Climate change poses significant threats to ecosystems, human health, and global stability. Despite international efforts to reduce greenhouse gas emissions, the Earth’s climate continues to warm, leading to extreme weather events, rising sea levels, and other detrimental impacts. In response to this crisis, scientists have begun exploring various strategies to mitigate climate change through geoengineering, which involves deliberate interventions in the Earth’s climate system. This article provides an overview of climate geoengineering research, focusing on key techniques, challenges, and ethical considerations, including actions being taken by the American Geophysical Union (AGU), a nonprofit professional scientific society, to develop an ethical framework to help guide research in this important area. AGU also is driving global engagement on this topic, including with leaders and members of faith communities.

Abstract The article proposes a novel model for ArtScience collaborations that is based on more equal roles. With better power balance, artists and scientists can together create projects that truly synthesize their fields. Additionally, it is suggested that these collaborations can significantly contribute to social change through socially engaged research. The article focuses on the transformative potential of the collaboration process itself. The presented case study is the authors’ collaboration in creating hybrids of participatory performance art and social psychology experiments. It contributes new methodological approaches to the expanding field of ArtScience collaborations.

The first descriptions of "non-specific" killing of tumor cells by lymphocytes were reported in 1973, and subsequently, the mediators of the activity were named "natural killer" (NK) cells by Rolf Kiessling and colleagues at the Karolinska Institute in 1975. The activity was detected in mice, rats, and humans that had no prior exposure to the tumors, major histocompatibility complex (MHC) antigen matching of the effectors and tumor cells was not required, and the cells responsible were distinct from MHC-restricted, antigen-specific T cells. In the ensuing five decades, research by many labs has extended knowledge of NK cells beyond an in vitro curiosity to demonstrate their in vivo relevance in host defense against tumors and microbial pathogens and their role in regulation of the immune system. This brief Perspective highlights a timeline of a few selected advancements in NK cell biology from a personal perspective of being involved in this quest.

The causal role of high-density lipoprotein (HDL) in atherosclerotic cardiovascular disease (CVD) remains debated. Considering recent evidence, the purpose of this review is to a provide a focused update and new perspectives on HDL and CVD. A Mendelian randomization study demonstrated an increased risk of CVD when HDL-cholesterol was predominantly transported in larger HDL particles and a decreased risk of CVD when HDL-cholesterol was predominantly transported in smaller HDL particles. Moreover, another Mendelian randomization study demonstrated that concentration and content of medium HDL particles is associated with CVD. A Mendelian randomization study that utilized stratified analyses demonstrated that individuals with HDL-cholesterol 50 mg/dl or less were at increased risk of CVD. Lastly, the AEGIS-II trial demonstrated that CSL112, a human apolipoprotein A-I that increases cholesterol efflux, did not significantly reduce cardiovascular events in patients at very high risk. Exploratory analyses showed that patients treated with CSL112 had numerically lower rates of cardiovascular events. Qualitative markers of HDL may be causally related to CVD. There is a need for ongoing research into HDL therapeutics that promote the biological properties of HDL. The optimal cohort or disease state that will benefit from these therapies needs to be identified.

Abstract This paper delineates the authors’ practice-based findings from The Algorithmic Pedestal exhibit, a practice-based research project examining the impact of algorithmic curation on visual ecology. Instagram, a platform that deploys algorithmic recommendations to select and display artworks, was instructed to choose a set of images from the Metropolitan Museum of Art’s collection to display. Fabienne Hess, a London-based artist, also chose images to display from the same collection. This article reflects on the process of producing an exhibit with curatorial inputs from both a machine and a human. It also shares and describes the selected images for the first time.

This study examined the impact of cannabis use disorder (CUD) on inpatient morbidity, length of stay (LOS), and inpatient cost (IC) of patients undergoing urologic oncologic surgery. The National Inpatient Sample (NIS) from 2003 to 2014 was analyzed for patients undergoing prostatectomy, nephrectomy, or cystectomy (n = 1,612,743). CUD was identified using ICD-9 codes. Complex-survey procedures were used to compare patients with and without CUD. Inpatient major complications, high LOS (4th quartile), and high IC (4th quartile) were examined as endpoints. Univariable and multivariable analysis (MVA) were performed to compare groups. The incidence of CUD increased from 51 per 100,000 admissions in 2003 to 383 per 100,000 in 2014 (p < 0.001). Overall, 3,503 admissions had CUD. Patients with CUD were more frequently younger (50 vs. 61), male (86% vs. 78.4%), Black (21.7% vs. 9.2%), and had 1st quartile income (36.1% vs. 20.6%); all p < 0.001. CUD had no impact on any complication rates (all p > 0.05). However, CUD patients had higher LOS (3 vs. 2days; p < 0.001) and IC ($15,609 vs. $12,415; p < 0.001). On MVA, CUD was not an independent predictor of major complications (p = 0.6). Conversely, CUD was associated with high LOS (odds ratio (OR) 1.31; 95% CI 1.08-1.59) and high IC (OR 1.33; 95% CI 1.12-1.59), both p < 0.01. The incidence of CUD at the time of urologic oncologic surgery is increasing. Future research should look into the cause of our observed phenomena and how to decrease LOS and IC in CUD patients.

Acute myeloid leukemia (AML) is a genetically diverse and challenging malignancy, with mutations in the FLT3 gene being particularly common and deleterious. Gilteritinib, a potent FLT3 inhibitor, has been approved by the U.S. Food and Drug Administration (FDA) for the treatment of relapsed/refractory AML with FLT3 mutations. Although gilteritinib was developed based on its inhibitory activity against FLT3 kinase, it is important to understand the precise mechanisms of its antileukemic activity in managing drug resistance and discovering biomarkers. This study was designed to elucidate the effect of gilteritinib on the FLT3 expression level. The results showed that gilteritinib induced a dose-dependent decrease in both FLT3 phosphorylation and expression. This reduction was particularly pronounced after 48 h of treatment. The decrease in FLT3 expression was found to be independent of changes in FLT3 mRNA transcription, suggesting post-transcriptional regulatory mechanisms. Further studies were performed in various AML cell lines and cells with both FLT3 wild-type and FLT3 mutant exhibited FLT3 reduction by gilteritinib treatment. In addition, other FLT3 inhibitors were evaluated for their ability to reduce FLT3 expression. Other FLT3 inhibitors, midostaurin, crenolanib, and quizartinib, also reduced FLT3 expression, consistent with the effect of gilteritinib. These findings hold great promise for optimizing gilteritinib treatment in AML patients. However, it is important to recognize that further research is warranted to gain a full understanding of these mechanisms and their clinical implications in the context of FLT3 reduction.

The role of Emergency Medical Services (EMS) is changing globally as ambulance crews respond to a shifting burden of disease as well as societal stressors such as violence and inequality. New ways of thinking about how to provide emergency care are required to shift EMS from a role primarily focused on clinical care and transporting patients to hospital. In this paper, we present the experience of the Philippi Project (PP), an innovative community-based model of care developed by front-line ambulance crews in a low-income neighborhood in Cape Town, South Africa. Our insights were developed through observational, interview and document review work, within an overall embedded research approach. Our analysis draws on the Everyday Health Systems Resilience framework, which sees resilience as an emergent process that may be stimulated through response to stress and shock. Responses take the form of absorptive, adaptive or transformative strategies and are underpinned by system capacities (cognitive, behavioral and contextual). We consider the PP as a potentially transformative resilience strategy, defined as a new way of working that offered the promise of long-term health system gains. We found that the PP's initial development was supported by a range of system capacity attributes (such as the intentional development of relationships, a sense of collective purpose, and creating spaces for constructive sensemaking). However, the PP was hard to sustain over time because emergent ways of working were undermined both by other capacity attributes rooted in pre-existing organizational routines, and two contextual shocks (Covid-19 and a violent incident). The paper adds a new empirical contribution to the still-small EHSR literature. In addition, the PP experience offers globally relevant lessons for developing community-based models of EMS care. It demonstrates that frontline staff can develop creative solutions to their stressful daily realities, but only if space is created and protected.

The extracellular matrix (ECM) is an abundant noncellular component of most solid tumors known to support tumor progression and metastasis. The interplay between the ECM and cancer therapeutics opens up new avenues in understanding cancer biology. While the ECM is known to protect the tumor from anticancer agents by serving as a biomechanical barrier, emerging studies show that various cancer therapies induce ECM remodeling, resulting in therapy resistance and tumor progression. This review discusses critical issues in this field including how the ECM influences treatment outcome, how cancer therapies affect ECM remodeling, and the challenges associated with targeting the ECM. Significance: The intricate relationship between the extracellular matrix (ECM) and cancer therapeutics reveals novel insights into tumor biology and its effective treatment. While the ECM may protect tumors from anti-cancer agents, recent research highlights the paradoxical role of therapy-induced ECM remodeling in promoting treatment resistance and tumor progression. This review explores the key aspects of the interplay between ECM and cancer therapeutics.