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The frequency and intensity of extreme climatic events such as heatwaves are predicted to increase under continued climate change and rising atmospheric CO2. Degraded and fragmented ecosystems are at particular risk of being greatly impacted by such extreme events. The longleaf pine (LLP) savanna ecosystem, once the dominant ecosystem throughout the Southeast Coastal Plains of the United States, has been reduced to a small percentage of its pre‐colonization range. While the effect of heatwaves on grassland systems has been well explored, less focus has been given to the legacy effects of previous climatic events. Through a greenhouse experiment using Schizachyrium scoparium (little bluestem), a dominant understory grass species in LLP savanna ecosystems, we aimed to study the legacy effects of heatwaves (i.e., higher temperatures and lower precipitation and humidity) across multiple plant performance metrics and stress responses. S. scoparium had a negative response to an early heatwave, showing increased mortality, smaller maximum leaf length, fewer leaves, decreased specific leaf area (SLA), decreased leaf thickness, and reduced belowground net primary productivity (NPP) when compared to plants that did not experience a heatwave. S. scoparium individuals exposed to a late heatwave had fewer leaves, reduced SLA, and thinner leaves when compared to plants that did not experience a heatwave. While plants exposed to both an early and late heatwave experienced an increase in some stress responses as observed by increased catalase activity and plant mortality, they exhibited no change in other stress responses studied (e.g., maximum leaf length, relative growth rate, productivity, leaf thickness, peroxidase levels, or fuel load). Overall, our study revealed that S. scoparium may show neutral‐to‐positive legacy effects in response to multiple heatwaves. This indicates that LLP savanna ecosystems dominated by S. scoparium may display resistance to the predicted increased frequency of heatwaves in the southeastern United States, an important outcome for the heavily degraded and endangered ecosystem.

Lesbian, gay, bisexual, transgender, and queer (LGBTQ) individuals face mental and physical health disparities. Fear of discrimination and organizational care incompetency promotes avoidance of care and nondisclosure of sexual orientation and gender identity. The purpose of this article is to evaluate the outcomes of cultural competency training for interprofessional staff to foster safe and inclusive LGBTQ cancer care and address this population's care needs. One-hour cultural competency training focused on assessing bias, increasing health knowledge, and creating a safe environment. Fifteen sessions trained 110 participants. Pre- and post-training surveys evaluated staff's LGBTQ health knowledge and cultural competency self-efficacy. Staff were significantly more likely to agree with the following statements post-training.

Autophagy is a highly conserved, intracellular recycling process by which cytoplasmic contents are degraded in the lysosome. This process occurs at a low level constitutively; however, it is induced robustly in response to stressors, in particular, starvation of critical nutrients such as amino acids and glucose. That said, the relative contribution of these inputs is ambiguous, and many starvation medias are poorly defined or devoid of multiple nutrients. Here, we set out to create a quantitative dataset of autophagy across multiple stages in single, living cells, measured under normal growth conditions and during nutrient starvation of amino acids or glucose. We found that autophagy is induced by starvation of amino acids, but not glucose, in U2OS cells, and that MTORC1-mediated ULK1 regulation and autophagy are tightly linked to amino acid levels. While autophagy is engaged immediately during amino acid starvation, a heightened response occurs during a period marked by transcriptional upregulation of autophagy genes during sustained starvation. Finally, we demonstrated that cells immediately return to their initial, low-autophagy state when nutrients are restored, highlighting the dynamic relationship between autophagy and environmental conditions.

Unusually warm conditions recently observed in the Pacific Arctic region included a dramatic loss of sea ice cover and an enhanced inflow of warmer Pacific-derived waters. Moored sediment traps deployed at three biological hotspots of the Distributed Biological Observatory (DBO) during this anomalously warm period collected sinking particles nearly continuously from June 2017 to July 2019 in the northern Bering Sea (DBO2) and in the southern Chukchi Sea (DBO3), and from August 2018 to July 2019 in the northern Chukchi Sea (DBO4). Fluxes of living algal cells, chlorophyll a (chl a ), total particulate matter (TPM), particulate organic carbon (POC), and zooplankton fecal pellets, along with zooplankton and meroplankton collected in the traps, were used to evaluate spatial and temporal variations in the development and composition of the phytoplankton and zooplankton communities in relation to sea ice cover and water temperature. The unprecedented sea ice loss of 2018 in the northern Bering Sea led to the export of a large bloom dominated by the exclusively pelagic diatoms Chaetoceros spp. at DBO2. Despite this intense bloom, early sea ice breakup resulted in shorter periods of enhanced chl a and diatom fluxes at all DBO sites, suggesting a weaker biological pump under reduced ice cover in the Pacific Arctic region, while the coincident increase or decrease in TPM and POC fluxes likely reflected variations in resuspension events. Meanwhile, the highest transport of warm Pacific waters during 2017–2018 led to a dominance of the small copepods Pseudocalanus at all sites. Whereas the export of ice-associated diatoms during 2019 suggested a return to more typical conditions in the northern Bering Sea, the impact on copepods persisted under the continuously enhanced transport of warm Pacific waters. Regardless, the biological pump remained strong on the shallow Pacific Arctic shelves.

Aim Community engagement plays a crucial role in preventing and managing Aedes -borne mosquito disease outbreaks, such as dengue. There is limited research on the engagement approaches used in high-income country contexts with existing research suggesting a preference for top-down vector control relying on one-way communication to engage and mobilize at-risk communities. The reasons behind why authorities use certain engagement approaches over others are underexplored. This study explores the community engagement approaches used in Aedes mosquito management in Townsville, Australia, and the factors influencing the choice of these approaches. Methods The study used a case study design employing two qualitative methodologies: semi-structured key informant interviews ( N  = 15) and a review of key documents ( N  = 13). Both inductive and deductive approaches were used to thematically analyse the data. Results A range of approaches were used to engage the community in Aedes mosquito management. From mass media campaigns and door-to-door inspections, to engaging the community in Wolbachia mosquito-releases, and helping authorities with indoor spraying during outbreak response. The factors influencing the choice of these approaches included legal obligations and regulatory compliance, vector control norms, leadership beliefs, human and financial resourcing. Conclusions This study provides new insights into why authorities adopt specific community engagement approaches in Aedes mosquito management, within a high-income country context. It identifies barriers to enhancing community engagement and suggests strategies for addressing them in future planning. These findings are particularly relevant given the increasing Aedes mosquito risk in similar high-income country settings.

Inhibitory extracellular matrices form around mature neurons as perineuronal nets containing chondroitin sulfate proteoglycans that limit axonal sprouting after CNS injury. The enzyme chondroitinase (Chase) degrades inhibitory chondroitin sulfate proteoglycans and improves axonal sprouting and functional recovery after spinal cord injury in rodents. We evaluated the effects of Chase in rhesus monkeys that had undergone C7 spinal cord hemisection. Four weeks after hemisection, we administered multiple intraparenchymal Chase injections below the lesion, targeting spinal cord circuits that control hand function. Hand function improved significantly in Chase-treated monkeys relative to vehicle-injected controls. Moreover, Chase significantly increased corticospinal axon growth and the number of synapses formed by corticospinal terminals in gray matter caudal to the lesion. No detrimental effects were detected. This approach appears to merit clinical translation in spinal cord injury.

In a nonhuman primate model of spinal cord injury, human neural progenitor cell grafts exhibit long-term survival, differentiation, and anatomical integration with host spinal circuitry. We grafted human spinal cord–derived neural progenitor cells (NPCs) into sites of cervical spinal cord injury in rhesus monkeys ( Macaca mulatta ). Under three-drug immunosuppression, grafts survived at least 9 months postinjury and expressed both neuronal and glial markers. Monkey axons regenerated into grafts and formed synapses. Hundreds of thousands of human axons extended out from grafts through monkey white matter and synapsed in distal gray matter. Grafts gradually matured over 9 months and improved forelimb function beginning several months after grafting. These findings in a 'preclinical trial' support translation of NPC graft therapy to humans with the objective of reconstituting both a neuronal and glial milieu in the site of spinal cord injury.

Background Aedes -borne disease risk is increasing in tropical and sub-tropical regions across the globe. While Aedes -borne disease continues to disproportionally affect low- and middle-income countries, parts of high-income countries, such as the Torres Strait region in Australia are also at risk. The Torres Strait is a group of islands located between Cape York Peninsula in far north Queensland, Australia and Papua New Guinea. The Torres Strait has both Aedes albopictus and Aedes aegypti and is close to Papua New Guinea where dengue fever is endemic. Managing Aedes-borne disease risk requires a range of strategies, including community participation. Existing research shows that high-income countries tend to favour government-led (top-down) informing approaches when engaging communities in Aedes mosquito management. Little is known about the factors that influence the choice of community participation approaches in Aedes mosquito management particularly in a high-income country setting, such as Australia. This research contributes to filling this knowledge gap by exploring the community participation approaches used in Aedes mosquito management and the factors influencing these choices in the Torres Strait. Methods 16 semi-structured interviews were conducted with local government and state government agencies working in Aedes mosquito management in the Torres Strait. Six key mosquito management plans and policies were also reviewed. Thematic analysis was used to identify, analyse and attribute meaning from the data collected. Results A range of community participation approaches were used within the two main Aedes mosquito management programs ( Aedes albopictus Elimination Program and the Torres Strait Island Regional Council, Environmental Health Program) in the Torres Strait. These approaches included door-to-door inspections, awareness raising strategies, and community clean-up events. Approaches were chosen for reasons related to regulations, attitude and beliefs, and resourcing. Conclusions This study revealed the use of both top-down and bottom-up approaches to engaging the community in Aedes mosquito management in the Torres Strait. These findings contribute to a better understanding of why bottom-up approaches are used, which is valuable for shaping future policy decisions. This study also provides suggestions on ways to enhance community participation in the Torres Strait, which could also be considered in other similar tropical regions.

Huntington’s disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in exon 1 of the HTT gene. HD usually manifests in mid-life with loss of GABAergic projection neurons from the striatum accompanied by progressive atrophy of the putamen followed by other brain regions, but linkages between the genetics and neurodegeneration are not understood. We measured metabolic perturbations in HD-human brain in a case-control study, identifying pervasive lowering of vitamin B5, the obligatory precursor of coenzyme A (CoA) that is essential for normal intermediary metabolism. Cerebral pantothenate deficiency is a newly-identified metabolic defect in human HD that could potentially: (i) impair neuronal CoA biosynthesis; (ii) stimulate polyol-pathway activity; (iii) impair glycolysis and tricarboxylic acid cycle activity; and (iv) modify brain-urea metabolism. Pantothenate deficiency could lead to neurodegeneration/dementia in HD that might be preventable by treatment with vitamin B5.

NEK7 is a serine-threonine kinase linked to mitosis. Beutler and colleagues show that NEK7 is required for assembly of the NLRP3 inflammasome and restricts NLRP3 activation to interphase of the cell cycle. The NLRP3 inflammasome responds to microbes and danger signals by processing and activating proinflammatory cytokines, including interleukin 1β (IL-1β) and IL-18. We found here that activation of the NLRP3 inflammasome was restricted to interphase of the cell cycle by NEK7, a serine-threonine kinase previously linked to mitosis. Activation of the NLRP3 inflammasome required NEK7, which bound to the leucine-rich repeat domain of NLRP3 in a kinase-independent manner downstream of the induction of mitochondrial reactive oxygen species (ROS). This interaction was necessary for the formation of a complex containing NLRP3 and the adaptor ASC, oligomerization of ASC and activation of caspase-1. NEK7 promoted the NLRP3-dependent cellular inflammatory response to intraperitoneal challenge with monosodium urate and the development of experimental autoimmune encephalitis in mice. Our findings suggest that NEK7 serves as a cellular switch that enforces mutual exclusivity of the inflammasome response and cell division.