Objective: This study evaluated the validity of self-reported smartphone usage data against objectively-measured smartphone usage data by directly tracking the activities in the participants’ smartphone among Chinese adolescents and young adults in Hong Kong. Methods: A total of 187 participants were recruited (mean age 19.4, 71.7% female) between 2017 and 2018. A smartphone usage tracking app was installed on all participants’ smartphone for 7 consecutive days. After the 7-day monitoring period, they completed a selfadministered questionnaire on smartphone usage habits. Results: Although the correlation between self-reported and objectively-measured total smartphone usage time was insignificant (ρ=-0.10, p=0.18), in three out of the four usage domains were positively and significantly correlated, namely social network (ρ=0.21, p=0.005), instant messaging (ρ=0.27, p<0.001), and games (ρ=0.64, p<0.001). Participants’ self-report of the total time spent on smartphones exceeded the objective data by around 760 min per week (self-reported 1,930.3 min/wk vs. objectively-measured 1,170.7 min/wk, p<0.001). Most of the over-reporting was contributed by the web browsing domain (self-reported 447.8 min/wk vs. objectively-measured 33.3 min/wk, p<0.001). Conclusion Our results showed large discrepancies between self-reported smartphone and objectively-measured smartphone usage except for self-reported usage on game apps.

Comparison of pancreaticoduodenal transplants (PDT) and duct-ligated pancreas transplant (DLPT) were performed using syngeneic and allogeneic studies in rats. Both DLPT and PDT allogeneic grafts showed mild rejection. DLPT groups showed disorganized pathology and acini replaced by fat. Eventually, massive fibrosis was seen in the Islets of Langerhans, as well as rejection cellular infiltrates. In both PDT groups, normal histology was observed in the same period. Thus the effect of duct occlusion is highly detrimental for the grafts.
Animals ; Graft Rejection/pathology ; Ligation/adverse effects ; Pancreas/*pathology ; Pancreas Transplantation/*adverse effects ; Pancreatic Ducts/surgery ; Postoperative Period ; Rats ; Rats, Inbred Lew ; Rats, Sprague-Dawley ; Research Support, Non-U.S. Gov't ; Transplantation, Homologous ; Transplantation, Isogeneic

Although genome-wide association studies have identified more than eighty genetic variants associated with non-small cell lung cancer (NSCLC) risk, biological mechanisms of these variants remain largely unknown. By integrating a large-scale genotype data of 15 581 lung adenocarcinoma (AD) cases, 8350 squamous cell carcinoma (SqCC) cases, and 27 355 controls, as well as multiple transcriptome and epigenomic databases, we conducted histology-specific meta-analyses and functional annotations of both reported and novel susceptibility variants. We identified 3064 credible risk variants for NSCLC, which were overrepresented in enhancer-like and promoter-like histone modification peaks as well as DNase I hypersensitive sites. Transcription factor enrichment analysis revealed that USF1 was AD-specific while CREB1 was SqCC-specific. Functional annotation and gene-based analysis implicated 894 target genes, including 274 specifics for AD and 123 for SqCC, which were overrepresented in somatic driver genes (ER = 1.95, P = 0.005). Pathway enrichment analysis and Gene-Set Enrichment Analysis revealed that AD genes were primarily involved in immune-related pathways, while SqCC genes were homologous recombination deficiency related. Our results illustrate the molecular basis of both well-studied and new susceptibility loci of NSCLC, providing not only novel insights into the genetic heterogeneity between AD and SqCC but also a set of plausible gene targets for post-GWAS functional experiments.
Adenocarcinoma of Lung/genetics* ; Carcinoma, Non-Small-Cell Lung/genetics* ; Carcinoma, Squamous Cell/genetics* ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Lung Neoplasms/genetics* ; Polymorphism, Single Nucleotide