Peer Priming? A Large-Scale Field Experiment Studying the Impact of Popular Rankings on Demand in Mobile Retail

Consumers on mobile retail apps face significant search costs due to the small screen size of devices. One of the search aid features to improve the search convenience is to show consumers a small set of frequently used searches conducted by peer consumers on the platform as a prime cue. We refer to this feature as the popular ranking search aid (PRSA). Collaborating with Meituan, a leading services mobile app in China, we implement a large-scale field experiment to explore how PRSA affects consumer search activities and purchases. Our analyses generate three key findings. First, PRSA leads to an increase of 18.6% in page views and a 6.4% increase in purchases. Second, the change in shopping behavior emerges through a change in search behavior with more non-directed searches and fewer directed searches. Third, our mediation analysis supports that search behavior mediates the business outcomes. We offer theoretical and managerial implications

Design of Partially Etched GaP-OI Microresonators for Two-Color Kerr Soliton Generation at NIR and MIR

We present and theoretically investigate a dispersion engineered GaP-OI microresonator containing a partially-etched gap of 250 nm x 410 nm in a 600 nm x 2990 nm waveguide. This gap enables a 3.25 {\mu}m wide anomalous dispersion spectral span covering both the near-infrared and the mid-infrared spectra. This anomalous dispersion is manifested by two mechanisms, being the hybridization of the fundamental TE modes around 1550 nm and the geometric dispersion of the higher order TE mode around the 3100 nm wavelengths, respectively. Two Kerr soliton combs can be numerically generated with 101 GHz and 97 GHz teeth spacings at these spectral windows. The proposed structure demonstrates the design flexibility thanks to the partially etched gap and paves the way towards potential coherent multicolor frequency comb generation in the emerging GaP-OI platform

The Mechanism of ATP-Dependent Allosteric Protection of Akt Kinase Phosphorylation

SummaryKinases use ATP to phosphorylate substrates; recent findings underscore the additional regulatory roles of ATP. Here, we propose a mechanism for allosteric regulation of Akt1 kinase phosphorylation by ATP. Our 4.7-μs molecular dynamics simulations of Akt1 and its mutants in the ATP/ADP bound/unbound states revealed that ATP occupancy of the ATP-binding site stabilizes the closed conformation, allosterically protecting pT308 by restraining phosphatase access and key interconnected residues on the ATP→pT308 allosteric pathway. Following ATP→ADP hydrolysis, pT308 is exposed and readily dephosphorylated. Site-directed mutagenesis validated these predictions and indicated that the mutations do not impair PDK1 and PP2A phosphatase recruitment. We further probed the function of residues around pT308 at the atomic level, and predicted and experimentally confirmed that Akt1H194R/R273H double mutant rescues pathology-related Akt1R273H. Analysis of classical Akt homologs suggests that this mechanism can provide a general model of allosteric kinase regulation by ATP; as such, it offers a potential avenue for allosteric drug discovery

Prevalence and factors associated with post-traumatic stress disorder in healthcare workers exposed to COVID-19 in Wuhan, China: a cross-sectional survey

BackgroundThe COVID-19 pandemic has posed significant threats to both the physical and psychological health of healthcare workers working in the front-line combating COVID-19. However, studies regarding the medium to long term impact of COVID-19 on mental health among healthcare workers are limited. Therefore, we conducted this cross-sectional survey to investigate the prevalence, factors and impact of post-traumatic stress disorder (PTSD) in healthcare workers exposed to COVID-19 8 months after the end of the outbreak in Wuhan, China.MethodsA web-based questionnaire was delivered as a link via the communication application WeChat to those healthcare workers who worked at several COVID-19 units during the outbreak (from December 2019 to April 2020) in Wuhan, China. The questionnaire included questions on social-demographic data, the post-traumatic stress disorder checklist-5 (PCL-5), the family care index questionnaire (Adaptation, Partnership, Growth, Affection and Resolve, APGAR), and the quality-of-life scale (QOL). The prevalence, risk and protective factors, and impact of PTSD on healthcare workers were subsequently analyzed.ResultsAmong the 659 participants, 90 healthcare workers were still suffering from PTSD 8 months after the end of the outbreak of COVID-19 in Wuhan, in which avoidance and negative impact were the most affected dimensions. Suffering from chronic disease, experiencing social isolation, and job dissatisfaction came up as independent risk factors for PTSD, while obtaining COVID-19 related information at an appropriate frequency, good family function, and working in well-prepared mobile cabin hospitals served as protective factors. The impact of PTSD on COVID-19 exposed healthcare workers was apparent by shortened sleeping time, feeling of loneliness, poorer quality of life and intention to resign.ConclusionsEight months after the end of the COVID-19 outbreak in Wuhan, the level of PTSD in healthcare workers exposed to COVID-19 was still high. Apart from the commonly recognized risk factors, comorbid chronic disease was identified as a new independent risk factor for developing PTSD. For countries where the pandemic is still ongoing or in case of future outbreaks of new communicable diseases, this study may contribute to preventing cases of PTSD in healthcare workers exposed to infectious diseases under such circumstances

Circulating Monocytes Act as a Common Trigger for the Calcification Paradox of Osteoporosis and Carotid Atherosclerosis via TGFB1-SP1 and TNFSF10-NFKB1 Axis

BackgroundOsteoporosis often occurs with carotid atherosclerosis and causes contradictory calcification across tissue in the same patient, which is called the “calcification paradox”. Circulating monocytes may be responsible for this unbalanced ectopic calcification. Here, we aimed to show how CD14+ monocytes contribute to the pathophysiology of coexisting postmenopausal osteoporosis and carotid atherosclerosis.MethodsWe comprehensively analyzed osteoporosis data from the mRNA array dataset GSE56814 and the scRNA-seq dataset GSM4423510. Carotid atherosclerosis data were obtained from the GSE23746 mRNA dataset and GSM4705591 scRNA-seq dataset. First, osteoblast and vascular SMC lineages were annotated based on their functional expression using gene set enrichment analysis and AUCell scoring. Next, pseudotime analysis was applied to draw their differentiated trajectory and identify the key gene expression changes in crossroads. Then, ligand–receptor interactions between CD14+ monocytes and osteoblast and vascular smooth muscle cell (SMC) lineages were annotated with iTALK. Finally, we selected calcification paradox-related expression in circulating monocytes with LASSO analysis.ResultsFirst, we found a large proportion of delayed premature osteoblasts in osteoporosis and osteogenic SMCs in atherosclerosis. Second, CD14+ monocytes interacted with the intermediate cells of the premature osteoblast and osteogenic SMC lineage by delivering TGFB1 and TNFSF10. This interaction served as a trigger activating the transcription factors (TF) SP1 and NFKB1 to upregulate the inflammatory response and cell senescence and led to a retarded premature state in the osteoblast lineage and osteogenic transition in the SMC lineage. Then, 76.49% of common monocyte markers were upregulated in the circulating monocytes between the two diseases, which were related to chemotaxis and inflammatory responses. Finally, we identified 7 calcification paradox-related genes on circulating monocytes, which were upregulated in aging cells and downregulated in DNA repair cells, indicating that the aging monocytes contributed to the development of the two diseases.ConclusionsOur work provides a perspective for understanding the triggering roles of CD14+ monocytes in the development of the calcification paradox in osteoporosis- and atherosclerosis-related cells based on combined scRNA and mRNA data. This study provided us with an elucidation of the mechanisms underlying the calcification paradox and could help in developing preventive and therapeutic strategies