A randomised single-blind comparison of the effectiveness of Tristel Fuse (chlorine dioxide) as an office-based fluid soak, with Cidex OPA (ortho-phthaldehyde) using an automated endoscopic reprocessor (AER) as high-level disinfection for flexible cystoscopes.

OBJECTIVE: To compare the effectiveness, safety and cost of Tristel Fuse (chlorine dioxide) with Cidex OPA (ortho-phthaldehyde; 1,2-benzenedicarboxaldehyde) in an automated endoscopic reprocessor (AER) for high-level disinfection of flexible cystoscopes. PATIENTS AND METHODS: A randomised single-blind study comparing the high-level disinfectants Tristel Fuse as a simple office-based soak and Cidex OPA using an AER was performed. Participants were 'blinded' to the agent used for disinfection of the flexible cystoscopes. All patients had negative mid-stream urine at baseline, (MSU) no symptoms suggestive of urinary tract infection (UTI) on the day of investigation, no recent antibiotic use or current indwelling urinary catheter. Patients who underwent cystoscopic biopsy during the procedure were excluded. A urine analysis was done before and 3-5 days after cystoscopy and multiple equipment cultures were performed. The Urogenital Distress Inventory (UDI-6 + two questions from the 'long-form'), symptom and quality-of-life scores were assessed before and after cystoscopy as were ease-of-use assessments and a full cost analysis. RESULTS: In all, 180 of 465 screened participants were randomised 1:1 and the mean age was 72.1 years, 17% were females and 57% of procedures were performed for bladder tumour surveillance. The urine analysis was positive in 5.4% of patients in each group and 29% (Tristel) vs 20% (Cidex) of patients had urinary leukocyturia (p = ns) after cystoscopy. The turnover (minutes per cycle) was 7.5 (Tristel) vs 26.7 (Cidex). The per-procedure costs were $11.67 (American dollars) for Tristel Fuse and $21.82 for Cidex OPA with fixed costs of $4788 for Tristel Fuse and $60,514 for Cidex OPA. CONCLUSIONS: Tristel Fuse appears to be as effective and more cost-effective than Cidex OPA for high-level disinfection of flexible cystoscopes. This has significant cost implications for the office urologist.

New Zealand's drug development industry--strengths and opportunities.

AIM: Globally the traditional model of drug development is changing and the large pharmaceutical companies are looking externally for innovative compounds, new technologies and cost-effective drug development services. New Zealand (NZ) can capitalise on its expertise in innovative drug discovery and development but needs to be able to define and promote its capabilities to the global drug development industry. An approach that will enable a ready assessment of NZ's expertise is presented. METHOD: Interviews will be carried out with key senior personnel from NZ drug discovery groups, drug development companies and organisations that provide a wide range of research and development services. The resulting data will be collated to document current capabilities and expertise, as well as limitations, in NZ's industry and assess their potential for the future. Participants will be asked to identify factors that support and factors that limit their organisation's progress in drug development and to suggest policies that could be implemented to positively influence future performance. CONCLUSION: A formal assessment of New Zealand's capabilities, strengths and limitations in drug development will aid in the promotion of its expertise to overseas organisations and enhance the economic benefits that could accrue to New Zealand.

A double-blind, placebo-controlled study to assess the mitochondria-targeted antioxidant MitoQ as a disease-modifying therapy in Parkinson's disease.

Multiple lines of evidence point to mitochondrial oxidative stress as a potential pathogenic cause for Parkinson's disease (PD). MitoQ is a powerful mitochondrial antioxidant. It is absorbed orally and concentrates within mitochondria where it has been shown to protect against oxidative damage. We enrolled 128 newly diagnosed untreated patients with PD in a double-blind study of two doses of MitoQ compared with placebo to explore the hypothesis that, over 12 months, MitoQ would slow the progression of PD as measured by clinical scores, particularly the Unified Parkinson Disease Rating Scale. We showed no difference between MitoQ and placebo on any measure of PD progression. MitoQ does not slow the progression of PD, and this finding should be taken into account when considering the oxidative stress hypothesis for the pathogenesis of PD.

The mitochondria-targeted anti-oxidant mitoquinone decreases liver damage in a phase II study of hepatitis C patients.

BACKGROUND: Increased oxidative stress and subsequent mitochondrial damage are important pathways for liver damage in chronic hepatitis C virus (HCV) infection; consequently, therapies that decrease mitochondrial oxidative damage may improve outcome. The mitochondria-targeted anti-oxidant mitoquinone combines a potent anti-oxidant with a lipophilic cation that causes it to accumulate several-hundred fold within mitochondria in vivo. AIMS: In this phase II study, we investigated the effect of oral mitoquinone on serum aminotransferases and HCV RNA levels in HCV-infected patients. METHODS: Thirty HCV patients who were either non-responders or unsuitable candidates for standard-of-care (pegylated interferon plus ribavirin) were randomized to receive mitoquinone (40 or 80 mg) or placebo once daily for 28 days, and serum aminotransferases and HCV RNA levels were measured. RESULTS: Both treatment groups showed significant decreases in absolute and percentage changes in serum alanine transaminase (ALT) from baseline to treatment day 28 (P<0.05). There was also a significant difference between incremental area under the curve for ALT between baseline and day 28 for the 40 mg treatment group against placebo (P<0.05). The differences in plasma ALT activity from baseline to day 28 in both mitoquinone groups compared with placebo did not reach significance (P>0.05). There was no change in HCV load on mitoquinone treatment. CONCLUSIONS: Administration of the mitochondria-targeted anti-oxidant mitoquinone significantly decreased plasma ALT and aspartate aminotransferase in patients with chronic HCV infection, and this suggests that mitoquinone may decrease necroinflammation in the liver in these patients. As mitochondrial oxidative damage contributes to many other chronic liver diseases, such as steatohepatitis, further studies using mitochondria-targeted anti-oxidants in HCV and other liver diseases are warranted.