, D., Pidgeon, C. N., Phillips, J., Rawluk, D., Young, S., Toland, J., Deveney, A. M., Waddington, J. L., O’Brien, D. P., Hickey, A., Maguire, E., Phillips, J. P., Al-Ansari, N., Cunney, R., Smyth, E., Sharif, S., Eljamel, M., Pidgeon, C., Maguire, E. A., Burke, E. T., Staunton, H., O’Riordan, J. 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G., Johnson, H., McQuoid, G., Gilmer, B., Browne, G., Keogh, J. A. B., Jefferson, A, Smith, M., Hennessy, S., Burke, C. M., Sreenan, S., Power, C. K., Pathmakanthan, S., Poulter, L. W., Chan, A., Sheehan, M., Maguire, M., O’Connor, C. M., FitzGerald, M. X., Southey, A., Costello, C. M., McQuaid, K., Urbach, V., Thomas, S., Horwitz, E. R., Mulherin, D., FitzGerald, O., Bresnihan, B., Kirk, G., Veale, D. J., Belch, J. J. F., Mofidi, A., Mofidi, R., Quigley, C., McLaren, M., Veale, D., D’Arrigo, C., Couto, J. Candal, Woof, J., Greer, M., Cree, I., Belch, J., Hone, S., Fenton, J., Hamilton, S., and McShane, D.

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1994
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71. Erratum to 'Choices of Stent and Cerebral Protection in the Ongoing ACST-2 Trial: A Descriptive Study' (European Journal of Vascular and Endovascular Surgery (2017) 53(5) (617–625) (S1078588417300424) (10.1016/j.ejvs.2016.12.034))

Author

de Waard, D. D., Halliday, A., de Borst, G. J., Bulbulia, R., Huibers, A., Casana, R., Bonati, L. H., Tolva, V., Fraedrich, G., Rantner, B., Gizewski, E., Gruber, I., Hendriks, J., Cras, P., Lauwers, P., van Scheil, P., Vermassen, F., Van Herzeele, I., Geenens, M., Hemelsoet, D., Lerut, P., Lambrecht, B., Saad, G., Peeters, A., Bosiers, M., da Silva, E., de Luccia, N., Sitrangulo, J. C., Estenssoro, A. E. V., Presti, C., Casella, I., Monteiro, J. A. T., Campos, W., Puech-Leao, P., Petrov, V., Bachvarov, C., Hill, M., Mitha, A., Wong, J., Liu, C. -W., Bao, L., Yu, C., Cvjetko, I., Vidjak, V., Fiedler, J., Ostry, S., Sterba, L., Kostal, P., Staffa, R., Vlachovsky, R., Privara, M., Kriz, Z., Vojtisek, B., Krupa, P., Reif, M., Benes, V., Buchvald, P., Endrych, L., Prochazka, V., Kuliha, M., Otahal, D., Hrbac, T., Netuka, D., Mohapl, M., Kramier, F., Eldessoki, M., Heshmat, H., Abd-Allah, F., Palmiste, V., Margus, S., Toomsoo, T., Becquemin, J. -P., Bergeron, P., Abdulamit, T., Cardon, J. -M., Debus, S., Thomalla, G., Fiehler, J., Gerloss, C., Grzyska, U., Storck, M., Lamacchia, E., Eckstein, H. H., Söllner, H., Berger, H., Kallmayer, M., Popert, H., Zimmermann, A., Guenther, A., Klingner, C., Mayer, T., Schubert, J., Zanow, J., Scheinert, D., Banning-Eichenseer, U., Bausback, Y., Branzan, D., Braünilch, S., Lenzer, J., Schidt, A., Staab, H., Ulirch, M., Barlinn, J., Haase, K., Abramyuk, A., Bodechtel, U., Gerber, J., Reeps, C., Pfeiffer, T., Torello, G., Cöster, A., Giannoukas, A., Spanos, K., Matsagkas, M., Koutias, S., Vasdekis, S., Kakisis, J., Moulakakis, K., Lazaris, A., Liapas, C., Brountzos, E., Lazarides, M., Ioannou, N., Polydorou, A., Fulop, B., Fako, E., Voros, E., Bodosi, M., Nemeth, T., Barzo, P., Pazdernyik, S., Entz, L., Szeberin, Z., Dosa, E., Nemes, B., Jaranyi, Z., Pazdernyia, S., Madhaban, P., Hoffman, A., Nikolsky, E., Beyar, R., Silingardi, R., Lauricella, A., Coppi, G., Nicoloci, E., Tusini, N., Strozzi, F., Vecchiati, E., Ferri, M., Ferrero, E., Psacharopulo, D., Gaggiano, A., Viazzo, A., Farchioni, L., Parlani, G., Caso, V., De Rangoy, P., Verzini, F., Castelli, P., Delodovici, M. 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Psacharopulo, D., Gaggiano, A., Viazzo, A., Farchioni, L., Parlani, G., Caso, V., De Rangoy, P., Verzini, F., Castelli, P., DeLodovici, M.L., Carrafiello, G., Ierardi, A.M., Piffaretti, G., Nano, G., Occhiuto, M.T., Malacrida, G., Tealdi, D., Steghter, S., Stella, A., Pini, R., Faggioli, G., Sacca, S., Negri, M.D., Palombo, M., Perfumo, M.C., Fadda, G.F., Kasemi, H., Cernetti, C., Tonello, D., Visonà, A., Mangialardi, N., Ronchey, S., Altavista, M.C., Michelagnoli, S., Chisci, E., Speziale, F., Capoccia, L., Veroux, P., Giaquinta, A., Patti, F., Pulli, R., Boggia, P., Angiletta, D., Amatucci, G., Spinetti, F., Mascoli, F., Tsolaki, E., Civilini, E., Reimers, B., Snoch-Ziólkiewicz, M., Gabriel, M., Odero, A., Accrocca, F., Bajardi, G., Takashi, I., Masayuki, E., Hidenori, E., Aidashova, B., Kospanov, N., Bakke, S., Skjelland, M., Czlonkowska, A., Kobayashi, A., Proczka, R., Dowzenko, A., Czepel, W., Polanski, J., Bialek, P., Ozkinis, G., Stanisic, M., Iwanowski, W., Andziak, P., Gonçalves, F.B., Starodubtsev, V., Ignatenko, P., Karpenko, A., Radak, D., Aleksic, N., Sagic, D., Davidovic, L., Koncar, I., Tomic, I., Colic, M., Bartkoy, D., Rusnak, F., Gaspirini, M., Praczek, P., Milosevic, Z., Flis, V., Bergauer, A., Kobilica, N., Miksic, K., Matela, J., Blanco, E., Guerra, M., Riambau, V., Gillgren, P., Skioldebrand, C., Nymen, N., Berg, B., Delle, M., Formgren, J., Kally, T.B., Qvarfordt, P., Plate, G., Pärson, H., Lindgren, H., Bjorses, K., Gottsäter, A., Warvsten, M., Kristmundsson, T., Forssell, C., Malina, M., Holst, J., Kuhme, T., Sonesson, B., Lindblad, B., Kolbel, T., Acosta, S., Bonati, L., Traenka, C., Mueller, M., Lattman, T., Wasner, M., Mujagic, E., Von Hessling, A., Isaak, A., Stierli, P., Eugster, T., Mariani, L., Stippich, C., Wolff, T., Kahles, T., Toorop, R., Moll, F., Lo, R., Meershoek, A., Jahrome, A.K., Vos, A.W.F., Schuiling, W., Keunen, R., Reijnen, M., Macsweeney, S., McConachie, N., Southam, A., Stansby, G., Lees, T., Lambert, D., Clarke, M., Wyatt, M., Kappadath, S., Wales, L., Jackson, R., Raudonaitis, A., MacDonald, S., Dunlop, P., Brown, A., Vetrivel, S., Bajoriene, M., Gopi, R., McCollum, C., Wolowczyk, L., Ghosh, J., Seriki, D., Ashleigh, R., Butterfield, J., Welch, M., Smyth, J.V., Briley, D., Schulz, U., Perkins, J., Hands, L., Kuker, W., Darby, C., Handa, A., Sekaran, L., Poskitt, K., Morrison, J., Guyler, P., Grunwald, I., Brown, J., Jakeways, M., Tysoe, S., Hargroves, D., Gunathilagan, G., Insall, R., Senaratne, J., Beard, J., Cleveland, T., Nawaz, S., Lonsdale, R., Turner, D., Gaines, P., Nair, R., Chetter, I., Robinson, G., Akomolafe, B., Hatfield, J., Saastamoinen, K., Crinnion, J., Egun, A.A., Thomas, J., Drinkwater, S., D'Souza, S., Thomson, G., Gregory, B., Babu, S., Joseph, T., Gibbs, R., Tebit, G., Mehrzad, A., Enevoldson, P., Mendalow, D., Parry, A., Tervitt, G., Clifton, A., Nazzel, M., Peto, R., Pan, H., Potter, J., Bullbulia, R., Ashley, S., Flather, M., Mansfield, A., Simpson, D., Thomas, D., Gray, W., Farrell, B., Davies, C., Rahimi, K., Gough, M., Cao, P., Rothwell, P., Belli, A., Mafham, M., Herrington, W., Sandercock, P., Gray, R., Shearman, C., Molyneux, A., Gray, A., Clarke, A., Sneade, M., Tully, L., Brudlo, W., Lay, M., Munday, A., Berry, C., Tochlin, S., Mihaylova, B., Cox, J., Kurien, R., and Chester, J.

Subjects
Surgery, Cardiology and Cardiovascular Medicine, Settore MED/22 - Chirurgia Vascolare
Abstract

Due to a miscommunication during the production of this article, the members of the ACST-2 Collaborative Group were not properly indexed in PubMed. This has now been corrected online. We apologize for any confusion or inconvenience that this oversight might have caused.

Published
2017

72. Erratum to “Choices of Stent and Cerebral Protection in the Ongoing ACST-2 Trial: A Descriptive Study” (European Journal of Vascular and Endovascular Surgery (2017) 53(5) (617–625) (S1078588417300424) (10.1016/j.ejvs.2016.12.034))

Author

de Waard, D. D., Halliday, A., de Borst, G. J., Bulbulia, R., Huibers, A., Casana, R., Bonati, L. H., Tolva, V., Fraedrich, G., Rantner, B., Gizewski, E., Gruber, I., Hendriks, J., Cras, P., Lauwers, P., van Scheil, P., Vermassen, F., Van Herzeele, I., Geenens, M., Hemelsoet, D., Lerut, P., Lambrecht, B., SAAD, GEORGE SAFWAT YOUSSEF, Peeters, A., Bosiers, M., COSTA DA SILVA, AMELIA ELISABETE, de Luccia, N., Sitrangulo, J. C., Estenssoro, A. E. V., PRESTI, CHIARA, Casella, I., Monteiro, J. A. T., Campos, W., Puech-Leao, P., Petrov, V., Bachvarov, C., Hill, M., Mitha, A., Wong, J., Liu, C. -W., BAO, LIYING, Yu, C., Cvjetko, I., Vidjak, V., Fiedler, J., Ostry, S., Sterba, L., Kostal, P., Staffa, R., Vlachovsky, R., Privara, M., Kriz, Z., Vojtisek, B., Krupa, P., Reif, M., Benes, V., Buchvald, P., Endrych, L., Prochazka, V., Kuliha, M., Otahal, D., Hrbac, T., Netuka, D., Mohapl, M., Kramier, F., Eldessoki, M., Heshmat, H., Abd-Allah, F., Palmiste, V., Margus, S., Toomsoo, T., Becquemin, J. -P., Bergeron, P., Abdulamit, T., Cardon, J. -M., Debus, S., Thomalla, G., Fiehler, J., Gerloss, C., Grzyska, U., Storck, M., LaMacchia, E., Eckstein, H. H., Söllner, H., Berger, H., Kallmayer, M., Popert, H., Zimmermann, A., Guenther, A., Klingner, C., Mayer, T., Schubert, J., Zanow, J., Scheinert, D., Banning-Eichenseer, U., Bausback, Y., Branzan, D., Braünilch, S., Lenzer, J., Schidt, A., Staab, H., Ulirch, M., Barlinn, J., Haase, K., Abramyuk, A., Bodechtel, U., Gerber, J., Reeps, C., Pfeiffer, T., Torello, G., Cöster, A., Giannoukas, A., Spanos, K., Matsagkas, M., Koutias, S., VASDEKIS, VASSILIS G.S., Kakisis, J., Moulakakis, K., Lazaris, A., Liapas, C., Brountzos, E., Lazarides, M., Ioannou, N., Polydorou, A., Fulop, B., Fako, E., Voros, E., Bodosi, M., Nemeth, T., Barzo, P., Pazdernyik, S., Entz, L., Szeberin, Z., Dosa, E., Nemes, B., Jaranyi, Z., Pazdernyia, S., Madhaban, P., Hoffman, A., Nikolsky, E., Beyar, R., Silingardi, R., Lauricella, A., COPPI, GIOACHINO, Nicoloci, E., Tusini, N., Strozzi, F., Vecchiati, E., Ferri, M., FERRERO, ELISA, Psacharopulo, D., Gaggiano, A., Viazzo, A., Farchioni, L., Parlani, G., Caso, V., De Rangoy, P., Verzini, F., CASTELLI, PAOLO, DeLodovici, M. L., Carrafiello, G., Ierardi, A. M., Piffaretti, G., Nano, G., Occhiuto, M. T., Malacrida, G., Tealdi, D., Steghter, S., Stella, A., Pini, R., Faggioli, G., SACCA', SALVATORE, Negri, M. D., Palombo, M., Perfumo, M. C., Fadda, G. F., Kasemi, H., CERNETTI, MARIA CHIARA, Tonello, D., Visonà, A., Mangialardi, N., Ronchey, S., Altavista, M. C., Michelagnoli, S., Chisci, E., Speziale, F., Capoccia, L., Veroux, P., Giaquinta, A., Patti, F., Pulli, R., Boggia, P., Angiletta, D., Amatucci, G., Spinetti, F., Mascoli, F., TSOLAKI, ELPINIKI, Civilini, E., Reimers, B., Setacci, C., Pogany, G., ODERO, ANDREA, Accrocca, F., Bajardi, G., Takashi, I., Masayuki, E., Hidenori, E., Aidashova, B., Kospanov, N., Bakke, S., Skjelland, M., Czlonkowska, A., Kobayashi, A., Proczka, R., Dowzenko, A., Czepel, W., Polanski, J., Bialek, P., Ozkinis, G., Snoch-Ziólkiewicz, M., Gabriel, M., Stanisic, M., Iwanowski, W., Andziak, P., Gonçalves, F. B., Starodubtsev, V., Ignatenko, P., Karpenko, A., Radak, D., Aleksic, N., Sagic, D., Davidovic, L., Koncar, I., Tomic, I., ČOLIC, MINA, Bartkoy, D., Rusnak, F., Gaspirini, M., Praczek, P., Milosevic, Z., Flis, V., Bergauer, A., Kobilica, N., Miksic, K., Matela, J., Blanco, E., Guerra, M., Riambau, V., Gillgren, P., Skioldebrand, C., Nymen, N., Berg, B., DELLE VERGINI, ANNA RITA MARIA, Formgren, J., Kally, T. B., Qvarfordt, P., Plate, G., Pärson, H., Lindgren, H., Bjorses, K., Gottsäter, A., Warvsten, M., Kristmundsson, T., Forssell, C., Malina, M., Holst, J., Kuhme, T., Sonesson, B., Lindblad, B., Kolbel, T., Acosta, S., BONATI, LISA, Traenka, C., Mueller, M., Lattman, T., Wasner, M., Mujagic, E., Von Hessling, A., Isaak, A., Stierli, P., Eugster, T., Mariani, L., Stippich, C., Wolff, T., Kahles, T., Toorop, R., Moll, F., Lo, R., Meershoek, A., Jahrome, A. K., Vos, A. W. F., Schuiling, W., Keunen, R., Reijnen, M., Macsweeney, S., McConachie, N., Southam, A., Stansby, G., Lees, T., Lambert, D., Clarke, M., Wyatt, M., Kappadath, S., Wales, L., Jackson, R., Raudonaitis, A., MacDonald, S., Dunlop, P., Brown, A., Vetrivel, S., Bajoriene, M., Gopi, R., McCollum, C., Wolowczyk, L., Ghosh, J., Seriki, D., Ashleigh, R., Butterfield, J., WELCH, MICHAEL, Smyth, J. V., Briley, D., Schulz, U., Perkins, J., Hands, L., Kuker, W., Darby, C., Handa, A., Sekaran, L., Poskitt, K., Morrison, J., Guyler, P., Grunwald, I., Brown, J., Jakeways, M., Tysoe, S., Hargroves, D., Gunathilagan, G., Insall, R., Senaratne, J., Beard, J., Cleveland, T., Nawaz, S., Lonsdale, R., Turner, D., Gaines, P., Nair, R., Chetter, I., Robinson, G., Akomolafe, B., Hatfield, J., Saastamoinen, K., Crinnion, J., Egun, A. A., Thomas, J., Drinkwater, S., D'Souza, S., Thomson, G., Gregory, B., Babu, S., Ashley, S., Joseph, T., Gibbs, R., Tebit, G., Mehrzad, A., Enevoldson, P., Mendalow, D., Parry, A., Tervitt, G., Clifton, A., Nazzel, M., Peto, R., Pan, H., Potter, J., Bullbulia, R., Bonati, L., Mihaylova, B., Flather, M., Mansfield, A., Simpson, D., Thomas, D., Gray, W., Farrell, B., Davies, C., Rahimi, K., Gough, M., Cao, P., Rothwell, P., Belli, A., Mafham, M., Herrington, W., Sandercock, P., Gray, R., Shearman, C., Molyneux, A., Gray, A., Clarke, A., Sneade, M., Tully, L., Brudlo, W., Lay, M., MUNDAY, SARA ANN, Berry, C., Tochlin, S., Cox, J., Kurien, R., Chester, J., de Waard, D. D., Halliday, A., de Borst, G. J., Bulbulia, R., Huibers, A., Casana, R., Bonati, L. H., Tolva, V., Fraedrich, G., Rantner, B., Gizewski, E., Gruber, I., Hendriks, J., Cras, P., Lauwers, P., van Scheil, P., Vermassen, F., Van Herzeele, I., Geenens, M., Hemelsoet, D., Lerut, P., Lambrecht, B., Saad, G., Peeters, A., Bosiers, M., da Silva, E., de Luccia, N., Sitrangulo, J. C., Estenssoro, A. E. V., Presti, C., Casella, I., Monteiro, J. A. T., Campos, W., Puech-Leao, P., Petrov, V., Bachvarov, C., Hill, M., Mitha, A., Wong, J., Liu, C. -W., Bao, L., Yu, C., Cvjetko, I., Vidjak, V., Fiedler, J., Ostry, S., Sterba, L., Kostal, P., Staffa, R., Vlachovsky, R., Privara, M., Kriz, Z., Vojtisek, B., Krupa, P., Reif, M., Benes, V., Buchvald, P., Endrych, L., Prochazka, V., Kuliha, M., Otahal, D., Hrbac, T., Netuka, D., Mohapl, M., Kramier, F., Eldessoki, M., Heshmat, H., Abd-Allah, F., Palmiste, V., Margus, S., Toomsoo, T., Becquemin, J. -P., Bergeron, P., Abdulamit, T., Cardon, J. -M., Debus, S., Thomalla, G., Fiehler, J., Gerloss, C., Grzyska, U., Storck, M., Lamacchia, E., Eckstein, H. H., Söllner, H., Berger, H., Kallmayer, M., Popert, H., Zimmermann, A., Guenther, A., Klingner, C., Mayer, T., Schubert, J., Zanow, J., Scheinert, D., Banning-Eichenseer, U., Bausback, Y., Branzan, D., Braünilch, S., Lenzer, J., Schidt, A., Staab, H., Ulirch, M., Barlinn, J., Haase, K., Abramyuk, A., Bodechtel, U., Gerber, J., Reeps, C., Pfeiffer, T., Torello, G., Cöster, A., Giannoukas, A., Spanos, K., Matsagkas, M., Koutias, S., Vasdekis, S., Kakisis, J., Moulakakis, K., Lazaris, A., Liapas, C., Brountzos, E., Lazarides, M., Ioannou, N., Polydorou, A., Fulop, B., Fako, E., Voros, E., Bodosi, M., Nemeth, T., Barzo, P., Pazdernyik, S., Entz, L., Szeberin, Z., Dosa, E., Nemes, B., Jaranyi, Z., Pazdernyia, S., Madhaban, P., Hoffman, A., Nikolsky, E., Beyar, R., Silingardi, R., Lauricella, A., Coppi, G., Nicoloci, E., Tusini, N., Strozzi, F., Vecchiati, E., Ferri, M., Ferrero, E., Psacharopulo, D., Gaggiano, A., Viazzo, A., Farchioni, L., Parlani, G., Caso, V., De Rangoy, P., Verzini, F., Castelli, P., Delodovici, M. L., Carrafiello, G., Ierardi, A. M., Piffaretti, G., Nano, G., Occhiuto, M. T., Malacrida, G., Tealdi, D., Steghter, S., Stella, A., Pini, R., Faggioli, G., Sacca, S., Negri, M. D., Palombo, M., Perfumo, M. C., Fadda, G. F., Kasemi, H., Cernetti, C., Tonello, D., Visonà, A., Mangialardi, N., Ronchey, S., Altavista, M. C., Michelagnoli, S., Chisci, E., Speziale, F., Capoccia, L., Veroux, P., Giaquinta, A., Patti, F., Pulli, R., Boggia, P., Angiletta, D., Amatucci, G., Spinetti, F., Mascoli, F., Tsolaki, E., Civilini, E., Reimers, B., Setacci, C., Pogany, G., Odero, A., Accrocca, F., Bajardi, G., Takashi, I., Masayuki, E., Hidenori, E., Aidashova, B., Kospanov, N., Bakke, S., Skjelland, M., Czlonkowska, A., Kobayashi, A., Proczka, R., Dowzenko, A., Czepel, W., Polanski, J., Bialek, P., Ozkinis, G., Snoch-Ziólkiewicz, M., Gabriel, M., Stanisic, M., Iwanowski, W., Andziak, P., Gonçalves, F. B., Starodubtsev, V., Ignatenko, P., Karpenko, A., Radak, D., Aleksic, N., Sagic, D., Davidovic, L., Koncar, I., Tomic, I., Colic, M., Bartkoy, D., Rusnak, F., Gaspirini, M., Praczek, P., Milosevic, Z., Flis, V., Bergauer, A., Kobilica, N., Miksic, K., Matela, J., Blanco, E., Guerra, M., Riambau, V., Gillgren, P., Skioldebrand, C., Nymen, N., Berg, B., M., Delle, Formgren, J., Kally, T. B., Qvarfordt, P., Plate, G., Pärson, H., Lindgren, H., Bjorses, K., Gottsäter, A., Warvsten, M., Kristmundsson, T., Forssell, C., Malina, M., Holst, J., Kuhme, T., Sonesson, B., Lindblad, B., Kolbel, T., Acosta, S., Bonati, L., Traenka, C., Mueller, M., Lattman, T., Wasner, M., Mujagic, E., Von Hessling, A., Isaak, A., Stierli, P., Eugster, T., Mariani, L., Stippich, C., Wolff, T., Kahles, T., Toorop, R., Moll, F., R., Lo, Meershoek, A., Jahrome, A. K., Vos, A. W. F., Schuiling, W., Keunen, R., Reijnen, M., Macsweeney, S., Mcconachie, N., Southam, A., Stansby, G., Lees, T., Lambert, D., Clarke, M., Wyatt, M., Kappadath, S., Wales, L., Jackson, R., Raudonaitis, A., Macdonald, S., Dunlop, P., Brown, A., Vetrivel, S., Bajoriene, M., Gopi, R., Mccollum, C., Wolowczyk, L., Ghosh, J., Seriki, D., Ashleigh, R., Butterfield, J., Welch, M., Smyth, J. V., Briley, D., Schulz, U., Perkins, J., Hands, L., Kuker, W., Darby, C., Handa, A., Sekaran, L., Poskitt, K., Morrison, J., Guyler, P., Grunwald, I., Brown, J., Jakeways, M., Tysoe, S., Hargroves, D., Gunathilagan, G., Insall, R., Senaratne, J., Beard, J., Cleveland, T., Nawaz, S., Lonsdale, R., Turner, D., Gaines, P., Nair, R., Chetter, I., Robinson, G., Akomolafe, B., Hatfield, J., Saastamoinen, K., Crinnion, J., Egun, A. A., Thomas, J., Drinkwater, S., D'Souza, S., Thomson, G., Gregory, B., Babu, S., Ashley, S., Joseph, T., Gibbs, R., Tebit, G., Mehrzad, A., Enevoldson, P., Mendalow, D., Parry, A., Tervitt, G., Clifton, A., Nazzel, M., Peto, R., Pan, H., Potter, J., Bullbulia, R., Mihaylova, B., Flather, M., Mansfield, A., Simpson, D., Thomas, D., Gray, W., Farrell, B., Davies, C., Rahimi, K., Gough, M., Cao, P., Rothwell, P., Belli, A., Mafham, M., Herrington, W., Sandercock, P., Gray, R., Shearman, C., Molyneux, A., Gray, A., Clarke, A., Sneade, M., Tully, L., Brudlo, W., Lay, M., Munday, A., Berry, C., Tochlin, S., Cox, J., Kurien, R., and Chester, J.

Subjects
Surgery, Cardiology and Cardiovascular Medicine
Abstract

Due to a miscommunication during the production of this article, the members of the ACST-2 Collaborative Group were not properly indexed in PubMed. This has now been corrected online. We apologize for any confusion or inconvenience that this oversight might have caused.

Published
2017

77. KDM6A Controls Genes Modulating Immune Surveillance in Multiple Myeloma

Author

Alberto Riva, José I. Martín-Subero, Gabrielle Quickstad, Jonathan D. Licht, Daphné Dupéré-Richer, Richard L. Bennett, Sayantan Maji, Darby C. Monagle, and Marta Kulis

Subjects
business.industry, Immunology, Medicine, Cell Biology, Hematology, business, medicine.disease, Biochemistry, Immune surveillance, Gene, Multiple myeloma
Abstract

Background: In multiple myeloma (MM), inactivating mutations and loss of the histone demethylase KDM6A (also named UTX, Ubiquitously transcribed Tetratricopeptide repeat, X chromosome) locus are found in up to 50% of patients and are associated with poorer prognosis. KDM6A belongs to a family of Jumonji-C (Jmj-C)-containing demethylases that work as a scaffold for a multiprotein complex containing H3K4 specific methyltransferases KMT2D and/or KMT2C (MLL2/3), the histone acetyltransferase CBP/p300 and members of the SWI/SNF chromatin-remodeling complex. In a concerted manner this complex activates enhancers by adding activation marks on histones and removing methylation of lysine 27 on histone H3 (H3K27me) associated with gene repression. The H3K27me3 methyltransferase EZH2 that catalyzes the reverse reaction of KDM6A, is often overexpressed in MM and this also correlates with poor prognosis. As well, KMT2C, KMT2D and SWI/SNF components of its complex are all found significantly mutated in MM which emphasize the importance of enhancer deregulation in myeloma. Aim: Our goal is to understand how loss of KDM6A affects gene transcription networks and enhancer function to affect MM pathogenesis or progression. Method: We explored the transcriptional consequences of KDM6A deficiency in patient tumors using the gene expression dataset included within the Multiple Myeloma Research Foundation (MMRF) Researcher Gateway and in MM cell lines using data from the Cancer Cell Line Encyclopedia (CCLE). We further modeled the loss of KDM6A in female MM cell lines using CRISPR-Cas9 ribonucleotide protein (RNP) technology and by re-expressing KDM6A in cells null for KDM6A. Using ChIP-sequencing analysis in isogenic KDM6A knockout or replete cell lines, we identified KDM6A binding site in MM and explored how KDM6A deficiency affects chromatin structure to regulate a transcriptional network. Results: Epithelial-to-mesenchymal-transition (EMT)-related pathways were downregulated in low KDM6A expressing tumor from the MMRF patient cohort. In both male and female patients, low expression of KDM6A was associated with decreased expression of genes involved in immune recognition. In MM cell lines, we observed a significant positive correlation between KDM6A expression level and expression of the transcriptional regulators of Major Histocompatibility complex I and II (MHCII and MCHII), NLRC5 and CIITA, respectively. With ChIP-sequencing analysis we find that KDM6A directly binds NLRC5 and CIITA genes, among many other genes involved in immune surveillance. KDM6A null MM cells displayed upregulation of pathways promoting EMT and downregulation of genes regulating immune function, such as HLA-A/B/C, CCL3/5, HHLA2 and ITGAL. Moreover, re-expression of KDM6A in KDM6A null cells upregulated the expression of these gene along with surface expression of MHCI proteins. Conclusion: Together, our data demonstrates that KDM6A modulates EMT and directly regulates expression of major regulators of immune surveillance. KDM6A deficiency may drive MM towards an EMT program to promote systemic spread and facilitate escape from the immune surveillance. Disclosures No relevant conflicts of interest to declare.

Published
2020
Full Text
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78. Abstract A19: Discovery and characterization of selective and nonselective inhibitors of ErbB4 signaling: Putative targeted melanoma therapeutics

Author

Mackenzie H. Harris, Laura J. Cook, Ram B. Gupta, David J. Riese, Allan E. David, John T. Piazza, Darby C. Taylor, Richard L. Cullum, David Z. Kaufmann, Cristina C. Rael, Logan Neel, Lauren M. Lucas, and Jared I. Senfeld

Subjects
Agonist, Cancer Research, biology, Akt/PKB signaling pathway, Cell growth, medicine.drug_class, Tyrosine phosphorylation, Receptor tyrosine kinase, chemistry.chemical_compound, Oncology, chemistry, Cancer research, medicine, biology.protein, Phosphorylation, Protein kinase B, PI3K/AKT/mTOR pathway
Abstract

Introduction: Gain-of-function mutations in the gene that encodes the ErbB4 receptor tyrosine kinase have been found in a significant fraction of melanoma samples. Melanoma cell lines that harbor some of these mutations are dependent on ErbB4 for proliferation. However, there is a scarcity of therapeutics for treating these ErbB4-dependent melanomas. Our drug discovery approach is based on the observation that the Q43L mutant of the ErbB4 agonist Neuregulin 2beta (NRG2b) functions as a partial agonist/antagonist at ErbB4. NRG2b/Q43L stimulates ErbB4 tyrosine phosphorylation, fails to stimulate ErbB4-dependent cell proliferation, and competitively antagonizes agonist stimulation of ErbB4-dependent cell proliferation. ErbB4 partial agonists that function as antagonists at ErbB4 may hold promise as targeted therapeutics for ErbB4-dependent melanomas. Experimental Procedures: Automated, high-throughput phospho-ErbB4 sandwich ELISA and ErbB4-dependent proliferation assays were developed and deployed to identify 19 small-molecule compounds that stimulate ErbB4 tyrosine phosphorylation, yet inhibit ErbB4-dependent cell proliferation. These compounds were prioritized on the basis of their potency, efficacy, and specificity for inhibition of ErbB4-dependent proliferation. Traditional immunoblotting approaches specific to candidate proteins have been deployed to identify targets for hit molecules of interest. Data: The single high-priority candidate (AU-05) inhibits agonist-induced ErbB4-dependent cellular proliferation with an IC50 of 6.8 uM, but inhibits IL3-dependent proliferation with an IC50 of ~2100 uM, suggesting that AU-05 possesses specificity for ErbB4-dependent proliferation. In contrast, AU-39 potently inhibits both ErbB4-dependent cell proliferation with an IC50 of 1.05 nM and IL3-dependent cellular proliferation with an IC50 of 2.61 nM. We have hypothesized that AU-39 targets the PI3K/Akt signaling pathway, which lies downstream of both ErbB4 and the IL3 receptor. We are testing this hypothesis in part by examining the effects of AU-39 on agonist-induced ErbB4 and IL3 receptor coupling to phosphorylation of Akt and other components of the PI3K/Akt pathway. Conclusions: AU-05 is a starting point for the development of specific ErbB4 inhibitors, whereas AU-39 is a candidate inhibitor of the PI3K/Akt signaling pathway. The inhibition of ErbB4-dependent cellular proliferation by these molecules justifies further development of both molecules. Citation Format: Lauren M. Lucas, Richard L. Cullum, Jared I. Senfeld, Laura J. Cook, Mackenzie H. Harris, David Z. Kaufmann, Cristina C. Rael, Darby C. Taylor, John T. Piazza, Logan T. Neel, Ram B. Gupta, Allan E. David, David J. Riese II. Discovery and characterization of selective and nonselective inhibitors of ErbB4 signaling: Putative targeted melanoma therapeutics [abstract]. In: Proceedings of the AACR Special Conference on Melanoma: From Biology to Target; 2019 Jan 15-18; Houston, TX. Philadelphia (PA): AACR; Cancer Res 2020;80(19 Suppl):Abstract nr A19.

Published
2020
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79. Beta‐cell‐specific Loss of the Inhibitory G protein, Gα z , has Sex‐dependent Effects on Development and Pathophysiology of Type 1 Diabetes

Author

Kathryn A. Carbajal, Darby C. Peter, Austin Reuter, Haley Wienkes, Michelle E. Kimple, and Rachel J. Fenske

Subjects
medicine.medical_specialty, Type 1 diabetes, Chemistry, medicine.disease, Biochemistry, Pathophysiology, Endocrinology, Internal medicine, Genetics, medicine, Beta cell, Inhibitory G-protein, Molecular Biology, Biotechnology
Published
2020
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80. Association of Serum Lipid Profile With Coronary Computed Tomographic Angiography-derived Morphologic and Functional Quantitative Plaque Markers

Author

Brian E. Jacobs, Matthias Renker, Christel Weiss, Ibrahim Akin, Christian Tesche, Stefan Baumann, Darby C Shuler, Stefan O. Schoenberg, Michael Behnes, Holger Haubenreisser, Martin Borggrefe, Chris Schwemmer, U. Joseph Schoepf, Tobias Becher, Ksenija Stach, Dirk Lossnitzer, Philipp Kryeziu, Marlon Rutsch, and Thomas Henzler

Subjects
Pulmonary and Respiratory Medicine, Male, medicine.medical_specialty, Computed Tomography Angiography, Coronary Artery Disease, 030204 cardiovascular system & hematology, Coronary Angiography, 030218 nuclear medicine & medical imaging, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Sex Factors, Internal medicine, Medicine, Humans, Radiology, Nuclear Medicine and imaging, In patient, Vascular Calcification, Aged, Retrospective Studies, medicine.diagnostic_test, business.industry, Serum lipid levels, Age Factors, Retrospective cohort study, Middle Aged, medicine.disease, Lipids, Plaque, Atherosclerotic, Computed tomographic angiography, Stenosis, Evaluation Studies as Topic, Cardiology, Female, business, Lipid profile, Biomarkers, Lipoprotein
Abstract

Recent advances in image quality of coronary computed tomographic angiography (cCTA) have enabled improved characterization of coronary plaques. Thus, we investigated the association between quantitative morphological plaque markers obtained by cCTA and serum lipid levels in patients with suspected or known coronary artery disease.We retrospectively analyzed data of 119 statin-naive patients (55±14 y, 66% men) who underwent clinically indicated cCTA between January 2013 and February 2017. Patients were subdivided into a plaque and a no-plaque group. Quantitative and morphologic plaque markers, such as segment involvement score, segment stenosis score, remodeling index, napkin-ring sign, total plaque volume, calcified plaque volume, and noncalcified plaque volume (NCPV) and plaque composition, were analyzed using a semiautomated plaque software prototype. Total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein, low-density lipoprotein/high-density lipoprotein ratio, and triglycerides were determine in both groups.Higher age (61±11 y vs. 52±14 y, P0.0001) and a higher likelihood of male gender (77% vs. 56%, P0.0001) were observed in the plaque group. Differences in lipid levels were neither observed for differentiation between plaque presence or absence, nor after subcategorization for plaque composition. LDL serum levels160 mg/dL correlated with higher NCPV compared with patients with LDL between 100 and 160 mg/dL (112 vs. 27 mm, P=0.037). Other markers were comparable between the different groups.Statin-naive patients with known or suspected coronary artery disease did not show differences in lipid levels related to plaque composition by cCTA. Patients with plaques tended to be men and were significantly older. High LDL levels correlated with high NCPV.

Published
2018

81. Age-Dependent Protection of Insulin Secretion in Diet Induced Obese Mice

Author

Brian A. Schmidt, Elizabeth R. De Leon, Jacqueline A. Brinkman, Rachel J. Fenske, Trillian Gregg, Michelle E. Kimple, Nicole E. Cummings, Matthew J. Merrins, Darby C. Peter, Dawn S. Sherman, and Dudley W. Lamming

Subjects
0301 basic medicine, Male, medicine.medical_specialty, Aging, medicine.medical_treatment, lcsh:Medicine, Type 2 diabetes, Article, 03 medical and health sciences, Mice, Internal medicine, Insulin-Secreting Cells, Glucose Intolerance, Insulin Secretion, medicine, Glucose homeostasis, Animals, Insulin, Prediabetes, Obesity, lcsh:Science, 2. Zero hunger, geography, Multidisciplinary, geography.geographical_feature_category, business.industry, lcsh:R, medicine.disease, Islet, 030104 developmental biology, Endocrinology, Diet, Western, lcsh:Q, medicine.symptom, business, Diet-induced obese, Weight gain
Abstract

Type 2 diabetes is an age-and-obesity associated disease driven by impairments in glucose homeostasis that ultimately result in defective insulin secretion from pancreatic β-cells. To deconvolve the effects of age and obesity in an experimental model of prediabetes, we fed young and aged mice either chow or a short-term high-fat/high-sucrose Western diet (WD) and examined how weight, glucose tolerance, and β-cell function were affected. Although WD induced a similar degree of weight gain in young and aged mice, a high degree of heterogeneity was found exclusively in aged mice. Weight gain in WD-fed aged mice was well-correlated with glucose intolerance, fasting insulin, and in vivo glucose-stimulated insulin secretion, relationships that were not observed in young animals. Although β-cell mass expansion in the WD-fed aged mice was only three-quarters of that observed in young mice, the islets from aged mice were resistant to the sharp WD-induced decline in ex vivo insulin secretion observed in young mice. Our findings demonstrate that age is associated with the protection of islet function in diet-induced obese mice, and furthermore, that WD challenge exposes variability in the resilience of the insulin secretory pathway in aged mice.

Published
2018

82. Loss of the Inhibitory G‐Protein, G α z , in the Cell Protects Against Spontaneous and Streptozotocin‐Induced Diabetes in NOD Mice

Author

Haley Wienkes and Darby C. Peter

Subjects
medicine.medical_specialty, Chemistry, Cell, Streptozotocin, medicine.disease, Biochemistry, medicine.anatomical_structure, Endocrinology, Internal medicine, Diabetes mellitus, Genetics, medicine, Inhibitory G-protein, Molecular Biology, Biotechnology, NOD mice, medicine.drug
Published
2018
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85. Irish endocrine society

Author

Gleeson, A., Owens, D., Collins, P., Johnson, A., Tomkin, G. H., Sexton, D. M., Creedon, G., Ledwith, M., Griffin, M., OʼMeara, N., Collins, P. B., Kilbane, M. T., Tuite, A. M., Shering, S. G., Smith, D. F., McDermott, F. W. M., OʼHiggins, N. J., Smyth, P. P. A., McKenna, K., Thompson, C. J., Kohler, W. M., OʼShea, D., Alaghband-Zadeh, J., Latham, K., Carter, G., McDermott, E. W. M., Lovell, S. L., Leslie, H., Doherty, C., Hadden, D. R., McGeown, Mary G., Kinsley, B. T., McKenna, T. J., Byrne, P. M., Gallagher, C., McKennal, M. J., Li Voon Chong, S. W., Darby, C., Freyne, P., Cullen, M. J., McKone, E., Heffernan, A., Darko, D. A., Kyrialcides, E., Burr, R., Armstrong, V. L., Ennis, C. N., Hunter, S. J., Sheridan, B., Atkinson, A. B., Bell, P. M., Giblin, L., Griffin, M. E., Otridge, B., OʼMeara, N. M., Weinger, K., Bajaj, M., Levy, C. J., Waters, M., Simonson, D. C., Cox, D. J., Jacobson, A. M., Traub, A. I., Sexton, D., Wiggam, M. I., Walmsley, A. E., Leary, A. C., Grealy, G., Higgins, T. M., Buckley, N., Barry, D. G., Murphy, D., Ferriss, J. B., McConnell, E. M., McCance, R., Nikookam, K., Suliman, M. E., Carroll, M., Webster, J., Wilson, R. M., Cullen, D. R., McAllister, A. S., McCance, D. R., Alavi, Z., OʼHare, J. A., Johnston, G. D., McKenna, M. J., and Freaney, R.

Published
1998
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89. Acute kidney injury in patients with nephrotic syndrome undergoing contrast-enhanced CT for suspected venous thromboembolism: a propensity score-matched retrospective cohort study

Author

Chang Sheng Zhou, U. Joseph Schoepf, Darby C Shuler, Julian L. Wichmann, Shu Min Tao, Long Jiang Zhang, Guangming Lu, and Xiang Kong

Subjects
Adult, Male, medicine.medical_specialty, Nephrotic Syndrome, Renal function, Contrast Media, 030204 cardiovascular system & hematology, urologic and male genital diseases, 030218 nuclear medicine & medical imaging, Cohort Studies, 03 medical and health sciences, Young Adult, 0302 clinical medicine, Iodinated contrast, Risk Factors, medicine, Humans, Radiology, Nuclear Medicine and imaging, Risk factor, Propensity Score, Retrospective Studies, business.industry, Incidence (epidemiology), Acute kidney injury, Retrospective cohort study, General Medicine, Venous Thromboembolism, Acute Kidney Injury, Middle Aged, medicine.disease, female genital diseases and pregnancy complications, Radiographic Image Enhancement, Propensity score matching, Female, Radiology, business, Tomography, X-Ray Computed, Nephrotic syndrome
Abstract

To determine whether intravenous iodinated contrast material administration increases the risk of acute kidney injury (AKI) in patients with nephrotic syndrome undergoing contrast-enhanced CT. Patients with nephrotic syndrome undergoing contrast-enhanced CT were retrospectively identified (n = 701). Control group consisted of patients with nephrotic syndrome receiving non-contrast CT (n = 1053). Two different 1:1 propensity score matching models using three or 10 variables were developed for each estimated glomerular filtration (eGFR) subgroup. Incidence of post-CT AKI for the two groups was assessed and compared by standard AKI criteria and Acute Kidney Injury Network (AKIN) criteria. After matching with three variables, the AKI incidence in the contrast-enhanced CT and non-contrast CT groups was 2.7% vs 2.5% (standard AKI criteria) and 4.2% vs. 6.7% (AKIN criteria) (p = 1.00 and 0.05), respectively. After matching with 10 variables, AKI incidences were 3.1% vs. 2.6% (standard AKI criteria) and 4.1% vs. 7.4% (AKIN criteria) (p = 0.72 and 0.03), respectively. AKI incidences of each eGFR subgroup in the contrast-enhanced CT group were not higher than in the non-contrast CT group (lowest p = 0.46). Intravenous contrast material administration during CT was not found to be a risk factor for AKI in this large cohort of patients with nephrotic syndrome. • AKI incidence of contrast-enhanced CT and non-contrast CT had no difference. • AKI incidences of eGFR subgroup in contrast-enhanced CT were not increased. • Studies without a non-contrast CT control group may overestimate CIN incidence.

Published
2017

90. Choices of Stent and Cerebral Protection in the Ongoing ACST-2 Trial: A Descriptive Study (vol 53, pg 617, 2017)

Author

de Waard, D. D., Halliday, A., de Borst, G. J., Bulbulia, R., Huibers, A., Casana, R., Bonati, L. H., Tolva, V., Fraedrich, G., Rantner, B., Gizewski, E., Gruber, I., Hendriks, J., Cras, P., Lauwers, P., van Scheil, P., Vermassen, F., Van Herzeele, I., Geenens, M., Hemelsoet, D., Lerut, P., Lambrecht, B., Saad, G., Peeters, A., Bosiers, M., da Silva, E., de Luccia, N., Sitrangulo, J. C., Estenssoro, A. E. V., Presti, C., Casella, I., Monteiro, J. A. T., Campos, W., Puech-Leao, P., Petrov, V., Bachvarov, C., Hill, M., Mitha, A., Wong, J., Liu, C. -W., Bao, L., Yu, C., Cvjetko, I., Vidjak, V., Fiedler, J., Ostry, S., Sterba, L., Kostal, P., Staffa, R., Vlachovsky, R., Privara, M., Kriz, Z., Vojtisek, B., Krupa, P., Reif, M., Benes, V., Buchvald, P., Endrych, L., Prochazka, V., Kuliha, M., Otahal, D., Hrbac, T., Netuka, D., Mohapl, M., Kramier, F., Eldessoki, M., Heshmat, H., Abd-Allah, F., Palmiste, V., Margus, S., Toomsoo, T., Becquemin, J. -P., Bergeron, P., Abdulamit, T., Cardon, J. -M., Debus, S., Thomalla, G., Fiehler, J., Gerloss, C., Grzyska, U., Storck, M., Lamacchia, E., Eckstein, H. H., Söllner, H., Berger, H., Kallmayer, M., Popert, H., Zimmermann, A., Guenther, A., Klingner, C., Mayer, T., Schubert, J., Zanow, J., Scheinert, D., Banning-Eichenseer, U., Bausback, Y., Branzan, D., Braünilch, S., Lenzer, J., Schidt, A., Staab, H., Ulirch, M., Barlinn, J., Haase, K., Abramyuk, A., Bodechtel, U., Gerber, J., Reeps, C., Pfeiffer, T., Torello, G., Cöster, A., Giannoukas, A., Spanos, K., Matsagkas, M., Koutias, S., Vasdekis, S., Kakisis, J., Moulakakis, K., Lazaris, A., Liapas, C., Brountzos, E., Lazarides, M., Ioannou, N., Polydorou, A., Fulop, B., Fako, E., Voros, E., Bodosi, M., Nemeth, T., Barzo, P., Pazdernyik, S., Entz, L., Szeberin, Z., Dosa, E., Nemes, B., Jaranyi, Z., Pazdernyia, S., Madhaban, P., Hoffman, A., Nikolsky, E., Beyar, R., Silingardi, R., Lauricella, A., Coppi, G., Nicoloci, E., Tusini, N., Strozzi, F., Vecchiati, E., Ferri, M., Ferrero, E., Psacharopulo, D., Gaggiano, A., Viazzo, A., Farchioni, L., Parlani, G., Caso, V., De Rangoy, P., Verzini, F., Castelli, P., Delodovici, M. L., Carrafiello, G., Ierardi, A. M., Piffaretti, G., Nano, G., Occhiuto, M. T., Malacrida, G., Tealdi, D., Steghter, S., Stella, A., Pini, R., Faggioli, G., Sacca, S., Negri, M. D., Palombo, M., Perfumo, M. C., Fadda, G. F., Kasemi, H., Cernetti, C., Tonello, D., Visonà, A., Mangialardi, N., Ronchey, S., Altavista, M. C., Michelagnoli, S., Chisci, E., Speziale, F., Capoccia, L., Veroux, P., Giaquinta, A., Patti, F., Pulli, R., Boggia, P., Angiletta, D., Amatucci, G., Spinetti, F., Mascoli, F., Tsolaki, E., Civilini, E., Reimers, B., Snoch-Ziólkiewicz, M., Gabriel, M., Odero, A., Accrocca, F., Bajardi, G., Takashi, I., Masayuki, E., Hidenori, E., Aidashova, B., Kospanov, N., Bakke, S., Skjelland, M., Czlonkowska, A., Kobayashi, A., Proczka, R., Dowzenko, A., Czepel, W., Polanski, J., Bialek, P., Ozkinis, G., Stanisic, M., Iwanowski, W., Andziak, P., Gonçalves, F. B., Starodubtsev, V., Ignatenko, P., Karpenko, A., Radak, D., Aleksic, N., Sagic, D., Davidovic, L., Koncar, I., Tomic, I., Colic, M., Bartkoy, D., Rusnak, F., Gaspirini, M., Praczek, P., Milosevic, Z., Flis, V., Bergauer, A., Kobilica, N., Miksic, K., Matela, J., Blanco, E., Guerra, M., Riambau, V., Gillgren, P., Skioldebrand, C., Nymen, N., Berg, B., Delle, M., Formgren, J., Kally, T. B., Qvarfordt, P., Plate, G., Pärson, H., Lindgren, H., Bjorses, K., Gottsäter, A., Warvsten, M., Kristmundsson, T., Forssell, C., Malina, M., Holst, J., Kuhme, T., Sonesson, B., Lindblad, B., Kolbel, T., Acosta, S., Bonati, L., Traenka, C., Mueller, M., Lattman, T., Wasner, M., Mujagic, E., Von Hessling, A., Isaak, A., Stierli, P., Eugster, T., Mariani, L., Stippich, C., Wolff, T., Kahles, T., Toorop, R., Moll, F., Lo, R., Meershoek, A., Jahrome, A. K., Vos, A. W. F., Schuiling, W., Keunen, R., Reijnen, M., Macsweeney, S., Mcconachie, N., Southam, A., Stansby, G., Lees, T., Lambert, D., Clarke, M., Wyatt, M., Kappadath, S., Wales, L., Jackson, R., Raudonaitis, A., Macdonald, S., Dunlop, P., Brown, A., Vetrivel, S., Bajoriene, M., Gopi, R., Mccollum, C., Wolowczyk, L., Ghosh, J., Seriki, D., Ashleigh, R., Butterfield, J., Welch, M., Smyth, J. V., Briley, D., Schulz, U., Perkins, J., Hands, L., Kuker, W., Darby, C., Handa, A., Sekaran, L., Poskitt, K., Morrison, J., Guyler, P., Grunwald, I., Brown, J., Jakeways, M., Tysoe, S., Hargroves, D., Gunathilagan, G., Insall, R., Senaratne, J., Beard, J., Cleveland, T., Nawaz, S., Lonsdale, R., Turner, D., Gaines, P., Nair, R., Chetter, I., Robinson, G., Akomolafe, B., Hatfield, J., Saastamoinen, K., Crinnion, J., Egun, A. A., Thomas, J., Drinkwater, S., D'Souza, S., Thomson, G., Gregory, B., Babu, S., Joseph, T., Gibbs, R., Tebit, G., Mehrzad, A., Enevoldson, P., Mendalow, D., Parry, A., Tervitt, G., Clifton, A., Nazzel, M., Peto, R., Pan, H., Potter, J., Bullbulia, R., Ashley, S., Flather, M., Mansfield, A., Simpson, D., Thomas, D., Gray, W., Farrell, B., Davies, C., Rahimi, K., Gough, M., Cao, P., Rothwell, P., Belli, A., Mafham, M., Herrington, W., Sandercock, P., Gray, R., Shearman, C., Molyneux, A., Gray, A., Clarke, A., Sneade, M., Tully, L., Brudlo, W., Lay, M., Munday, A., Berry, C., Tochlin, S., Mihaylova, B., Cox, J., Kurien, R., and Chester, J.

Subjects
Surgery, Cardiology and Cardiovascular Medicine
Published
2017

95. Initial results of BMS-986012, a first-in-class fucosyl-GM1 mAb, in combination with nivolumab, in pts with relapsed/refractory (rel/ ref) small-cell lung cancer (SCLC).

Author

Darby C., Kollia G., Williams D., Ready N., Kolaitis G., Chu Q.S-C., Van Herpen C., Leighl N.B., Markman B., Clarke S., Juergens R.A., Basciano P., Lathers D., Tannenbaum-Dvir S., Urbanska K., Darby C., Kollia G., Williams D., Ready N., Kolaitis G., Chu Q.S-C., Van Herpen C., Leighl N.B., Markman B., Clarke S., Juergens R.A., Basciano P., Lathers D., Tannenbaum-Dvir S., and Urbanska K.

Abstract

Background: Given the burden of comorbidities, lack of curative agents, and high mortality in pts with SCLC, novel treatment options with limited toxicity are needed. BMS-986012 is a first-in-class, fully human mAb with enhanced antibody-dependent cellmediated cytotoxicity that binds to fucosyl-GM1, a ganglioside highly expressed on SCLC. BMS-986012 monotherapy is well tolerated and has shown evidence of antitumor activity in some pts with rel/ref SCLC in a phase 1/2 study (NCT02247349; Chu et al. Ann Oncol. 2016;27(6 suppl) [abstract 1427PD]). Here we present initial results of BMS-986012 + nivolumab (anti-programmed death-1 mAb) in pts with rel/ref SCLC (NCT02247349). Method(s): Pts with SCLC who relapsed after or were refractory to first-line therapy received BMS-986012 400 or 1000 mg +nivolumab 360 mg IV Q3W. Dose escalation was based on a modified toxicity probability interval design. Primary objectives were safety and tolerability and determination of dose-limiting toxicities (DLT) and maximum tolerated dose. Secondary objectives included pharmacokinetics, antitumor activity, and immunogenicity. Result(s): To date, 16 pts received BMS-986012 (400 mg, n=8; 1000 mg, n=8)+nivolumab. Demographic and safety data are based on 14 pts treated as of the April 3, 2017 cutoff. Median age was 64 y (range, 49-79 y), ECOG status was 0 (29%) or 1 (71%), and all pts were current (29%) or former (71%) smokers. All pts had prior platinum-based first-line therapy. The most common treatment-related AEs (TRAEs) were generalized pruritus (71%), vulvovaginal pruritus (21%), and dry skin (21%). Only 2 pts, both treated with 1000/360 mg, had G3/4 TRAEs (G3 pruritus with G4 lipase increase; G3 hepatic failure [DLT; led to discontinuation]). As of May 1, 2017, 4 of the 16 pts evaluable for efficacy achieved partial responses (2 unconfirmed). Updated efficacy data as well as data from ongoing biomarker analyses will be presented. Conclusion(s): BMS-986012 in combination with nivolumab is

Published
2017

97. Status update and interim results from the asymptomatic carotid surgery trial-2 (ACST-2)

Author

Bulbulia, R, Gray, W, Naughten, A, den Hartog, A, Delmestri, A, Wallis, C, le Conte, S, Macdonald, S, Radak, D, Nessi, F, Torsello, G, Hendriks, J, Bjorses, K, Davidovic, L, Tusini, N, Gillgren, P, Casana, R, Tolva, V, Bausback, Y, Mehrzad, A, Gottsäter, A, Esisi, B, Cras, P, Hendriks, Jm, Lauwers, P, Hertoghs, M, Van Schil, P, De Jaegher, L, Peeters, P, Verbist, J, Dendooven, D, De Letter, J, Vanhooren, G, Astarci, P, Capron, I, Choghari, C, Hammer, F, Lacroix, V, Peeters, A, Verhelst, R, Bosiers, M, De Meester, K, Deloose, K, Van Buggenhout, E, Vinck, E, Geenens, M, Hemelsoet, D, Van Herzeele, I, Vermassen, F, De Koster, G, Desiron, Q, Maertens de Noordhout, A, Malmendier, D, Massoz, M, Saad, G, Cirelli, S, Dormal, P, Lerut, P, Thues, E, Coutts, S, Demchuk, A, Hill, M, Hudon, M, Klein, G, Mcclelland, M, Morrish, W, Samis, G, Sutherland, G, Watson, T, Wong, J, Liu, B, Liu, Cw, Barankova, L, Chlouba, V, Fiedler, J, Priban, V, Sterba, L, Kalabova, L, Kriz, Z, Krupa, P, Privara, M, Reif, M, Souckova, L, Staffa, R, Vlachovsky, R, Vojtisek, B, Hrbac, T, Kuliha, M, Prochazka, V, Roubec, M, Skoloudik, D, Abd Allah, F, Eldessoki, Mh, Kassem, Hh, Gharieb, Hs, Cardon, Jm, Le Gallou Wittenberg, A, Allaire, E, Becquemin, Jp, Cochennec, F, Desgranges, P, Hosseini, H, Kobeiter, H, Marzelle, J, Bergeron, P, Padovani, R, Trastour, Jc, Biermaier, B, Gissler, Hm, Klotzsch, C, Pfeiffer, T, Schneider, R, Soehl, L, Wennrih, M, Botsios, S, Branzan, D, Braunlich, S, Holzer, H, Lenzer, J, Reichenbecher, C, Piorkowski, C, Schuster, J, Scheinert, D, Schmidt, A, Ulrich, M, Werner, M, Coster, A, Engelhardt, A, Ratusinski, Cm, Berekoven, B, Frerker, K, Gordon, V, Bellenis, I, Polydorou, A, Polydorou, V, Tavernarakis, A, Ioannou, N, Terzoudi, M, Chatzinikou, E, Giannoukas, A, Hadjigeorgiou, G, Koutsias, S, Ralli, S, Rousas, N, Nemes, B, Jàrànyi, Z, Szabo, A, Varga, D, Barzo, P, Bodosi, M, Fako, E, Fulop, B, Kuncz, A, Nagy, E, Nemeth, T, Pazdernyik, S, Skoba, K, Voros, E, Haider, Sn, Harbison, J, Madhavan, P, Moore, D, Beyar, R, Hoffman, A, Karram, T, Kerner, A, Nikolsky, E, Nitecki, S, Amatucci, G, Vittorio, P, Frederico, Marinazzo, D, Regina, G, Giaquinta, A, Patti, F, Veroux, M, Veroux, P, Adobbati, L, Bertoni, G, Bianchi, P, Cireni, L, Martello, L, Arcuri, L, Casoni, F, Coppi, G, Moratto, R, Veronesi, J, Bajardi, G, Savettieri, G, Corbetta, R, Odero, A, Quaretti, P, Thyrion, Z, Cao, P, Caso, V, Derango, P, Farchioni, L, Parlani, G, Malferrari, G, Strozzi, F, Vecchiati, E, Biello, Antonella, Capoccia, Laura, Menna, Danilo, Rizzo, ANNA RITA, Sbarigia, Enrico, Speziale, Francesco, Toni, D, Giovanni, M, Meola, G, Nano, G, Occiuto, Mt, Stegher, S, Tealdi, D, Accrocca, F, Ambrogi, C, Barbazza, R, Marcucci, G, Cappelli, A, de Donato, G, Palasciano, G, Pieragalli, D, Setacci, C, Settaci, F, Labate, C, Ferrero, E, Ferri, M, Viazzo, A, Castelli, P, Delodovici, Ml, Ferrario, M, Piffaretti, G, Tomei, G, Furui, E, Inoue, T, Kondo, R, Matsumoto, Y, Shimizu, H, Aidashova, B, Kospanov, N, 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Subjects
Male, Time Factors, Carotid artery stenosis, Carotid artery stenting, Carotid endarterectomy, Randomized controlled trial, Stroke, medicine.medical_treatment, Myocardial Infarction, Severity of Illness Index, law.invention, law, Risk Factors, MED/22 - CHIRURGIA VASCOLARE, Carotid Stenosis, Endarterectomy, Endarterectomy, Carotid, Middle Aged, Treatment Outcome, Female, Stents, medicine.symptom, Cardiology and Cardiovascular Medicine, medicine.medical_specialty, Aged, Angioplasty, Asymptomatic Diseases, Cardiovascular Agents, Humans, Patient Selection, Risk Assessment, Asymptomatic, medicine, Carotid, business.industry, Vascular surgery, medicine.disease, Surgery, Cardiovascular agent, Human medicine, business
Abstract

Objectives: ACST-2 is currently the largest trial ever conducted to compare carotid artery stenting (CAS) with carotid endarterectomy (CEA) in patients with severe asymptomatic carotid stenosis requiring revascularization. Methods: Patients are entered into ACST-2 when revascularization is felt to be clearly indicated, when CEA and CAS are both possible, but where there is substantial uncertainty as to which is most appropriate. Trial surgeons and interventionalists are expected to use their usual techniques and CE-approved devices. We report baseline characteristics and blinded combined interim results for 30-day mortality and major morbidity for 986 patients in the ongoing trial up to September 2012. Results: A total of 986 patients (687 men, 299 women), mean age 68.7 years (SD ± 8.1) were randomized equally to CEA or CAS. Most (96%) had ipsilateral stenosis of 70-99% (median 80%) with contralateral stenoses of 50-99% in 30% and contralateral occlusion in 8%. Patients were on appropriate medical treatment. For 691 patients undergoing intervention with at least 1-month follow-up and Rankin scoring at 6 months for any stroke, the overall serious cardiovascular event rate of periprocedural (within 30 days) disabling stroke, fatal myocardial infarction, and death at 30 days was 1.0%. Conclusions: Early ACST-2 results suggest contemporary carotid intervention for asymptomatic stenosis has a low risk of serious morbidity and mortality, on par with other recent trials. The trial continues to recruit, to monitor periprocedural events and all types of stroke, aiming to randomize up to 5,000 patients to determine any differential outcomes between interventions. Clinical trial: ISRCTN21144362. © 2013 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.

Published
2016

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