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As populations worldwide show increasing levels of stress, understanding emerging links among stress, inflammation, cognition, and behavior is vital to human and planetary health. We hypothesize that inflammation is a multiscale driver connecting stressors that affect individuals to large-scale societal dysfunction and, ultimately, to planetary-scale environmental impacts. We propose a “central inflammation map” hypothesis to explain how the brain regulates inflammation and how inflammation impairs cognition, emotion, and action. According to our hypothesis, these interdependent inflammatory and neural processes, and the inter-individual transmission of environmental, infectious, and behavioral stressors—amplified via high-throughput digital global communications—can culminate in a multiscale, runaway, feed-forward process that could detrimentally affect human decision-making and behavior at scale, ultimately impairing the ability to address these same stressors. This perspective could provide non-intuitive explanations for behaviors and relationships among cells, organisms, and communities of organisms, potentially including population-level responses to stressors as diverse as global climate change, conflicts, and the COVID-19 pandemic. To illustrate our hypothesis and elucidate its mechanistic underpinnings, we present a mathematical model applicable to the individual and societal levels to test the links among stress, inflammation, control, and healing, including the implications of transmission, intervention (e.g., via lifestyle modification or medication), and resilience. Future research is needed to validate the model’s assumptions and conclusions against empirical benchmarks and to expand the factors/variables employed. Our model illustrates the need for multilayered, multiscale stress mitigation interventions, including lifestyle measures, precision therapeutics, and human ecosystem design. Our analysis shows the need for a coordinated, interdisciplinary, international research effort to understand the multiscale nature of stress. Doing so would inform the creation of interventions that improve individuals’ lives; enhance communities’ resilience to stress; and mitigate the adverse effects of stress on the world. 

Stress is a feeling of being worried, scared, or overwhelmed, caused by challenging situations or big life changes. Not all stress is bad, and some kinds of stress, like exercise, can even be good for us. However, when stress is severe or lasts a long time, it can harm our health. Severe stress causes inflammation, which is the body’s way of protecting itself. Inflammation helps the body heal, but long-lasting inflammation can lead to health problems. Stress can also affect the brain, making it hard to think clearly or make good decisions. In our work, we linked all these stress-related factors together (using math) to explain our hypothesis that stress can spread from person to person through our actions, words, and body language—and even over social media—until it affects whole societies and eventually the entire planet! This is a dangerous cycle that can lead to evenmorestress and inflammation, making problems worse. To break the cycle, we each need to focus on reducing stress in our own lives. 

Reliance on water production by desalination as a solution to water scarcity is growing worldwide. High energy demands of seawater desalination raise new challenges for both water and energy management and highlight the importance of understanding the operational dependencies of the water sector on energy supplies. This study provides an in-depth analysis of the impact of the water-energy nexus in a desalination-based water sector, using Israel as a case study. Being large energy consumers, desalination plants are part of the Electricity Load Shedding Program (ELSP), which government energy regulators invoke in times of energy shortage. We focus on the interdependency between the two sectors as manifested at the time of ELSP utilization during an extreme heat wave. We show that energy shedding compensation is 6 to 14 times greater than the economic loss to the desalination plant from no water production, creating an obvious economic incentive to participate in ELSPs. However, this imbalance has a substantial negative impact on the water sector, which may compromise the level of service. Our evaluation concludes that the government authorities regulating water and energy need an official mechanism and policy for joint management strategies that can ensure economic efficiency and reduce the risk of power and water shortages during extreme events. 

ABSTRACT Measurements of the optical turbulence profile are critical for selecting a potential new solar observational site or for characterizing an existing solar observatory. To measure the turbulence distribution to a moderate altitude above an existing observatory, current techniques use a large facility telescope with an aperture size larger than 1.0 m. This limits their application, especially in surveys to find a new potential site where no large facility telescope is available and where a portable measurement device is needed for such measurements. To address the above issues, we propose a new technique, termed the Advanced Multiple Aperture Seeing Profiler (A-MASP), which uses solar granulation to measure the daytime optical turbulence profile. The A-MASP is a portable system and thus can fully address the fundamental limitation of current optical turbulence profile measurement techniques. The A-MASP consists of two small telescopes, each with an aperture of the order of 100 mm, which can measure the turbulence profile to an altitude up to 20 km. Here, we present our A-MASP development work and its initial on-site measurements at the Big Bear Solar Observatory. In a proof-of-concept experiment, it was successfully demonstrated that the A-MASP can reliably measure the turbulence profile up to 12 km with a vector separation of 0.7 m between the two telescopes. The A-MASP could be used for future surveys to find potentially good observational sites. 

Abstract Maternal reprogramming of histone methylation is critical for reestablishing totipotency in the zygote, but how histone-modifying enzymes are regulated during maternal reprogramming is not well characterized. To address this gap, we asked whether maternal reprogramming by the H3K4me1/2 demethylase SPR-5/LSD1/KDM1A, is regulated by the chromatin co-repressor protein, SPR-1/CoREST, in Caenorhabditis elegans and mice. In C. elegans, SPR-5 functions as part of a reprogramming switch together with the H3K9 methyltransferase MET-2. By examining germline development, fertility, and gene expression in double mutants between spr-1 and met-2, as well as fertility in double mutants between spr-1 and spr-5, we find that loss of SPR-1 results in a partial loss of SPR-5 maternal reprogramming function. In mice, we generated a separation of function Lsd1 M448V point mutation that compromises CoREST binding, but only slightly affects LSD1 demethylase activity. When maternal LSD1 in the oocyte is derived exclusively from this allele, the progeny phenocopy the increased perinatal lethality that we previously observed when LSD1 was reduced maternally. Together, these data are consistent with CoREST having a conserved function in facilitating maternal LSD1 epigenetic reprogramming. 

ABSTRACT Formation of a zygote is coupled with extensive epigenetic reprogramming to enable appropriate inheritance of histone methylation and prevent developmental delays. In Caenorhabditis elegans, this reprogramming is mediated by the H3K4me2 demethylase SPR-5 and the H3K9 methyltransferase, MET-2. In contrast, the H3K36 methyltransferase MES-4 maintains H3K36me2/3 at germline genes between generations to facilitate re-establishment of the germline. To determine whether the MES-4 germline inheritance pathway antagonizes spr-5; met-2 reprogramming, we examined the interaction between these two pathways. We found that the developmental delay of spr-5; met-2 mutant progeny is associated with ectopic H3K36me3 and the ectopic expression of MES-4-targeted germline genes in somatic tissues. Furthermore, the developmental delay is dependent upon MES-4 and the H3K4 methyltransferase, SET-2. We propose that MES-4 prevents crucial germline genes from being repressed by antagonizing maternal spr-5; met-2 reprogramming. Thus, the balance of inherited histone modifications is necessary to distinguish germline versus soma and prevent developmental delay. This article has an associated ‘The people behind the papers’ interview. 

In Caenorhabditis elegans, mutations in WDR-5 and other components of the COMPASS H3K4 methyltransferase complex extend lifespan and enable its inheritance. Here, we show that wdr-5 mutant longevity is itself a transgenerational trait that corresponds with a global enrichment of the heterochromatin factor H3K9me2 over twenty generations. In addition, we find that the transgenerational aspects of wdr-5 mutant longevity require the H3K9me2 methyltransferase MET-2, and can be recapitulated by removal of the putative H3K9me2 demethylase JHDM-1. Finally, we show that the transgenerational acquisition of longevity in jhdm-1 mutants is associated with accumulating genomic H3K9me2 that is inherited by their long-lived wild-type descendants at a subset of loci. These results suggest that heterochromatin facilitates the transgenerational establishment and inheritance of a complex trait. Based on these results, we propose that transcription-coupled H3K4me via COMPASS limits lifespan by encroaching upon domains of heterochromatin in the genome.