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4. Development of competent children’s ward co-ordinators

Author

Scaife C, Kellett, and October M

Subjects
Nursing staff, Nursing, education, Workforce, Newly qualified, Job description, General Medicine, Psychology
Abstract

Taking charge of a clinical shift on a ward is daunting for newly qualified staff nurses. This article describes the co-ordinators competency pathway, written to guide and assess band 5 ward nurses, and a co-ordinators development day, which is a simulation-based training day developed by a team of senior nurses to prepare band 5 nurses to become competent children's ward co-ordinators. Each of two groups - of either experienced or less experienced band 5s - starts with the training day as a base for either 12 or 18 months of in-work training that follow. A new job description matching the trust's workforce reorganisation enabled this development of the band 5 nurse's role. A service evaluation has found staff are more competent and confident as a result of this initiative.

Published
2014
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5. The Clinical Utility of CA 19-9 in Pancreatic Adenocarcinoma: Diagnostic and Prognostic Updates

Author

Poruk, K. E., Gay, D. Z., Brown, K., Mulvihill, J. D., Kenneth Boucher, Scaife, C. L., Firpo, M. A., and Mulvihill, S. J.

Subjects
Oncology, medicine.medical_specialty, Pancreatic disease, CA-19-9 Antigen, Adenocarcinoma, Sensitivity and Specificity, Biochemistry, Article, Diagnosis, Differential, Internal medicine, Pancreatic cancer, Biomarkers, Tumor, medicine, Humans, Pancreatic carcinoma, Single institution, Molecular Biology, business.industry, Pancreatic Diseases, General Medicine, Prognosis, medicine.disease, Carcinoembryonic Antigen, Pancreatic Neoplasms, Molecular Medicine, Biomarker (medicine), CA19-9, Differential diagnosis, business
Abstract

CA 19-9 and CEA are the most commonly used biomarkers for diagnosis and management of patients with pancreatic cancer. Since the original compendium by Steinberg in 1990, numerous studies have reported the use of CA 19-9 and, to a lesser extent, CEA in the diagnosis of pancreatic cancer. Here we update an evaluation of the accuracy of CA 19-9 and CEA, and, unlike previous reviews, focus on discrimination between malignant and benign disease instead of normal controls. In 57 studies involving 3,285 pancreatic carcinoma cases, the combined sensitivity of CA 19-9 was 78.2% and in 37 studies involving 1,882 cases with benign pancreatic disease the specificity of CA 19-9 was 82.8%. From the combined analysis of studies reporting CEA, the sensitivity was 44.2% (1,324 cases) and the specificity was 84.8% (656 cases). These measurements more appropriately reflect the expected biomarker accuracy in the differential diagnosis of patients with periampullary diseases. We also present a summary of the use of CA 19-9 as a prognostic tool and evaluate CA 19-9 diagnostic and prognostic utility in a 10-year, single institution experience.

Published
2013
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12. A proteomic analysis of the functional effects of fatty acids in NIH 3T3 fibroblasts

Author

Magdalon, J., Hatanaka, E., Romanatto, T., Rodrigues, H., Kuwabara, W., Scaife, C., Newsholme, Philip, Curi, R., Magdalon, J., Hatanaka, E., Romanatto, T., Rodrigues, H., Kuwabara, W., Scaife, C., Newsholme, Philip, and Curi, R.

Abstract

Previous studies have demonstrated that long chain fatty acids influence fibroblast function at sub-lethal concentrations. This study is the first to assess the effects of oleic, linoleic or palmitic acids on protein expression of fibroblasts, as determined by standard proteomic techniques. The fatty acids were not cytotoxic at the concentration used in this work as assessed by membrane integrity, DNA fragmentation and the MTT assay but significantly increased cell proliferation. Subsequently, a proteomic analysis was performed using two dimensional difference gel electrophoresis (2D-DIGE) and MS based identification. Cells treated with 50 μM oleic, linoleic or palmitic acid for 24 h were associated with 24, 22, 16 spots differentially expressed, respectively. Among the identified proteins, α-enolase and far upstream element binding protein 1 (FBP-1) are of importance due to their function in fibroblast-associated diseases. However, modulation of α-enolase and FBP-1 expression by fatty acids was not validated by the Western blot technique.

Published
2011

15. Muscle disorders * 111. The impact of fatigue in patients with idiopathic inflammatory myopathy: a mixed method study

Author

Campbell, R., primary, Hofmann, D., additional, Hatch, S., additional, Gordon, P., additional, Lempp, H., additional, Das, L., additional, Blumbergs, P., additional, Limaye, V., additional, Vermaak, E., additional, McHugh, N., additional, Edwards, M. H., additional, Jameson, K., additional, Sayer, A. A., additional, Dennison, E., additional, Cooper, C., additional, Salvador, F. B., additional, Huertas, C., additional, Isenberg, D., additional, Jackson, E. J., additional, Middleton, A., additional, Churchill, D., additional, Walker-Bone, K., additional, Worsley, P. R., additional, Mottram, S., additional, Warner, M., additional, Morrissey, D., additional, Gadola, S., additional, Carr, A., additional, Stokes, M., additional, Srivastava, R. N., additional, Sanghi, D., additional, Elbaz, A., additional, Mor, A., additional, Segal, G., additional, Drexler, M., additional, Norman, D., additional, Peled, E., additional, Rozen, N., additional, Goryachev, Y., additional, Debbi, E. M., additional, Haim, A., additional, Wolf, A., additional, Debi, R., additional, Cohen, M. S., additional, Igolnikov, I., additional, Bar Ziv, Y., additional, Benkovich, V., additional, Bernfeld, B., additional, Collins, J., additional, Moots, R. J., additional, Clegg, P. D., additional, Milner, P. I., additional, Ejtehadi, H. D., additional, Nelson, P. N., additional, Wenham, C., additional, Balamoody, S., additional, Hodgson, R., additional, Conaghan, P., additional, Wilkie, R., additional, Blagojevic, M., additional, Jordan, K. P., additional, Mcbeth, J., additional, Peffers, M. J., additional, Beynon, R. J., additional, Thornton, D. J., additional, Chapman, R., additional, Chapman, V., additional, Walsh, D., additional, Kelly, S., additional, Hui, M., additional, Zhang, W., additional, Doherty, S., additional, Rees, F., additional, Muir, K., additional, Maciewicz, R., additional, Doherty, M., additional, Snelling, S., additional, Davidson, R. K., additional, Swingler, T., additional, Price, A., additional, Clark, I., additional, Stockley, E., additional, Hathway, G., additional, Faas, H., additional, Auer, D., additional, Hirsch, G., additional, Hale, E., additional, Kitas, G., additional, Klocke, R., additional, Abraham, A., additional, Pearce, M. S., additional, Mann, K. D., additional, Francis, R. M., additional, Birrell, F., additional, Tucker, M., additional, Mellon, S. J., additional, Jones, L., additional, Price, A. J., additional, Dieppe, P. A., additional, Gill, H. S., additional, Ashraf, S., additional, Walsh, D. A., additional, McCollum, D., additional, McCabe, C., additional, Grieve, S., additional, Shipley, J., additional, Gorodkin, R., additional, Oldroyd, A. G., additional, Evans, B., additional, Greenbank, C., additional, Bukhari, M., additional, Rajak, R., additional, Bennett, C., additional, Williams, A., additional, Martin, J. C., additional, Abdulkader, R., additional, MacNicol, C., additional, Brixey, K., additional, Stephenson, S., additional, Clunie, G., additional, Andrews, R. N., additional, Clark, E. M., additional, Gould, V. C., additional, Carter, L., additional, Morrison, L., additional, Tobias, J. H., additional, Pye, S. R., additional, Vanderschueren, D., additional, O'Neill, T. W., additional, Lee, D. M., additional, Jans, I., additional, Billen, J., additional, Gielen, E., additional, Laurent, M., additional, Claessens, F., additional, Adams, J. E., additional, Ward, K. A., additional, Bartfai, G., additional, Casanueva, F., additional, Finn, J. D., additional, Forti, G., additional, Giwercman, A., additional, Han, T. S., additional, Huhtaniemi, I., additional, Kula, K., additional, Lean, M. E., additional, Pendleton, N., additional, Punab, M., additional, Wu, F. C., additional, Boonen, S., additional, Mercieca, C., additional, Webb, J., additional, Bhalla, A., additional, Fairbanks, S., additional, Moss, K. E., additional, Collins, C., additional, Sedgwick, P., additional, Parker, J., additional, Harvey, N. C., additional, Cole, Z. A., additional, Crozier, S. R., additional, Ntani, G., additional, Mahon, P. A., additional, Robinson, S. M., additional, Inskip, H. M., additional, Godfrey, K. M., additional, Dennison, E. M., additional, Bridges, M., additional, Ruddick, S., additional, Holroyd, C. R., additional, Mahon, P., additional, Godfrey, K., additional, McNeilly, T., additional, McNally, C., additional, Beringer, T., additional, Finch, M., additional, Coda, A., additional, Davidson, J., additional, Walsh, J., additional, Fowlie, P., additional, Carline, T., additional, Santos, D., additional, Patil, P., additional, Rawcliffe, C., additional, Olaleye, A., additional, Moore, S., additional, Fox, A., additional, Sen, D., additional, Ioannou, Y., additional, Nisar, S., additional, Rankin, K., additional, Birch, M., additional, Finnegan, S., additional, Rooney, M., additional, Gibson, D. S., additional, Malviya, A., additional, Ferris, C. M., additional, Rushton, S. P., additional, Foster, H. E., additional, Hanson, H., additional, Muthumayandi, K., additional, Deehan, D. J., additional, Birt, L., additional, Poland, F., additional, MacGregor, A., additional, Armon, K., additional, Pfeil, M., additional, McErlane, F., additional, Beresford, M. W., additional, Baildam, E. M., additional, Thomson, W., additional, Hyrich, K., additional, Chieng, A., additional, Gardner-Medwin, J., additional, Lunt, M., additional, Wedderburn, L., additional, Newell, K., additional, Evans, A., additional, Manning, G., additional, Scaife, C., additional, McAllister, C., additional, Pennington, S. R., additional, Duncan, M., additional, Moore, T., additional, Pericleous, C., additional, Croca, S. C., additional, Giles, I., additional, Alber, K., additional, Yong, H., additional, Midgely, A., additional, Rahman, A., additional, Rzewuska, M., additional, Mallen, C., additional, Strauss, V. Y., additional, Belcher, J., additional, Peat, G., additional, Byng-Maddick, R., additional, Wijendra, M., additional, Penn, H., additional, Roddy, E., additional, Muller, S., additional, Hayward, R., additional, Kamlow, F., additional, Pakozdi, A., additional, Jawad, A., additional, Green, D. J., additional, Hider, S. L., additional, Singh Bawa, S., additional, Bawa, S., additional, Turton, A., additional, Palmer, M., additional, Lewis, J., additional, Moss, T., additional, Goodchild, C. E., additional, Tang, N., additional, Scott, D., additional, Salkovskis, P., additional, Selvan, S., additional, Williamson, L., additional, Thalayasingam, N., additional, Higgins, M., additional, Saravanan, V., additional, Rynne, M., additional, Hamilton, J. D., additional, Heycock, C., additional, Kelly, C., additional, Norton, S., additional, Sacker, A., additional, Done, J., additional, Young, A., additional, Smolen, J. S., additional, Fleischmann, R. M., additional, Emery, P., additional, van Vollenhoven, R. F., additional, Guerette, B., additional, Santra, S., additional, Kupper, H., additional, Redden, L., additional, Kavanaugh, A., additional, Keystone, E. C., additional, van der Heijde, D., additional, Weinblatt, M. E., additional, Mozaffarian, N., additional, Liu, S., additional, Zhang, N., additional, Wilkinson, S., additional, Riaz, M., additional, Ostor, A. J., additional, Nisar, M. K., additional, Burmester, G., additional, Mariette, X., additional, Navarro-Blasco, F., additional, Oezer, U., additional, Kary, S., additional, Unnebrink, K., additional, Jobanputra, P., additional, Maggs, F., additional, Deeming, A., additional, Carruthers, D., additional, Rankin, E., additional, Jordan, A., additional, Faizal, A., additional, Goddard, C., additional, Pugh, M., additional, Bowman, S., additional, Brailsford, S., additional, Nightingale, P., additional, Tugnet, N., additional, Cooper, S. C., additional, Douglas, K. M., additional, Edwin Lim, C. S., additional, Bee Lian Low, S., additional, Joy, C., additional, Hill, L., additional, Davies, P., additional, Mukherjee, S., additional, Cornell, P., additional, Westlake, S. L., additional, Richards, S., additional, Rahmeh, F., additional, Thompson, P. W., additional, Breedveld, F., additional, Keystone, E., additional, Landewe, R., additional, McIlraith, M., additional, Dharmapalaiah, C., additional, Shand, L., additional, Rose, G., additional, Watts, R., additional, Eldashan, A., additional, Dasgupta, B., additional, Borg, F. A., additional, Bell, G. M., additional, Anderson, A. E., additional, Harry, R. A., additional, Stoop, J. N., additional, Hilkens, C. M., additional, Isaacs, J., additional, Dickinson, A., additional, McColl, E., additional, Banik, S., additional, Smith, L., additional, France, J., additional, Rutherford, A., additional, Scott Russell, A., additional, Smith, J., additional, Jassim, I., additional, Withrington, R., additional, Bacon, P., additional, De Lord, D., additional, McGregor, L., additional, Morrison, I., additional, Stirling, A., additional, Porter, D. R., additional, Saunders, S. A., additional, Else, S., additional, Semenova, O., additional, Thompson, H., additional, Ogunbambi, O., additional, Kallankara, S., additional, Baguley, E., additional, Patel, Y., additional, Alzabin, S., additional, Abraham, S., additional, Taher, T. E., additional, Palfeeman, A., additional, Hull, D., additional, McNamee, K., additional, Pathan, E., additional, Kinderlerer, A., additional, Taylor, P., additional, Williams, R. O., additional, Mageed, R. A., additional, Iaremenko, O., additional, Mikitenko, G., additional, Ferrari, M., additional, Kamalati, T., additional, Pitzalis, C., additional, Pearce, F., additional, Tosounidou, S., additional, Obrenovic, K., additional, Erb, N., additional, Packham, J., additional, Sandhu, R., additional, White, C., additional, Cardy, C. M., additional, Justice, E., additional, Frank, M., additional, Li, L., additional, Lloyd, M., additional, Ahmed, A., additional, Readhead, S., additional, Ala, A., additional, Fittall, M., additional, Manson, J., additional, Sibilia, J., additional, Marc Flipo, R., additional, Combe, B., additional, Gaillez, C., additional, Le Bars, M., additional, Poncet, C., additional, Elegbe, A., additional, Westhovens, R., additional, Hassanzadeh, R., additional, Mangan, C., additional, Fleischmann, R., additional, van Vollenhoven, R., additional, Huizinga, T. W. J., additional, Goldermann, R., additional, Duncan, B., additional, Timoshanko, J., additional, Luijtens, K., additional, Davies, O., additional, Dougados, M., additional, Hewitt, J., additional, Owlia, M., additional, Schiff, M., additional, Alten, R., additional, Kaine, J. L., additional, Nash, P. T., additional, Delaet, I., additional, Qi, K., additional, Genovese, M. C., additional, Clark, J., additional, Kardash, S., additional, Wong, E., additional, Hull, R., additional, McCrae, F., additional, Shaban, R., additional, Thomas, L., additional, Young-Min, S., additional, Ledingham, J., additional, Covarrubias Cobos, A., additional, Leon, G., additional, Mysler, E. F., additional, Keiserman, M. W., additional, Valente, R. M., additional, Abraham Simon Campos, J., additional, Porawska, W., additional, Box, J. H., additional, Legerton, C. W., additional, Nasonov, E. L., additional, Durez, P., additional, Pappu, R., additional, Teng, J., additional, Edwards, C. J., additional, Arden, N., additional, Campbell, J., additional, van Staa, T., additional, Housden, C., additional, Sargeant, I., additional, Choy, E., additional, McAuliffe, S., additional, Roberts, K., additional, Sarzi-Puttini, P., additional, Andrianakos, A., additional, Sheeran, T. P., additional, Choquette, D., additional, Finckh, A., additional, Desjuzeur, M.-L., additional, Gemmen, E. K., additional, Mpofu, C., additional, Gottenberg, J.-E., additional, Shah, P., additional, Cox, M., additional, Nye, A., additional, O'Brien, A., additional, Jones, P., additional, Jones, G. T., additional, Paudyal, P., additional, MacPherson, H., additional, Sim, J., additional, Ernst, E., additional, Fisken, M., additional, Lewith, G., additional, Tadman, J., additional, Macfarlane, G. J., additional, Bertin, P., additional, Arendt, C., additional, Terpstra, I., additional, VanLunen, B., additional, de Longueville, M., additional, Zhou, H., additional, Cai, A., additional, Lacy, E., additional, Kay, J., additional, Matteson, E., additional, Hu, C., additional, Hsia, E., additional, Doyle, M., additional, Rahman, M., additional, Shealy, D., additional, Scott, D. L., additional, Ibrahim, F., additional, Abozaid, H., additional, Hassell, A., additional, Plant, M., additional, Walker, D., additional, Simpson, G., additional, Kowalczyk, A., additional, Prouse, P., additional, Brown, A., additional, George, M., additional, Kumar, N., additional, Mackay, K., additional, Marshall, S., additional, Ludivico, C. L., additional, Murthy, B., additional, Corbo, M., additional, Samborski, W., additional, Berenbaum, F., additional, Ambrugeat, J., additional, Bennett, B., additional, Burkhardt, H., additional, Bykerk, V., additional, Roman Ivorra, J., additional, Wollenhaupt, J., additional, Stancati, A., additional, Bernasconi, C., additional, Scott, D. G. I., additional, Claydon, P., additional, Ellis, C., additional, Buchan, S., additional, Pope, J., additional, Bingham, C. O., additional, Massarotti, E. M., additional, Coteur, G., additional, Weinblatt, M., additional, Ball, C., additional, Ainsworth, T., additional, Kermik, J., additional, Woodham, J., additional, Haq, I., additional, Quesada-Masachs, E., additional, Carolina Diaz, A., additional, Avila, G., additional, Acosta, I., additional, Sans, X., additional, Alegre, C., additional, Marsal, S., additional, McWilliams, D., additional, Kiely, P. D., additional, Bolce, R., additional, Wang, J., additional, Ingham, M., additional, Dehoratius, R., additional, Decktor, D., additional, Rao, V., additional, Pavlov, A., additional, Klearman, M., additional, Musselman, D., additional, Giles, J., additional, Bathon, J., additional, Sattar, N., additional, Lee, J., additional, Baxter, D., additional, McLaren, J. S., additional, Gordon, M.-M., additional, Thant, K. Z., additional, Williams, E. L., additional, Earl, S., additional, White, P., additional, Williams, J., additional, Jan, A. K., additional, Bhatti, A. I., additional, Stafford, C., additional, Carolan, M., additional, and Ramakrishnan, S. A., additional

Published
2012
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17. Multimodal Perfluorocarbon Nanoemulsions for [sup 19]F MRI, Ultrasonography, and Catalysis of MRgFUS-Mediated Drug Delivery

Author

Rapoport, N., primary, Nam, K.-H., additional, Christensen, D. A., additional, Kennedy, A. M., additional, Parker, D. L., additional, Payne, A. H., additional, Todd, N., additional, Shea, J. E., additional, Scaife, C. L., additional, Matsumoto, Yoichiro, additional, Crum, Lawrence A., additional, and ter Haar, Gail Reinette, additional

Published
2011
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19. Paediatric and Adolescent Rheumatology [143-150]: 143. Knee Joint in JIA: A Prospective Evaluation of Clinical Examination, Ultrasound and Mri Assessment. A Newly Developed Knee MRI Scoring System in JIA

Author

Pascoli, L., primary, Napier, N. J., additional, Wray, M., additional, Mc Carron, M., additional, Mc Allister, C., additional, Rooney, M. E., additional, Gibson, D. S., additional, Pascoli, L., additional, McAlilister, C., additional, Scaife, C., additional, Dunn, M., additional, Pennington, S., additional, Rooney, M., additional, Wright, S., additional, Hinks, A., additional, Martin, P., additional, Flynn, E., additional, Eyre, S., additional, Packham, J., additional, Barton, A., additional, Worthington, J., additional, Thomson, W., additional, McErlane, F., additional, Kulkarni, P., additional, Nicholl, K., additional, Foster, H. E., additional, Pain, C., additional, Baildam, E., additional, Foster, H., additional, Harrison, M., additional, and Symmonds, D., additional

Published
2010
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25. Multimodal Perfluorocarbon Nanoemulsions for 19F MRI, Ultrasonography, and Catalysis of MRgFUS-Mediated Drug Delivery.

Author

Rapoport, N., Nam, K. -H., Christensen, D. A., Kennedy, A. M., Parker, D. L., Payne, A. H., Todd, N., Shea, J. E., and Scaife, C. L.

Subjects
PERFLUOROCARBONS, MAGNETIC resonance imaging, DIAGNOSTIC ultrasonic imaging, DRUG delivery systems, TARGETED drug delivery
Abstract

Perfluorocarbon nanoemulsions can target lipophilic therapeutic agents to solid tumors and simultaneously provide for monitoring nanocarrier biodistribution via ultrasonography and/or 19F MRI. In the first generation of block copolymer stabilized perfluorocarbon nanoemulsions, perfluoropentane (PFP) was used as the droplet forming compound. Although manifesting excellent therapeutic and ultrasound imaging properties, PFP nanoemulsions were unstable at storage, difficult to handle, and underwent droplet-to-bubble transition upon injection that was hard to control. To solve the above problems, perfluoro-15-crown-5-ether (PFCE) was used as a core forming compound in the second generation of block copolymer stabilized perfluorocarbon nanoemulsions. In the present paper, acoustic, imaging, and therapeutic properties of unloaded and paclitaxel (PTX) loaded PFCE nanoemulsions are reported. The size of paclitaxel-loaded PFCE nanodroplets (300 nm to 500 nm depending on emulsification conditions) favors their passive accumulation in tumor tissue. PFCE nanodroplets manifest both ultrasound and 19F MR contrast properties, which allows the use of multimodal imaging to monitor nanodroplet biodistribution. Ultrasonography and 19F MRI produced consistent results on nanodroplet biodistribution. Sonication with 1-MHz therapeutic ultrasound triggered reversible droplet-to-bubble transition in PFCE nanoemulsions. Microbubbles formed by acoustic vaporization underwent stable cavitation. In a pilot study on ultrasound-mediated therapy of a large breast cancer tumor, paclitaxelloaded PFCE nanoemulsions combined with 1-MHz ultrasound (MI = 1.75) showed excellent therapeutic properties. Anticipated mechanisms of the observed effects are discussed. [ABSTRACT FROM AUTHOR]

Published
2011
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36. A proteomic analysis of the functional effects of fatty acids in NIH 3T3 fibroblasts

Author

Magdalon Juliana, Hatanaka Elaine, Romanatto Talita, Rodrigues Hosana G, Kuwabara Wilson MT, Scaife Caitriona, Newsholme Philip, and Curi Rui

Subjects
oleic acid, linoleic acid, palmitic acid, enolase, FBP, c-myc, protein expression, proliferation, Nutritional diseases. Deficiency diseases, RC620-627
Abstract

Abstract Previous studies have demonstrated that long chain fatty acids influence fibroblast function at sub-lethal concentrations. This study is the first to assess the effects of oleic, linoleic or palmitic acids on protein expression of fibroblasts, as determined by standard proteomic techniques. The fatty acids were not cytotoxic at the concentration used in this work as assessed by membrane integrity, DNA fragmentation and the MTT assay but significantly increased cell proliferation. Subsequently, a proteomic analysis was performed using two dimensional difference gel electrophoresis (2D-DIGE) and MS based identification. Cells treated with 50 μM oleic, linoleic or palmitic acid for 24 h were associated with 24, 22, 16 spots differentially expressed, respectively. Among the identified proteins, α-enolase and far upstream element binding protein 1 (FBP-1) are of importance due to their function in fibroblast-associated diseases. However, modulation of α-enolase and FBP-1 expression by fatty acids was not validated by the Western blot technique.

Published
2011
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40. Early and Late Complications After Radiofrequency Ablation of Malignant Liver Tumors in 608 Patients

Author

Francesco Izzo, Eddie K. Abdalla, Paolo Marra, Paolo Vallone, Fabrizio Scordino, Bruno Daniele, Courtney L Scaife, Vincenzo De Rosa, Lee M. Ellis, J. Nicolas Vauthey, Chan Raut, Francesco Fiore, Evelyne M. Loyer, Raffaele Orlando, Karen A. Beaty, Robert A. Wolff, Haesun Choi, Steven A. Curley, Sandro Pignata, Curley, Sa, Marra, P, Beaty, K, Ellis, Lm, Vauthey, Jn, Abdalla, Ek, Scaife, C, Raut, C, Wolff, R, Choi, H, Loyer, E, Vallone, P, Fiore, F, Scordino, Fabrizio, De Rosa, V, Orlando, R, Pignata, S, Daniele, B, and Izzo, F.

Subjects
medicine.medical_specialty, Chemotherapy, business.industry, Radiofrequency ablation, medicine.medical_treatment, Catheter ablation, Neuroendocrine tumors, medicine.disease, Metastasis, Hypertonic saline, Surgery, law.invention, surgical procedures, operative, law, Hepatocellular carcinoma, medicine, Radiology, Complication, business, therapeutics, Features
Abstract

A burgeoning number of direct intratumoral therapies are being used to treat human solid tumors. One of the most common sites of application of these tumor-directed treatments has been the liver. The liver is second only to lymph nodes as a common site of metastasis from nonhepatic malignancies.1 Primary liver cancer, specifically hepatocellular carcinoma (HCC), is 1 of the most common human solid malignancies worldwide, with an annual incidence of over 1 million new diagnoses.2 A proportion of patients with primary or secondary hepatic malignancies with disease confined to the liver will derive long-term survival benefit from surgical resection of their disease. Unfortunately, less than 10%–30% of patients with primary or secondary hepatic malignancies are candidates for surgical resection because of the number of tumors, location of tumors that preclude a margin-negative resection, or because of coexistent chronic liver dysfunction producing an unacceptable risk of liver failure after partial hepatectomy.3–7 Patients with liver-only malignant disease who are not candidates for resection may be offered a rapidly evolving menu of direct tumor cytodestructive treatments. The in situ destruction of unresectable primary and secondary hepatic malignancies can potentially improve the median survival of patients and provide palliative relief of symptoms. The latter is particularly true in patients with pain related to tumor displacement of the hepatic capsule or in patients with symptoms related to excess hormone production from metastatic neuroendocrine tumors. Destruction of unresectable hepatic tumors has been performed by direct intratumoral injection of cytotoxic substances, including absolute ethanol, acetic acid, heated hypertonic saline, or chemotherapy agents; by intratumoral placement of cryoprobes to freeze tumors; or more recently by intratumoral placement of needles or fibers that generate heat with radiofrequency electrical current, microwaves, or laser to produce thermal tissue necrosis. An ideal direct in situ antitumor therapy would produce complete destruction of all malignant cells with no significant side effects or complications. Clearly, no such treatment exists and all in situ cytodestructive treatments must be evaluated based on improvements in patient survival rates, local tumor control rates, and complications associated with treatment. Thermal ablation techniques, particularly radiofrequency ablation (RFA), to treat primary and secondary hepatic malignancies have gained widespread availability and use over the past 5 years.8–11 The local control and complication rates associated with microwave and laser ablation have been reported rarely; thus, it is difficult to assess the treated tumor control efficacy and risk to patients using these treatment modalities.8 Treatment-related complications are not always reported in hepatic tumor RFA studies and the complication types and incidence rates in a large, prospective series of patients have not been previously reported.10–12

Published
2004

41. Plasma proteomic signature of chronic psychosocial stress in mice.

Author

O'Connor LA, Melo TG, Golubeva AV, Donoso F, Scaife C, English JA, Nolan YM, and O'Leary OF

Abstract

Chronic stress significantly impacts both physical and mental wellbeing, increasing risk of cardiovascular disease, immune dysregulation, and psychiatric conditions such as depression and anxiety disorders. The plasma proteome is a valuable source of biomarkers of health and disease, but the limited number of studies exploring the potential of the plasma proteome as a biomarker for stress-related disorders underscores the importance of further investigation of the effects of chronic stress on the plasma proteome. The aim of this study was to examine the effect of a 5-week chronic psychosocial stress paradigm on the plasma proteome in mice and to determine if any affected proteins correlated with stress-induced changes in behaviour and physiology, and thus might represent biomarkers of negative impacts of chronic stress. Using LC-MS/MS proteomic analysis, 38 proteins in the mouse plasma proteome were identified to be affected by chronic psychosocial stress. Functional analysis revealed that these proteins clustered into biological functions including inflammatory response, regulation of the immune response, complement and coagulation cascades, lipid metabolic process, and high-density lipoprotein particles Correlation analyses of the identified proteins with stress-induced behavioural or physiological changes stress revealed significant correlations between stress-induced anxiety-like behaviour and Phosphatidylinositol-glycan-specific phospholipase D, Complement C2, Epidermal growth factor receptor, Prosaposin, Actin-related protein 2/3 complex subunit 1B, Maltase-glucoamylase, Mannosyl-oligosaccharide 1,2-alpha-mannosidase IA and Fibrinogen-like protein 1. Chronic psychosocial stress blunted acute stress-induced corticosterone release, and this correlated with abundance of Pyrethroid hydrolase Ces2a; N-fatty-acyl-amino acid synthase/hydrolase Pm20d1, Mannosyl-oligosaccharide 1,2-alpha-mannosidase IA, Alpha-2-macroglobulin-P and L-selectin. Finally, stress-induced reductions in both brown and epididymal fat correlated with Phosphatidylinositol-glycan-specific phospholipase D, Complement C2, Epidermal growth factor receptor, Kininogen-1, Apolipoprotein M, Angiopoietin-related protein 3, Proprotein convertase subtilisin/kexin type 9, and Lipopolysaccharide-binding protein. These findings demonstrate that chronic psychosocial stress induces alterations in plasma proteins implicated in key biological processes and pathways related to stress response, immune function, and lipid metabolic regulation. Further investigation into these proteins may provide new avenues for identification of biomarkers or mediators of stress-induced pathology., (Copyright © 2024. Published by Elsevier Inc.)

Published
2024
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42. Motif mapping during chickpea germination reveals a complex sequential activation of different proteolytic activities.

Author

Bera I, O'Sullivan M, Scaife C, Cagney G, and Shields DC

Subjects
Plant Proteins metabolism, Amino Acid Sequence, Amino Acid Motifs, Tandem Mass Spectrometry, Peptide Hydrolases metabolism, Cicer metabolism, Cicer enzymology, Cicer growth & development, Germination, Proteolysis, Seeds metabolism, Seeds growth & development
Abstract

Despite the importance of grains and legumes in the human diet, little is known regarding peptide release and the temporal changes of protease activities during seed germination. LC/MS-MS peptidomic analysis of two cultivars of germinating chickpea followed by computational analyses indicated cleavage dominated by proteases with a single position preference (mainly before (P1) or after cleavage (P1'): L at P2 (cysEP-like); R or K at P1 (vignain-like), N or Q at P1 (legumain-like); and previously unidentified K, R, A and S at P1'; A at P2'). While P1 N cleavages were relatively constant, P1' K/R preferences were high in soaked garbanzo (kabuli) seeds, declined by four days, and returned at six days, but were much rarer in the brown (desi) cultivar. Late Embryogenesis Associated (LEA) peptides were markedly released during early germination. Vicilin peptides rich in glutamic acid near their N-termini markedly increased with germination, consistent with strong proteolytic resistance, even to human digestion, as indicated by analyses of separate datasets. Thus, this first peptidomics study of seed germination proteolytic profiles unveils a complex cultivar-specific programme of sequential activation and inactivation of a series of proteases, associated with the differential release of peptides from different protein groups., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Bera et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Published
2024
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43. Platelet proteomic profiling reveals potential mediators of immunothrombosis and proteostasis in myeloproliferative neoplasms.

Author

Kelliher S, Gamba S, Weiss L, Shen Z, Marchetti M, Schieppati F, Scaife C, Madden S, Bennett K, Fortune A, Maung S, Fay M, Ní Áinle F, Maguire P, Falanga A, Kevane B, and Krishnan A

Subjects
Humans, Thrombosis etiology, Proteome, Myeloproliferative Disorders metabolism, Myeloproliferative Disorders blood, Myeloproliferative Disorders etiology, Proteomics methods, Blood Platelets metabolism, Proteostasis
Published
2024
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44. Evolution of the Genetic Code in the Ascoideales (CUG-Ser2) Yeast Clade: The Ancestral tRNA-Leu(CAG) Gene Is Retained in Most Saccharomycopsis Species but Is Nonessential and Not Used for Translation.

Author

Ó Cinnéide E, Scaife C, Dillon ET, and Wolfe KH

Subjects
Genetic Code, Saccharomycopsis genetics, Protein Biosynthesis, Phylogeny, RNA, Transfer, Leu genetics, Anticodon genetics, RNA, Transfer, Ser genetics, Evolution, Molecular
Abstract

In the yeast genera Saccharomycopsis and Ascoidea, which comprise the taxonomic order Ascoideales, nuclear genes use a nonstandard genetic code in which CUG codons are translated as serine instead of leucine, due to a tRNA-Ser with the unusual anticodon CAG. However, some species in this clade also retain an ancestral tRNA-Leu gene with the same anticodon. One of these species, Ascoidea asiatica, has been shown to have a stochastic proteome in which proteins contain ∼50% Ser and 50% Leu at CUG codon sites, whereas previously examined Saccharomycopsis species translate CUG only as Ser. Here, we investigated the presence, conservation, and possible functionality of the tRNA-Leu(CAG) gene in the genus Saccharomycopsis. We sequenced the genomes of 23 strains that, together with previously available data, include almost every known species of this genus. We found that most Saccharomycopsis species have genes for both tRNA-Leu(CAG) and tRNA-Ser(CAG). However, tRNA-Leu(CAG) has been lost in Saccharomycopsis synnaedendra and Saccharomycopsis microspora, and its predicted cloverleaf structure is aberrant in all the other Saccharomycopsis species. We deleted the tRNA-Leu(CAG) gene of Saccharomycopsis capsularis and found that it is not essential. Proteomic analyses in vegetative and sporulating cultures of S. capsularis and Saccharomycopsis fermentans showed only translation of CUG as Ser. Despite its unusual structure, the tRNA-Leu(CAG) gene shows evidence of sequence conservation among Saccharomycopsis species, particularly in its acceptor stem and leucine identity elements, which suggests that it may have been retained in order to carry out an unknown nontranslational function., (© The Author(s) 2024. Published by Oxford University Press on behalf of Society for Molecular Biology and Evolution.)

Published
2024
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45. Risk factors and health behaviors associated with loneliness among cancer survivors during the COVID-19 pandemic.

Author

Aßmann ES, Ose J, Hathaway CA, Oswald LB, Hardikar S, Himbert C, Chellam V, Lin T, Daniels B, Kirchhoff AC, Gigic B, Grossman D, Tward J, Varghese TK Jr, Shibata D, Figueiredo JC, Toriola AT, Beck A, Scaife C, Barnes CA, Matsen C, Ma DS, Colman H, Hunt JP, Jones KB, Lee CJ, Larson M, Onega T, Akerley WL, Li CI, Grady WM, Schneider M, Dinkel A, Islam JY, Gonzalez BD, Otto AK, Penedo FJ, Siegel EM, Tworoger SS, Ulrich CM, and Peoples AR

Subjects
Humans, Female, Loneliness psychology, Pandemics, Risk Factors, Health Behavior, COVID-19, Cancer Survivors, Neoplasms
Abstract

Loneliness may exacerbate poor health outcomes particularly among cancer survivors during the COVID-19 pandemic. Little is known about the risk factors of loneliness among cancer survivors. We evaluated the risk factors of loneliness in the context of COVID-19 pandemic-related prevention behaviors and lifestyle/psychosocial factors among cancer survivors. Cancer survivors (n = 1471) seen at Huntsman Cancer Institute completed a survey between August-September 2020 evaluating health behaviors, medical care, and psychosocial factors including loneliness during COVID-19 pandemic. Participants were classified into two groups: 'lonely' (sometimes, usually, or always felt lonely in past month) and 'non-lonely' (never or rarely felt lonely in past month). 33% of cancer survivors reported feeling lonely in the past month. Multivariable logistic regression showed female sex, not living with a spouse/partner, poor health status, COVID-19 pandemic-associated lifestyle factors including increased alcohol consumption and marijuana/CBD oil use, and psychosocial stressors such as disruptions in daily life, less social interaction, and higher perceived stress and financial stress were associated with feeling lonely as compared to being non-lonely (all p < 0.05). A significant proportion of participants reported loneliness, which is a serious health risk among vulnerable populations, particularly cancer survivors. Modifiable risk factors such as unhealthy lifestyle behaviors and psychosocial stress were associated with loneliness. These results highlight the need to screen for unhealthy lifestyle factors and psychosocial stressors to identify cancer survivors at increased risk of loneliness and to develop effective management strategies., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2024
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46. Unveiling the Role of Endoplasmic Reticulum Stress Pathways in Canine Demodicosis.

Author

Kelly PA, McHugo GP, Scaife C, Peters S, Stevenson ML, McKay JS, MacHugh DE, Saez IL, and Breathnach R

Subjects
Humans, Dogs, Animals, Cytokines, Macrophages, Phenotype, Proteomics, Endoplasmic Reticulum Stress
Abstract

Canine demodicosis is a prevalent skin disease caused by overpopulation of a commensal species of Demodex mite, yet its precise cause remains unknown. Research suggests that T-cell exhaustion, increased immunosuppressive cytokines, induction of regulatory T cells and increased expression of immune checkpoint inhibitors may contribute to its pathogenesis. This study aimed to gain a deeper understanding of the molecular changes occurring in canine demodicosis using mass spectrometry and pathway enrichment analysis. The results indicate that endoplasmic reticulum stress promotes canine demodicosis through regulation of three linked signalling pathways: eIF2, mTOR, and eIF4 and p70S6K. These pathways are involved in the modulation of Toll-like receptors, most notably TLR2, and have been shown to play a role in the pathogenesis of skin diseases in both dogs and humans. Moreover, these pathways are also implicated in the promotion of immunosuppressive M2 phenotype macrophages. Immunohistochemical analysis, utilising common markers of dendritic cells and macrophages, verified the presence of M2 macrophages in canine demodicosis. The proteomic analysis also identified immunological disease, organismal injury and abnormalities and inflammatory response as the most significant underlying diseases and disorders associated with canine demodicosis. This study demonstrates that Demodex mites, through ER stress, unfolded protein response and M2 macrophages contribute to an immunosuppressive microenvironment, thereby assisting in their proliferation., (© 2024 The Authors. Parasite Immunology published by John Wiley & Sons Ltd.)

Published
2024
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47. Platelet proteo-transcriptomic profiling validates mediators of thrombosis and proteostasis in patients with myeloproliferative neoplasms.

Author

Kelliher S, Gamba S, Weiss L, Shen Z, Marchetti M, Schieppati F, Scaife C, Madden S, Bennett K, Fortune A, Maung S, Fay M, Ní Áinle F, Maguire P, Falanga A, Kevane B, and Krishnan A

Abstract

Patients with chronic Myeloproliferative Neoplasms (MPN) including polycythemia vera (PV) and essential thrombocythemia (ET) exhibit unique clinical features, such as a tendency toward thrombosis and hemorrhage, and risk of disease progression to secondary bone marrow fibrosis and/or acute leukemia. Although an increase in blood cell lineage counts (quantitative features) contribute to these morbid sequelae, the significant qualitative abnormalities of myeloid cells that contribute to vascular risk are not well understood. Here, we address this critical knowledge gap via a comprehensive and untargeted profiling of the platelet proteome in a large (n= 140) cohort of patients (from two independent sites) with an established diagnosis of PV and ET (and complement prior work on the MPN platelet transcriptome from a third site). We discover distinct MPN platelet protein expression and confirm key molecular impairments associated with proteostasis and thrombosis mechanisms of potential relevance to MPN pathology. Specifically, we validate expression of high-priority candidate markers from the platelet transcriptome at the platelet proteome ( e.g. , calreticulin (CALR), Fc gamma receptor (FcγRIIA) and galectin-1 (LGALS1) pointing to their likely significance in the proinflammatory, prothrombotic and profibrotic phenotypes in patients with MPN. Together, our proteo-transcriptomic study identifies the peripherally-derived platelet molecular profile as a potential window into MPN pathophysiology and demonstrates the value of integrative multi-omic approaches in gaining a better understanding of the complex molecular dynamics of disease.

Published
2023
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48. Comparative Genomic Analysis of Pancreatic Acinar Cell Carcinoma (PACC) and Pancreatic Ductal Adenocarcinoma (PDAC) Unveils New Actionable Genomic Aberrations in PACC.

Author

Florou V, Elliott A, Bailey MH, Stone D, Affolter K, Soares HP, Nevala-Plagemann C, Scaife C, Walker P, Korn WM, Lou E, Shroff RT, Hosein PJ, and Garrido-Laguna I

Subjects
Humans, Precision Medicine, Mutation, Genomics, Carcinoma, Acinar Cell genetics, Carcinoma, Acinar Cell pathology, Pancreatic Neoplasms drug therapy, Pancreatic Neoplasms genetics, Pancreatic Neoplasms pathology, Carcinoma, Pancreatic Ductal genetics, Carcinoma, Pancreatic Ductal drug therapy
Abstract

Purpose: Pure pancreatic acinar cell carcinomas (PACC) are rare malignancies with no established treatment. PACC demonstrates significant genetic intertumoral heterogeneity with multiple pathways involved, suggesting using targeted cancer therapeutics to treat this disease. We aggregated one of the largest datasets of pure PACC to examine the genomic variability and explore patient-specific therapeutic targets., Experimental Design: PACC specimens (n = 51) underwent next-generation sequencing of DNA (n = 29) or whole exome (n = 22) and RNA (whole transcriptome, n = 29) at a commercial laboratory. We performed comparative analyses of a genomic cohort of pancreatic ductal adenocarcinomas (PDAC; n = 4,205). In parallel, we conducted a retrospective review of patients with PACC treated at Huntsman Cancer Institute (HCI)., Results: The real-world dataset included samples from 51 patients with PACC. We found key molecular differences between pure PACC and PDAC, highlighting the unique characteristics of pure PACC. Major differences in PACC include lower MAPK signaling and less stromal cell abundance compared with PDAC. Pure PACC showed genomic loss-of-heterozygosity to largely coincide with mutations in BRCA1, BRCA2, and PALB2. Of the 7 patients treated at HCI, one had a tumor that harbored a BRAF-V600E mutation. Leveraging precision oncology, this patient is being treated with encorafenib plus binimetinib, achieving an exceptionally durable and ongoing complete response of more than 3 years., Conclusions: There are major differences between PACC and PDAC, including downregulation of the MAPK signaling pathway, and less stromal cell abundance. In addition, genomic characterization of pure PACC revealed frequent targetable alterations, which can guide patient treatment., (©2023 American Association for Cancer Research.)

Published
2023
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49. Ampullary Adenocarcinoma, Version 1.2023, NCCN Clinical Practice Guidelines in Oncology.

Author

Chiorean EG, Chiaro MD, Tempero MA, Malafa MP, Benson AB, Cardin DB, Christensen JA, Chung V, Czito B, Dillhoff M, Donahue TR, Dotan E, Fountzilas C, Glazer ES, Hardacre J, Hawkins WG, Klute K, Ko AH, Kunstman JW, LoConte N, Lowy AM, Masood A, Moravek C, Nakakura EK, Narang AK, Nardo L, Obando J, Polanco PM, Reddy S, Reyngold M, Scaife C, Shen J, Truty MJ, Vollmer C, Wolff RA, Wolpin BM, Rn BM, Lubin S, and Darlow SD

Subjects
Humans, Pancreatic Neoplasms, Ampulla of Vater, Common Bile Duct Neoplasms diagnosis, Common Bile Duct Neoplasms therapy, Duodenal Neoplasms diagnosis, Duodenal Neoplasms therapy, Adenocarcinoma diagnosis, Adenocarcinoma therapy
Abstract

Ampullary cancers refer to tumors originating from the ampulla of Vater (the ampulla, the intraduodenal portion of the bile duct, and the intraduodenal portion of the pancreatic duct), while periampullary cancers may arise from locations encompassing the head of the pancreas, distal bile duct, duodenum, or ampulla of Vater. Ampullary cancers are rare gastrointestinal malignancies, and prognosis varies greatly based on factors such as patient age, TNM classification, differentiation grade, and treatment modality received. Systemic therapy is used in all stages of ampullary cancer, including neoadjuvant therapy, adjuvant therapy, and first-line or subsequent-line therapy for locally advanced, metastatic, and recurrent disease. Radiation therapy may be used in localized ampullary cancer, sometimes in combination with chemotherapy, but there is no high-level evidence to support its utility. Select tumors may be treated surgically. This article describes NCCN recommendations regarding management of ampullary adenocarcinoma.

Published
2023
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50. The Implications of Treatment Delays in Adjuvant Therapy for Resected Cholangiocarcinoma Patients.

Author

Parsons M, Lloyd S, Johnson S, Scaife C, Soares H, Kim R, Kim R, Garrido-Laguna I, and Tao R

Subjects
Humans, Time-to-Treatment, Radiotherapy, Adjuvant, Chemotherapy, Adjuvant, Bile Ducts, Intrahepatic pathology, Proportional Hazards Models, Retrospective Studies, COVID-19, Cholangiocarcinoma surgery, Cholangiocarcinoma pathology, Bile Duct Neoplasms surgery, Bile Duct Neoplasms pathology
Abstract

Purpose: The purpose of this study is to understand factors associated with timing of adjuvant therapy for cholangiocarcinoma and the impact of delays on overall survival (OS)., Methods: Data from the National Cancer Database (NCDB) for patients with non-metastatic bile duct cancer from 2004 to 2015 were analyzed. Patients were included only if they underwent surgery and adjuvant chemotherapy and/or radiotherapy (RT). Patients who underwent neoadjuvant or palliative treatments were excluded. Pearson's chi-squared test and multivariate logistic regression analyses were used to assess the distribution of demographic, clinical, and treatment factors. After propensity score matching with inverse probability of treatment weighting, OS was compared between patients initiating therapy past various time points using Kaplan Meier analyses and doubly robust estimation with multivariate Cox proportional hazards modeling., Results: In total, 7,733 of 17,363 (45%) patients underwent adjuvant treatment. The median time to adjuvant therapy initiation was 59 days (interquartile range 45-78 days). Age over 65, black and Hispanic race, and treatment with RT alone were associated with later initiation of adjuvant treatment. Patients with larger tumors and high-grade disease were more likely to initiate treatment early. After propensity score weighting, there was an OS decrement to initiation of treatment beyond the median of 59 days after surgery., Conclusions: We identified characteristics that are related to the timing of adjuvant therapy in patients with biliary cancers. There was an OS decrement associated with delays beyond the median time point of 59 days. This finding may be especially relevant given the treatment delays seen as a result of COVID-19., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2023
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