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We demonstrated a stable and spectrum-selective self-powered UV photodetector based on lead-free Cs3Cu2I5 films with excellent photodetection performance.

We demonstrated a polarization-sensitive and flexible ultraviolet photodetector based on one-dimensional CsCu2I3 nanowires with a photocurrent anisotropy ratio of 3.16.

Hydrochromic materials have attracted widespread attention in the fields of anti-counterfeiting because of their ability of the reversible light absorption and/or emission properties in response to water. Here, for the first it is demonstrated that the ternary copper halides Cs 3 Cu 2 I 5 nanocrystals (NCs) possess excellent hydrochromic properties. The prepared Cs 3 Cu 2 I 5 NCs films can dynamically extract and insert CsI by exposing/removing water to realize the reversible conversion between blue-emissive Cs 3 Cu 2 I 5 and yellow-emissive CsCu 2 I 3 . Interestingly, polymethyl methacrylate (PMMA) coated Cs 3 Cu 2 I 5 can effectively avoid the extraction of CsI and maintain long-term stability in the water. Further, the hydrochromic Cs 3 Cu 2 I 5 and water-resistant Cs 3 Cu 2 I 5 @PMMA are used as the inks to synergistically act on anti-counterfeiting information to achieve multiple encryption effects, which can clearly identify and authenticate the effective information after moisture decryption. Importantly, the pattern can be re-encrypted to the invalid pattern after water evaporation. In addition, the anti-counterfeiting pattern has excellent stability during repeated encryption/decryption conversion cycles, which can not only balance the accessibility of anti-counterfeiting information but also effectively improve the security of information. This new discovery may not only deepen the understanding of Cs 3 Cu 2 I 5 but also provide new options for the design of hydrochromic materials for anti-counterfeiting information.

U14 is a conserved small nucleolar RNA (snoRNA) required for processing of yeast 18S rRNA. The presence of two long sequences (13 and 14 nucleotides) with strong complementarity to 18S rRNA suggests that U14 base-pairs with pre-rRNA. Evidence of direct binding was developed by showing that mutations in these U14 elements mimic U14 depletion and that function can be rescued by a compensatory sequence change in 18S RNA. The U14 elements are functionally interdependent, indicating that both participate in binding. Folding models predict that binding might occur through both rRNA elements simultaneously. Potential roles of U14 in rRNA folding, maturation, and ribosome assembly are discussed. U14 is one of several snoRNAs with long complementarities to rRNA and the first snoRNA in this class shown to interact directly with rRNA.

The transcription factor glioma-associated oncogene 1 (Gli1) has been recognized as a very important nuclear executor at the distal end of the Hedgehog (Hh) signal pathway, which has crucial roles in regulating many developmental processes, such as pattern formation, differentiation, proliferation, and apoptosis. Overexpression of patched 1 protein and Gli1 or constitutively active Indian Hedgehog (IHh)-parathyroid hormone-related protein signal pathway may lead to musculoskeletal tumorigenesis. However, for chondrosarcoma few studies have paid close attention to the IHh-Gli1 signal transduction cascade and more work needs to be carried out to fully elucidate Gli1 protein functions. Here we show that the IHh signal pathway was activated in chondrosarcoma, and knocking down the expression of Gli1 attenuated the disturbed IHh signal pathway, which not only suppressed cell proliferation and promoted G2/M cell cycle arrest but also enhanced cell apoptosis by downregulating Bcl-2 and Bcl-xl expression. Furthermore, Gli1 downregulation, not cyclopamine, induced autophagy by regulating mTOR phosphorylation, and inhibition of autophagy prevented Gli1 small interfering RNA-mediated cell death. We also demonstrated that extracellular signal-regulated kinase 1/2 activity may mediate these antiproliferative events induced by Gli1 inhibition. These results indicate that Gli1 inhibition could ultimately provide a promising new approach for chondrosarcoma treatment.

Mesenchymal stem cells (MSCs) show homing capacity towards tumor sites. Numerous reports indicate that they are involved in multiple tumor-promoting processes through several mechanisms, including immunosuppression; stimulation of angiogenesis; transition to cancer-associated fibroblasts; inhibition of cancer cell apoptosis; induction of epithelial–mesenchymal transition (EMT); and increase metastasis and chemoresistance. However, other studies have shown that MSCs suppress tumor growth by suppressing angiogenesis, incrementing inflammatory infiltration, apoptosis and cell cycle arrest, and inhibiting the AKT and Wnt signaling pathways. In this review, we discuss the supportive and suppressive impacts of MSCs on tumor progression and metastasis. We also discuss MSC-based therapeutic strategies for cancer based on their potential for homing to tumor sites.

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