White paper on 6G drivers and the UN SDGs

Executive summary The commercial launch of 6G communications systems and the United Nations’ Sustainable Development Goals (UN SDGs) are both targeted for 2030. 6G communications are expected to boost global growth and productivity, create new business models and transform many aspects of society. The UN SDGs are a way of framing opportunities and challenges of a desirable future world and cover topics as broad as ending poverty, building gender equality, the fight against climate change and developing smart cities. The relationship between these potentially mutually reinforcing forces is currently under-defined. Building on the vision for 6G, and a review of megatrends, ongoing studies on the relation of mobile communications to the UN SDGs and existing indicators, a novel linkage between 6G and the UN SDGs is proposed. This linkage is via a set of indicators. This white paper also initiates work on a new set of 6G related indicators to guide research on 6G systems. The novel linkage is built on the envisaged three-fold role of 6G as 1) a provider of services to help steer and support communities and countries towards reaching the UN SDGs, 2) a measuring tool for data collection to help the reporting of indicators with hyperlocal granularity, and 3) a reinforcer of new ecosystems based on 6G technology enablers and 6G networks of networks to be developed in line with the UN SDGs which incorporates future mobile communication technologies which will be available in 2030. Related challenges are also identified. An action plan is presented along with prioritized focus areas within the mobile communication sector technology and industry evolution to best support the achievement of the UN SDGs

Susceptibility of low-density lipoprotein particles to aggregate depends on particle lipidome, is modifiable, and associates with future cardiovascular deaths

Abstract Aims: Low-density lipoprotein (LDL) particles cause atherosclerotic cardiovascular disease (ASCVD) through their retention, modification, and accumulation within the arterial intima. High plasma concentrations of LDL drive this disease, but LDL quality may also contribute. Here, we focused on the intrinsic propensity of LDL to aggregate upon modification. We examined whether inter-individual differences in this quality are linked with LDL lipid composition and coronary artery disease (CAD) death, and basic mechanisms for plaque growth and destabilization. Methods and results: We developed a novel, reproducible method to assess the susceptibility of LDL particles to aggregate during lipolysis induced ex vivo by human recombinant secretory sphingomyelinase. Among patients with an established CAD, we found that the presence of aggregation-prone LDL was predictive of future cardiovascular deaths, independently of conventional risk factors. Aggregation-prone LDL contained more sphingolipids and less phosphatidylcholines than did aggregation-resistant LDL. Three interventions in animal models to rationally alter LDL composition lowered its susceptibility to aggregate and slowed atherosclerosis. Similar compositional changes induced in humans by PCSK9 inhibition or healthy diet also lowered LDL aggregation susceptibility. Aggregated LDL in vitro activated macrophages and T cells, two key cell types involved in plaque progression and rupture. Conclusion: Our results identify the susceptibility of LDL to aggregate as a novel measurable and modifiable factor in the progression of human ASCVD