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Wildfire and the threat it poses to society represents an example of the complex, dynamic relationship between social and ecological systems. Increasingly, wildfire adaptation is posited as a pathway to shift the approach to fire from a suppression paradigm that seeks to control fire to a paradigm that focuses on “living with” and “adapting to” wildfire. In this study, we seek insights into what it means to adapt to wildfire from a range of stakeholders whose efforts contribute to the management of wildfire. Study participants provided insights into the meaning, relevance, and use of the concept of fire adaptation as it relates to their wildfire-related activities. A key finding of this investigation suggests that social scale is of key importance in the conceptualization and understanding of adaptation for participating stakeholders. Indeed, where you stand in terms of understandings of fire adaptation depends in large part on where you sit.

The purpose of this study was to test the hypothesis that higher levels of systemic inflammation in a community sample of non-demented subjects older than seventy years of age are associated with reduced diffusion anisotropy in brain white matter and lower cognition. Ninety-five older persons without dementia underwent detailed clinical and cognitive evaluation and magnetic resonance imaging, including diffusion tensor imaging. Systemic inflammation was assessed with a composite measure of commonly used circulating inflammatory markers (C-reactive protein and tumor necrosis factor-alpha). Tract-based spatial statistics analyses demonstrated that diffusion anisotropy in the body and isthmus of the corpus callosum was negatively correlated with the composite measure of systemic inflammation, controlling for demographic, clinical and radiologic factors. Visuospatial ability was negatively correlated with systemic inflammation, and diffusion anisotropy in the body and isthmus of the corpus callosum was shown to mediate this association. The findings of the present study suggest that higher levels of systemic inflammation may be associated with lower microstructural integrity in the corpus callosum of non-demented elderly individuals, and this may partially explain the finding of reduced higher-order visual cognition in aging.

Parcel-level risk (PLR) describes how wildfire risk varies from home to home based on characteristics that relate to likely fire behavior, the susceptibility of homes to fire, and the ability of firefighters to safely access properties. Here, we describe the WiRē Rapid Assessment (RA), a parcel-level rapid wildfire risk assessment tool designed to evaluate PLR with a small set of measures for all homes in a community. We investigate the relationship between 2019 WiRē RA data collected in the Columbine Lake community in Grand County, Colorado, and whether assessed homes were destroyed in the 2020 East Troublesome Fire. We find that the overall parcel-level risk scores, as well as many individual attributes, relate to the chance that a home was destroyed. We also find strong evidence of risk spillovers across neighboring properties. The results demonstrate that even coarsely measured RA data capture meaningful differences in wildfire risk across a community. The findings also demonstrate the importance of accounting for multiple aspects of PLR, including both hazards and susceptibility, when assessing the risk of wildfire to homes and communities. Finally, the results underscore that relatively small actions by residents before a fire can influence wildfire outcomes.

The objective of this work was to test the hypotheses that a) more frequent cognitive activity in late life is associated with higher brain diffusion anisotropy and lower trace of the diffusion tensor, and b) brain diffusion characteristics partially mediate the association of late life cognitive activity with cognition. As part of a longitudinal cohort study, 379 older people without dementia rated their frequency of participation in cognitive activities, completed a battery of cognitive function tests, and underwent diffusion tensor imaging. We used tract-based spatial statistics to test the association between late life cognitive activity and brain diffusion characteristics. Clusters with statistically significant findings defined regions of interest in which we tested the hypothesis that diffusion characteristics partially mediate the association of late life cognitive activity with cognition. More frequent cognitive activity in late life was associated with higher level of global cognition after adjustment for age, sex, education, and indicators of early life cognitive enrichment ( p  = 0.001). More frequent cognitive activity was also related to higher fractional anisotropy in the left superior and inferior longitudinal fasciculi, left fornix, and corpus callosum, and lower trace in the thalamus ( p  < 0.05, FWE-corrected). After controlling for fractional anisotropy or trace from these regions, the regression coefficient for the association of late life cognitive activity with cognition was reduced by as much as 26 %. These findings suggest that the association of late life cognitive activity with cognition may be partially mediated by brain diffusion characteristics.

Often, factors that determine the risk of an environmental hazard occur at landscape scales, and risk mitigation requires action by multiple private property owners. How property owners respond to risk mitigation on neighboring lands depends on whether mitigation actions are strategic complements or strategic substitutes. We test for these neighbor interactions with a case study on wildfire risk mitigation on private properties. We use two measures of wildfire risk mitigation—an assessment by a wildfire professional and a self-assessment by homeowners. Taken together, the two assessments provide the first empirical explanation for strategic complements in wildfire risk mitigation and a more complete picture of how homeowners respond to this landscape-scale risk. We find homeowners that mitigate risk on their land are more likely to have neighbors that do the same, and homeowners that fail to mitigate risk are more likely to have neighbors that fail to do so as well. Due to spatial spillovers, motivating a few key residents to take action could reduce risk across the landscape.

Private landowners are important actors in landscape-level wildfire risk management. Accordingly, wildfire programs and policy encourage wildland–urban interface homeowners to engage with local organizations to properly mitigate wildfire risk on their parcels. We investigate whether parcel-level wildfire risk assessment data, commonly used to inform community-level planning and resource allocation, can be used to “nudge” homeowners to engage further with a regional wildfire organization. We sent 4564 households in western Colorado a letter that included varying combinations of risk information about their community, their parcels, and their neighbors’ parcels, and we measured follow-up visits to a personalized “Web site”. We find that the effect of providing parcel-specific information depends on baseline conditions: Informing homeowners about their property’s wildfire risk increases information-seeking among homeowners of the highest-risk parcels by about 5 percentage points and reduces information-seeking among homeowners of lower-risk parcels by about 6 percentage points. Parcel-specific information also increases the overall response in the lowest risk communities by more than 10 percentage points. Further, we find evidence of a 6-percentage point increase in response rate associated with receiving a social comparison treatment that signals neighboring properties as being either low or moderate risk on average. These results, especially considered against the 13 percent overall average response rate, offer causal evidence that providing parcel-specific wildfire risk information can influence behavior. As such, we demonstrate the effectiveness of simple outreach in engaging wildland–urban interface homeowners with wildfire risk professionals in ways that leverage existing data.

Wildland–urban interface (WUI) homeowners who do not mitigate the wildfire risk on their properties impose a negative externality on society. To reduce the social costs of wildfire and incentivise homeowners to take action, cost sharing programs seek to reduce the barriers that impede wildfire risk mitigation. Using survey data from a WUI community in western Colorado and a two-stage decision framework, we examine residents’ willingness to participate in a cost sharing program for removing vegetation on their properties and the amount they are willing to contribute to the cost of that removal. We find that different factors motivate decisions about participation and about how much to pay. Willingness to participate correlates with both financial and non-monetary considerations, including informational barriers and wildfire risk perceptions, but not with concerns about effectiveness or visual impacts. Residents of properties with higher wildfire risk levels are less likely to participate in the cost sharing than those with lower levels of wildfire risk. We find widespread, positive willingness to pay for vegetation removal, with the amount associated negatively with property size and positively with respondent income. These results can inform the development of cost sharing programs to encourage wildfire risk mitigation on private property.

Acidity, defined as pH, is a central component of aqueous chemistry. In the atmosphere, the acidity of condensed phases (aerosol particles, cloud water, and fog droplets) governs the phase partitioning of semivolatile gases such as HNO3, NH3, HCl, and organic acids and bases as well as chemical reaction rates. It has implications for the atmospheric lifetime of pollutants, deposition, and human health. Despite its fundamental role in atmospheric processes, only recently has this field seen a growth in the number of studies on particle acidity. Even with this growth, many fine-particle pH estimates must be based on thermodynamic model calculations since no operational techniques exist for direct measurements. Current information indicates acidic fine particles are ubiquitous, but observationally constrained pH estimates are limited in spatial and temporal coverage. Clouds and fogs are also generally acidic, but to a lesser degree than particles, and have a range of pH that is quite sensitive to anthropogenic emissions of sulfur and nitrogen oxides, as well as ambient ammonia. Historical measurements indicate that cloud and fog droplet pH has changed in recent decades in response to controls on anthropogenic emissions, while the limited trend data for aerosol particles indicate acidity may be relatively constant due to the semivolatile nature of the key acids and bases and buffering in particles. This paper reviews and synthesizes the current state of knowledge on the acidity of atmospheric condensed phases, specifically particles and cloud droplets. It includes recommendations for estimating acidity and pH, standard nomenclature, a synthesis of current pH estimates based on observations, and new model calculations on the local and global scale.

Background Converging evidence suggests a role for microglia-mediated neuroinflammation in Parkinson’s disease (PD). Animal models of PD can serve as a platform to investigate the role of neuroinflammation in degeneration in PD. However, due to features of the previously available PD models, interpretations of the role of neuroinflammation as a contributor to or a consequence of neurodegeneration have remained elusive. In the present study, we investigated the temporal relationship of neuroinflammation in a model of synucleinopathy following intrastriatal injection of pre-formed alpha-synuclein fibrils (α-syn PFFS). Methods Male Fischer 344 rats ( N  = 114) received unilateral intrastriatal injections of α-syn PFFs, PBS, or rat serum albumin with cohorts euthanized at monthly intervals up to 6 months. Quantification of dopamine neurons, total neurons, phosphorylated α-syn (pS129) aggregates, major histocompatibility complex-II (MHC-II) antigen-presenting microglia, and ionized calcium-binding adaptor molecule-1 (Iba-1) immunoreactive microglial soma size was performed in the substantia nigra. In addition, the cortex and striatum were also examined for the presence of pS129 aggregates and MHC-II antigen-presenting microglia to compare the temporal patterns of pSyn accumulation and reactive microgliosis. Results Intrastriatal injection of α-syn PFFs to rats resulted in widespread accumulation of phosphorylated α-syn inclusions in several areas that innervate the striatum followed by significant loss (~ 35%) of substantia nigra pars compacta dopamine neurons within 5–6 months. The peak magnitudes of α-syn inclusion formation, MHC-II expression, and reactive microglial morphology were all observed in the SN 2 months following injection and 3 months prior to nigral dopamine neuron loss. Surprisingly, MHC-II immunoreactivity in α-syn PFF injected rats was relatively limited during the later interval of degeneration. Moreover, we observed a significant correlation between substantia nigra pSyn inclusion load and number of microglia expressing MHC-II. In addition, we observed a similar relationship between α-syn inclusion load and number of microglia expressing MHC-II in cortical regions, but not in the striatum. Conclusions Our results demonstrate that increases in microglia displaying a reactive morphology and MHC-II expression occur in the substantia nigra in close association with peak numbers of pSyn inclusions, months prior to nigral dopamine neuron degeneration, and suggest that reactive microglia may contribute to vulnerability of SNc neurons to degeneration. The rat α-syn PFF model provides an opportunity to examine the innate immune response to accumulation of pathological α-syn in the context of normal levels of endogenous α-syn and provides insight into the earliest neuroinflammatory events in PD.

Background: Biomarkers for predicting response to immune checkpoint inhibitors (ICI) are scarce and often lack external validation. This study provides a comprehensive investigation of pretreatment C-reactive protein (CRP) levels as well as its longitudinal trajectories as a marker of treatment response and disease outcome in patients with advanced non-small cell lung cancer (NSCLC) undergoing immunotherapy with anti PD-1 or anti PD-L1 agents. Methods: We performed a retrospective bi-center study to assess the association between baseline CRP levels and anti PD-(L)1 treatment outcomes in the discovery cohort (n = 90), confirm these findings in an external validation cohort (n = 101) and explore the longitudinal evolution of CRP during anti PD-(L)1 treatment and the potential impact of dynamic CRP changes on treatment response and disease outcome in the discovery cohort. Joint models were implemented to evaluate the association of longitudinal CRP trajectories and progression risk. Primary treatment outcomes were progression-free survival (PFS) and overall survival (OS), while the objective response rate (ORR) was a secondary outcome, respectively. Results: In the discovery cohort, elevated pretreatment CRP levels emerged as independent predictors of worse PFS (HR per doubling of baseline CRP = 1.37, 95% CI: 1.16–1.63, p < 0.0001), worse OS (HR per doubling of baseline CRP = 1.42, 95% CI: 1.18–1.71, p < 0.0001) and a lower ORR ((odds ratio (OR) of ORR per doubling of baseline CRP = 0.68, 95% CI: 0.51–0.92, p = 0.013)). In the validation cohort, pretreatment CRP could be fully confirmed as a predictor of PFS and OS, but not ORR. Elevated trajectories of CRP during anti PD-(L)1 treatment (adjusted HR per 10 mg/L increase in CRP = 1.22, 95% CI: 1.15–1.30, p < 0.0001), as well as a faster increases of CRP over time (HR per 10 mg/L/month faster increase in CRP levels = 13.26, 95% CI: 1.14–154.54, p = 0.039) were strong predictors of an elevated progression risk, whereas an early decline of CRP was significantly associated with a reduction in PFS risk (HR = 0.91, 95% CI: 0.83–0.99, p = 0.036), respectively. Conclusion: These findings support the concept that CRP should be further explored by future prospective studies as a simple non-invasive biomarker for assessing treatment benefit during anti PD-(L)1 treatment in advanced NSCLC.