Redox flow batteries are promising for large-scale energy storage, but some long-standing problems such as safety issues, system cost and cycling stability must be resolved. Here we demonstrate a type of redox flow battery that is based on all-polymer particulate slurry electrolytes. Micro-sized and uniformly dispersed all-polymer particulate suspensions are utilized as redox-active materials in redox flow batteries, breaking through the solubility limit and facilitating the application of insoluble redox-active materials. Expensive ion-exchange membranes are replaced by commercial dialysis membranes, which can simultaneously realize the rapid shuttling of H + ions and cut off the migration of redox-active particulates across the separator via size exclusion. In result, the all-polymer particulate slurry redox flow batteries exhibit a highly reversible multi-electron redox process, rapid electrochemical kinetics and ultra-stable long-term cycling capability.

For the first time, 4-alkyl Hantzsch esters were used to construct molecules with all-carbon quaternary centers by visible light-induced photoredox catalysis via transfer alkylation. Up to a 1500 h(-1) turnover frequency was achieved in this reaction. Reactions of 4-alkyl Hantzsch nitriles as tertiary radical donors joined two contiguous all-carbon quaternary centers intermolecularly, and this chemistry was used to synthesize a common precursor of a class of hydroxysteroid dehydrogenase inhibitors.

As of February 11, 2020, all prefecture-level cities in mainland China have reported confirmed cases of 2019 novel coronavirus (2019-nCoV), but the city-level epidemical dynamics is unknown. The aim of this study is to model the current dynamics of 2019-nCoV at city level and predict the trend in the next 30 days under three possible scenarios in mainland China. We developed a spatially explicit epidemic model to consider the unique characteristics of the virus transmission in individual cities. Our model considered that the rate of virus transmission among local residents is different from those with Wuhan travel history due to the self-isolation policy. We introduced a decay rate to quantify the effort of each city to gradually control the disease spreading. We used mobile phone data to obtain the number of individuals in each city who have travel history to Wuhan. This city-level model was

INPH patients present hyperdynamic flow with increased velocity and volume both in systole and diastole phase. Degree of rising in diastole phase exceeds that of systole phase. The resulting reversal of netflow direction may play a key role in the occurrence of ventriculomegaly in iNPH patients.

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The second-generation antiandrogen enzalutamide, targeting androgen receptor (AR), was approved to treat castration resistant prostate cancer (CRPC) in 2012. Its resistance was observed when it was in the clinical research stage. AR mutation is the main factor of enzalutamide resistance. AR F876L and F876L_T877A mutations were reported to switch enzalutamide from AR antagonist to agonist, but W741C cannot. There are various mutations in the ligand binding domain of AR LBD, such as L701H, W741L, H874Y, T877A, and M895T, if these mutations can lead to drug resistance problem or not is not known. In this work, molecular dynamics (MD) simulations and molecular mechanics Generalized Born (GB) surface area (MM-GBSA) calculations were employed to explore the interaction mechanisms between enzalutamide and wild-type (WT)/mutant ARs. The simulation results indicate that helix 12 (H12), which lies on the top of the AR LBD like a cover, plays a vital role for the function of enzalutamide. When C-ring of enzalutamide locates near to H12, the distance between enzalutamide and H12 is reduced, which prevents H12 from closing and distort the coactivator binding site, resulting in the inactivation of transcription. In this case, enzalutamide acts as an AR antagonist. However, when the C-ring of enzalutamide is near to helix H11 or the Loop 11-12, H12 tends to close to form a coactivator binding site to facilitate transcription, enzalutamide acts as an AR agonist. Moreover, per-residue free energy decomposition analysis indicates that M895 and I899 are key residues in the antagonist mechanism of enzalutamide. J. Cell. Biochem. 118: 2792-2801, 2017. © 2017 Wiley Periodicals, Inc.

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Background and Purpose: It is still not clear whether Notch1 signaling inhibition can promote functional outcomes after stroke, given that it plays time-dependent roles in the sequential process of endogenous neurogenesis. The purpose of this study was to identify the appropriate time frame for Notch1 signaling inhibition according to the temporal evolution of Notch1 signaling activation and the responses of neural stem cells (NSCs), in order to target it for therapeutic intervention and stimulate neurorestorative strategies after stroke.Methods: Sprague-Dawley (SD) rats were subjected to 90-min of middle cerebral artery occlusion (MCAO). Rats were sacrificed before, and at day 1, day 2, day 3, day 4, and day 7 after ischemia for immunohistochemical analysis of the Notch intracellular domain (NICD), Nestin and doublecortin (Dcx). Next, MCAO rats were treated with the γ-secretase inhibitor N-[N-(3,5-di uorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester (DAPT) or with saline at day 4 after ischemia, and subsequently evaluated with behavioral test analysis and magnetic resonance imaging (MRI). The rat brains were then harvested for immunohistochemical analysis of Dcx, NeuN and myelin basic protein (MBP) at 2, 3, 4, and 8 weeks.Results: Notch1 signaling was maximally activated at day 3 after ischemia in parallel with the temporal evolution of NSCs. Inhibiting Notch1 signaling at day 4 after reperfusion with DAPT further promoted recovery of MRI parameters of the corticospinal tract (CST) and the functional outcomes, concomitantly with an increase in neuroblasts, their migration to the ischemic boundary, and potential differentiation to mature neurons, as well as the amelioration of axonal bundle integrity.Conclusion: Inhibition of Notch1 signaling at the subacute stage of stroke could maximally promote endogenous neurogenesis and axonal reorganization.