The descriptions of the built environment are combined with various HPH goals and population groups. To utilize the built environment as a resource for HPHs, the networks should consider incorporating the built environment in documents and action plans at all organizational levels.

In older adults, elevated gait variability when walking has been associated with both cognitive impairment and future falls. This study leveraged three existing datasets to determine relationships between gait variability and the strength of functional connectivity within and between large-scale brain networks in healthy older adults, those with mild-to-moderate functional impairment, and those with Parkinson’s disease (PD).

Gait and resting-state fMRI data were extracted from existing datasets on 1) 12 older adults without overt disease yet with slow gait and mild executive dysfunction; 2) 12 older adults with intact cognitive-motor function and age- and sex-matched to the first cohort; and 3) 15 individuals with PD. Gait variability (%, coefficient of variation of stride time) during preferred walking speed was measured and correlated with the degree of functional connectivity within and between seven established large-scale functional brain networks.

Regression models adjusted for age and sex revealed that in each cohort, those with less gait variability exhibited greater negative correlation between fluctuations in resting-state brain activity between the default network and the dorsal attention network (Functionally-limited older β=4.38, p=.027; Healthy older β=1.66, p=.032; PD β=1.65, p=.005). No other within- or between- network connectivity outcomes were consistently related to gait variability across all three cohorts.

These results provide strong evidence that gait variability is uniquely related to functional connectivity between the default network and the dorsal attention network, and that this relationship may be independent of both functional status and underlying brain disease.

These results provide strong evidence that gait variability is uniquely related to functional connectivity between the default network and the dorsal attention network, and that this relationship may be independent of both functional status and underlying brain disease.

Genome-wide profiling of transcription factor binding and chromatin states is a widely-used approach for mechanistic understanding of gene regulation. Recent technology development has enabled such profiling at single-cell resolution. However, an end-to-end computational pipeline for analyzing such data is still lacking.

Here, we have developed a flexible pipeline for analysis and visualization of single-cell CUT&Tag and CUT&RUN data, which provides functions for sequence alignment, quality control, dimensionality reduction, cell clustering, data aggregation, and visualization. Furthermore, it is also seamlessly integrated with the functions in original CUT&RUNTools for population-level analyses. As such, this provides a valuable toolbox for the community.

https//github.com/fl-yu/CUT-RUNTools-2.0.

Supplementary data are available at Bioinformatics online.

Supplementary data are available at Bioinformatics online.

Randomized-controlled trials of mRNA vaccine protection against SARS-CoV-2 included few elderly participants. Telratolimod in vitro We assess single-dose mRNA vaccine effectiveness (VE) in adults ≥70-years-old in British Columbia (BC), Canada where second doses were deferred by up to 16 weeks and where a spring 2021 wave uniquely included co-dominant circulation of Alpha (B.1.1.7) and Gamma (P.1) variants of concern (VOC).

Analyses included community-dwelling adults ≥70-years-old with specimen collection between April 4 (epidemiological week 14) and May 1 (week 17) 2021. Adjusted VE was estimated by test-negative design. Cases were RT-PCR test-positive for SARS-CoV-2 and controls were test-negative. Vaccine status was defined by receipt of a single-dose ≥21 days before specimen collection, but a range of intervals was assessed. Variant-specific VE was estimated against viruses genetically characterized as Alpha, Gamma or non-VOC lineages.

VE analyses included 16,993 specimens 1,226 (7.2%) test-positive cases and 15,767 test-negative controls. Of 1,131 (92%) genetically-characterized viruses, 509 (45%), 314 (28%) and 276 (24%) were Alpha, Gamma and non-VOC lineages, respectively. At 0-13 days post-vaccination, VE was negligible at 14% (95% CI 0-26) but increased from 43% (95% CI 30-53) at 14-20 days to 75% (95% CI 63-83) at 35-41 days post-vaccination. VE at ≥21 days post-vaccination was 65% (95% CI 58-71) overall 72% (95% CI 58-81), 67% (95% CI 57-75) and 61% (95% CI 45-72) for non-VOC, Alpha and Gamma variants, respectively.

A single dose of mRNA vaccine reduced the risk of SARS-CoV-2 by about two-thirds in adults ≥70-years-old, with protection only minimally reduced against Alpha and Gamma variants.

A single dose of mRNA vaccine reduced the risk of SARS-CoV-2 by about two-thirds in adults ≥70-years-old, with protection only minimally reduced against Alpha and Gamma variants.

Pneumonic plague (PP), caused by Yersinia pestis, is the most feared clinical form of plague due to its rapid lethality and potential to cause outbreaks. PP outbreaks are now rare due to antimicrobial therapy.

A PP outbreak in Madagascar involving transmission of a Y. pestis strain resistant to streptomycin, the current recommended first-line treatment in Madagascar, was retrospectively characterized using epidemiology, clinical diagnostics, molecular characterization, and animal studies.

The outbreak occurred in February 2013 in the Faratsiho district of Madagascar and involved 22 cases, including three untreated fatalities. The 19 other cases participated in funeral practices for the fatal cases and fully recovered after combination antimicrobial therapy intramuscular streptomycin followed by oral co-trimoxazole. The Y. pestis strain that circulated during this outbreak is resistant to streptomycin resulting from a spontaneous point mutation in the 30S ribosomal protein S12 (rpsL) gene. This same mutation causes streptomycin resistance in two unrelated Y.