Benjamin W. Turney
University of Oxford
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Publication
Featured researches published by Benjamin W. Turney.
BJUI | 2012
Benjamin W. Turney; John Reynard; Jeremy G. Noble; Stephen R. Keoghane
Study Type – Therapy (case series)
BJUI | 2006
Benjamin W. Turney; Jonathan M.G. Willatt; David Nixon; Jeremy P. Crew; Nigel C. Cowan
To evaluate the use of computed tomography urography (CTU) for diagnosing bladder tumours in patients with macroscopic haematuria and aged >40 years.
BJUI | 2012
Christopher Blick; Sarfraz A. Nazir; Susan Mallett; Benjamin W. Turney; Natasha N. Onwu; Ian S. Roberts; Jeremy P. Crew; Nigel C. Cowan
Study Type – Diagnostic (exploratory cohort)
BJUI | 2007
Mark A. Rochester; Nilay Patel; Benjamin W. Turney; David R. Davies; Ian S. Roberts; Jeremy P. Crew; Andrew Protheroe; Valentine M. Macaulay
To analyse bladder cancer biopsies and investigate the pattern of expression of the type 1 insulin‐like growth factor receptor (IGF1R), a receptor tyrosine kinase that mediates tumour cell proliferation, motility and protection from apoptosis.
BJUI | 2006
Eleanor Ray; Benjamin W. Turney; Rajinder Singh; Ashish Chandra; David Cranston; Tim O'Brien
To define the current achievable outcomes from open partial nephrectomy (OPN) in the UK at a time when other treatments for small kidney tumours are increasingly being advocated. Current knowledge of the effectiveness of OPN is limited by the fact that published data are almost exclusively derived from a very few centres of established world renown.
Radiotherapy and Oncology | 2012
Benjamin W. Turney; Martin Kerr; Meenali M. Chitnis; Kunal A. Lodhia; Yong Wang; Johann Riedemann; Mark A. Rochester; Andrew Protheroe; Simon Brewster; Valentine M. Macaulay
BACKGROUND AND PURPOSE IGF-1R depletion sensitizes prostate cancer cells to ionizing radiation and DNA-damaging cytotoxic drugs. This study investigated the hypothesis that IGF-1R regulates DNA double strand break (DSB) repair. METHODS We tested effects of IGF-1R siRNA transfection on the repair of radiation-induced DSBs by immunoblotting and immunofluorescence for γH2AX, and pulsed-field gel electrophoresis. Homologous recombination (HR) was quantified by reporter assays, and cell cycle distribution by flow cytometry. RESULTS We confirmed that IGF-1R depletion sensitized DU145 and PC3 prostate cancer cells to ionizing radiation. DU145 control transfectants resolved radiation-induced DSBs within 24 h, while IGF-1R depleted cells contained 30-40% unrepaired breaks at 24 h. IGF-1R depletion induced significant reduction in DSB repair by HR, although the magnitude of the repair defect suggests additional contributory factors. Radiation-induced G2-M arrest was attenuated by IGF-1R depletion, potentially suppressing cell cycle-dependent processes required for HR. In contrast, IGF-1R depletion induced only minor radiosensitization in LNCaP cells, and did not influence repair. Cell cycle profiles were similar to DU145, so were unlikely to account for differences in repair responses. CONCLUSIONS These data indicate a role for IGF-1R in DSB repair, at least in part via HR, and support use of IGF-1R inhibitors with DNA damaging cancer treatments.
BJUI | 2016
Hendrik Heers; Benjamin W. Turney
To provide a 5‐year follow‐on update on the changes in prevalence and treatment of upper urinary tract (UUT) stone disease in England.
Annals of Neurology | 2012
Alexander L. Green; Ella Stone; Holly Sitsapesan; Benjamin W. Turney; John H. Coote; Tipu Z. Aziz; Jonny A. Hyam; Thelma A. Lovick
Most of the time the bladder is locked in storage mode, switching to voiding only when it is judged safe and/or socially appropriate to urinate. Here we show, in humans and rodents, that deep brain stimulation in the periaqueductal gray matter can rapidly and reversibly manipulate switching within the micturition control circuitry, to defer voiding and maintain urinary continence, even when the bladder is full. Manipulation of neural continence pathways by deep brain stimulation may offer new avenues for the treatment of urinary incontinence of central origin. Ann Neurol 2012;72:144–147
Journal of Endourology | 2014
Benjamin W. Turney
BACKGROUND AND PURPOSE Obtaining renal access is one of the most important and complex steps in learning percutaneous nephrolithotomy (PCNL). Ideally, this skill should be practiced outside the operating room. There is a need for anatomically accurate and cheap models for simulated training. The objective was to develop a cost-effective, anatomically accurate, nonbiologic training model for simulated PCNL access under fluoroscopic guidance. METHODS Collecting systems from routine computed tomography urograms were extracted and reformatted using specialized software. These images were printed in a water-soluble plastic on a three-dimensional (3D) printer to create biomodels. These models were embedded in silicone and then the models were dissolved in water to leave a hollow collecting system within a silicone model. These PCNL models were filled with contrast medium and sealed. A layer of dense foam acted as a spacer to replicate the tissues between skin and kidney. RESULTS 3D printed models of human collecting systems are a useful adjunct in planning PCNL access. The PCNL access training model is relatively low cost and reproduces the anatomy of the renal collecting system faithfully. A range of models reflecting the variety and complexity of human collecting systems can be reproduced. The fluoroscopic triangulation process needed to target the calix of choice can be practiced successfully in this model. CONCLUSIONS This silicone PCNL training model accurately replicates the anatomic architecture and orientation of the human renal collecting system. It provides a safe, clean, and effective model for training in accurate fluoroscopy-guided PCNL access.
BJUI | 2011
Benjamin W. Turney; Gareth D. H. Turner; Simon Brewster; Valentine M. Macaulay
What’s known on the subject? and What does the study add?