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Abstract Background Many felid species are of high conservation concern, and with increasing human disturbance the situation is worsening. Small isolated populations are at risk of genetic impoverishment decreasing within-species biodiversity. Movement is known to be a key behavioural trait that shapes both demographic and genetic dynamics and affects population survival. However, we have limited knowledge on how different manifestations of movement behaviour translate to population processes. In this study, we aimed to 1) understand the potential effects of movement behaviour on the genetic diversity of small felid populations in heterogeneous landscapes, while 2) presenting a simulation tool that can help inform conservation practitioners following, or considering, population management actions targeting the risk of genetic impoverishment. Methods We developed a spatially explicit individual-based population model including neutral genetic markers for felids and applied this to the example of Eurasian lynx. Using a neutral landscape approach, we simulated reintroductions into a three-patch system, comprising two breeding patches separated by a larger patch of differing landscape heterogeneity, and tested for the effects of various behavioural movement syndromes and founder population sizes. We explored a range of movement syndromes by simulating populations with various movement model parametrisations that range from ‘shy’ to ‘bold’ movement behaviour. Results We find that movement syndromes can lead to a higher loss of genetic diversity and an increase in between population genetic structure for both “bold” and “shy” movement behaviours, depending on landscape conditions, with larger decreases in genetic diversity and larger increases in genetic differentiation associated with bold movement syndromes, where the first colonisers quickly reproduce and subsequently dominate the gene pool. In addition, we underline the fact that a larger founder population can offset the genetic losses associated with subpopulation isolation and gene pool dominance. Conclusions We identified a movement syndrome trade-off for population genetic variation, whereby bold-explorers could be saviours - by connecting populations and promoting panmixia, or sinks - by increasing genetic losses via a ‘founder takes all’ effect, whereas shy-stayers maintain a more gradual genetic drift due to their more cautious behaviour. Simulations should incorporate movement behaviour to provide better projections of long-term population viability and within-species biodiversity, which includes genetic diversity. Simulations incorporating demographics and genetics have great potential for informing conservation management actions, such as population reintroductions or reinforcements. Here, we present such a simulation tool for solitary felids.

Abstract Background The cytokine IL-17 is a key player in autoimmune processes, while the cytokine IL-6 is responsible for the chronification of inflammation. However, their roles in type 1 diabetes development are still unknown. Methods Therefore, therapies for 5 days with anti-IL-17A or anti-IL-6 in combination with a T cell-specific antibody, anti-TCR, or in a triple combination were initiated immediately after disease manifestation to reverse the diabetic metabolic state in the LEW.1AR1-iddm (IDDM) rat, a model of human type 1 diabetes. Results Monotherapies with anti-IL-6 or anti-IL-17 showed no sustained anti-diabetic effects. Only the combination therapy of anti-TCR with anti-IL-6 or anti-IL-17 at starting blood glucose concentrations up to 12 mmol/l restored normoglycaemia. The triple antibody combination therapy was effective even up to very high initial blood glucose concentrations (17 mmol/l). The β cell mass was raised to values of around 6 mg corresponding to those of normoglycaemic controls. In parallel, the apoptosis rate of β cells was reduced and the proliferation rate increased as well as the islet immune cell infiltrate was strongly reduced in double and abolished in triple combination therapies. Conclusions The anti-TCR combination therapy with anti-IL-17 preferentially raised the β cell mass as a result of β cell proliferation while anti-IL-6 strongly reduced β cell apoptosis and the islet immune cell infiltrate with a modest increase of the β cell mass only. The triple combination therapy achieved both goals in a complimentary anti-autoimmune and anti-inflammatory action resulting in sustained normoglycaemia with normalized serum C-peptide concentrations.