Early-stage loss of ecological integrity drives the risk of zoonotic disease emergence.

Anthropogenic pressures have increasingly disrupted the integrity of ecosystems worldwide, jeopardizing their capacity to provide essential contributions to human well-being. Recently, the role of natural ecosystems in reducing disease emergence risk has gained prominence in decision-making processes, as scientific evidence indicates that human-driven pressure, such as habitat destruction and deforestation, can trigger the emergence of zoonotic infectious diseases. However, the intricate relationship between biodiversity and emerging infectious diseases (EIDs) remains only partially understood. Here, we updated the most comprehensive zoonotic EID event database with the latest reported events to analyse the relationship between EIDs of wildlife origin (zoonoses) and various facets of ecological integrity. We found EID risk was strongly predicted by structural integrity metrics such as human footprint and ecoregion intactness, in addition to environmental variables such as tropical rainforest density and mammal species richness. EID events were more likely to occur in areas with intermediate levels of compositional and structural integrity, underscoring the risk posed by human encroachment into pristine, undisturbed lands. Our study highlights the need to identify novel indicators and targets that can effectively address EID risk alongside other pressing global challenges in sustainable development, ultimately informing strategies for preserving both human and environmental health.

The oral microbiome in the pathophysiology of cardiovascular disease.

Despite advances in our understanding of the pathophysiology of many cardiovascular diseases (CVDs) and expansion of available therapies, the global burden of CVD-associated morbidity and mortality remains unacceptably high. Important gaps remain in our understanding of the mechanisms of CVD and determinants of disease progression. In the past decade, much research has been conducted on the human microbiome and its potential role in modulating CVD. With the advent of high-throughput technologies and multiomics analyses, the complex and dynamic relationship between the microbiota, their 'theatre of activity' and the host is gradually being elucidated. The relationship between the gut microbiome and CVD is well established. Much less is known about the role of disruption (dysbiosis) of the oral microbiome; however, interest in the field is growing, as is the body of literature from basic science and animal and human investigations. In this Review, we examine the link between the oral microbiome and CVD, specifically coronary artery disease, stroke, peripheral artery disease, heart failure, infective endocarditis and rheumatic heart disease. We discuss the various mechanisms by which oral dysbiosis contributes to CVD pathogenesis and potential strategies for prevention and treatment.

Tuning the Electronic Response of Metallic Graphene by Potassium Doping.

Electron doping of graphene has been extensively studied on graphene-supported surfaces, where the metallicity is influenced by the substrate. Herewith we propose potassium adsorption on free-standing nanoporous graphene, thus eluding any effect due to the substrate. We monitor the electron migration in the π* downward-shifted conduction band. In this rigid band shift, we correlate the spectral density of the π* state in the upper Dirac cone with the associated plasmon, blue-shifted with increasing K dose, as deduced by electron energy loss spectroscopy. These results are confirmed by the Dirac plasmon activated by the C 1s emitted electrons, thanks to spatially resolved photoemission. This crosscheck constitutes a reference on the correlation between the electronic π* states in the conduction band and the Dirac plasmon evolution upon in situ electron doping of fully free-standing graphene.