Background Consumer-wearable activity trackers are small electronic devices that record fitness and health-related measures. Objective The purpose of this systematic review was to examine the validity and reliability of commercial wearables in measuring step count, heart rate, and energy expenditure. Methods We identified devices to be included in the review. Database searches were conducted in PubMed, Embase, and SPORTDiscus, and only articles published in the English language up to May 2019 were considered. Studies were excluded if they did not identify the device used and if they did not examine the validity or reliability of the device. Studies involving the general population and all special populations were included. We operationalized validity as criterion validity (as compared with other measures) and construct validity (degree to which the device is measuring what it claims). Reliability measures focused on intradevice and interdevice reliability. Results We included 158 publications examining nine different commercial wearable device brands. Fitbit was by far the most studied brand. In laboratory-based settings, Fitbit, Apple Watch, and Samsung appeared to measure steps accurately. Heart rate measurement was more variable, with Apple Watch and Garmin being the most accurate and Fitbit tending toward underestimation. For energy expenditure, no brand was accurate. We also examined validity between devices within a specific brand. Conclusions Commercial wearable devices are accurate for measuring steps and heart rate in laboratory-based settings, but this varies by the manufacturer and device type. Devices are constantly being upgraded and redesigned to new models, suggesting the need for more current reviews and research.

Zika virus (ZIKV) is an emerging arbovirus of the Flaviviridae family. Although ZIKV infection is typically mild and self-limiting in healthy adults, infection has been associated with neurological symptoms such as Guillain-Barré syndrome, and a causal link has been established between fetal microcephaly and ZIKV infection during pregnancy. These risks, and the magnitude of the ongoing ZIKV pandemic, have created an urgent need for the development of animal models to study the immune response to ZIKV infection. Previous animal models have primarily focused on pathogenesis in immunocompromised mice. In this study, we provide a model of ZIKV infection in wild-type immunocompetent C57BL/6 mice, and have provided an analysis of the immune response to infection. We evaluated the activation of several innate immune cell types, and studied the kinetics, phenotype, and functionality of T cell responses to ZIKV infection. Our results demonstrate that ZIKV infection is mild in wild-type immunocompetent C57BL/6 mice, resulting in minimal morbidity. Our data establish that at the peak of the adaptive response, antigen-experienced CD4+ T cells polarize to a Th1 phenotype, and antigen-experienced CD8+ T cells exhibit an activated effector phenotype, producing both effector cytokines and cytolytic molecules. Furthermore, we have identified a novel ZIKV CD8+ T cell epitope in the envelope protein that is recognized by the majority of responding cells. Our model provides an important reference point that will help dissect the impact of polymorphisms in the circulating ZIKV strains on the immune response and ZIKV pathogenesis. In addition, the identification of a ZIKV epitope will allow for the design of tetramers to study epitope-specific T cell responses, and will have important implications for the design and development of ZIKV vaccine strategies.

Purpose of ReviewUpdate the state of evidence on the effectiveness of retail food environment interventions in influencing diet and explore the underlying role of public policy, through a systematic review of population-level interventions to promote health in the retail food environment, including community and consumer environments. Diet-related outcomes included purchasing, dietary intakes, diet quality, and health including weight. We coded studies for enabling public policy levers underpinning the intervention, using two widely used conceptual frameworks.Recent FindingsOf 86 articles (1974–2018), the majority (58 articles, 67%) showed at least one positive effect on diet. Thirteen articles (15%) discussed natural experiments, 27 articles (31%) used a design involving comparison groups including 23 articles (27%) specifically describing randomized controlled trials, and 46 (53%) were quasi-experimental (cross-sectional) evaluations. Across the “4Ps” of marketing (product, promotion, placement, and price), promotion comprised the greatest proportion of intervention strategies, especially in earlier literature (pre-2008). Few studies combined geographic access interventions with 4P strategies, and few used robust dietary intake assessments. Behavior change communication remains an intervention mainstay, but recent work has also incorporated environmental and social planning, and fiscal strategies. More recent interventions were multi-component.SummaryThe retail food environment intervention literature continues to grow and has become more robust overall, with clearer evidence of the effect of interventions on diet-related outcomes, including consumer purchasing, dietary intakes, and health. There is still much scope for development in the field. Attention to enabling public policy could help to strengthen intervention implementation and evaluation in the retail food environment.

Individuals infected with hepatitis C virus (HCV) are at high risk of developing progressive liver disease, including cirrhosis and hepatocellular carcinoma (HCC). How HCV infection causes liver destruction has been of significant interest for many years, and apoptosis has been proposed as one operative mechanism. In this study, we employed a tissue culture-adapted strain of HCV (JFH1T) to test effects of HCV infection on induction of programmed cell death (PCD) in Huh-7.5 cells. We found that HCV infection reduced the proliferation rate and induced caspase-3-mediated apoptosis in the infected cell population. However, in addition to apoptosis, we also observed infected cells undergoing caspase-1-mediated pyroptosis, which was induced by NLRP3 inflammasome activation. By co-culturing HCV-infected Huh-7.5 cells with an HCV-non-permissive cell line, we also demonstrated induction of both apoptosis and pyroptosis in uninfected cells. Bystander apoptosis, but not bystander pyroptosis, required cell-cell contact between infected and bystander cells. In summary, these findings provide new information on mechanisms of cell death in response to HCV infection. The observation that both apoptosis and pyroptosis can be induced in bystander cells extends our understanding of HCV-induced pathogenesis in the liver.

Immune regulation of cellular metabolism can be responsible for successful responses to invading pathogens. Viruses alter their hosts' cellular metabolism to facilitate infection. Conversely, the innate antiviral responses of mammalian cells target these metabolic pathways to restrict viral propagation. We identified miR-130b and miR-185 as hepatic microRNAs (miRNAs) whose expression is stimulated by 25-hydroxycholesterol (25-HC), an antiviral oxysterol secreted by interferon-stimulated macrophages and dendritic cells, during hepatitis C virus (HCV) infection. However, 25-HC only directly stimulated miR-185 expression, whereas HCV regulated miR-130b expression. Independently, miR-130b and miR-185 inhibited HCV infection. In particular, miR-185 significantly restricted host metabolic pathways crucial to the HCV life cycle. Interestingly, HCV infection decreased miR-185 and miR-130b levels to promote lipid accumulation and counteract 25-HC's antiviral effect. Furthermore, miR-185 can inhibit other viruses through the regulation of immunometabolic pathways. These data establish these microRNAs as a key link between innate defenses and metabolism in the liver.