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Background Evidence of the effects of the built environment on children has mainly focused on disease outcomes; however, quality of life (QoL) has gained increasing attention as an important health and policy endpoint itself. Research on built environment effects on children’s QoL could inform public health programs and urban planning and design. Objective We aimed to review and synthesize the evidence of the relationship between built environment features and children’s QoL. Methods Five research databases were searched for quantitative peer-reviewed studies on children between 2 and 18 years, published in English or German between January 2010 and August 2023. Only primary research was considered. Included studies ( n  = 17) were coded and methodologically assessed with the Joanna Briggs Critical Appraisal Checklists, and relevant data were extracted, analyzed, and synthesized, using the following built environment framework: (1) neighborhood green and blue space, (2) neighborhood infrastructure, and (3) neighborhood perception. Results Green space was positively associated with children’s QoL. Infrastructure yielded inconclusive results across all measured aspects. Overall neighborhood satisfaction was positively correlated with higher QoL but results on perceived environmental safety were mixed. Conclusions Most studies are correlational, making it difficult to infer causality. While the positive findings of green space on QoL are consistent, specific features of the built environment show inconsistent results. Overall perception of the built environment, such as neighborhood satisfaction, also shows more robust results compared to perceptions of specific features of the built environment. Due to the heterogeneity of both built environment and QoL measures, consistent measures of both concepts will help advance this area of research.

The roles given Carl Van Doren in the Melville revival’s opening chapter have so far been either too big or not big enough. Although Van Doren did not launch the revival, as some persons claim, he nevertheless played a larger part than asserted by others in making a Melvillean of the one who is credited with launching it, Raymond Weaver. By emending the record of Van Doren’s role in originating the revival, moreover, this narrative also emends the record of the revival’s origins story itself.

Brain-machine interfaces (BMIs) record and translate neural activity into a control signal for assistive or other devices. Intracortical microelectrode arrays (MEAs) enable high degree-of-freedom BMI control for complex tasks by providing fine-resolution neural recording. However, chronically implanted MEAs are subject to a dynamic environment where transient or systematic disruptions can interfere with neural recording and degrade BMI performance. Typically, neural implant failure modes have been categorized as biological, material, or mechanical. While this categorization provides insight into a disruption's causal etiology, it is less helpful for understanding degree of impact on BMI function or possible strategies for compensation. Therefore, we propose a complementary classification framework for intracortical recording disruptions that is based on duration of impact on BMI performance and requirement for and responsiveness to interventions: (1) interfere with recordings on the time scale of minutes to hours and can resolve spontaneously; (2) cause persistent interference in recordings but the root cause can be remedied by an appropriate intervention; (3) cause persistent or progressive decline in signal quality, but their effects on BMI performance can be mitigated algorithmically; and (4) cause permanent signal loss that is not amenable to remediation or compensation. This conceptualization of intracortical BMI disruption types is useful for highlighting specific areas for potential hardware improvements and also identifying opportunities for algorithmic interventions. We review recording disruptions that have been reported for MEAs and demonstrate how biological, material, and mechanical mechanisms of disruption can be further categorized according to their impact on signal characteristics. Then we discuss potential compensatory protocols for each of the proposed disruption classes. Specifically, transient disruptions may be minimized by using robust neural decoder features, data augmentation methods, adaptive machine learning models, and specialized signal referencing techniques. Statistical Process Control methods can identify reparable disruptions for rapid intervention. diagnostics such as impedance spectroscopy can inform neural feature selection and decoding models to compensate for irreversible disruptions. Additional compensatory strategies for irreversible disruptions include information salvage techniques, data augmentation during decoder training, and adaptive decoding methods to down-weight damaged channels.

Macrophages activated with interferon-γ (IFN-γ) in combination with other proinflammatory stimuli, such as lipopolysaccharide or tumor necrosis factor-α (TNF-α), respond with transcriptional and cellular changes that enhance clearance of intracellular pathogens at the risk of damaging tissues. IFN-γ effects must therefore be carefully balanced with inhibitory mechanisms to prevent immunopathology. We performed a genome-wide CRISPR knockout screen in a macrophage cell line to identify negative regulators of IFN-γ responses. We discovered an unexpected role of the ubiquitin-fold modifier (Ufm1) conjugation system (herein UFMylation) in inhibiting responses to IFN-γ and lipopolysaccharide. Enhanced IFN-γ activation in UFMylation-deficient cells resulted in increased transcriptional responses to IFN-γ in a manner dependent on endoplasmic reticulum stress responses involving Ern1 and Xbp1. Furthermore, UFMylation in myeloid cells is required for resistance to influenza infection in mice, indicating that this pathway modulates in vivo responses to infection. These findings provide a genetic roadmap for the regulation of responses to a key mediator of cellular immunity and identify a molecular link between the UFMylation pathway and immune responses.

Host inflammatory responses must be tightly regulated to ensure effective immunity while limiting tissue injury. IFN gamma (IFNγ) primes macrophages to mount robust inflammatory responses. However, IFNγ also induces cell death, and the pathways that regulate IFNγ-induced cell death are incompletely understood. Using genome-wide CRISPR/Cas9 screening, we identified autophagy genes as central mediators of myeloid cell survival during the IFNγ response. Hypersensitivity of autophagy gene-deficient cells to IFNγ was mediated by tumor necrosis factor (TNF) signaling via receptor interacting protein kinase 1 (RIPK1)- and caspase 8-mediated cell death. Mice with myeloid cell-specific autophagy gene deficiency exhibited marked hypersensitivity to fatal systemic TNF administration. This increased mortality in myeloid autophagy gene-deficient mice required the IFNγ receptor, and mortality was completely reversed by pharmacologic inhibition of RIPK1 kinase activity. These findings provide insight into the mechanism of IFNγ-induced cell death via TNF, demonstrate a critical function of autophagy genes in promoting cell viability in the presence of inflammatory cytokines, and implicate this cell survival function in protection against mortality during the systemic inflammatory response.

Disparities in vaccine confidence and uptake among racial and ethnic minorities have resulted in a disproportionate burden of COVID-19 in these populations. Social media campaigns have shown promise in public health promotion and behavioral interventions. In January 2022, an academic-community partnership launched #Vax4Community, a 6-month social media campaign centered around the use of digital storytelling videos. The campaign purpose was to decrease vaccine hesitancy, combat vaccine misinformation and disinformation, and increase vaccine confidence within three distinct target communities: the justice-involved population, South Asian residents, and public housing youth in the metropolitan area of New York City (NYC). Our approach included the production and dissemination of digital storytelling videos featuring personal vaccine experiences from target populations. We evaluated key performance indicators (KPIs) of the campaign, including post impressions, reach and engagement across social media platforms, and shares from partner organizations. Overall, we received 1,910,662 post impressions, 699,722 unique users reached, and 2,880 post engagements across Instagram, Facebook, LinkedIn, and Twitter, and 147 shares from 48 partner organizations. Social media campaigns require strategic design in branding, messaging and outreach channels and could serve as an important tool to disseminate emotionally relatable content and trusted information to prime target populations to respond more optimally to public health interventions. The purpose of this paper is to describe the process of creating and disseminating these digital stories and the KPIs of the social media campaign.

Despite increasing interest in the role of parks on children's health, there has been little empirical research on the impact of park interventions. We used a quasi-experimental pre-post study design with matched controls to evaluate the effects of park redesign and renovation on children's health-related quality of life (QoL) in underserved neighborhoods in New York City, with predominantly Hispanic and Black populations. Utilizing longitudinal data from the Physical Activity and Redesigned Community Spaces (PARCS) Study, we examined the parent-reported health-related QoL of 201 children aged 3-11 years living within a 0.3-mile radius of 13 renovated parks compared to 197 children living near 11 control parks before and after the park intervention. Health-related QoL was measured using a modified version of the KINDL questionnaire that assessed children's physical and emotional well-being, self-esteem, and well-being in home, peer, and school functioning. Linear mixed regression model was used to examine the difference in difference (DID) between the intervention vs. control group for QoL. We found a significant differential improvement in the physical well-being subscale of KINDL in the intervention vs. control group (DID = 6.35, 95% confidence interval [CI] = 0.85-11.85, p = 0.024). The effect was particularly strong among girls (DID = 7.88, p = 0.023) and children of the lowest socio-economic background (p < 0.05). No significant DID was found in other KINDL domains. Our study indicated a beneficial impact of improving park quality on the physical well-being of children residing in underserved neighborhoods. These findings lend support for investments in neighborhood parks to advance health equity.

Preparations enriched in plastics were used to investigate the location of ADP-glucose pyrophosphorylase (AGPase) in the developing endosperm of maize (Zea mays L.). These preparations contained more than 25% of the total activity of the plastic marker enzymes alkaline pyrophosphatase and soluble starch synthase, less than 2% of the cytosolic marker enzymes alcohol dehydrogenase and pyrophosphate, fructose 6-phosphate 1-phosphotransferase, and approximately 3% of the AGPase activity. Comparison with the marker enzyme distribution suggests that more than 95% of the activity of AGPase in maize endosperm is extra-plastidial. Two proteins were recognized by antibodies to the small subunit of AGPase from maize endosperm Brittle-2 (Bt2). The larger of the two proteins was the major small subunit in homogenates of maize endosperm, and the smaller, less abundant of the two proteins was enriched in preparations containing plastics. These results suggest that there are distinct plastidial and cytosolic forms of AGPase, which are composed of different subunits. Consistent with this was the finding that the bt2 mutation specifically eliminated the extra-plastidial AGPase activity and the larger of the two proteins recognized by the antibody to the Bt2 subunit

Curriculum mapping initiatives are started with the essential goal of improving student achievement, yet the mapping process can be challenging to navigate or lead. While the main work of curriculum mapping is conducted by classroom teachers, administrators must be actively involved, and they must also take into account the demands curriculum mapping places on teachers. This book provides administrators with the foundational understandings and specific guidance and strategies to effectively support a curriculum mapping initiative in their schools and districts. The authors discuss administrative leadership for curriculum mapping, including the roles and responsibilities of various administrative positions, such as the superintendent, headteacher, and curriculum director, and provide protocols and procedures for writing administrative maps. A Leader's Guide to Curriculum Mapping offers concrete information and suggestions for moving a curriculum mapping initiative forward in a positive manner and ultimately ensuring that curriculum mapping is not only sustained, but is embedded in the cultural consciousness and becomes the natural way of conducting professional curriculum work throughout a learning organization. The book: - Includes brief but necessary coverage of theory and foundational concept - Focuses on administrative leadership with curriculum design in mind and administrative support for systemic change - Provides administrators with guidance, protocols, and step-by-step directions for the stages of a curriculum mapping initiative - Offers practical applications, realistic expectations, and real-life examples - Addresses significant concerns such as time and resources necessary for sustainability.

We describe a model to calculate the buffering capacity of bicarbonate in the rumen. The addition of NaHCO3 results in the release of CO2 from solution and eventually from the rumen via eructation. This process directly neutralizes ruminal acidity. The degree to which the process continues depends on the partial pressure of CO2 in the gas phase, the pH, and a constant (7.74), according to the Henderson-Hasselbalch equation: pH = 7.74 + log([HCO3-]/pressure of CO2 in atmospheres). The addition of NaHCO3 to buffer solutions and ruminal fluid under high pressure of CO2 increased pH as predicted. The buffering capacity of ruminal fluid under CO2 was greater at low pH than was previously determined by titration in air. In contrast, in vitro systems in which CO2 is not permitted to escape may result in reduced buffering capacity. In vitro systems in which excess CO2 may escape (under N2 gas pressure) may result in uncontrolled pH elevation. Dilution of ruminal fluid under constant pressure of CO2 decreased ruminal pH as predicted by the model. The pH under different pressures at equilibrium and the buffering capacity are easily calculated for in vitro and in vivo systems.