The
development of simple, rapid-response sensors for water detection
in organic solvents is highly desirable in the chemical industry.
Here we demonstrate a unique luminescence water sensor based on a
dual-emitting europium-organic framework (Eu-MOF), which is assembled
from a purposely selected 2-aminoterephthalic acid ligand with responsive
fluorescence inherent in its intramolecular charge transfer (ICT)
process. This ICT process can be rapidly switched-on in the presence
of water owing to its ability to boost and stabilize the ICT state.
In contrast, the Eu3+ emission within the framework is
insensitive to water and can serve as a reference, thus enabling highly
sensitive water detection in a turn-on and ratiometric way. In addition,
the significant ratiometric luminescence response induced by water
makes Eu-MOF undergo a distinct change of emitting color from red
to blue, which is favorable for visual analysis with the naked eye.
Sensitive determination of water content (0.05–10% v/v) in
various organic solvents is achieved in multiple readouts including
ratiometric emission intensity, emission color, or the Commission
Internationale de l’Eclairage (CIE) chromaticity coordinate.
The present Eu-MOF sensor featuring high sensitivity and reusability,
self-calibration, simple fabrication and operation, and capability
for real-time and in situ detection is expected to
have practical applications in water analysis for industrial processes.
Background: The analysis of cancer diversity based on a logical framework of hallmarks has greatly improved our understanding of the occurrence, development and metastasis of various cancers. Methods: We designed Cancer Hallmark Genes (CHG) database which focuses on integrating hallmark genes in a systematic, standard way and annotates the potential roles of the hallmark genes in cancer processes. Following the conceptual criteria description of hallmark function the keywords for each hallmark were manually selected from the literature. Candidate hallmark genes collected were derived from 301 pathways of KEGG database by Lucene and manually corrected. Results: Based on the variation data, we finally identified the hallmark genes of various types of cancer and constructed CHG. And we also analyzed the relationships among hallmarks and potential characteristics and relationships of hallmark genes based on the topological structures of their networks. We manually confirm the hallmark gene identified by CHG based on literature and database. We also predicted the prognosis of breast cancer, glioblastoma multiforme and kidney papillary cell carcinoma patients based on CHG data. Conclusions: In summary, CHG, which was constructed based on a hallmark feature set, provides a new perspective for analyzing the diversity and development of cancers.
BackgroundConstructing and modeling the gene regulatory network is one of the central themes of systems biology. With the growing understanding of the mechanism of microRNA biogenesis and its biological function, establishing a microRNA-mediated gene regulatory network is not only desirable but also achievable.MethodologyIn this study, we propose a bioinformatics strategy to construct the microRNA-mediated regulatory network using genome-wide binding patterns of transcription factor(s) and RNA polymerase II (RPol II), derived using chromatin immunoprecipitation following next generation sequencing (ChIP-seq) technology. Our strategy includes three key steps, identification of transcription start sites and promoter regions of primary microRNA transcripts using RPol II binding patterns, selection of cooperating transcription factors that collaboratively function with the transcription factors targeted by ChIP-seq assay, and construction of the network that contains regulatory cascades of both transcription factors and microRNAs.Principal FindingsUsing CAMDA (Critical Assessment of Massive Data Analysis) 2009 data set that includes ChIP-seq data on RPol II and STAT1 (signal transducers and activators of transcription 1) in HeLa S3 cells in control condition and with interferon γ stimulation, we first identified promoter regions of 83 microRNAs in HeLa cells. We then identified two potential STAT1 collaborating factors, AP-1 and C/EBP (CCAAT enhancer-binding proteins), and further established eight feedback network elements that may regulate cellular response during interferon γ stimulation.ConclusionsThis study offers a bioinformatics strategy to provide testable hypotheses on the mechanisms of microRNA-mediated transcriptional regulation, based upon genome-wide protein-DNA interaction data derived from ChIP-seq experiments.
Chemotherapy agents can cause serious adverse effects by attacking both cancer tissues and normal tissues. Therefore, we proposed a synthetic lethality (SL) concept-based computational method to identify specific anticancer drug targets. First, a 3-step screening strategy (network-based, frequency-based and function-based screening) was proposed to identify the SL gene pairs by mining 697 cancer genes and the human signaling network, which had 6306 proteins and 62937 protein-protein interactions. The network-based screening was composed of a stability score constructed using a network information centrality measure (the average shortest path length) and the distance-based screening between the cancer gene and the non-cancer gene. Then, the non-cancer genes were extracted and annotated using drug-target interaction and drug description information to obtain potential anticancer drug targets. Finally, the human SL data in SynLethDB, the existing drug sensitivity data and text-mining were utilized for target validation. We successfully identified 2555 SL gene pairs and 57 potential anticancer drug targets. Among them, CDK1, CDK2, PLK1 and WEE1 were verified by all three aspects and could be preferentially used in specific targeted therapy in the future.
Alzheimer's disease is a multifactorial neurodegenerative disorder with many drug targets contributing to its etiology. Despite the devastating effects of this disease, therapeutic methods for treating Alzheimer's disease remain limited. The multifactorial nature of Alzheimer's disease strongly supports a multi-target rationale as a drug design strategy. Glycogen synthase kinase-3 beta and cyclin-dependent kinase 5 have been identified as being involved in the pathological hyperphosphorylation of tau proteins, which leads to the formation of neurofibrillary tangles and causes Alzheimer's disease. In this study, using a molecular docking method to screen a virtual library, we discovered molecules that can simultaneously inhibit Glycogen synthase kinase-3 beta and cyclin-dependent kinase 5 as lead compounds for the treatment of Alzheimer's disease. The docking results revealed the key residues in the substrate binding sites of both Glycogen synthase kinase-3 beta and cyclin-dependent kinase 5. A receiver operating characteristic curve indicated that the docking model consistently and selectively scored the majority of active compounds above decoys. The pre-treatment of cells with screened compounds protected them against Aβ25-35- induced cell death by up to 80%. Collectively, these findings suggest that some compounds have potential to be promising multifunctional agents for Alzheimer's disease treatment.
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