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Background: Quality measures influence patient outcomes, yet related education is not standardized in undergraduate nursing programs. This study examined how accredited programs teach quality measure content and the cognitive rigor of instruction. Method: A three-phase, descriptive study included development and validation of the Quality Education and Standards Training–Preparing for Quality Measure Performance (QUEST-PQMP) instrument, followed by national deployment to 1,830 programs. Results: Of the 175 responses, 75 reported a dedicated curriculum and 57 completed the QUEST-PQMP (Cronbach's α = .92). Programs reporting greater perceived student preparedness had higher QUEST-PQMP scores, though instruction emphasized lower-order rather than higher-order cognition. Limited curricular time and faculty expertise were common barriers. Conclusion: Undergraduate nursing curricula vary widely in quality measure content. Integrating this topic with intentional cognitive rigor and faculty development may strengthen graduates' readiness for data-informed, quality-driven nursing practice.

Small-molecule inhibitor of apoptosis (IAP) antagonists, called Smac mimetic compounds (SMCs), sensitize tumours to TNF-α-induced killing while simultaneously blocking TNF-α growth-promoting activities. SMCs also regulate several immunomodulatory properties within immune cells. We report that SMCs synergize with innate immune stimulants and immune checkpoint inhibitor biologics to produce durable cures in mouse models of glioblastoma in which single agent therapy is ineffective. The complementation of activities between these classes of therapeutics is dependent on cytotoxic T-cell activity and is associated with a reduction in immunosuppressive T-cells. Notably, the synergistic effect is dependent on type I IFN and TNF-α signalling. Furthermore, our results implicate an important role for TNF-α-producing cytotoxic T-cells in mediating the anti-cancer effects of immune checkpoint inhibitors when combined with SMCs. Overall, this combinatorial approach could be highly effective in clinical application as it allows for cooperative and complimentary mechanisms in the immune cell-mediated death of cancer cells. Smac mimetics sensitize cancer cells to the extrinsic cell death pathway and stimulate anti-tumour immunity. In this study, the authors show that Smac mimetics can synergize with immune checkpoint inhibitors to control tumour growth in mouse cancer models, including aggressive CNS tumours, in a cytotoxic CD8 + T-cell- and TNFα-dependent manner.

Objectives. To examine the impact of school shootings on indicators of adolescent school safety in the United States. Methods. We linked 2009–2019 Youth Risk Behavior Survey data on 211 236 adolescents aged 14 to 18 years from 24 school districts with data on high school shootings from the Center for Homeland Defense and Security. We conducted 2-way fixed-effects logistic regression models to assess the impact of shootings on self-report of 3 indicators of school safety: avoiding school because of feeling unsafe, carrying a weapon at school, and being threatened or injured with a weapon at school. Results. High school shootings were associated with adolescents having 20% greater odds of avoiding school because of feeling unsafe (adjusted odd ratio [AOR] = 1.20; 95% confidence interval [CI] = 1.11, 1.29) than those who had not. Findings were slightly attenuated in sensitivity analyses that tested exposure to shootings at any school in the district or state. High school shootings were associated with a statistically nonsignificant (P = .08) elevated risk of carrying a weapon at school (AOR = 1.11; 95% CI = 0.99, 1.25). Conclusions. The negative ramifications of school shootings extend far beyond the event itself to adolescents’ concerns about school safety. (Am J Public Health. 2023;113(4):438–441. https://doi.org/10.2105/AJPH.2022.307206 )

Growing apart together What drives evolutionary change? The Red Queen hypothesis predicts that coevolution of species should increase the rate of evolution at the molecular level. Here, genome sequencing in an experimental phage–bacteria system is used to show that this is true, but that the effect is concentrated on specific loci. In addition, coevolution is found to drive greater diversification of phage populations. The Red Queen hypothesis predicts that coevolution should increase the rate of evolution at the molecular level. Here, genome sequencing in an experimental phage–bacteria system is used to show that this is true, but the effect is concentrated on specific loci, and also that coevolution drives greater diversification of phage populations. The Red Queen hypothesis proposes that coevolution of interacting species (such as hosts and parasites) should drive molecular evolution through continual natural selection for adaptation and counter-adaptation 1 , 2 , 3 . Although the divergence observed at some host-resistance 4 , 5 , 6 and parasite-infectivity 7 , 8 , 9 genes is consistent with this, the long time periods typically required to study coevolution have so far prevented any direct empirical test. Here we show, using experimental populations of the bacterium Pseudomonas fluorescens SBW25 and its viral parasite, phage Φ2 (refs 10 , 11 ), that the rate of molecular evolution in the phage was far higher when both bacterium and phage coevolved with each other than when phage evolved against a constant host genotype. Coevolution also resulted in far greater genetic divergence between replicate populations, which was correlated with the range of hosts that coevolved phage were able to infect. Consistent with this, the most rapidly evolving phage genes under coevolution were those involved in host infection. These results demonstrate, at both the genomic and phenotypic level, that antagonistic coevolution is a cause of rapid and divergent evolution, and is likely to be a major driver of evolutionary change within species.

Zoological environments aim to promote natural behaviours and optimal welfare conditions. Over the past decade, research on the use of artificial ultraviolet-B (UV-B) exposure has improved vitamin D3 levels and reduced incidences of metabolic bone disease in diurnal primates; however, this has not been investigated in nocturnals. Aye-ayes (Daubentonia madagascariensis), nocturnal lemurs often housed indoors in zoos with little to no exposure to natural sunlight, have been reported to have low vitamin D3 levels. This study aims to investigate the impacts of artificial UV-B as a supplemental healthcare strategy for aye-ayes, examining its influences on vitamin D3 levels and positional sleeping behaviour. The 25-hydroxy-vitamin D3 (25OHD3) blood levels were tested before and after exposure to different levels of artificial UV-B and heat sources. Statistical analysis showed no correlation between UV-B and 25OHD3 at group parameter levels. However, one individual showed a positive correlation. Sleeping position duration analysis showed a potential basking behaviour with the use of increased ear exposure and other thermoregulatory responses. Despite representing 8.06% of the European captive aye-aye population, these findings highlight the need for further research on vitamin D3 parameters and responses to UV-B to optimise captive conditions and support the species’ long-term health.

The genus Yersinia has been used as a model system to study pathogen evolution. Using whole-genome sequencing of all Yersinia species, we delineate the gene complement of the whole genus and define patterns of virulence evolution. Multiple distinct ecological specializations appear to have split pathogenic strains from environmental, nonpathogenic lineages. This split demonstrates that contrary to hypotheses that all pathogenic Yersinia species share a recent common pathogenic ancestor, they have evolved independently but followed parallel evolutionary paths in acquiring the same virulence determinants as well as becoming progressively more limited metabolically. Shared virulence determinants are limited to the virulence plasmid pYV and the attachment invasion locus ail . These acquisitions, together with genomic variations in metabolic pathways, have resulted in the parallel emergence of related pathogens displaying an increasingly specialized lifestyle with a spectrum of virulence potential, an emerging theme in the evolution of other important human pathogens.

Clostridium difficile has rapidly emerged as the leading cause of antibiotic-associated diarrheal disease, with the transcontinental spread of various PCR ribotypes, including 001, 017, 027 and 078. However, the genetic basis for the emergence of C. difficile as a human pathogen is unclear. Whole genome sequencing was used to analyze genetic variation and virulence of a diverse collection of thirty C. difficile isolates, to determine both macro and microevolution of the species. Horizontal gene transfer and large-scale recombination of core genes has shaped the C. difficile genome over both short and long time scales. Phylogenetic analysis demonstrates C. difficile is a genetically diverse species, which has evolved within the last 1.1–85 million years. By contrast, the disease-causing isolates have arisen from multiple lineages, suggesting that virulence evolved independently in the highly epidemic lineages.

Subtelomeric regions are often under-represented in genome sequences of eukaryotes. One of the best known examples of the use of telomere proximity for adaptive purposes are the bloodstream expression sites (BESs) of the African trypanosome Trypanosoma brucei. To enhance our understanding of BES structure and function in host adaptation and immune evasion, the BES repertoire from the Lister 427 strain of T. brucei were independently tagged and sequenced. BESs are polymorphic in size and structure but reveal a surprisingly conserved architecture in the context of extensive recombination. Very small BESs do exist and many functioning BESs do not contain the full complement of expression site associated genes (ESAGs). The consequences of duplicated or missing ESAGs, including ESAG9, a newly named ESAG12, and additional variant surface glycoprotein genes (VSGs) were evaluated by functional assays after BESs were tagged with a drug-resistance gene. Phylogenetic analysis of constituent ESAG families suggests that BESs are sequence mosaics and that extensive recombination has shaped the evolution of the BES repertoire. This work opens important perspectives in understanding the molecular mechanisms of antigenic variation, a widely used strategy for immune evasion in pathogens, and telomere biology.

As a result of the COVID-19 pandemic and the Black Lives Matter movement, leaders in the field of interprofessional (IP) education have encouraged faculty to explore online adaptations to curriculum and examine strategies that enhance students’ structural competence. Structural competence is broadly defined as the ability to understand how oppression, governmental policies, and environmental inputs impact the health and well-being of an individual. With these changes in mind, a team of IP health science faculty developed two online curricular activities guided by the “common reading” book, Five Days at Memorial: Life and Death in a Storm-Ravaged Hospital by Sheri Fink. This article describes the development and findings of a mixed-methods evaluation of the two IP learning activities: (a) The Interprofessional Common Reading Experience (IPCRE) and (b) The IPCRE follow-up. The activities engaged over 250 students across multiple health professions (i.e., social work, nursing, athletic training, speech-language pathology, nutrition, and public health) attending three different universities. Our findings contribute to a greater understanding of how to develop online IP activities and curricular innovations that help to train equity-minded and anti-racist practitioners.

Background Of the > 2000 serovars of Salmonella enterica subspecies I, most cause self-limiting gastrointestinal disease in a wide range of mammalian hosts. However, S. enterica serovars Typhi and Paratyphi A are restricted to the human host and cause the similar systemic diseases typhoid and paratyphoid fever. Genome sequence similarity between Paratyphi A and Typhi has been attributed to convergent evolution via relatively recent recombination of a quarter of their genomes. The accumulation of pseudogenes is a key feature of these and other host-adapted pathogens, and overlapping pseudogene complements are evident in Paratyphi A and Typhi. Results We report the 4.5 Mbp genome of a clinical isolate of Paratyphi A, strain AKU_12601, completely sequenced using capillary techniques and subsequently checked using Illumina/Solexa resequencing. Comparison with the published genome of Paratyphi A ATCC9150 revealed the two are collinear and highly similar, with 188 single nucleotide polymorphisms and 39 insertions/deletions. A comparative analysis of pseudogene complements of these and two finished Typhi genomes (CT18, Ty2) identified several pseudogenes that had been overlooked in prior genome annotations of one or both serovars, and identified 66 pseudogenes shared between serovars. By determining whether each shared and serovar-specific pseudogene had been recombined between Paratyphi A and Typhi, we found evidence that most pseudogenes have accumulated after the recombination between serovars. We also divided pseudogenes into relative-time groups: ancestral pseudogenes inherited from a common ancestor, pseudogenes recombined between serovars which likely arose between initial divergence and later recombination, serovar-specific pseudogenes arising after recombination but prior to the last evolutionary bottlenecks in each population, and more recent strain-specific pseudogenes. Conclusion Recombination and pseudogene-formation have been important mechanisms of genetic convergence between Paratyphi A and Typhi, with most pseudogenes arising independently after extensive recombination between the serovars. The recombination events, along with divergence of and within each serovar, provide a relative time scale for pseudogene-forming mutations, affording rare insights into the progression of functional gene loss associated with host adaptation in Salmonella .