Internet-of-Things (IoT) systems have become pervasive for smart homes. In recent years, many of these IoT sensing systems are developed to enable in-home long-term monitoring applications, such as personalized services in smart homes, elderly/patient monitoring, etc. However, these systems often require complicated and expensive installation processes, which are some of the main concerns affecting users' adoption of smart home systems. In this work, we focus on floor vibration-based occupant monitoring systems, which enables non-intrusive in-home continuous occupant monitoring, such as patient step tracking and gait analysis. However, to enable these applications, the system would require known locations of vibration sensors placed in the environment. Current practice relies on manually input of location, which makes the installation labor-intensive, time consuming, and expensive. On the other hand, without known location of vibration sensors, the output of the system does not have intuitive physical meaning and is incomprehensive to users, which limits the systems' usability. We present AutoLoc, a scheme to estimate the location of the vibration sensors in a two-dimensional space in the view of a nearby camera, which has spatial physical meaning. AutoLoc utilizes occupants' walking events captured by both vibration sensors and the co-located camera to estimate the vibration sensors' location in the camera view. First, AutoLoc detects and localizes the occupant's footsteps in the vision data. Then, it associates the time and location of the event to the floor vibration data. Next, the extracted vibration data of the given event from multiple vibration sensors are used to estimate the sensors' locations in the camera view coordinates. We conducted real-world experiments and achieved up to 0.07 meters localization accuracy.

Background and aims

The California Tobacco-Use Prevention Education (TUPE) program promotes the use of evidence-based tobacco-specific prevention and cessation programs for adolescents within the school setting. Through a competitive grant process, schools are funded to provide programs for grades 6-12. This research evaluates the association between TUPE funding and tobacco prevention activities and tobacco use prevalence.

Methods

This study utilized two data sources: (1) 2016 California Educator Tobacco Survey (CETS), and (2) 2015-2016 California Student Tobacco Survey (CSTS). The CETS collected data from educators about school prevention efforts, priority of tobacco prevention, and confidence in addressing tobacco issues with students. A total of 3,564 educators from 590 schools participated in CETS. The CSTS collected data from 8th, 10th, and 12th graders in California on their exposure to, attitudes about, and utilization of tobacco products. A total of 47,981 students from 117 schools participated in CSTS.

Results

This study found that TUPE-funded schools were more likely to provide tobacco-specific health education programs, to place a priority on tobacco-prevention efforts, and to prepare educators to address tobacco use than non-TUPE schools. Educators at both types of schools felt better prepared to talk with students about traditional tobacco products than about emerging products such as e-cigarettes. Overall, students at TUPE-funded schools were more likely to report receiving anti-tobacco messages from school-based programs than those at non-TUPE schools. The former were also less likely to use tobacco products, even when the analysis controlled for demographics and school-level characteristics (OR = 0.82 [95% CI = 0.70-0.96]).

Conclusions

TUPE funding was associated with an increase in schools' tobacco-specific prevention activities and these enhanced activities were associated with lower tobacco use among students. This study also found that education and prevention efforts regarding emerging tobacco products need to be strengthened across all schools.

In this study, the impact of the apolipoprotein B mRNA-editing catalytic subunit-like (APOBEC) enzyme APOBEC3B (A3B) on epidermal growth factor receptor (EGFR)-driven lung cancer was assessed. A3B expression in EGFR mutant (EGFRmut) non-small-cell lung cancer (NSCLC) mouse models constrained tumorigenesis, while A3B expression in tumors treated with EGFR-targeted cancer therapy was associated with treatment resistance. Analyses of human NSCLC models treated with EGFR-targeted therapy showed upregulation of A3B and revealed therapy-induced activation of nuclear factor kappa B (NF-κB) as an inducer of A3B expression. Significantly reduced viability was observed with A3B deficiency, and A3B was required for the enrichment of APOBEC mutation signatures, in targeted therapy-treated human NSCLC preclinical models. Upregulation of A3B was confirmed in patients with NSCLC treated with EGFR-targeted therapy. This study uncovers the multifaceted roles of A3B in NSCLC and identifies A3B as a potential target for more durable responses to targeted cancer therapy.

Epigenetic modifications, including DNA methylation, represent a potential mechanism for environmental impacts on human disease. Maternal smoking in pregnancy remains an important public health problem that impacts child health in a myriad of ways and has potential lifelong consequences. The mechanisms are largely unknown, but epigenetics most likely plays a role. We formed the Pregnancy And Childhood Epigenetics (PACE) consortium and meta-analyzed, across 13 cohorts (n = 6,685), the association between maternal smoking in pregnancy and newborn blood DNA methylation at over 450,000 CpG sites (CpGs) by using the Illumina 450K BeadChip. Over 6,000 CpGs were differentially methylated in relation to maternal smoking at genome-wide statistical significance (false discovery rate, 5%), including 2,965 CpGs corresponding to 2,017 genes not previously related to smoking and methylation in either newborns or adults. Several genes are relevant to diseases that can be caused by maternal smoking (e.g., orofacial clefts and asthma) or adult smoking (e.g., certain cancers). A number of differentially methylated CpGs were associated with gene expression. We observed enrichment in pathways and processes critical to development. In older children (5 cohorts, n = 3,187), 100% of CpGs gave at least nominal levels of significance, far more than expected by chance (p value < 2.2 × 10(-16)). Results were robust to different normalization methods used across studies and cell type adjustment. In this large scale meta-analysis of methylation data, we identified numerous loci involved in response to maternal smoking in pregnancy with persistence into later childhood and provide insights into mechanisms underlying effects of this important exposure.