Abstract The current decline of the highly endangered African wild dog ( Lycaon pictus ) may be partly due to the population dynamics induced by their social system. African wild dogs are obligate co‐operators, and their need for helpers could generate inverse density dependence at the pack level. We show, through a mathematical model, that this can create an Allee effect, leading to a lower population size and a higher risk of population extinction, compared to populations with direct density dependence. This is due to three different processes. All three processes can increase population extinction individually and probably occur simultaneously in African wild dogs. First, inverse density dependence causes significantly higher rates of pack extinction. Second, it also increases the probability of failure to colonize territories by founders. Third, the Allee effect at the pack level (with a critical number of individuals), generates an Allee effect at the population level (with a critical number of packs). These three processes are likely to apply to other obligate co‐operative breeders. Furthermore, our results suggest that habitat fragmentation and destruction, as well as increased human pressure, increase the effects of inverse density dependence. Direct and indirect anthropogenic effects may thus be more detrimental to obligate co‐operative breeders than to other species.

1. Many vertebrates that live in seasonal climates moult once or twice a year, with the effect of refreshing worn coat or plumage, increasing insulation or improving camouflage. The timing of moult may be in response to a variety of cues, but because it is costly, it is also likely to reflect the health and wellbeing of individuals, here referred to as their condition. 2. Here, in the individually-monitored red deer from the Isle of Rum, in which summer and winter coats are easily distinguished, we a) test for traits that are predictive of moult timing, b) explore traits that moult timing is predictive of and c) analyse covariances between moult timings and calving dates at the individual, annual and residual level. 3. We show that adult female moult timing in July and November is associated with age, reproductive status and parasite burden, and has been getting earlier over time in November. A female’s moult status also predicts the overwinter survival of herself and her current calf as well as her future fecundity. Moult timing varies among individuals and years, and covariances between calving dates and the timing of each moult sheds light on the temporal patterns of condition within individuals and across years. 4. The timing of moult appears to be a non-invasive measure of condition. Monitoring moult timing across years at the population level may shed light on year-to year variation in population health and variation within populations is likely indicative of the relative conditions among individuals. Increased knowledge of population and individual condition may be of benefit for ungulate population management and conservation.

Rejoinder to separate Discussions by David Blockley, D.G. Elms, and Colin B. Brown of ‘Structural reliability theory in the context of structural safety’ by R.E. Melchers, Civil Engineering and Environmental Systems, Volume 24, Number 1, March 2007, pp. 55–69.

In 2002, the 45 year old Sorell Causeway Bridge in Tasmania’s south east was demolished due to fears surrounding the serviceability of the prestressed concrete beams, in relation to the corrosion of the post-tensioning strands. Attempts were made to determine the extent and severity of the corrosion prior to its demolition by employing a number of conventional non-destructive and diagnostic techniques, yet a firm conclusion could not be reached regarding the structure’s condition. To further investigate the degree of correlation between these conventional assessment techniques and the physical condition of the embedded steel in relation to corrosion risk guidelines recommended in the literature, a number of beams of varying condition were salvaged from the bridge demolition and subjected to further detailed investigations. The current paper focuses on the half-cell potential and chloride profile results obtained for two such beams in good and poor condition relating to the reinforcing and prestressing steel condition. In summary, the comparison of results yielded inconsistencies with the literature guidelines. Survey areas showing highly negative potentials and elevated chloride concentrations did not necessarily indicate corrosion activity or severity. In contrast, instances of severe corrosion were found on both reinforcing and prestressing steel where literature guidelines for these tests recommend that the risk of corrosion is low.

Abstract Background: Atezolizumab+bevacizumab (atezo+bev) is a first-line therapy for advanced hepatocellular carcinoma (aHCC) with ∼30% objective responses. Single-cell studies identified responses linked to CD8⁺ T effector cells (CD8_Tex and Temra) and CXCL10⁺ macrophages (Macro_CXCL10), and resistance to TREM2⁺ macrophages (Macro_TREM2) and CD14⁺ monocytes (Mono_CD14). We hypothesized that, beyond cell composition, immune spatial organization within the tumor microenvironment (TME) determines response to atezo+bev. Methods: Single-cell spatial transcriptomics (ST) was performed on 27 aHCCs (9 atezo+bev responders and 18 resistant) using the Xenium Prime 5.000-gene panel (10x Genomics) customized with 100 additional genes. For local tissue organization, distances between cells were computed using the dbscan package [radius(r)=300µm]. Immune cell clusters were defined as groups of ≥3 immune cells within 100 µm, and were identified through a density-based algorithm. This spatial clustering was assessed using both ST and multiplexed immunohistochemistry (mIHC) data. Cell-to-cell interactions (neighborhoods) were analyzed (r=25µm). Ligand-receptor interactions were evaluated using a spatial neighborhood-based approach. Results: ST of 27 aHCCs yielded 4.6 million cells. In responders, CD8_Tex and Temra, and Macro_CXCL10 cells localized within the tumor and were closer to cancer cells (p=0.02, p=0.08, and p=0.1, respectively). Furthermore, in responders, tumor hepatocytes exhibited a significantly enriched lymphoid neighborhood composition and significantly higher rates of immune-recruting interactions, including PDL1-PD1, CXCL9-CXCR3 and CXCL10-CXCR3 (p<0.05). Non-responders were enriched in TREM2⁺ macrophage-containing clusters. Specifically, they showed Macro_TREM2-pure clusters (10% vs 0%, p=0.009), mixed Macro_TREM2-Mono_CD14 clusters (27% vs 5%, p=0.03), and mixed Macro_TREM2-CD8⁺ T-cell clusters (38% vs 22%, p=0.04). This was accompanied by enrichment of the CXCL12-CXCR4 chemokine axis, consistent with an immunosuppressive TME. Using mIHC, we confirmed enrichment of Macro_TREM2-pure (p=0.02) and Macro_TREM2-CD8⁺ mixed clusters (p=0.03). Conclusions: Atezo+bev response in HCC is marked by intratumoral effector CD8⁺ T cells and CXCL10_Macro, tumor hepatocytes enriched in lymphoid neighborhoods, and immune-recruiting ligand-receptor interactions, whereas resistance is driven by TREM2_Macro clusters and CXCL12-CXCR4 signaling. These findings identify spatial immune organization as a key determinant of response to atezo+bev. Citation Format: Anna Vila-Escoda, Marta Piqué-Gili, Marta Casado-Pelaez, Roser Pinyol, Ana Hernández de Sande, Verónica Davalos, Albert Gris-Oliver, Carla Montironi, Judit Peix, Daniela Grases, Ezequiel Mauro, Guillem Cano-Segarra, Sarah Cappuyns, Igor Figueiredo, Giorgio Ioannou, Edgar Gonzalez-Kozlova, Tim Meyer, Anja Lachenmayer, Jens U Marquardt, Helen L Reeves, Julien Edeline, Fabian Finkelmeier, Jörg Trojan, Sacha Gnjatic, Jean-Frederic Blanc, Richard A Hubner, Matthias Pinter, Tom Luedde, Arndt Vogel, Daniela Sia, Vincenzo Mazzaferro, Manel Esteller, Jeroen Dekervel, Eduard Porta-Pardo, Josep M Llovet. Spatial immune architecture at single-cell resolution predicts response to atezolizumab plus bevacizumab in advanced HCC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(8_Suppl):Abstract nr LB123.