Uncovering User Interest from Biased and Noised Watch Time in Video Recommendation

In the video recommendation, watch time is commonly adopted as an indicator of user interest. However, watch time is not only influenced by the matching of users' interests but also by other factors, such as duration bias and noisy watching. Duration bias refers to the tendency for users to spend more time on videos with longer durations, regardless of their actual interest level. Noisy watching, on the other hand, describes users taking time to determine whether they like a video or not, which can result in users spending time watching videos they do not like. Consequently, the existence of duration bias and noisy watching make watch time an inadequate label for indicating user interest. Furthermore, current methods primarily address duration bias and ignore the impact of noisy watching, which may limit their effectiveness in uncovering user interest from watch time. In this study, we first analyze the generation mechanism of users' watch time from a unified causal viewpoint. Specifically, we considered the watch time as a mixture of the user's actual interest level, the duration-biased watch time, and the noisy watch time. To mitigate both the duration bias and noisy watching, we propose Debiased and Denoised watch time Correction (D$^2$Co), which can be divided into two steps: First, we employ a duration-wise Gaussian Mixture Model plus frequency-weighted moving average for estimating the bias and noise terms; then we utilize a sensitivity-controlled correction function to separate the user interest from the watch time, which is robust to the estimation error of bias and noise terms. The experiments on two public video recommendation datasets and online A/B testing indicate the effectiveness of the proposed method.Comment: Accepted by Recsys'2

Enhanced and shortened Mn 2+ emissions by Cu + co-doping in borosilicate glasses for W-LEDs

A novel pair of transition metal ions Cu+, Mn2+ is co-doped in borosilicate glasses. Both copper and manganese ions exist in lower valence states (Cu+, Mn2+) in the as-prepared glasses. Around 5-time enhanced Mn2+ emission under the UV excitation is observed, which, as demonstrated by excitation spectra and emission decay curves, is due to an energy transfer from Cu+ ions resulting in greatly increased absorption of Mn2+ ions in the UV region, and relaxation on doubly-forbidden transition of Mn2+ leading to the much shortened Mn2+ emission lifetime from millisecond to microsecond level. Besides, a composite white emission is generated by combining the blue-green part from Cu+ ions with the green-red part from Mn2+ ions and it can be effectively tuned from cold to warm by adjusting host glass composition and altering excitation wavelength. Relevant mechanisms are discussed

Network medicine links SARS-CoV-2/COVID-19 infection to brain microvascular injury and neuroinflammation in dementia-like cognitive impairment

Background Dementia-like cognitive impairment is an increasingly reported complication of SARS-CoV-2 infection. However, the underlying mechanisms responsible for this complication remain unclear. A better understanding of causative processes by which COVID-19 may lead to cognitive impairment is essential for developing preventive and therapeutic interventions. Methods In this study, we conducted a network-based, multimodal omics comparison of COVID-19 and neurologic complications. We constructed the SARS-CoV-2 virus-host interactome from protein-protein interaction assay and CRISPR-Cas9-based genetic assay results and compared network-based relationships therein with those of known neurological manifestations using network proximity measures. We also investigated the transcriptomic profiles (including single-cell/nuclei RNA-sequencing) of Alzheimer’s disease (AD) marker genes from patients infected with COVID-19, as well as the prevalence of SARS-CoV-2 entry factors in the brains of AD patients not infected with SARS-CoV-2. Results We found significant network-based relationships between COVID-19 and neuroinflammation and brain microvascular injury pathways and processes which are implicated in AD. We also detected aberrant expression of AD biomarkers in the cerebrospinal fluid and blood of patients with COVID-19. While transcriptomic analyses showed relatively low expression of SARS-CoV-2 entry factors in human brain, neuroinflammatory changes were pronounced. In addition, single-nucleus transcriptomic analyses showed that expression of SARS-CoV-2 host factors (BSG and FURIN) and antiviral defense genes (LY6E, IFITM2, IFITM3, and IFNAR1) was elevated in brain endothelial cells of AD patients and healthy controls relative to neurons and other cell types, suggesting a possible role for brain microvascular injury in COVID-19-mediated cognitive impairment. Overall, individuals with the AD risk allele APOE E4/E4 displayed reduced expression of antiviral defense genes compared to APOE E3/E3 individuals. Conclusion Our results suggest significant mechanistic overlap between AD and COVID-19, centered on neuroinflammation and microvascular injury. These results help improve our understanding of COVID-19-associated neurological manifestations and provide guidance for future development of preventive or treatment interventions, although causal relationship and mechanistic pathways between COVID-19 and AD need future investigations