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This paper is concerned with the large-time behavior of solutions to the Cauchy problem for the one-dimensional unipolar Euler-Poisson equations with critical time-dependent over-damping. We prove that the Cauchy problem admits a unique global smooth solution which time-asymptotically converges to the stationary solution in the logarithmic form $ O(\ln^{-\frac{k}{2}}(1+t)) $ for the integer $ k\in[1, +\infty) $. In particular, the integer $ k $ can be large enough as the initial perturbation is small enough. This convergence rate is much better than the previous studies with critical over-damping. The proof is based on the technical time-weighted energy estimates and the mathematical induction. [ABSTRACT FROM AUTHOR]

Metal‐organic framework materials (MOFs) have the characteristics of versatile composition, high specific surface area, rich and orderly pore structure and adjustable pore size, which provide an ideal platform to develop desulfurization adsorbent and investigate the factors influencing the mercaptan removal performance. In this study, five kinds of MOFs with different adsorption sites (Cu, Ni, Zn), topological structure, pore size and defect degree were prepared and evaluated the desulfurization performance. The mercaptan adsorption capacity followed the order of CuBDC‐D>CuBDC>NiBDC>ZIF‐8>MOF‐5, and the metal site and defect were considered the main influence factors. The present study suggested that defect engineering of Cu based MOFs is a promising strategy to design efficient adsorbent for mercaptan removal. [ABSTRACT FROM AUTHOR]

Genomic studies have linked mTORC1 pathway-activating mutations with exceptional response to treatment with allosteric inhibitors of mTORC1 called rapalogs. Rapalogs are approved for selected cancer types, including kidney and breast cancers. Here, we used sequencing data from 22 human kidney cancer cases to identify the activating mechanisms conferred by mTOR mutations observed in human cancers and advance precision therapeutics. mTOR mutations that clustered in focal adhesion kinase targeting domain (FAT) and kinase domains enhanced mTORC1 kinase activity, decreased nutrient reliance, and increased cell size. We identified 3 distinct mechanisms of hyperactivation, including reduced binding to DEP domaincontaining MTOR-interacting protein (DEPTOR), resistance to regulatory associated protein of mTOR-mediated (RAPTOR-mediated) suppression, and altered kinase kinetics. Of the 28 mTOR double mutants, activating mutations could be divided into 6 complementation groups, resulting in synergistic Rag- and Ras homolog enriched in brain-independent (RHEB-independent) mTORC1 activation. mTOR mutants were resistant to DNA damage-inducible transcript 1-mediated (REDD1=mediated) inhibition, confirming that activating mutations can bypass the negative feedback pathway formed between HIF1 and mTORC1 in the absence of von Hippel-Lindau (VHL) tumor suppressor expression. Moreover, VHL-deficient cells that expressed activating mTOR mutants grew tumors that were sensitive to rapamycin treatment. These data may explain the high incidence of mTOR mutations observed in clear cell kidney cancer, where VHL loss and HIF activation is pathognomonic. Our study provides mechanistic and therapeutic insights concerning mTOR mutations in human diseases., Introduction mTOR is a serine-threonine kinase that forms 2 distinct signaling complexes, mTORC1 and mTORC2 (1, 2), which are composed of common subunits (mTOR, mLST8, DEPTOR) (3, 4) and uniquely [...]