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This study reports a comprehensive empirical investigation of the nature and correlates of anti-mask attitudes during the COVID-19 pandemic. Accumulating evidence underscores the importance of facemasks, as worn by the general public, in limiting the spread of infection. Accordingly, mask wearing has become increasingly mandatory in public places such as stores and on public transit. Although the public has been generally adherent to mask wearing, a small but vocal group of individuals refuse to wear masks. Anti-mask protest rallies have occurred in many places throughout the world, sometimes erupting violently. Few empirical studies have examined the relationship between anti-mask attitudes and mask non-adherence and little is known about how such attitudes relate to one another or other factors (e.g., non-adherence to social distancing, anti-vaccination attitudes). To investigate these issues, the present study surveyed 2,078 adults from the US and Canada. Consistent with other surveys, we found that most (84%) people wore masks because of COVID-19. The 16% who did not wear masks scored higher on most measures of negative attitudes towards masks. Network analyses indicated that negative attitudes about masks formed an intercorrelated network, with the central nodes in the network being (a) beliefs that masks are ineffective in preventing COVID-19, and (b) psychological reactance (PR; i.e., an aversion to being forced to wear masks). These central nodes served as links, connecting the network of anti-masks attitudes to negative attitudes toward SARSCoV2 vaccination, beliefs that the threat of COVID-19 has been exaggerated, disregard for social distancing, and political conservatism. Findings regarding PR are important because, theoretically, PR is likely to strengthen other anti-masks attitudes (e.g., beliefs that masks are ineffective) because people with strong PR react with anger and counter-arguments when their beliefs are challenged, thereby leading to a strengthening of their anti-mask beliefs. Implications for improving mask adherence are discussed.

The need for high-throughput, precise, and meaningful methods for measuring behavior has been amplified by our recent successes in measuring and manipulating neural circuitry. The largest challenges associated with moving in this direction, however, are not technical but are instead conceptual: what numbers should one put on the movements an animal is performing (or not performing)? In this review, I will describe how theoretical and data analytical ideas are interfacing with recently-developed computational and experimental methodologies to answer these questions across a variety of contexts, length scales, and time scales. I will attempt to highlight commonalities between approaches and areas where further advances are necessary to place behavior on the same quantitative footing as other scientific fields.

The interaction of programmed cell death 1 ligand 1 (PDL1) with its receptor programmed cell death 1 (PD1) inhibits T cell responses, and blockade of this interaction has proven to be an effective immunotherapy for several different cancers. PDL1 can be expressed on the surface of tumour cells, immune cells and other cells in the tumour microenvironment but is also found in extracellular forms. Recent studies have explored the importance of different forms of extracellular PDL1, such as on exosomes or as a freely soluble protein, and have shown that PDL1-expressing exosomes can inhibit antitumour immune responses. In patients with melanoma, exosomal PDL1 is also a marker of immune activation early after initiation of therapy with PD1-blocking antibodies and predicts a clinical response to PD1 blockade. In this Progress article, we highlight recent insights into the role of exosomal PDL1 in immune oncology and how it may be useful as a biomarker for the management of cancer or to define a subset of patients who would benefit from therapeutics that block exosome production.Freeman and colleagues draw our attention to the existence of different forms of PDL1 — cell bound and various extracellular forms. Recent studies show that PDL1 on exosomes can inhibit antitumour immune responses and may be a useful biomarker for the management of cancer immunotherapy.

\"Cities are playing an ever more important role in the mitigation and adaption to climate change. This book examines the politics shaping whether, how and to what extent cities engage in global climate governance. By studying the C40 Cities Climate Leadership Group, and drawing on scholarship from international relations, social movements, global governance and field theory, the book introduces a theory of global urban governance fields. This theory links observed increases in city engagement and coordination to the convergence of C40 cities around particular ways of understanding and enforcing climate governance. The collective capacity of cities to produce effective and socially equitable global climate governance is also analysed. Highlighting the constraints facing city networks and the potential pitfalls associated with a city-driven global response, this assessment of the transformative potential of cities will be of great interest to researchers, graduate students and policymakers in global environmental politics and policy\"-- Provided by publisher.

Key Points Tumours actively inhibit the antitumour immune response. The programmed cell death protein 1–programmed cell death 1 ligand 1 (PD1–PDL1) pathway has a natural role in regulating peripheral tolerance and restraining over-exuberant immune responses. PDL1 is a critical dominant immunoinhibitor in many tumour types, leading to immune evasion by the tumour. PD1 pathway blockade unleashes a previously exhausted immune response that is focused on tumour neoantigens. Immunotherapies that increase the antitumour immune response, such as interleukin-2, or blockade of cytotoxic T lymphocyte antigen 4 (CTLA4), PD1 or PDL1 can benefit a moderate number of patients with cancer, with a durable clinical benefit in some. Many patients fail to develop tumour shrinkage when blocking only one immune checkpoint, and increasing response rates is a major and achievable goal. Given the tolerability and efficacy of PD1 pathway blockade in clinical trials it is a good foundation for combination therapies seeking to increase response rates. Once PD1 or CTLA4 are blocked, many other therapies can augment their efficacy, including blockade of other immunoinhibitory pathways, stimulation by activating pathways such as tumour necrosis factor receptor superfamily members, some chemotherapies, radiation, epigenetic modifiers, targeted therapies, angiogenesis blockade, augmentation of natural killer cell activity, chimeric antigen receptor T cell therapies, and vaccines. Therapeutics may work by blocking immunoinhibitory targets or stimulating immunoactivating targets not only on lymphocytes but also on macrophage, natural killer and stromal cells to overcome failure to respond to single checkpoint blockade. Anticancer immunotherapy through checkpoint blockade enables the patient to mount active antitumour responses and can dramatically improve survival. In this Review, Mahoney, Rennert and Freeman examine targets for next-generation immunomodulators and discuss how these may be integrated in rational combination therapies with existing and upcoming immune-targeted drugs. Targeting immune checkpoints such as programmed cell death protein 1 (PD1), programmed cell death 1 ligand 1 (PDL1) and cytotoxic T lymphocyte antigen 4 (CTLA4) has achieved noteworthy benefit in multiple cancers by blocking immunoinhibitory signals and enabling patients to produce an effective antitumour response. Inhibitors of CTLA4, PD1 or PDL1 administered as single agents have resulted in durable tumour regression in some patients, and combinations of PD1 and CTLA4 inhibitors may enhance antitumour benefit. Numerous additional immunomodulatory pathways as well as inhibitory factors expressed or secreted by myeloid and stromal cells in the tumour microenvironment are potential targets for synergizing with immune checkpoint blockade. Given the breadth of potential targets in the immune system, critical questions to address include which combinations should move forward in development and which patients will benefit from these treatments. This Review discusses the leading drug targets that are expressed on tumour cells and in the tumour microenvironment that allow enhancement of the antitumour immune response.

For several decades, understanding ageing and the processes that limit lifespan have challenged biologists. Thirty years ago, the biology of ageing gained unprecedented scientific credibility through the identification of gene variants that extend the lifespan of multicellular model organisms. Here we summarize the milestones that mark this scientific triumph, discuss different ageing pathways and processes, and suggest that ageing research is entering a new era that has unique medical, commercial and societal implications. We argue that this era marks an inflection point, not only in ageing research but also for all biological research that affects the human healthspan. The milestones that mark the advances in ageing research, the medical, commercial and societal implications of ageing and the different ageing pathways and processes that are associated with ageing are discussed.