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Background and Aims Falls remain a major health challenge in aging, yet little is known about how personality traits influence falls risk and related psychological concerns. This scoping review mapped existing evidence on relationships among personality traits, falls, fear of falling, and fall self‐efficacy in older adults to identify key associations and research gaps. Methods A comprehensive search of five databases (MEDLINE, APA PsycINFO, Web of Science, CINAHL, SPORTDiscus) was conducted from inception (1945) through December 2024. Eligible studies examined personality traits, assessed with validated instruments, in relation to falls, fear of falling, or fall self‐efficacy in older adults (≥ 50 years). All empirical designs were included. Data extraction followed PRISMA‐ScR guidance, and findings were synthesized descriptively. Results Of 8060 records screened, eight studies met the inclusion criteria (three longitudinal, five cross‐sectional). High neuroticism and low conscientiousness were the most consistently associated with greater fall risk and higher fear of falling. Extraversion showed generally protective associations with fear of falling, while Type A behaviour predicted higher fall incidence among men but not women. Openness and agreeableness showed no consistent patterns. Evidence on fall self‐efficacy was limited to one study, and none addressed balance confidence. Measurement heterogeneity across personality and fall‐related constructs limited comparability across studies. Conclusion Personality traits, particularly emotional instability and conscientiousness, appear relevant to fall risk and psychological concerns, though evidence remains sparse. Key gaps include limited work on fall self‐efficacy and balance confidence, under‐representation of clinical populations, and inconsistent measurement approaches. Future studies should use standardized instruments, longitudinal designs, and broader personality frameworks to inform personalised fall prevention strategies. Summary Neuroticism (emotional instability) and conscientiousness are consistently linked to fall risk and fear of falling in older adults. Extraversion showed a generally protective association with fear of falling, though evidence remains limited in scope. Standardized personality and fall‐related assessments are needed to guide personality‐informed fall‐prevention interventions.

Background: The COVID-19 pandemic disrupted primary health care systems worldwide, prompting rapid changes in how care was delivered. In Alberta, this included a significant shift from in-person to virtual care. This study examines trends in primary care utilization among Albertans during COVID-19 and the shift toward virtual care. Methods: Repeated cross-sectional analyses were conducted from 2018/19 to 2022/23 using Alberta Health Practitioner Claims data. Utilization was measured as the proportion of Albertans with at least one visit and the annual visit rate per person. Annual percent change (APC) was calculated relative to the pre-pandemic year (2019/20) and stratified by demographics. Findings: The proportion of Albertans with a primary care visit decreased by −9.55% in 2020/21 but recovered to −4.62% by 2022/23. Annual visit rates remained stable post-pandemic. The largest declines in 2020/21 were among children aged 5 to 11 (−38.42%), ≤4 (−33.42%), newborns (−30.36% to −25.49%), and those without health conditions (−20.9%). Virtual care accounted for 23.77% of visits in 2020/21, dropping to 14.43% by 2022/23. Conclusions: While fewer Albertans accessed primary care, visit rates remained stable due to virtual care. Further research is needed to assess the long-term impacts of COVID-19 on primary healthcare delivery.

Whole-genome sequence analysis of cells from a patient with acute myeloid leukemia (AML) revealed a mutation in DNMT3A, which encodes an enzyme that methylates DNA. Subsequent analyses showed that DNMT3A was mutated in 33.7% of patients with AML with an intermediate-risk cytogenetic profile. Whole-genome sequencing is an unbiased approach for discovering somatic variations in cancer genomes. We recently reported the DNA sequence and analysis of the genomes of two patients with acute myeloid leukemia (AML) with a normal karyotype. 1 , 2 We did not find new recurring mutations in the first study but did observe a recurrent mutation in IDH1, encoding isocitrate dehydrogenase 1, in the second study. 2 Subsequent work has confirmed and extended this finding, showing that mutations in IDH1 and related gene IDH2 are highly recurrent in patients with an intermediate-risk cytogenetic profile (20 to 30% frequency) and are associated with a . . .

Complexity and risk adjustment are two strategies employed to understand chronic disease and healthcare cost within patient populations. There is a general assumption that the data applied to risk adjustment models, such as the clinical risk groups (CRG) is sufficient to infer patient complexity. Our aim in this study was to compare the calculated complexity of a patient population using the 3 M™ CRG software to complexity data extracted from community-based primary care electronic medical records (EMR). We found that the distribution of the 3 M™ CRG health status was significantly different from the primary care EMR health status distribution, and that the number and type of chronic conditions identified differed between the two methods. We calculated a new variable that combined the information from the 3 M™ CRG software with the primary care EMR data. The distribution of the Combined-CRG distribution was significantly different from the 3 M™ CRG software; specifically, we saw many patients originally classified as being healthy or having minor chronic condition(s) re-categorized into having significant chronic condition(s). The CRG health statuses alone may be sufficient to predict future health expenditures, but caution is warranted if CRGs are to be used to infer complexity of the patient population.

In Schizosaccharomyces pombe, three genes, sir2+, hst2+, and hst4+, encode members of the Sir2 family of conserved NAD+-dependent protein deacetylases. The S. pombe sir2+ gene encodes a nuclear protein that is not essential for viability or for resistance to treatment with UV or a microtubule-destabilizing agent. However, sir2+ is essential for full transcriptional silencing of centromeres, telomeres, and the cryptic mating-type loci. Chromatin immunoprecipitation results suggest that the Sir2 protein acts directly at these chromosomal regions. Enrichment of Sir2p at silenced regions does not require the HP1 homolog Swi6p; instead, Swi6-GFP localization to telomeres depends in part on Sir2p. The phenotype of sir2 swi6 double mutants supports a model whereby Sir2p functions prior to Swi6p at telomeres and the silent mating-type loci. However, Sir2p does not appear to be essential for the localization of Swi6p to centromeric foci. Cross-complementation experiments showed that the Saccharomyces cerevisiae SIR2 gene can function in place of S. pombe sir2+, suggesting overlapping deacetylation substrates in both species. These results also suggest that, despite differences in most of the other molecules required, the two distantly related yeast species share a mechanism for targeting Sir2p homologs to silent chromatin.

We used proteins with randomized transmembrane (TM) domains to explore the role of hydrophobic amino acids in mediating specific interactions between transmembrane helices. The 44-aa bovine papillomavirus E5 protein, which binds to the TM domain of the PDGFβ receptor (PDGFβR) was used as a scaffold to construct a library encoding small dimeric proteins with randomized, strictly hydrophobic TM domains, and proteins were selected that induced focus formation in mouse C127 cells by activating the PDGFβR. Analysis of these proteins identified a motif of two hydrophobic residues that, when inserted into a 17-residue polyleucine TM domain, generated a protein that activated the PDGFβR and transformed cells. In addition, we identified transforming proteins that activated the wild-type PDGFβR but did not activate a series of PDGFβR TM point mutants that were efficiently activated by the E5 protein, indicating that these proteins were more specific than the E5 protein. Our results implied that multiple van der Waals interactions distributed along the entire length of the TM domains were required for productive interaction between the PDGFβR and some small proteins lacking hydrophilic TM residues. Our results also suggested that excluding hydrophilic residues from small TM proteins and peptides is a strategy to increase the specificity of heteromeric TM helix-helix interactions.

Viruses have been subjected to intense study because of their medical importance and because they can provide fundamental insights into normal and pathological cellular processes. Indeed, much of our knowledge about basic cellular biology and biochemistry was acquired through the study of viruses, and some of medicine's greatest triumphs and challenges involve viruses. Since viruses have evolved to exploit important cell processes, they can provide tools and approaches to manipulate cell function. The small transmembrane E5 protein of bovine papillomavirus type 1 transforms cells by a unique mechanism involving ligand-independent activation of the platelet-derived growth factor β receptor. Experiments summarized in this review suggest that it may be possible to use the E5 protein as a model to design an entirely new class of small, modular transmembrane proteins with novel biological activities.

We used proteins with randomized transmembrane (TM) domains to explore the role of hydrophobic amino acids in mediating specific interactions between transmembrane helices. The 44-aa bovine papillomavirus E5 protein, which binds to the TM domain of the PDGFb receptor (PDGFbR) was used as a scaffold to construct a library encoding small dimeric proteins with randomized, strictly hydrophobic TM domains, and proteins were selected that induced focus formation in mouse C127 cells by activating the PDGFbR. Analysis of these proteins identified a motif of two hydrophobic residues that, when inserted into a 17-residue polyleucine TM domain, generated a protein that activated the PDGFbR and transformed cells. In addition, we identified transforming proteins that activated the wild-type PDGFbR but did not activate a series of PDGFbR TM point mutants that were efficiently activated by the E5 protein, indicating that these proteins were more specific than the E5 protein. Our results implied that multiple van der Waals interactions distributed along the entire length of the TM domains were required for productive interaction between the PDGFbR and some small proteins lacking hydrophilic TM residues. Our results also suggested that excluding hydrophilic residues from small TM proteins and peptides is a strategy to increase the specificity of heteromeric TM helix-helix interactions.

The human genome holds an extraordinary trove of information about human development, physiology, medicine and evolution. Here we report the results of an international collaboration to produce and make freely available a draft sequence of the human genome. We also present an initial analysis of the data, describing some of the insights that can be gleaned from the sequence.

Human chromosome 7 has historically received prominent attention in the human genetics community, primarily related to the search for the cystic fibrosis gene and the frequent cytogenetic changes associated with various forms of cancer. Here we present more than 153 million base pairs representing 99.4% of the euchromatic sequence of chromosome 7, the first metacentric chromosome completed so far. The sequence has excellent concordance with previously established physical and genetic maps, and it exhibits an unusual amount of segmentally duplicated sequence (8.2%), with marked differences between the two arms. Our initial analyses have identified 1,150 protein-coding genes, 605 of which have been confirmed by complementary DNA sequences, and an additional 941 pseudogenes. Of genes confirmed by transcript sequences, some are polymorphic for mutations that disrupt the reading frame.