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A porous organic cage crystal, α-CC2, shows unexpected adsorption of sulphur hexafluoride (SF6) in its cage cavities analysis of the static crystal structure indicates that SF6 is occluded, as even the smallest diatomic gas, H2, is larger than the window of the cage pore. Herein, we use in situ powder X-ray diffraction (PXRD) experiments to provide unequivocal evidence for the presence of SF6 inside the 'occluded' cage voids, pointing to a mechanism of dynamic flexibility of the system. By combining PXRD results with molecular dynamics simulations, we build a molecular level picture of the cooperative porosity in α-CC2 that facilitates the passage of SF6 into the cage voids.Conventional conductive hydrogels usually lack self-healing properties, but might be favorable for smart electronic applications. Therefore, we present the fabrication of conductive self-healing hydrogels that merge the merits of electrical conductivity and self-healing properties. The conductive self-healing hydrogel composite was prepared by using single-walled carbon nanotubes (SWCNTs), poly(vinyl alcohol) (PVA), and a poly(N,N-dimethyl acrylamide) copolymer derivative modified with pyrene and borate functional moieties. While the tethered pyrene groups of the copolymer facilitated an even dispersion of the conductive components, i.e., SWCNTs, in aqueous solution viaπ-π stacking, the hydrogel system was formed via covalent dynamic cross-linking through tetrahedral borate ion interaction with the -OH group of PVA. The hydrogel composites exhibited bulk conductivity (1.27 S m-1 with 8 mg mL-1 SWCNTs) with a fast and autonomous self-healing ability that restored 95% of the original conductivity within 10 s under ambient conditions. Accordingly, due to their outstanding properties, we postulate that these composites may have potential in biomedical applications, such as tissue engineering, wound healing or electronic skins.The reactive oxygen species (ROS)-mediated anti-cancer therapy that shows the advantages of tumor specificity, high curative effect, and less toxic side-effects has powerful potential for cancer treatment. However, hypoxia in the tumor microenvironment (TME) and low penetrability of photosensitizers further limit their clinical application. Here, we present a composite core-shell-structured nanozyme (MS-ICG@MnO2@PEG) that consists of a mesoporous silica nanoparticle (MS) core and a MnO2 shell loaded with the photosensitizer indocyanine green (ICG) and then coated with PEG as the photodynamic/chemodynamic therapeutic agent for the ROS-mediated cancer treatment. On the one hand, MS-ICG@MnO2@PEG catalyzes H2O2 to produce O2 for enhanced photodynamic therapy (PDT), and on the other hand, it consumes GSH to trigger a Fenton-like reaction that generates *OH, thus enhancing the chemodynamic therapy (CDT). At the cellular level, MS-ICG@MnO2@PEG nanozymes exhibit good biocompatibility and induce the production of ROS in 4T1 tumor cells. It disrupts the redox balance in tumor cells affecting the mitochondrial function, and specifically kills the tumor cells. In vivo, the MS-ICG@MnO2@PEG nanozymes selectively accumulate at tumor sites and inhibit tumor growth and metastasis in 4T1 tumor-bearing mice. Accordingly, this study shows that the core-shell nanozymes can serve as an effective platform for the ROS-mediated breast cancer treatment by enhancing the combination of PDT and CDT.Selenium vacancy engineering has been realized in Co0.85Se nanoparticles via an anoxic melting strategy, where the vacancy content can be continuously controlled to modulate atomic disordering. The resulting Co0.85Se-30 catalyst requires a super low overpotential of 243 mV to achieve 10 mA cm-2 for the OER with a Tafel slope of 45.5 mV dec-1 and 70 h stability. In-depth electrochemical analysis finds that the outstanding properties are chiefly attributed to the dynamic Co-centers, giving the highest intrinsic activity (jCo = 6.49 A g-1 at η = 270 mV) and lowest apparent activation energy (42.43 kJ mol-1).Two Pt complexes with high quantum yields and photostability, and low cytotoxicity, were developed to track RNA G-quadruplexes (GQs) in live cells. Higher number and intensity, and longer lifetime of fluorescent foci in cancer cells than those in healthy cells suggest that the quantity and folding dynamics of RNA GQs could not only correlate to their biological functions, but be two novel biomarkers to characterize cancerous cells.In this study, the detailed kinetic mechanism of the trans-decalin + OH reaction is firstly investigated for a wide range of conditions (i.e., T = 200-2000 K & P = 0.76-76 000 Torr) using the M06-2X/aug-cc-pVTZ level and stochastic Rice-Ramsperger-Kassel-Marcus based master equation (RRKM-ME) rate model, which includes corrections of the hindered internal rotor (HIR) and tunneling effects. Panobinostat supplier Our predicted global rate constant excellently matches with the scarce experimental measurement (R. Atkinson, et al. Int. J. Chem. Kinet., 1983, 15, 37-50). The H-abstraction channel from Cα of trans-decalin is found to be dominant at low temperatures. A U-shaped temperature-dependent behavior and slightly positive pressure-dependence at low temperatures (e.g., T ≤ 400 K & P = 760 Torr) of the total rate constants are also observed. Detailed analysis reveals that the HIR treatment is essential to capture the kinetic behavior while the tunneling correction only plays a minor role.Senescence of smooth muscle cells (SMCs) has a crucial role in the pathogenesis of abdominal aortic aneurysm (AAA), a disease of vascular degeneration. Perturbation of cellular ribosomal DNA (rDNA) transcription triggers nucleolar stress response. Previously we demonstrated that induction of nucleolar stress in SMCs elicited cell cycle arrest via the ataxia-telangiectasia mutated (ATM)/ATM- and Rad3-related (ATR)-p53 axis. However, the specific roles of nucleolar stress in vascular degeneration remain unexplored. In the present study, we demonstrated for the first time that in both human and animal AAA tissues, there were non-coordinated changes in the expression of RNA polymerase I machinery components, including a downregulation of transcription initiation factor-IA (TIF-IA). Genetic deletion of TIF-IA in SMCs in mice (smTIF-IA-/-) caused spontaneous aneurysm-like lesions in the aorta. In vitro, induction of nucleolar stress triggered a non-canonical DNA damage response, leading to p53 phosphorylation and a senescence-like phenotype in SMCs.
Here's my website: https://www.selleckchem.com/products/LBH-589.html
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