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Gaze-adaptive interfaces can enable intuitive hands-free augmented reality (AR) interaction but unintentional selection (i.e. "Midas Touch") can have serious consequences during high-stakes real-world AR use. In the present study, we assessed how simulated gaze-adaptive AR interfaces, implementing single and dual gaze inputs, influence Soldiers' human performance and user experience (UX) in a fast-paced virtual reality marksmanship task. In Experiment 1, we investigated 1- and 2-stage dwell-based interfaces, finding confirmatory dual gaze dwell input effectively reduced Midas Touch but also reduced task performance and UX compared to an always-on (AO) interface. In Experiment 2, we investigated gaze depth-based interfaces, finding similar negative impacts of confirmatory dwell on Midas Touch, task performance, and UX. Overall, compared to the AO interface, single gaze input interfaces (e.g. single dwell or gaze depth threshold) reduced viewing of task-irrelevant information and yielded similar task performance and UX despite being prone to Midas Touch. Broadly, our findings demonstrate that AR users performing fast-paced dynamic tasks can tolerate some unintentional activation of AR displays if reliable and rapid information access is maintained and point to the need to develop and refine gaze depth estimation algorithms and novel gaze depth-based interfaces that provide rapid access to AR display content. [ABSTRACT FROM AUTHOR]

Based on the mixed ligands of 1,4‐bis(2,4,6‐tricarboxylpyrid‐5‐yl)benzene (H6BTPB) and 1,4‐bis(imidazol‐1‐yl)benzene (bib), a new cadmium(II) coordination polymer with the molecular formula of {[Cd(bib)(μ2‐H2O)(H2O)2](H4BTPB)0.5(bib)0.5}n (CdCP) was constructed under solvothermal condition, and displayed a 3D supramolecular structure expanded by the hydrogen bonds between the 1D [Cd(bib)(μ2‐H2O)(H2O)2]n ladder chain and the guests. Profiting from its superior stability and inherent luminescence, the prepared CdCP dispalyed great potential as a highly sensitive and selective luminescent sensor in trace detection of 3‐NT biomarker in both water and real bodily fluids through the luminescence quenching effects, with the Ksv and LODs being 2.408×105 M−1 and 30.3 nM in water, 2.230×105 M−1 and 44.7 nM in diluted urine, 2.249×105 M−1 and 43.9 nM in diluted serum, respectively. Subsequent mechanism studies indicated the synergistic effect of internal filtering effect, photo‐induced electron transfer, and fluorescence resonance energy transfer determining the luminescence quenching response of CdCP towards 3‐NT biomarker. [ABSTRACT FROM AUTHOR]

Hypoxia has been highly proven a hallmark of tumor micro‐environment, promoting the malignant phenotypes, playing a crucial role from tumor initiation, progression, invasion, and intravasation to metastatic dissemination and outgrowth. Increasing evidence also showed that hypoxia mediated the abnormal lipid metabolism in cancer by regulating various oncogenic signal pathways. However, it is still unclear but attractive how hypoxia specifically functioned and changed the condition of the tumor micro‐environment. In present study, we find that hypoxia promoted the methylation degree of CBR4 promoter region thus downgraded the expression of CBR4, which promoted GEP‐NETs progression and increased the sensitivity of GEP‐NETs cells to everolimus. Further, CBR4 interacted with fatty acid synthase (FASN), displaying a down‐regulation of FASN by activating the ubiquitin proteasome pathway and suppressed mTOR signaling. Overall, our results uncovers the CBR4/FASN/mTOR axis as a mechanism for tumor development and inspires us a new molecular guide for the therapeutic strategies for GEP‐NETs treatment. [ABSTRACT FROM AUTHOR]

Exosomes play significant roles in the communications between tumor cells and tumor microenvironment. However, the specific mechanisms by which exosomes modulate tumor development under hypoxia in pancreatic neuroendocrine tumors (pNETs) are not well understood. This study aims to investigate these mechanisms and made several important discoveries. We found that hypoxic exosomes derived from pNETs cells can activate tumor‐associated macrophages (TAM) to the M2 phenotype, in turn, the M2‐polarized TAM, facilitate the migration and invasion of pNETs cells. Further investigation revealed that CEACAM5, a protein highly expressed in hypoxic pNETs cells, is enriched in hypoxic pNETs cell‐derived exosomes. Hypoxic exosomal CEACAM5 was observed to induce M2 polarization of TAM through activation of the MAPK signaling pathway. Coculturing pNETs cells with TAM or treated with hypoxic exosomes enhanced the metastatic capacity of pNETs cells. In conclusion, these findings suggest that pNETs cells generate CEACAM5‐rich exosomes in a hypoxic microenvironment, which in turn polarize TAM promote malignant invasion of pNETs cells. Targeting exosomal CEACAM5 could potentially serve as a diagnostic and therapeutic strategy for pNETs. [ABSTRACT FROM AUTHOR]