Mobile Internet Access Patterns for Travel: Comparison of Desktops, Tablets, and Phones

This study investigated information access patterns on desktops, tablets, and phones of a few different travel related websites through web log analysis. The results show that the three types of devices have different ratios of search traffic, referral traffic, and direct traffic. With a smaller screen on mobile devices, users visit fewer pages per visit, stay less time on the website per session, and have higher bounce rates. Content analysis revealed that travelers requested more specific information on mobile devices and general information on desktop computers, indicating information needs in late decision making stages on mobile devices

Fish species-specific TRIM gene FTRCA1 negatively regulates interferon response through attenuating IRF7 transcription

In mammals and fish, emerging evidence highlights that TRIM family members play important roles in the interferon (IFN) antiviral immune response. Fish TRIM family has undergone an unprecedented expansion leading to generation of finTRIM subfamily, which is exclusively specific to fish. Our recent results have shown that FTRCA1 (finTRIM C. auratus 1) is likely a fish species-specific finTRIM member in crucian carp C. auratus and acts as a negative modulator to downregulate fish IFN response by autophage-lysosomal degradation of protein kinase TBK1. In the present study, we found that FTRCA1 also impedes the activation of crucian carp IFN promoter by IRF7 but not by IRF3. Mechanistically, FTRCA1 attenuates IRF7 transcription levels likely due to enhanced decay of IRF7 mRNA, leading to reduced IRF7 protein levels and subsequently reduced fish IFN expression. E3 ligase activity is required for FTRCA1 to negatively regulate IRF7-mediated IFN response, because ligase-inactive mutants and the RING-deleted mutant of FTRCA1 lose the ability to block the activation of crucian carp IFN promoter by IRF7. These results together indicate that FTRCA1 is a multifaceted modulator to target different signaling factors for shaping fish IFN response in crucian carp.</p

Robotic Assembly Control Reconfiguration Based on Transfer Reinforcement Learning for Objects with Different Geometric Features

Robotic force-based compliance control is a preferred approach to achieve high-precision assembly tasks. When the geometric features of assembly objects are asymmetric or irregular, reinforcement learning (RL) agents are gradually incorporated into the compliance controller to adapt to complex force-pose mapping which is hard to model analytically. Since force-pose mapping is strongly dependent on geometric features, a compliance controller is only optimal for current geometric features. To reduce the learning cost of assembly objects with different geometric features, this paper is devoted to answering how to reconfigure existing controllers for new assembly objects with different geometric features. In this paper, model-based parameters are first reconfigured based on the proposed Equivalent Theory of Compliance Law (ETCL). Then the RL agent is transferred based on the proposed Weighted Dimensional Policy Distillation (WDPD) method. The experiment results demonstrate that the control reconfiguration method costs less time and achieves better control performance, which confirms the validity of proposed methods

MiRNA-145 increases therapeutic sensibility to gemcitabine treatment of pancreatic adenocarcinoma cells.

Pancreatic adenocarcinoma is one of the most leading causes of cancer-related deaths worldwide. Although recent advances provide various treatment options, pancreatic adenocarcinoma has poor prognosis due to its late diagnosis and ineffective therapeutic multimodality. Gemcitabine is the effective first-line drug in pancreatic adenocarcinoma treatment. However, gemcitabine chemoresistance of pancreatic adenocarcinoma cells has been a major obstacle for limiting its treatment effect. Our study found that p70S6K1 plays an important role in gemcitabine chemoresistence. MiR-145 is a tumor suppressor which directly targets p70S6K1 for inhibiting its expression in pancreatic adenocarcinoma, providing new therapeutic scheme. Our findings revealed a new mechanism underlying gemcitabine chemoresistance in pancreatic adenocarcinoma cells