DataSheet_1_Coastal vulnerability modelling and social vulnerability assessment under anthropogenic impacts.pdf

Coastal regions are highly vulnerable to the impacts of human activities, land cover change, sea level rise (SLR), and climate extremes. In this study, we attempt to address this issue by simulating the spatial interactions among natural hazards, ever-increasing human activities, and social vulnerability in the south coast of the Bohai Sea, China. It is found that the activities occurring on land, especially within coastal environments, such as agricultural pond and ports, and those in the ocean (tide and residual current) both impose disaster risks on the marine environment. In 2020, 25.2% of the total study area is highly vulnerable, which is 21% larger than that in 1997. The socially vulnerable areas are mainly distributed in the southeast coast of the Laizhou Bay. These areas should be strengthened to reduce and prevent the storm surge and flood disasters. Ultimately, we emphasize the urgent needs to implement effective policy measures for reducing tomorrow’s risks from natural hazards.</p

Enhanced Stability and Catalytic Performance of Active Rh Sites on Al₂O₃ Via Atomic Layer Deposited ZrO₂

Modulating the Rh active sites on surfaces of Al2O3 is crucial to developing effective three-way catalysts. Herein, an ultralow amount of ZrO2 (0.0179%) was deposited onto Al2O3 nanorods via atomic layer deposition (ALD) to form a catalyst with both thermal stability and low-temperature activity. The results demonstrate that the ALD-ZrO2 is conducive to improve the catalytic activity of the Rh site and inhibit the formation of irreducible Rh species at high temperature. The obtained catalysts show satisfactory performance for a model NO–CO reaction even after thermal aging at 1050 °C. This strategy shows that a molecularly precise synthesis can lead to the robust promotion of Rh activity under low temperature and provide a promising path toward reducing the deactivation of catalysts at high temperature

Effect of Nano-Silver on Formation of Marine Snow and the Underlying Microbial Mechanism

Roller experiments were conducted to explore the effect of nano-silver on the formation of marine snow and the underlying microbial mechanism. With the increasing concentration of nano-Ag from 1 ng/L to 1 mg/L, the formation and aggregation of marine snow particles were solidly suppressed in a dose-dependent pattern. Moreover, the formed marine snows tended to be thinner fibrous particles with smaller size and increased edge smoothness and compactness in the presence of nano-Ag. The microbial analyses indicated that nano-Ag not only inhibited the development of biomass but also changed the species composition and functional profile of the microbial community. Nano-Ag obviously inhibited most of the abundant species, except for some myxobacteria, which is unfavorable for the microbial community stability. For the microbial functions, some major biological processes including the growth, metabolic, and cellular processes were also inhibited by the high dosage of nano-Ag. The strong microbial inhibition of nano-Ag would contribute to the suppression on the formation of marine snow. Specifically, the function genes of extracellular polymeric substance synthesis and secretion were significantly reduced by nano-Ag, which might be the key and straight microbial factor in suppressing the formation of marine snow

Positive Surface Charge Enhances Selective Cellular Uptake and Anticancer Efficacy of Selenium Nanoparticles

Surface charge plays a key role in cellular uptake and biological actions of nanomaterials. Selenium nanoparticles (SeNPs) are novel Se species with potent anticancer activity and low toxicity. This study constructed positively charged SeNPs by chitosan surface decoration to achieve selective cellular uptake and enhanced anticancer efficacy. The results of structure characterization revealed that hydroxyl groups in chitosan reacted with SeO32– ion to form special chain-shaped intermediates, which could be decomposed to form crystals upon reduction by ascorbic acid. The initial colloids nucleated and then assembled into spherical SeNPs. The positive charge of the NH3+ group on the outer surface of the nanoparticles contributed to the high stability in aqueous solutions. Moreover, a panel of four human cancer cell lines were found to be susceptible to SeNPs, with IC50 values ranging from 22.7 to 49.3 μM. Chitosan surface decoration of SeNPs significantly enhanced the selective uptake by endocytosis in cancer cells and thus amplified the anticancer efficacy. Treatment of the A375 melanoma cells with chitosan–SeNPs led to dose-dependent apoptosis, as evidenced by DNA fragmentation and phosphatidylserine translocation. Our results suggest that the use of positively charged chitosan as a surface decorator could be a simple and attractive approach to achieve selective uptake and anticancer action of nanomaterials in cancer cells

NKp46 deficiency does not affect ILC2s and ILC3s.

(A) Gating strategy for ILC2s and ILC3s. ILC2s were gated on CD45+Lin─CD127+Gata3+, and ILC3s were gated on CD45+Lin─CD127+RORγt+. (B) Percentages of ILC2s or ILC3s were analyzed by flow cytometry in SI in Ncr1gfp/gfp mice and Ncr1+/+ littermates. ILC2s were gated on CD45+Lin─CD127+Gata3+RORγt─ lymphocytes. ILC3s were gated on CD45+Lin─CD127+RORγt+Gata3─ lymphocytes. (C) Quantities of ILC2s or ILC3s were determined in SI of Ncr1gfp/gfp mice and their Ncr1+/+ littermates (n = 4). (D) Lin─(or CD3─CD19─)NK1.1+NKp46+(or GFP+ for Ncr1gfp/gfp mice)CD49b+ NK cells were sorted from the spleen of Ncr1gfp/gfp mice or Ncr1+/+ littermates and were co-stimulated with IL-12 (10 ng/ml) and IL-18 (10 ng/ml) for 16 h, followed by the measurement of IFN-γ production by intracellular flow cytometric analysis (D, left panel, n = 3) or ELISA assays (D, right panel, n = 3). Golgi Plug was added at a 1:1,000 dilution to the culture 4 h prior to cell harvesting. (E) Homogenized SI cells isolated from Ncr1gfp/gfp mice or Ncr1+/+ littermates were stimulated with IL-23 (10 ng/ml) for 4 h, followed by the measurement of IL-22 production by flow cytometric analysis after gating ILC3s on CD45+Lin─CD127+RORγt+. Golgi Plug was added at a 1:1,000 dilution to the culture 3 h prior to cell harvesting. Error bars, standard deviations. The numerical data for panel C and D can be found in S1 Data. ELISA, Enzyme-linked immunosorbent assay; FSC-A, forward scatter area; FSC-H, FSC height; IFN, interferon; IL, interleukin; ILC, innate lymphoid cell; Ncr1, natural cytotoxicity receptor 1; NK, natural killer; NS, no significance; RORγt, retinoic acid receptor (RAR) related orphan receptor gamma t; SI, small intestine; SSC-A, side scatter area; SSC-H, SSC height; SSC-W, SSC width.</p

Transport Properties of Some 1‑Butyl-3-methylimidazolium Carboxylate Ionic Liquids

In this work, we have synthesized four 1-butyl-3-methylimidazolium carboxylate ionic liquids (ILs): 1-butyl-3-methylimidazolium glycolate ([C₄mim]­[HOCH₂COO]), lactate ([C₄mim]­[CH₃CHOHCOO]), benzoate ([C₄mim]­[C₆H₅COO]), and glycinate ([C₄mim]­[H₂NCH₂COO]). The transport properties such as viscosities and conductivities have been experimentally determined for these ILs at (303.15 to 343.15) K. From these data, the influences of substituent group in carboxylate anion and system temperature on viscosities and conductivities of the ILs have been examined. In addition, Walden plots have been plotted to investigate ionicity of the ILs, and the viscosity and conductivity data have been correlated by Vogel–Fulcher–Tammann (VFT) and Arrhenius equations

Nanometer-Mesa Inverted-Pyramid Photonic Crystals for Thin Silicon Solar Cells

The usage of ultrathin flexible silicon foil can further extend the functionality of silicon and emerging silicon-based tandem solar cells particularly in building and vehicle-integrated photovoltaics where high-efficiency, lightweight, and flexible solar panels are highly desired. However, silicon’s relatively weak optical absorption coefficient especially in the near infrared (NIR) region limits its optoelectronic applications with a reduced wafer thickness. Herein, we seek to overcome this limitation by exploring the wave interference phenomenon for effective absorption of NIR light in ultrathin silicon. Particularly, inverted pyramid photonic crystals (PhCs) with nano–micrometer-scale feature sizes are carved directly on silicon. Detailed experimental and theoretical studies are presented by systematically examining the optical properties of PhC-integrated thin silicon substrates (down to a 10 μm thickness). The corresponding maximum photocurrent density for a thin absorber is projected and compared with that predicted by Lambertian’s limit. In contrast to traditionally configured microscale inverse pyramids, we show that a small mesa width is critical to achieving high optical performance for a wave-interference-based absorption enhancement. Mesa widths as small as 35 nm are realized over a large wafer-scale fabrication using facile techniques. The optical performance of 10 μm silicon indicates that an ideal photocurrent density approaching 40 mA/cm2 is feasible. This study indicates that photonic crystals provide strong wave interference in ultrathin silicon, and in particular, we observe high optical absorption even after removing more than 90% of the silicon from conventional “thick” Si wafers

NKp46 plays a cell-intrinsic role in regulating ILC1 development.

<p>(A) Scheme of BM transplantation using BM cells of CD45.2 <i>Ncr1</i>^gfp/gfp mice or <i>Ncr1</i>^+/+ littermate controls as donor cells to inject into CD45.1 recipients via tail vein. Development of ILC subsets was analyzed 2 weeks after transplantation. (B) Percentages of CD45.2⁺ NK cells or CD45.2⁺ ILC1s were analyzed by flow cytometric analysis in the liver of CD45.1 recipients, which were engrafted with BM cells of <i>Ncr1</i>^gfp/gfp mice (<i>n</i> = 5) or <i>Ncr1</i>^+/+ littermates (<i>n</i> = 4). (C) Percentages of CD45.2⁺ NK cells or CD45.2⁺ ILC1s were analyzed in the spleen or BM of CD45.1 recipient mice, which were engrafted with BM cells of <i>Ncr1</i>^gfp/gfp mice (<i>n</i> = 5) or their <i>Ncr1</i>^+/+ littermates (<i>n</i> = 4). (D and E) Data shown are representative dot plots of flow cytometric analysis (left panel) and summary data (right panel) of CD45.2⁺ILC2 (D) or CD45.2⁺ ILC3 (E) in SI in CD45.1 recipients, which were engrafted with BM cells of <i>Ncr1</i>^gfp/gfp mice (<i>n</i> = 4) or their <i>Ncr1</i>^+/+ littermates (<i>n</i> = 4). Error bars, standard deviations; ***, <i>p</i> < 0.001; **, <i>p</i> < 0.01; *, <i>p</i> < 0.05. The numerical data for panels B, C, D and E can be found in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.2004867#pbio.2004867.s007" target="_blank">S1 Data</a>. Lin^─, CD3^─CD19^─; BM, bone marrow; ILC, innate lymphoid cells; <i>Ncr1</i>, natural cytotoxicity receptor 1; NK, natural killer; RORγt, retinoic acid receptor (RAR) related orphan receptor gamma t; SI, small intestine.</p

Dependence of innate lymphoid cell 1 development on NKp46

<div><p>NKp46, a natural killer (NK) cell–activating receptor, is involved in NK cell cytotoxicity against virus-infected cells or tumor cells. However, the role of NKp46 in other NKp46⁺ non-NK innate lymphoid cell (ILC) populations has not yet been characterized. Here, an NKp46 deficiency model of natural cytotoxicity receptor 1 (<i>Ncr1</i>)^gfp/gfp and <i>Ncr1</i>^gfp/+ mice, i.e., homozygous and heterozygous knockout (KO), was used to explore the role of NKp46 in regulating the development of the NKp46⁺ ILCs. Surprisingly, our studies demonstrated that homozygous NKp46 deficiency resulted in a nearly complete depletion of the ILC1 subset (ILC1) of group 1 ILCs, and heterozygote KO decreased the number of cells in the ILC1 subset. Moreover, transplantation studies confirmed that ILC1 development depends on NKp46 and that the dependency is cell intrinsic. Interestingly, however, the cell depletion specifically occurred in the ILC1 subset but not in the other ILCs, including ILC2s, ILC3s, and NK cells. Thus, our studies reveal that NKp46 selectively participates in the regulation of ILC1 development.</p></div