Traditional fluorescence-based tags, used for anticounterfeiting, rely on primitive pattern matching and visual identification; additional covert security features such as fluorescent lifetime or pattern masking are advantageous if fraud is to be deterred. Herein, we present an electrohydrodynamically printed unicolour multi-fluorescent-lifetime security tag system composed of lifetime-tunable lead-halide perovskite nanocrystals that can be deciphered with both existing time-correlated single-photon counting fluorescence-lifetime imaging microscopy and a novel time-of-flight prototype. We find that unicolour or matching emission wavelength materials can be prepared through cation-engineering with the partial substitution of formamidinium for ethylenediammonium to generate "hollow" formamidinium lead bromide perovskite nanocrystals; these materials can be successfully printed into fluorescence-lifetime-encoded-quick-read tags that are protected from conventional readers.  https://www.selleckchem.com/products/nvp-bgt226.html  Furthermore, we also demonstrate that a portable, cost-effective time-of-flight fluorescence-lifetime imaging prototype can also decipher these codes. A single comprehensive approach combining these innovations may be eventually deployed to protect both producers and consumers.Glioblastoma (GBM) is a deadly cancer in which cancer stem cells (CSCs) sustain tumor growth and contribute to therapeutic resistance. Protein arginine methyltransferase 5 (PRMT5) has recently emerged as a promising target in GBM. Using two orthogonal-acting inhibitors of PRMT5 (GSK591 or LLY-283), we show that pharmacological inhibition of PRMT5 suppresses the growth of a cohort of 46 patient-derived GBM stem cell cultures, with the proneural subtype showing greater sensitivity. We show that PRMT5 inhibition causes widespread disruption of splicing across the transcriptome, particularly affecting cell cycle gene products. We identify a GBM splicing signature that correlates with the degree of response to PRMT5 inhibition. Importantly, we demonstrate that LLY-283 is brain-penetrant and significantly prolongs the survival of mice with orthotopic patient-derived xenografts. Collectively, our findings provide a rationale for the clinical development of brain penetrant PRMT5 inhibitors as treatment for GBM.How can deceptive communication signals exist in an evolutionarily stable signalling system? To resolve this age-old honest signalling paradox, researchers must first establish whether deception benefits deceivers. However, while vocal exaggeration is widespread in the animal kingdom and assumably adaptive, its effectiveness in biasing listeners has not been established. Here, we show that human listeners can detect deceptive vocal signals produced by vocalisers who volitionally shift their voice frequencies to exaggerate or attenuate their perceived size. Listeners can also judge the relative heights of cheaters, whose deceptive signals retain reliable acoustic cues to interindividual height. Importantly, although vocal deception biases listeners' absolute height judgments, listeners recalibrate their height assessments for vocalisers they correctly and concurrently identify as deceptive, particularly men judging men. Thus, while size exaggeration can fool listeners, benefiting the deceiver, its detection can reduce bias and mitigate costs for listeners, underscoring an unremitting arms-race between signallers and receivers in animal communication.Erythropoietin (EPO) is not only an erythropoiesis hormone but also an immune-regulatory cytokine. The receptors of EPO (EPOR)2 and tissue-protective receptor (TPR), mediate EPO's immune regulation. Our group firstly reported a non-erythropoietic peptide derivant of EPO, cyclic helix B peptide (CHBP), which could inhibit macrophages inflammation and dendritic cells (DCs) maturation. As a kind of innate immune regulatory cell, myeloid-derived suppressor cells (MDSCs) share a common myeloid progenitor with macrophages and DCs. In this study, we investigated the effects on MDSCs differentiation and immunosuppressive function via CHBP induction. CHBP promoted MDSCs differentiate toward M-MDSCs with enhanced immunosuppressive capability. Infusion of CHBP-induced M-MDSCs significantly prolonged murine skin allograft survival compared to its counterpart without CHBP stimulation. In addition, we found CHBP increased the proportion of CD11b+Ly6G-Ly6Chigh CD127+ M-MDSCs, which exerted a stronger immunosuppressive function compared to CD11b+Ly6G-Ly6Chigh CD127- M-MDSCs. In CHBP induced M-MDSCs, we found that EPOR downstream signal proteins Jak2 and STAT3 were upregulated, which had a strong relationship with MDSC function. In addition, CHBP upregulated GATA-binding protein 3 (GATA-3) protein translation level, which was an upstream signal of CD127 and regulator of STAT3. These effects of CHBP could be reversed if Epor was deficient. Our novel findings identified a new subset of M-MDSCs with better immunosuppressive capability, which was induced by the EPOR-mediated Jak2/GATA3/STAT3 pathway. These results are beneficial for CHBP clinical translation and MDSC cell therapy in the future.Multiple myeloma (MM) is a heterogeneous haematological disease that remains clinically challenging. Increased activity of the epigenetic silencer EZH2 is a common feature in patients with poor prognosis. Previous findings have demonstrated that metabolic profiles can be sensitive markers for response to treatment in cancer. While EZH2 inhibition (EZH2i) has proven efficient in inducing cell death in a number of human MM cell lines, we hereby identified a subset of cell lines that despite a global loss of H3K27me3, remains viable after EZH2i. By coupling liquid chromatography-mass spectrometry with gene and miRNA expression profiling, we found that sensitivity to EZH2i correlated with distinct metabolic signatures resulting from a dysregulation of genes involved in methionine cycling. Specifically, EZH2i resulted in a miRNA-mediated downregulation of methionine cycling-associated genes in responsive cells. This induced metabolite accumulation and DNA damage, leading to G2 arrest and apoptosis. Altogether, we unveiled that sensitivity to EZH2i in human MM cell lines is associated with a specific metabolic and gene expression profile post-treatment.