A Heat Emergency: Urban Heat Exposure and Access to Refuge in Richmond, VA.

The urban heat island effect exacerbates independent climate change-induced shifts toward longer, stronger, and more frequent heat extremes. Environmental inequity, driven by a history of racially motivated urban planning policies, has led particular demographics to bear the worst impacts of urban heat exposure and thus also climate change. These impacts cause adverse health outcomes in the form of heat emergencies. Through a novel demographic and spatial analysis of heat-related illness Emergency Medical Services data from Richmond, Virginia, this study investigates the relationships between heat health emergencies and intra-urban heat islands quantified through three heat exposure metrics. We also evaluate the accessibility of built refuge from urban heat in the form of public transit infrastructure, libraries, and government cooling centers in relation to these emergencies. We found that heat emergencies are inequitably distributed among racial, age, and socioeconomic groups in Richmond, particularly among residents identified as Male, Black or African American, 50+ years old, and experiencing mental health, intoxication, and/or homelessness. We found significant associations between the location of these heat emergencies and urban heat islands as estimated from remotely-sensed surface and community science-derived air temperature metrics, but not a co-estimated heat index. We also found that available refuge facilities are insufficiently located to protect individuals with reduced mobility across areas with the highest number of heat-related health emergencies. Community involvement in the mitigation and management of extreme heat threats, especially for those disproportionately impacted, is necessary to decrease the number of summertime heat illnesses.

Episodic Past, Future, and counterfactual thinking in Relapsing-Remitting Multiple sclerosis.

Multiple sclerosis (MS) is a progressive disease characterized by widespread white matter lesions in the brain and spinal cord. In addition to well-characterized motor deficits, MS results in cognitive impairments in several domains, notably in episodic autobiographical memory. Recent studies have also revealed that patients with MS exhibit deficits in episodic future thinking, i.e., our capacity to imagine possible events that may occur in our personal future. Both episodic memory and episodic future thinking have been shown to share cognitive and neural mechanisms with a related kind of hypothetical simulation known as episodic counterfactual thinking: our capacity to imagine alternative ways in which past personal events could have occurred but did not. However, the extent to which episodic counterfactual thinking is affected in MS is still unknown. The current study sought to explore this issue by comparing performance in mental simulation tasks involving either past, future or counterfactual thoughts in relapsing-remitting MS. Diffusion weighted imaging (DWI) measures were also extracted to determine whether changes in structural pathways connecting the brain's default mode network (DMN) would be associated with group differences in task performance. Relative to controls, patients showed marked reductions in the number of internal details across all mental simulations, but no differences in the number of external and semantic-based details. It was also found that, relative to controls, patients with relapsing-remitting MS reported reduced composition ratings for episodic simulations depicting counterfactual events, but not so for actual past or possible future episodes. Additionally, three DWI measures of white matter integrity-fractional anisotropy, radial diffusivity and streamline counts-showed reliable differences between patients with relapsing-remitting MS and matched healthy controls. Importantly, DWI measures associated with reduced white matter integrity in three association tracts on the DMN-the right superior longitudinal fasciculus, the left hippocampal portion of the cingulum and the left inferior longitudinal fasciculus-predicted reductions in the number of internal details during episodic counterfactual simulations. Taken together, these results help to illuminate impairments in episodic simulation in relapsing-remitting MS and show, for the first time, a differential association between white matter integrity and deficits in episodic counterfactual thinking in individuals with relapsing-remitting MS.

Cyclophilin inhibitor NIM811 ameliorates experimental allergic encephalomyelitis.

Cyclophilins have diverse functions that may affect the course of central nervous system (CNS) inflammatory disorders. Anti-inflammatory and neuroprotective mechanisms may be targeted by inhibition of cyclophilin A-dependent and cyclophilin D-dependent functions, respectively. We tested the effect of cyclophilin inhibition on CNS inflammation by administering N-methyl-4-isoleucine-cyclosporin (NIM811) to mice undergoing experimental allergic encephalomyelitis (EAE). Treatment with NIM811 resulted in significant reduction of EAE clinical severity. Analysis of mitochondrial calcium retention capacity and the course of EAE in cyclophilin D knockout mice indicated that the effect of NIM811 on EAE was not entirely cyclophilin D-dependent. NIM811-treated EAE animals showed reduction in interleukin-2 expression and reduction in CNS inflammatory infiltrates. These results indicate that anti-inflammatory rather than neuroprotective mechanisms associated with cyclophilins are likely involved in the mechanism of NIM811 in EAE.