Robin Weston
Royal Melbourne Hospital
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Publication
Featured researches published by Robin Weston.
BJUI | 2009
Vivek K. Wadhwa; Robin Weston; Rahul Mistry; Nigel J. Parr
To study the long‐term effects of androgen‐deprivation therapy (ADT) using luteinizing hormone‐releasing hormone (LHRH) agonists or antiandrogen therapy with bicalutamide on bone mineral density (BMD) of selected groups of patients with newly diagnosed advanced prostate cancer, stratified by BMD at presentation and to predict alterations in fracture risk.
BJUI | 2010
Benjamin J. Challacombe; Robin Weston; Geoff Coughlin; Declan Murphy; Prokar Dasgupta
© 2 0 1 0 T H E A U T H O R S B J U I N T E R N A T I O N A L
The Journal of Urology | 2011
Emma E. Clarebrough; Benjamin J. Challacombe; Christopher Briggs; Benjamin Namdarian; Robin Weston; Declan Murphy; Anthony J. Costello
PURPOSE An accurate, complete understanding of the prostate neuroanatomy is required to optimize nerve sparing techniques during radical prostatectomy. However, the precise topography and function of the periprostatic nerves remain contentious and there is uncertainty about which nerve sparing technique is most optimal. We accurately quantified the distribution, precise localization and cross-sectional area of periprostatic neural tissue using cadaveric specimens. MATERIALS AND METHODS We analyzed 13 cadaveric hemipelves using hematoxylin and eosin stained sections from the base, mid zone and apex of each prostate. Each section was digitized and divided into 6 sectors numbered clockwise. Analysis was performed using National Institutes of Health ImageJ software to calculate the total periprostatic neural cross-sectional area per sector. RESULTS Calculating the total neural cross-sectional area highlighted a decrease from prostate base to mid zone to apex of 24.7, 19.7 and 13.7 mm(2), respectively. Most neural tissue was located in the posterolateral region. However, the proportion surrounding the anterior part of the prostate increased toward the apex with a median of 6.0% and 7.6% at the base and mid zone regions, respectively, increasing to 11.2% at the apex. CONCLUSIONS Simple numerical nerve quantification may be insufficient to accurately describe the periprostatic neural distribution. Calculating nerve bundle cross-sectional area confirmed that most neural tissue is in the posterolateral region, although the proportion located anterior increases from base to apex. Thus, higher release of the periprostatic fascia may be indicated toward the apex.
BJUI | 2011
Vivek K. Wadhwa; Robin Weston; Nigel J. Parr
Study Type – Therapy (case series)
BJUI | 2010
Vivek K. Wadhwa; Robin Weston; Nigel J. Parr
Study Type – Therapy (RCT) Level of Evidence 1b
British Journal of Medical and Surgical Urology | 2009
Vivek K. Wadhwa; Robin Weston; Nigel J. Parr
Objective: This study was conducted to determine the cause of death in patients receiving ADT for PCa in the PSA era. Patients and methods: We followed 618 patients (mean age 73 years) with PCa initiating ADT from October 1999 to October 2007. Patients were recruited from urology clinics. Patients were regularly reviewed in a dedicated PCa clinic. Cause of death was recorded prospectively, after review of medical case notes and biochemical parameters. Results: At median follow-up of 6.7 years, there were 377 deaths (61% mortality). Of these, 176 (47%) were attributable to PCa. Non-cancer deaths (n = 201) were predominantly cardiovascular (n = 125) and respiratory (n = 43). Overall median presenting PSA was 37 ng/ml (range 0.4–5599), significantly higher (P < 0.001) in those dying from PCa (115 ng/ml) than from other causes (18 ng/ml). PCa specific mortality increased with PSA at presentation (14% for PSA < 50 ng/ml, 45% for 50–100 ng/ml and 69% for > 100 ng/ml). When stratified for presenting age, PCa deaths were 70% (46/66) for men 60–69 years, 47% (85/180) for 70–79 years and 34% (45/131) for >80 years. Conclusions: Many patients with PCa initiating ADT continue to die from non-cancer causes in an era of widespread PSA testing, the proportion increasing with older age at presentation. This may justify deferring hormonal treatment in suitable older asymptomatic men, sparing the burden of long-term ADT. Patients with PCa who require hormonal therapy should be assessed for cardiovascular and respiratory risk factors at the time of presentation.
Anz Journal of Surgery | 2011
Robin Weston; Declan Murphy; Anthony J. Costello
I applaud Dr T B Hugh on his article and letter. I add a system error perspective. The issue is that there was a failure to warn of the risk of R vocal cord palsy (VCP) in 1983, and not whether there was a breach in 1994 when the trial occurred. I agree that the incidence of R VCP because of a Dohlman operation before 1983 was not established at trial and I agree it was zero, unlike the known incidence of 1:14 000 in Rogers v Whitaker. With respect, even the trial judge’s objected question was not referenced to the period before 1983. Expert opinion after 1983 or in 1991 is not relevant. It is probable that the expert opinion in 1994 as to ‘vocal cord paralysis has been described’ referred to Dr Benjamin’s 1991 article, which is presumed to be Mrs Hart. There was no evidence as to the incidence of R VCP before 1983. The number of Dohlman operations by Professor Benjamin before 1983 is relevant, not the total in 1994 including different techniques. In 1993, he reported 34 cases treated by a different technique (laser) rather than Dohlman diathermy. The specific number of Dohlman cases undertaken by Professor Benjamin before 1983 was not established but is probably at least 34 less than the number Professor Benjamin stated at a trial in 1994. I submit that at trial 11 years later, there was a system error. The relevant 1983 facts needed to determine a breach were not established.
Anz Journal of Surgery | 2011
Robin Weston; Declan Murphy; Anthony J. Costello
I applaud Dr T B Hugh on his article and letter. I add a system error perspective. The issue is that there was a failure to warn of the risk of R vocal cord palsy (VCP) in 1983, and not whether there was a breach in 1994 when the trial occurred. I agree that the incidence of R VCP because of a Dohlman operation before 1983 was not established at trial and I agree it was zero, unlike the known incidence of 1:14 000 in Rogers v Whitaker. With respect, even the trial judge’s objected question was not referenced to the period before 1983. Expert opinion after 1983 or in 1991 is not relevant. It is probable that the expert opinion in 1994 as to ‘vocal cord paralysis has been described’ referred to Dr Benjamin’s 1991 article, which is presumed to be Mrs Hart. There was no evidence as to the incidence of R VCP before 1983. The number of Dohlman operations by Professor Benjamin before 1983 is relevant, not the total in 1994 including different techniques. In 1993, he reported 34 cases treated by a different technique (laser) rather than Dohlman diathermy. The specific number of Dohlman cases undertaken by Professor Benjamin before 1983 was not established but is probably at least 34 less than the number Professor Benjamin stated at a trial in 1994. I submit that at trial 11 years later, there was a system error. The relevant 1983 facts needed to determine a breach were not established.
The Journal of Urology | 2007
Vivek K. Wadhwa; Robin Weston; Nigel J. Parr
The Journal of Urology | 2005
Vivek K. Wadhwa; Robin Weston; Asad Hussain; Nigel J. Parr