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1. Early years postgraduate surgical training programmes in the UK are failing to meet national quality standards: An analysis from the ASiT/BOTA Lost Tribe prospective cohort study of 2,569 surgical trainees

Author

Glasbey, James C., Harries, Rhiannon L., Beamish, Andrew J., Gokani, Vimal J., Mohan, Helen, Williams, Adam P., Fleming, Simon, Chai, Aaron, Singh, Abhinav, Stoneham, Adam C.S., Lunt, Adam J., Rehman, Adeeb H., Dhahri, Adeel A., Yvon, Adrien R.A., Dutta, Agneish, Abou-Foul, Ahmad K., Abdelrahman, Ahmed, Daoub, Ahmed, Sanalla, Ahmed, de Gea Rico, Aitor, Konarski, Alastair, Ward, Alex E., Wilkin, Alex J., Winter, Alexandra K., Arnaout, Ali, Bakhsh, Ali, Esfandiari, Alireza, Hardy, Alistair W., Khan, Amad N., Thacoor, Amitabh, Gavrila, Ana D., Nedea, Anca-Mihaela, Fontalis, Andreas, Hall, Andrew J., Williamson, Andrew J., Kosti, Angeliki, Harlinska, Anna, Adimonye, Anthony, Egglestone, Anthony, Thaventhiran, Anthony J., Myatt, Antonia, Vusirikala, Anuhya, Rawashdeh, Arab S., Paramasivan, Arjun C., Cotton, Arthur E., Scrimshire, Ashley B., Ramesh, Ashwanth C., Krishnamoorthy, Ashwin K., Ahmed, Asif, Abdul-Hamid, Ayeshah, Khan, Ayushah, Oremule, Babatunde, Ho, Beatrice, Barkham, Ben, Collard, Ben, Edgar, Ben F., Drake, Benjamin, John, Bethan E., Gordon, Catherine R., Rossborough, Catherine, Park, Chang Y., Seretis, Charalampos, Johnson, Charles H.N., Gill, Charn, Serino, Chiara, Ogbuokiri, Chinomso I., Swords, Chloe, Kang, Chong Y., McKinnon, Chris, Brown, Christopher E., Manning, Christopher J., Marusza, Christopher J., Jones, Christopher P., Forde, Cillian T., Wilson, Claire L., Koh, Claudia, Horgan, Conal, Lin, Daniel J., Ashmore, Daniel L., Ness, Daniel, Akhtar, Daniel O., Doherty, Daniel T., Scholfield, Daniel W., Ensor, David C., Bratt, David G., Spence, David J.R., Thomson, David R., Ferguson, David W., Apparau, Denish, Navaratnam, Devaraj M., Mai, Dinh, Rutherford, Duncan G., Karam, Edward, Wu, Eiling, Zimmermann, Eleanor F., Douka, Eleftheria, Flatt, Elinor, Kane, Elizabeth G., Thornhill, Elizabeth L., Gammeri, Emanuele, Littlehales, Emma G., Valsamis, Epaminondas M., Hankin, Erin J., Meenan, Erin R.M., Botha, Etienne N., Khalid, Farhan, Patel, Fatema, Power, Fiachra R., Rutherford, Fiona M., Saeed, Fozia, Guest, Francesca L., Barbosa, Francisco J., Cameron, Fraser G., Raja, Furqan R., Thiruchandran, Gajendiran, Munbauhal, Gavish, Dovey, Gemma E., Hogg, Gemma E., Dovell, George E., Matheron, George, Hill, George T., Layton, Georgia R., Jong, Georgiana G.S., Hicks, Georgina, Millward, Graham J., Shaw, Grahame A., Stamp, Gregory F.W., Parwaiz, Hammad, Chong, Han Hong, Copley, Hannah C., Lennox-Warburton, Hannah C., Emerson, Hannah M., Dean, Harry F., Eltyeb, Hazim, Chu, Howard O., Sadien, Iannish, Mohamed, Imran M., Parwaiz, Iram, Drummond, Isabella M.H., Pearce, Jack C.H., Ahmed, Jacob J., Koris, Jacob, Rait, Jaideep S., Bailey, James A., Cohen, James A., Kennedy, James A., Olivier, James B., Bailey, James, Archer, James E., Stewart, James J., de Barros, James N.J.Monteiro, Allen, James R., O'Brien, James W., James, McGhee, T., Quarcoopome, Jared N., Winyard, Jasmine C., Roberts, Jason L., Barwell, Jennifer S., Rodrigues, Jeremy, Chapman, Jessica A.R., Fairbanks, Jessica Y., Voll, Jessika, Lim, Jie Q., Chang, Jin H., Bovis, Joanna L., Ferns, John, Tam, Johnson Pok Him, Herron, Jonathan B.T., Macdonald, Jonathan D.R., Ducey, Jonathan R., DIxon, Joseph W., Luck, Joshua T., Hewage, Kalon, Yakoub, Kamal M., Bhopal, Kamran F., Vejsbjerg, Karen A., Aboelmagd, Karim, Bera, Katarzyna D., Hamlett, Katharine E., Fok, Katherine E., Hurst, Katherine V., Gillams, Kathryn L., Siggens, Katie L., Young, Katie, Burns, Kenneth M., Burke, Kerry A., Seebah, Kevin, Shah, Khalid A., Bentick, Kieran R., Majid, Kiran, Davies, Kirsty L., Tan, Krystal, Baryeh, Kwaku W., Phillips, Laura A.F., Ellerton, Laura N., Giet, Leeying J., Monaghan, Liam, Ka Cheung, Lok, Shen, Louise L., Paramore, Louise, Arrowsmith, Lucy J., Attwell, Lukas A., Thornton, Luke, Xu, Luting, Leadon, Madeline L., Natarajan, Madhavi, Houlihan, Maria C.R., Cheah, Marisa, Sagmeister, Markus L., Abubakar, Maryam, Flynn, Matthew F., Harris, Matthew, Stone, Matthew J., Young, Matthew J., Gray, Matthew P., Horner, Matthew P., Schembri, Matthew, Trail, Matthew, Joy, Melvin, Rice, Michael J., Thomas, Michael P., Poon, Michael T.C., Stoddart, Michael T., Fong, Michelle L., Foster, Mitchell T., Mohamud, Mohamed F., Hoque, Mohammed N., Remtulla, Mohammedabbas, Javed Karim, Mohsin, Rezacova, Monika, Siddiqui, Muhammad B., Iqbal, Muhammad R., Mensa, Mussa, McCauley, Nadine, Bauer, Natasha J., Walker, Nathan, Hakim, Navid A., Knight, Ngonidzashe, O'Hara, Niall, Fawcett, Nicholas A., Wong, Nicholas, Allen, Nicola F.D., Husnoo, Nilofer, Vallabh, Nimisha, Srikandarajah, Nisaharan, Chidumije, Nnaemeka, Elamin, Obaiy, Akinlaja, Odunayo O., Griffiths, Olga, Brown, Oliver D., Shastri, Oliver, Cameron, Olivia J., Kenyon, Olivia, Javed, Omar A., Sogaolu, Opeyemi O., Birmpili, Panagiota, Haylock-Vize, Patricia, Green, Patrick A., Carroll, Patrick J., Yang, Peiming, Beak, Philip, Persson, Pia, Tam, Pok Him Johnson, Waqar, Rabia, Morley, Rachael L., Bowden, Rachel Clare, Eyre, Rachel L., Pankhania, Rahul M., Sahemey, Rajpreet S., Kabariti, Rakan, Rawashdeh, M., Arab, Rawashdeh S., Rollett, Rebecca A., Nicholas, Rebecca S., Morgan, Rebecca V., Limb, Richard, Robinson, Richard Mark, Hayes, Richard S., Daureeawoo, Ridwan, Cooke, Robert A., Espey, Robert A.J., Chessman, Robert, Whitham, Robert D.J., Payne, Robert E., Staruch, Robert, Alho, Roberto J.R., Gordon, Robin, Cuthbert, Rory, Harrison, Roseanna B., Scott, Rupert A., Parks, Ruth M., Cheong, Ryan C.T., Hillier-Smith, Ryan L., Moffatt, Ryan, Rehman, Saad, Ambren, Sabah, Abdulal, Sabria, Kulkarni, Sagar, Hopwood, Sam, Greenfield, Samantha H., Mehta, Samir K., Haines, Samuel, AlSaati, Sarah A., Williams, Sarah A., El-Badawy, Sarah, Barlow, Sarah L., Pywell, Sarah, Pollock, Sarah-jayne, Lampridis, Savvas, Nazarian, Scarlet, Rezvani, Sean, Scattergood, Sean, Toescu, Sebastian M., Hotonu, Sesi, Shaikh, Shafaque, Rupani, Shamil, Hasan, Shumaila, Pradeep, Shwetha, Cole, Simon J., Growcott, Siona A., Bedoya, Sofia E., Ike, Sonia I., Bodnarescu, Stefan V., Seppings, Stella C., Poyntz, Stephanie A., Jordan, Stevan J., Iqbal, Sundas, Das, Suparna, Chatterjee-Woolman, Suravi, Shumon, Syed, Morrison, Tamsin E.M., Sibartie, Tara, Aboelmagd, Tariq, Russell, Thomas B., Seddon, Thomas C., Stringfellow, Thomas D., Goldsmith, Thomas, Banks, Thomas H.F., Tolley, Thomas, Oputa, Tobenna J., Kanzara, Todd T., Challoner, Tom, Urbonas, Tomas, Richards, Tomos B., Morrison-Jones, Victoria J., Garikapati, Vivek, Al-Azzani, Waheeb A.K., Zahra, Wajiha, Ho, Weiguang, Al-Dhahir, Wesam, Gibson, William G.W., Grant, Yasmin, Hijazi, Yasser, Chiang, Yayganeh, Gundkalli, Zobia K., Seymour, Zoe M., and Panayi, Zoe

Published
2018
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2. A systems approach reveals species differences in hepatic stress response capacity.

Author

Russomanno, Giusy, Sison-Young, Rowena, Livoti, Lucia A, Coghlan, Hannah, Jenkins, Rosalind E, Kunnen, Steven J, Fisher, Ciarán P, Reddyhoff, Dennis, Gardner, Iain, Rehman, Adeeb H, Fenwick, Stephen W, Jones, Andrew R, Conchard, Guy Vermeil De, Simonin, Gilles, Bertheux, Helene, Weaver, Richard J, Johnson, Robert L, Liguori, Michael J, Clausznitzer, Diana, and Stevens, James L

Subjects
SPECIES, OXIDATIVE stress, TISSUE analysis, LIVER injuries, CONDITIONED response
Abstract

To minimize the occurrence of unexpected toxicities in early phase preclinical studies of new drugs, it is vital to understand fundamental similarities and differences between preclinical species and humans. Species differences in sensitivity to acetaminophen (APAP) liver injury have been related to differences in the fraction of the drug that is bioactivated to the reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI). We have used physiologically based pharmacokinetic modeling to identify oral doses of APAP (300 and 1000 mg/kg in mice and rats, respectively) yielding similar hepatic burdens of NAPQI to enable the comparison of temporal liver tissue responses under conditions of equivalent chemical insult. Despite pharmacokinetic and biochemical verification of the equivalent NAPQI insult, serum biomarker and tissue histopathology analyses revealed that mice still exhibited a greater degree of liver injury than rats. Transcriptomic and proteomic analyses highlighted the stronger activation of stress response pathways (including the Nrf2 oxidative stress response and autophagy) in the livers of rats, indicative of a more robust transcriptional adaptation to the equivalent insult. Components of these pathways were also found to be expressed at a higher basal level in the livers of rats compared with both mice and humans. Our findings exemplify a systems approach to understanding differential species sensitivity to hepatotoxicity. Multiomics analysis indicated that rats possess a greater basal and adaptive capacity for hepatic stress responses than mice and humans, with important implications for species selection and human translation in the safety testing of new drug candidates associated with reactive metabolite formation. [ABSTRACT FROM AUTHOR]

Published
2023
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3. Identification of flucloxacillin-modified hepatocellular proteins: implications in flucloxacillin-induced liver injury.

Author

Ali, Serat-E, Waddington, James C, Lister, Adam, Sison-Young, Rowena, Jones, Robert P, Rehman, Adeeb H, Goldring, Chris E P, Naisbitt, Dean J, and Meng, Xiaoli

Subjects
TRANSFER RNA, MULTIDRUG resistance-associated proteins, MITOCHONDRIAL proteins, LIVER injuries, MEMBRANE transport proteins, PROTEINS, ADAPTOR proteins
Abstract

Flucloxacillin is a β-lactam antibiotic associated with a high incidence of drug-induced liver injury. Although expression of HLA-B*57:01 is associated with increased susceptibility, little is known of the pathological mechanisms involved in the induction of the clinical phenotype. Irreversible protein modification is suspected to drive the reaction through the provision of flucloxacillin-modified peptides that are presented to T-cells by the protein encoded by the risk allele. In this study, we have shown that flucloxacillin binds to multiple proteins within human primary hepatocytes, including major hepatocellular proteins (hemoglobin and albumin) and mitochondrial proteins. Inhibition of membrane transporters multidrug resistance-associated protein 2 (MRP2) and P-glycoprotein (P-gp) appeared to reduce the levels of covalent binding. A diverse range of proteins with different functions was found to be targeted by flucloxacillin, including adaptor proteins (14-3-3), proteins with catalytic activities (liver carboxylesterase 1, tRNA-splicing endonuclease subunit Sen2, All-trans-retinol dehydrogenase ADH1B, Glutamate dehydrogenase 1 mitochondrial, Carbamoyl-phosphate synthase [ammonia] mitochondrial), and transporters (hemoglobin, albumin, and UTP-glucose-1-phosphate uridylyltransferase). These flucloxacillin-modified intracellular proteins could provide a potential source of neoantigens for HLA-B*57:01 presentation by hepatocytes. More importantly, covalent binding to critical cellular proteins could be the molecular initiating events that lead to flucloxacillin-induced cholestasis Data are available via ProteomeXchange with identifier PXD038581. [ABSTRACT FROM AUTHOR]

Published
2023
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5. Prognostic and predictive markers in liver limited stage IV colorectal cancer.

Author

Rehman, Adeeb H., Jones, Robert P., and Poston, Graeme

Subjects
COLORECTAL cancer, LIVER metastasis, METASTASIS, BIOLOGY, DISEASE progression
Abstract

Colorectal cancer is the third most commonly diagnosed cancer among both men and women. Personalised treatment options remain complex, although there is broad agreement over which patients with colorectal liver metastases (CRLM) should and should not be offered resection. Decisions on an optimal management strategy involves careful assessment of both technical and oncological factors. In this review we aim to summarise current prognostic biomarkers for metastatic colorectal cancers, specifically patients considered for resection. A number of clinico-pathological factors have been identified as prognostically important with good internal validity, but limited external validity. Furthermore, these prognostic scoring systems do not take factor in modern chemotherapeutic agents and the disease modification these agents produce. Histopathological response to chemotherapy is of significant prognostic importance. Molecular markers can help predict the efficacy of a biological agent. An important prognostic factor of liver metastasis is the recognition that location of the primary colorectal cancer impacts on metastatic phenotype and represents difference in genotype, i.e. proximal tumours are more aggressive than distal tumours with an increased likelihood of disease progression. Several mutational molecular markers identified include microsatellite instability, BRAF, and KRAS/NRAS and combination mutations, which confer poorer outcomes. Accurate prognostication in patients with liver limited colorectal metastases remains crucial, as this allows tailoring treatment options to each disease and improving outcomes. Access to tissue before treatment remains a limitation although advances in ability to assess tumour biology by non-invasive methods are promising. [ABSTRACT FROM AUTHOR]

Published
2019
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