Luminescent Organic–Inorganic Hybrids of Functionalized Mesoporous Silica SBA-15 by Thio-Salicylidene Schiff Base

Novel organic–inorganic mesoporous luminescent hybrid material N, N′-bis(salicylidene)-thiocarbohydrazide (BSTC-SBA-15) has been obtained by co-condensation of tetraethyl orthosilicate and the organosilane in the presence of Pluronic P123 surfactant as a template. N,N′-bis(salicylidene)-thiocarbohydrazide (BSTC) grafted to the coupling agent 3-(triethoxysilyl)-propyl isocyanate (TESPIC) was used as the precursor for the preparation of mesoporous materials. In addition, for comparison, SBA-15 doped with organic ligand BSTC was also synthesized, denoted as BSTC/SBA-15. This organic–inorganic hybrid material was well-characterized by X-ray diffraction, Fourier transform infrared spectroscopy, transmission electron microscopy (HRTEM), and photoluminescence spectra, which reveals that they all have high surface area, uniformity in the mesostructure. The resulting materials (BSTC-SBA-15 and BSTC/SBA-15) exhibit regular uniform microstructures, and no phase separation happened for the organic and the inorganic compounds was covalently linked through Si–O bonds via a self-assemble process. Furthermore, the two materials have different luminescence range: BSTC/SBA-15 presents the strong dominant green luminescence, while BSTC-functionalized material BSTC-SBA-15 shows the dominant blue emission

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field