Cosolvent or Antisolvent? A Molecular View of the Interface between Ionic Liquids and Cellulose upon Addition of Another Molecular Solvent

Ionic liquids (ILs) are promising nonderivatizing solvents for the dissolution of cellulose and lignin in biomass pretreatment processes, which are, however, retarded by sluggish dynamics. Recent investigations showed that cosolvents such as dimethyl sulfoxide (DMSO) can accelerate the dissolution dramatically. On the other hand, water is used as a common antisolvent to regenerate cellulose from solutions. To understand the co-/antisolvent effects in dissolving cellulose by ILs, we performed molecular dynamics simulations of the interfaces between an I_β cellulose crystal and different solvent systems, including ILs, DMSO, water, and mixed solvent systems. The density profiles and pair energy distributions (PEDs) show that the anions interact much more strongly with the cellulose surface than the cations, which is responsible for the dissolution of cellulose. It was found that the number of chloride ions in contact with cellulose does not cause the co-/antisolvent effect. In contrast, the cellulose–chloride PEDs are sensitive to the addition of molecular solvents, such as DMSO and water. Detailed analyses show that multiple hydrogen-bond (HB) patterns are formed between chloride and the hydroxyl groups of cellulose that are noticeably changed in the presence of DMSO or water. A combined analyses of both the PEDs and HB patterns can provide valuable information about the enhancement of cellulose dissolution. The simulation results in this work present useful knowledge for the design of solvent systems for dissolving cellulose or other types of biomass

Local Structure Evolution and its Connection to Thermodynamic and Transport Properties of 1-Butyl-3-methylimidazolium Tetrafluoroborate and Water Mixtures by Molecular Dynamics Simulations

Our recently developed improved united atom force field shows a good quality to reproduce both the static and transport properties of neat ionic liquids (ILs). Combined with the TIP4P-Ew water model, the force field is used to simulate the mixture of 1-butyl-3-methylimidazolium tetrafluoroborate ([C₄mim]­[BF₄]) and water without further optimization to adjust any cross parameters. Liquid densities of the mixture are well predicted over the entire concentration range at temperatures from 298.15 to 353.15 K. Simulations also reproduce the positive values of excess volumes and excess enthalpies, as well as their increase with temperature. The simulated viscosities are in good agreement with experimental values, especially in the water-rich region. We found three distinct regions by analyzing the concentration dependent self-diffusion coefficients via Stokes–Einstein (SE) relation, indicating the mixture experiences significant microheterogeneity with the adding of water. This observation is well connected to the structure features obtained in simulations, such as radial distribution functions (RDFs), spatial distribution functions (SDFs) and water clustering analysis. At the water mole fraction (<i>x</i>₂) less than 0.2, most of the water molecules are isolated in the polar cation–anion network in ionic liquids. With the increase of <i>x</i>₂ from 0.2 to 0.8, large water cluster forms and eventually percolates the whole system. When <i>x</i>₂ > 0.8, ionic liquids show a moderate degree of aggregation (with maximum around 0.9 to 0.95) before the cations and anions are fully dissolved in water

real ice accumulation

the excel for velocity and ice thickness analysis <br><br

Adsorption and Diffusion of <i>n</i>‑Heptane and Toluene over Mesoporous ZSM‑5 Zeolites

ZSM-5 zeolites with different mesoporosities were prepared by alkaline treatment and characterized by powder XRD and nitrogen adsorption. Two C₇ hydrocarbons of <i>n</i>-heptane and toluene were employed as probe molecules to investigate the effects of the introduction of mesopore on the adsorption and diffusion properties of ZSM-5 zeolites by comparing the experimental results of the samples treated and untreated by using NaOH. Adsorption isotherms were measured gravimetrically in the pressure range 0–32 mbar and from 293 to 338 K. The isotherms of microporous and mesoporous ZSM-5 were successfully fitted by using the Langmuir–Freundlich model and the dual-site Langmuir–Freundlich model, respectively. Henry’s constants and the initial heats of adsorption calculated from the adsorption isotherms as well as the fitting parameters displayed that the interactions between adsorbent and adsorbate were weakened after the introduction of mesopore, and the interactions between the adsorbates with microporous surface are much stronger than that between them with the mesoporous surface. Diffusion measurements were undertaken using the zero length column (ZLC) technique at partial pressure of <i>p</i>/<i>p</i>₀ < 0.000 15 from 333 to 393 K. The results showed that the effective diffusion constants (<i>D</i>_eff/<i>R</i>²) of the two C₇ hydrocarbons increased greatly in the presence of mesopores, while the corresponding activation energy decreased due to the reduced diffusion resistance and the shortened diffusion path in the mesoporous zeolites. Also, higher and much more dramatic enhancement of the efficient diffusivities as a function of mesoporous volume for toluene relative to that for <i>n</i>-heptane were found, indicating that the diffusion of <i>n</i>-heptane is controlled by the micropore diffusion and that the diffusion of toluene is exclusively determined by mass transfer through the mesopores

Noncanonical autophagy is a new strategy to inhibit HSV-1 through STING1 activation

STING1 (stimulator of interferon response cGAMP interactor 1) plays an essential role in immune responses for virus inhibition via inducing the production of type I interferon, inflammatory factors and macroautophagy/autophagy. In this study, we found that STING1 activation could induce not only canonical autophagy but also non-canonical autophagy (NCA) which is independent of the ULK1 or BECN1 complexes to form MAP1LC3/LC3-positive structures. Whether STING1-induced NCA has similar characters and physiological functions to canonical autophagy is totally unknown. Different from canonical autophagy, NCA could increase single-membrane structures and failed to degrade long-lived proteins, and could be strongly suppressed by interrupting vacuolar-type H+-translocating ATPase (V-ATPase) activity. Importantly, STING1-induced NCA could effectively inhibit DNA virus HSV-1 in cell model. Moreover, STING1[1-340], a STING1 mutant lacking immunity and inflammatory response due to deletion of the tail end of STING1, could degrade virus through NCA alone, suggesting that the antiviral effect of activated STING1 could be separately mediated by inherent immunity, canonical autophagy, and NCA. In addition, the translocation and dimerization of STING1 do not rely on its immunity function and autophagy pathway. Similar to canonical autophagy, LC3-positive structures of NCA induced by STING1 could finally fuse with lysosomes, and the degradation of HSV-1 could be reverted by inhibition of lysosome function, suggesting that the elimination of DNA virus via NCA still requires the lysosome pathway. Collectively, we proved that besides its classical immunity function and canonical autophagy pathway, STING1-induced NCA is also an efficient antiviral pathway for the host cell.</p

RIP2 regulates the caspase-11 non-canonical inflammasome.

<p><b>(A–B)</b> WT and <i>Rip2^−/−</i> BMDM were infected with 20MOI of <i>C. rodentium</i> for 18 h and combined supernatant and lysates were examined by Western blot for caspase-11 cleavage (casp-11p30) visually (A) and by densitometry (B). <b>(C–D)</b> WT and <i>Rip2^−/−</i> BMDM were infected with 20MOI of <i>C. rodentium</i> for 2 h and <i>Rip2^−/−</i> cells were subsequently treated with NAC or mock treated as a control. Samples were collected at 18 h and caspase-11 activation was examined as in panels A–B. <b>(E)</b> Densitometry was performed on pro-Caspase-11 p43 band from 3 independent experiments. <b>(F–G)</b> WT and <i>Rip2^−/−</i> BMDM were infected with 20MOI of <i>C. rodentium</i> for 4 h and cells were subsequently treated with 1 µM MG-132 or mock treated as a control. Samples were collected at the indicated time points and pro-caspase-11 levels examined by Western blot and densitometry. <b>(H)</b> WT and <i>Rip2^−/−</i> BMDM were infected with 20MOI of <i>C. rodentium</i> and RNA collected at the indicated time points and analyzed by qRT-PCR for fold induction and normalized to GAPDH. (A–H) Data are representative of three independent experiments with n = 2–3 wells per experiment and displayed as the mean ± SEM. (**, p<0.01; ***, p<0.001).</p

RIP2 regulates caspases-11 expression through a ROS-JNK pathway.

<p><b>(A)</b> WT and <i>Rip2^−/−</i> BMDM were infected with 20MOI of <i>C. rodentium</i> for 18 h and supernatants collected and examined for type-I interferon using a reporter cell line (U = Units). <b>(B–C)</b> WT or <i>Rip2^−/−</i> BMDM were infected with 20MOI of <i>C. rodentium</i> and mock treated or treated with H₂O₂. Samples were collected at the indicated times and examined for total JNK or phosphorylated JNK by Western blot. <b>(D)</b> WT or <i>Rip2^−/−</i> BMDM were infected with 20MOI of <i>C. rodentium</i> and mock treated or treated with the JNK inhibitor SP600125 (JNKi). Samples were collected at the indicated times and examined for total JNK, phosphorylated JNK and caspase-11 by western blot. <b>(E)</b> Proposed signaling pathway that regulates inflammasome activation. (A) Data are combined from 9 independent experiments and displayed as the mean ± SEM. (B–D) Data are representative of 3 independent experiments. (n.s. = not significant).</p

Enhanced inflammasome activation in <i>Nod2^−/−</i> and <i>Rip2^−/−</i> BMDMs.

<p>BMDM were generated from WT, <i>Nod2^−/−</i> and <i>Rip2^−/−</i> mice and infected with 20MOI of <i>Citrobacter rodentium</i> for 18 h. <b>(A–F)</b> Combined supernatant and lysates were examined by Western blot for caspase-1 cleavage (casp-1p20) visually (A,D) and by densitometry (B,E), or (C,F) supernatants were examined for IL-18 secretion by ELISA. <b>(G)</b> BMDM were infected with <i>C. rodentium</i> and assayed for intracellular growth at the indicated times post-infection. (A–F) Data are representative of five independent experiments with n = 2–3 wells per experiment. (G) Data are representative of two independent experiments with n = 2–3 wells per experiment. (B,C,E,F,G) Data are shown as the mean ± SEM. (*, p<0.05; **, p<0.01; ***, p<0.001).</p

NOD2 and RIP2 specifically regulate NLRP3 inflammasome activation.

<p><b>(A–B)</b> WT, <i>Nod2^−/−</i> and <i>Rip2^−/−</i> BMDM were infected with 1MOI <i>Salmonella typhimurium</i> for 4 h and combined supernatant and lysates were examined by Western blot for caspase-1 cleavage (casp-1p20) visually (A) and by densitometry (B). <b>(C)</b> Supernatants were examined 4 h after <i>S. typhimurium</i> infection for IL-18 secretion. <b>(D–F)</b> WT, <i>Nod2^−/−</i> and <i>Rip2^−/−</i> BMDM were infected with 10MOI <i>S typhimurium Δfljb/flic</i> mutant for 18 h. Caspase-1 activation and IL-18 were examined as in panels A–C. <b>(G–I)</b> WT and <i>Rip2^−/−</i> BMDM were infected with 20MOI of <i>C. rodentium</i> for 2 h and <i>Rip2^−/−</i> cells were subsequently treated with the NLRP3 specific inhibitor glyburide or mock treated as a control. Caspase-1 activation and IL-18 were examined as in panels A–C. <b>(J–L)</b> WT and <i>Rip2^−/−</i> BMDM were infected with 1MOI of <i>S. typhimurium</i> and <i>Rip2^−/−</i> cells were simultaneously treated with the NLRP3 specific inhibitor glyburide or mock treated as a control. Caspase-1 activation and IL-18 were examined as in panels A–C. (A–L) Data are representative of three independent experiments with n = 2–3 wells per experiment and displayed as the mean ± SEM. (*, p<0.05; **, p<0.01; ***, p<0.001).</p

Primer sequences used for RT-PCR.

<p>Primer sequences used for RT-PCR.</p