Improving the science-policy dialogue to meet the challenges of biodiversity conservation: having conversations rather than talking at one-another

A better, more effective dialogue is needed between biodiversity science and policy to underpin the sustainable use and conservation of biodiversity. Many initiatives exist to improve communication, but these largely conform to a ‘linear’ or technocratic model of communication in which scientific “facts” are transmitted directly to policy advisers to “solve problems”. While this model can help start a dialogue, it is, on its own, insufficient, as decision taking is complex, iterative and often selective in the information used. Here, we draw on the literature, interviews and a workshop with individuals working at the interface between biodiversity science and government policy development to present practical recommendations aimed at individuals, teams, organisations and funders. Building on these recommendations, we stress the need to: (a) frame research and policy jointly; (b) promote inter- and trans-disciplinary research and “multi-domain” working groups that include both scientists and policy makers from various fields and sectors; (c) put in place structures and incentive schemes that support interactive dialogue in the long-term. These are changes that are needed in light of continuing loss of biodiversity and its consequences for societal dependence on and benefits from nature

Improved molecular typing of toxigenic <i>Clostridium difficile</i> strains affecting animal and human health

Clostridium difficile is a Gram-positive, spore forming bacterium, which remains a formidable pathogen as the etiological agent of C. difficile infection (CDI). Substantial effort goes into diagnosis of CDI and characterisation of circulating toxigenic C. difficile strains for epidemiology and infection prevention and control. Currently, molecular typing of C. difficile requires 9 days following diagnosis through PCR ribotyping and multilocus variable number tandem repeat (VNTR) analysis. There is a need for more rapid typing methods to investigate possible linkage between CDI cases in healthcare settings. This study developed a one-step, closed tube real-time PCR and high resolution melt (HRM) assay targeting the intergenic spacer region (ISR) and several VNTR loci, with results generated in 2.5 h. The discriminatory power of the PCR-HRM assay was investigated by typing previously characterised toxigenic clinical and animal C. difficile isolates (n=90). Through comparison of HRM profiles targeting the ISR of isolates belonging to 17 PCR ribotypes, 13 HRM genotypes were recognised with 11 PCR ribotypes resolved from each other. Using correlation between HRM data and known VNTR repeat numbers at the B7, C6 and G8 loci, VNTR repeat numbers for isolates could be predicted within an average absolute difference of 1.8 at the B7 locus, 2.1 at the C6 locus, and 2.5 at the G8 locus. These results suggest that a PCR-HRM assay with a multilocus panel targeting ISR and selected VNTR loci could form part of an improved molecular typing scheme for toxigenic C. difficile strains that is faster than currently available methods.<br/

Clinical characteristics and survival in systemic sclerosis-mixed connective tissue disease and systemic sclerosis-overlap syndrome

Objective: To describe the clinical characteristics and outcomes of systemic sclerosis–mixed connective tissue disease (SSc–MCTD) and SSc overlap syndrome. Methods: We included patients from the Australian Scleroderma Cohort Study who met American College of Rheumatology/European Alliance of Associations for Rheumatology criteria for SSc. Three mutually exclusive groups were created: SSc–MCTD, SSc overlap, and SSc only. Univariate comparison of clinical features was performed by analysis of variance or chi-square test. Survival analysis was performed using Kaplan-Meier (KM) curves and Cox proportional hazards regression models. Results: Of 1,728 patients, 97 (5.6%) had SSc–MCTD, and 126 (7.3%) had SSc overlap. Those with MCTD–SSc were more commonly Asian (18.3% versus 10.1% in SSc overlap, and 3.6% in SSc only; P < 0.0001) and younger at disease onset (38.4 years versus 46.5 or 46.8 years, P < 0.0001). Those with SSc–MCTD or SSc overlap were more likely to have limited cutaneous SSc. All 3 groups had similar frequency of interstitial lung disease (ILD), although pulmonary arterial hypertension (PAH) was less common in SSc overlap. Synovitis and myositis were more common in SSc overlap and SSc–MCTD than in SSc only. KM curves showed better survival in SSc–MCTD than SSc overlap or SSc only (P = 0.011), but this was not significant after adjustment for sex and age at disease onset. SSc-specific antibodies were survival prognostic markers, with antinuclear antibody centromere or anti-RNP conferring better survival than anti–Scl-70 or anti–RNA polymerase III (P = 0.005). Patients with SSc–MCTD and SSc overlap had lower mortality following diagnosis of ILD and PAH than patients with SSc only. Conclusion: This study provides insights into the clinical characteristics of patients with SSc–MCTD, SSc overlap, and SSc only and shows that anti-RNP antibodies are associated with better survival than anti–Scl-70 and anti-RNA polymerase III antibodies.Jessica L. Fairley, Dylan Hansen, Susanna Proudman, Joanne Sahhar, Gene-Siew Ngian, Jenny Walker, Gemma Strickland, Michelle Wilson, Kathleen Morrisroe, Nava Ferdowsi, Gabor Major, Janet Roddy, Wendy Stevens, and Mandana Nikpour, for the Australian Scleroderma Interest Grou