Revolutionaries and spies: Spy-good and spy-bad graphs

We study a game on a graph $G$ played by $r$ {\it revolutionaries} and $s$ {\it spies}. Initially, revolutionaries and then spies occupy vertices. In each subsequent round, each revolutionary may move to a neighboring vertex or not move, and then each spy has the same option. The revolutionaries win if $m$ of them meet at some vertex having no spy (at the end of a round); the spies win if they can avoid this forever. Let $\sigma(G,m,r)$ denote the minimum number of spies needed to win. To avoid degenerate cases, assume |V(G)|\ge r-m+1\ge\floor{r/m}\ge 1. The easy bounds are then \floor{r/m}\le \sigma(G,m,r)\le r-m+1. We prove that the lower bound is sharp when $G$ has a rooted spanning tree $T$ such that every edge of $G$ not in $T$ joins two vertices having the same parent in $T$. As a consequence, \sigma(G,m,r)\le\gamma(G)\floor{r/m}, where $\gamma(G)$ is the domination number; this bound is nearly sharp when $\gamma(G)\le m$. For the random graph with constant edge-probability $p$, we obtain constants $c$ and $c'$ (depending on $m$ and $p$) such that $\sigma(G,m,r)$ is near the trivial upper bound when $r<c\ln n$ and at most $c'$ times the trivial lower bound when $r>c'\ln n$. For the hypercube $Q_d$ with $d\ge r$, we have $\sigma(G,m,r)=r-m+1$ when $m=2$, and for $m\ge 3$ at least $r-39m$ spies are needed. For complete $k$-partite graphs with partite sets of size at least $2r$, the leading term in $\sigma(G,m,r)$ is approximately $\frac{k}{k-1}\frac{r}{m}$ when $k\ge m$. For $k=2$, we have \sigma(G,2,r)=\bigl\lceil{\frac{\floor{7r/2}-3}5}\bigr\rceil and \sigma(G,3,r)=\floor{r/2}, and in general $\frac{3r}{2m}-3\le \sigma(G,m,r)\le\frac{(1+1/\sqrt3)r}{m}$.Comment: 34 pages, 2 figures. The most important changes in this revision are improvements of the results on hypercubes and random graphs. The proof of the previous hypercube result has been deleted, but the statement remains because it is stronger for m<52. In the random graph section we added a spy-strategy resul

TRY plant trait database – enhanced coverage and open access

Plant traits - the morphological, anatomical, physiological, biochemical and phenological characteristics of plants - determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits - almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

31st Annual Meeting and Associated Programs of the Society for Immunotherapy of Cancer (SITC 2016) : part two

Background The immunological escape of tumors represents one of the main ob- stacles to the treatment of malignancies. The blockade of PD-1 or CTLA-4 receptors represented a milestone in the history of immunotherapy. However, immune checkpoint inhibitors seem to be effective in specific cohorts of patients. It has been proposed that their efficacy relies on the presence of an immunological response. Thus, we hypothesized that disruption of the PD-L1/PD-1 axis would synergize with our oncolytic vaccine platform PeptiCRAd. Methods We used murine B16OVA in vivo tumor models and flow cytometry analysis to investigate the immunological background. Results First, we found that high-burden B16OVA tumors were refractory to combination immunotherapy. However, with a more aggressive schedule, tumors with a lower burden were more susceptible to the combination of PeptiCRAd and PD-L1 blockade. The therapy signifi- cantly increased the median survival of mice (Fig. 7). Interestingly, the reduced growth of contralaterally injected B16F10 cells sug- gested the presence of a long lasting immunological memory also against non-targeted antigens. Concerning the functional state of tumor infiltrating lymphocytes (TILs), we found that all the immune therapies would enhance the percentage of activated (PD-1pos TIM- 3neg) T lymphocytes and reduce the amount of exhausted (PD-1pos TIM-3pos) cells compared to placebo. As expected, we found that PeptiCRAd monotherapy could increase the number of antigen spe- cific CD8+ T cells compared to other treatments. However, only the combination with PD-L1 blockade could significantly increase the ra- tio between activated and exhausted pentamer positive cells (p= 0.0058), suggesting that by disrupting the PD-1/PD-L1 axis we could decrease the amount of dysfunctional antigen specific T cells. We ob- served that the anatomical location deeply influenced the state of CD4+ and CD8+ T lymphocytes. In fact, TIM-3 expression was in- creased by 2 fold on TILs compared to splenic and lymphoid T cells. In the CD8+ compartment, the expression of PD-1 on the surface seemed to be restricted to the tumor micro-environment, while CD4 + T cells had a high expression of PD-1 also in lymphoid organs. Interestingly, we found that the levels of PD-1 were significantly higher on CD8+ T cells than on CD4+ T cells into the tumor micro- environment (p < 0.0001). Conclusions In conclusion, we demonstrated that the efficacy of immune check- point inhibitors might be strongly enhanced by their combination with cancer vaccines. PeptiCRAd was able to increase the number of antigen-specific T cells and PD-L1 blockade prevented their exhaus- tion, resulting in long-lasting immunological memory and increased median survival