Tongji University

About: Tongji University is a education organization based out in Shanghai, China. It is known for research contribution in the topics: Population & Adsorption. The organization has 76116 authors who have published 81176 publications receiving 1248911 citations. The organization is also known as: Tongji & Tóngjì Dàxué.

Eu(III)-functionalized MIL-124 as fluorescent probe for highly selectively sensing ions and organic small molecules especially for Fe(III) and Fe(II).

Abstract: A layerlike MOF (MIL-124, orGa2(OH)4(C9O6H4)) has been prepared and chosen as a parent compound to encapsulate Eu3+ cations by one uncoordinated carbonyl group in its pores. The Eu3+-incorporated sample (Eu3+@MIL-124) is fully characterized, which shows excellent luminescence and good fluorescence stability in water or other organic solvents. Subsequently, we choose Eu3+@MIL-124 as sensitive probe for sensing metal ions, anions, and organic small molecules because of its robust framework. Studying of the luminescence properties reveals that the complex Eu3+@MIL-124 was developed as a highly selective and sensitive probe for detection of Fe3+ (detection limit, 0.28 μM) and Fe2+ ions through fluorescence quenching of Eu3+ and MOF over other metal ions. In connection to this, a probable sensing mechanism was also discussed in this paper. In addition, when Eu3+@MIL-124 was immersed in the different anions solutions and organic solvents, it also shows highly selective for Cr2O72–(detection limit, 0.15 μM)and a...

Chromatin signature of embryonic pluripotency is established during genome activation

Abstract: After fertilization the embryonic genome is inactive until transcription is initiated during the maternal-zygotic transition. This transition coincides with the formation of pluripotent cells, which in mammals can be used to generate embryonic stem cells. To study the changes in chromatin structure that accompany pluripotency and genome activation, we mapped the genomic locations of histone H3 molecules bearing lysine trimethylation modifications before and after the maternal-zygotic transition in zebrafish. Histone H3 lysine 27 trimethylation (H3K27me3), which is repressive, and H3K4me3, which is activating, were not detected before the transition. After genome activation, more than 80% of genes were marked by H3K4me3, including many inactive developmental regulatory genes that were also marked by H3K27me3. Sequential chromatin immunoprecipitation demonstrated that the same promoter regions had both trimethylation marks. Such bivalent chromatin domains also exist in embryonic stem cells and are thought to poise genes for activation while keeping them repressed. Furthermore, we found many inactive genes that were uniquely marked by H3K4me3. Despite this activating modification, these monovalent genes were neither expressed nor stably bound by RNA polymerase II. Inspection of published data sets revealed similar monovalent domains in embryonic stem cells. Moreover, H3K4me3 marks could form in the absence of both sequence-specific transcriptional activators and stable association of RNA polymerase II, as indicated by the analysis of an inducible transgene. These results indicate that bivalent and monovalent domains might poise embryonic genes for activation and that the chromatin profile associated with pluripotency is established during the maternal-zygotic transition.

Repulsion Loss: Detecting Pedestrians in a Crowd

Abstract: Detecting individual pedestrians in a crowd remains a challenging problem since the pedestrians often gather together and occlude each other in real-world scenarios. In this paper, we first explore how a state-of-the-art pedestrian detector is harmed by crowd occlusion via experimentation, providing insights into the crowd occlusion problem. Then, we propose a novel bounding box regression loss specifically designed for crowd scenes, termed repulsion loss. This loss is driven by two motivations: the attraction by target, and the repulsion by other surrounding objects. The repulsion term prevents the proposal from shifting to surrounding objects thus leading to more crowd-robust localization. Our detector trained by repulsion loss outperforms the state-of-the-art methods with a significant improvement in occlusion cases.

Nuclear cGAS suppresses DNA repair and promotes tumorigenesis.

Abstract: Accurate repair of DNA double-stranded breaks by homologous recombination preserves genome integrity and inhibits tumorigenesis. Cyclic GMP–AMP synthase (cGAS) is a cytosolic DNA sensor that activates innate immunity by initiating the STING–IRF3–type I IFN signalling cascade1,2. Recognition of ruptured micronuclei by cGAS links genome instability to the innate immune response3,4, but the potential involvement of cGAS in DNA repair remains unknown. Here we demonstrate that cGAS inhibits homologous recombination in mouse and human models. DNA damage induces nuclear translocation of cGAS in a manner that is dependent on importin-α, and the phosphorylation of cGAS at tyrosine 215—mediated by B-lymphoid tyrosine kinase—facilitates the cytosolic retention of cGAS. In the nucleus, cGAS is recruited to double-stranded breaks and interacts with PARP1 via poly(ADP-ribose). The cGAS–PARP1 interaction impedes the formation of the PARP1–Timeless complex, and thereby suppresses homologous recombination. We show that knockdown of cGAS suppresses DNA damage and inhibits tumour growth both in vitro and in vivo. We conclude that nuclear cGAS suppresses homologous-recombination-mediated repair and promotes tumour growth, and that cGAS therefore represents a potential target for cancer prevention and therapy.