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It is a vital technical challenge to extract lithium from salt-lake brine which has very high Mg2+ / Li+ mass ratio via green and low-cost methods, as these two cations have quite similar ionic hydration radius. Positively charged nanofiltration membranes can separate Li+ and Mg2+ through Donnan exclusion. In this work, a kind of hollow fiber nanofiltration membrane with positively charged skin layer was successfully fabricated via interfacial polymerization followed by a surface modification with branched polyethyleneimine (BPEI). The resultant membrane has a large number of amine groups, and thus shows positively charged surface with high rejection for divalent cation ions via Donnan exclusion. This gives it very high selectivity for the separation of Li+ ions from salt-lake brine. Under optimized conditions, it achieves a water permeance of up to 126.2 L m-2 h-1 MPa−1 at a transmembrane pressure difference of 4 bar, and a MgCl2 rejection of 94.6% with 2000 mg L-1 aqueous MgCl2 solution as feed. Meanwhile, it achieves a Mg2+ / Li+ selectivity of nearly 24 for MgCl2 and LiCl salt mixture solution with an overall concentration of 2000 mg L-1 and a Mg2+ / Li+ mass ratio of 150 : 1 as feed, which is high as compared with most of the literature, demonstrating its potential in the practical application of Mg2+ and Li+ separation.

Positively charged nanofiltration (NF) technology is considered a green and low-cost method for mono/divalent cation separation. Nevertheless, the separation rejection mechanisms of these NF membranes have yet to be extensively investigated. In this work, we fabricated a thin-film composite (TFC) hollow-fiber (HF) NF membrane with a positively charged surface via modification of the nascent interfacial polymerization layer using a branched polyethyleneimine (BPEI)/ethanol solution. Then, we extensively investigated its selective separation mechanism for mono/divalent cations. We proposed and proved that there exists a double-charged layer near the membrane surface, which helps to repel the divalent cations selectively via Donnan exclusion while promoting the fast penetration of monovalent cations. Meanwhile, the membrane skin layer is loose and hydrophilic due to the loose BPEI structure and the abundance of amine groups, as well as the changed fabrication conditions. In this way, we achieved very good mono/divalent cation selectivity and relatively high water permeance for the as-prepared HF NF membrane. We also obtained good anti-fouling, anti-scaling, and acid resistance, and long-term stability as well, which are urgently needed during practical application. Furthermore, we successfully amplified this HF NF membrane and proved that it has broad application prospects in mono/divalent cation separation.

A dual-polarized Ka-band feed based on gap waveguide (GW) technology for an ultra-high-gain reflector antenna is presented. The feed provides SUM-beams for data transfer and DIFF-beams for tracking. The whole reflector antenna is composed of the feed and a dual-reflector Cassegraine antenna. The feed has been prototyped, and the measured reflection coefficients for the horizontally and the vertically polarized SUM-beam ports are below −10 dB and −8 dB over 30.8–38 GHz, respectively. The measured feed radiation patterns agree well with the simulated ones. The dual-reflector Cassegraine antenna has been designed and simulated by using GRASP with the simulated far-field function of the proposed feed, showing that the reflector antenna achieves SUM-beam gains above 50 dBi and the null depth of the DIFF-beams are more than 30 dB below the maximum of SUM-beams.

Organic solvents take up 80% of the total chemicals used in pharmaceutical and related industries, while their reuse rate is less than 50%. Traditional solvent treatment methods such as distillation and evaporation have many disadvantages such as high cost, environmental unfriendliness, and difficulty in recovering heat-sensitive, high-value molecules. Organic solvent nanofiltration (OSN) has been a prevalent research topic for the separation and purification of organic solvent systems since the beginning of this century with the benefits of no-phase change, high operational flexibility, low cost, as well as environmental friendliness. Especially, hollow fiber (HF) OSN membranes have gained a lot of attention due to their high packing density and easy scale-up as compared with flat-sheet OSN membranes. This paper critically reviewed the recent research progress in the preparation of HF OSN membranes with high performance, including different materials, preparation methods, and modification treatments. This paper also predicts the future direction of HF OSN membrane development.

Although all murine MDSCs are defined as Gr1+CD11b+, their true immunophenotype remains elusive. In this study, we found murine Gr1+CD11b+ cells can be divided into two subsets: Gr1+CD11b+B220− and Gr1+CD11b+B220+, especially in the spleen tissues. Unlike the dominant B220− subset, the B220+ subpopulation was not induced by tumor in vivo. Moreover, Gr1+CD11b+B220+ cells from tumor-bearing mice spleens were unable to induce arginase 1 and inducible nitric oxide synthase expression, inhibit T cell proliferation, or promote tumor growth in primary tumor site. Nevertheless, these cells suppressed tumor metastasis in vivo and reduced cancer cell motility in vitro, while Gr1+CD11b+B220− cells from tumor-bearing mice spleens promoted tumor metastasis and enhanced cancer cell motility. Furthermore, both the polymorphonuclear (PMN-MDSCs) and monocytic MDSCs (Mo-MDSCs) could be further divided into B220− and B220+ subsets; interestingly, tumor only induced the expansion of B220− PMN-MDSCs and B220− Mo-MDSCs, but not the B220+ counterparts. Compared with B220− PMN-MDSCs and B220− Mo-MDSCs, the Ly6G+Ly6C−CD11b+B220+ and Ly6G−Ly6C+CD11b+B220+ cells from tumor-bearing mice spleens exhibited a more mature phenotype without immunosuppressive activity. Additionally, IL-6 deficiency attenuated the tumor-induced accumulation of MDSCs, B220− MDSCs and B220− PMN-MDSCs but increased the percentages of Gr1+CD11b+B220+, Ly6G+Ly6C−CD11b+B220+, and Ly6G−Ly6C+CD11b+B220+ cells, indicating the opposing roles of the IL-6 signaling pathway in the expansion of B220− MDSCs and their B220+ counterparts. Taken together, our findings indicate that the B220+ subset is a distinct subset of Gr1+CD11b+ cells functionally different from the B220− subpopulation during tumorigenesis and induction of MDSCs to B220+ cells may be helpful for cancer therapy.

Commensal microbes are necessary for a healthy gut immune system. However, the mechanism involving these microbes that establish and maintain gut immune responses is largely unknown. Here, we have found that the gut immune receptor leucine-rich repeat (LRR) C19 is involved in host-microbiota interactions. LRRC19 deficiency not only impairs the gut immune system but also reduces inflammatory responses in gut tissues. We demonstrate that the LRRC19-associated chemokines CCL6, CCL9, CXCL9, and CXCL10 play a critical role in immune cell recruitment and intestinal inflammation. The expression of these chemokines is associated with regenerating islet-derived (REG) protein-mediated microbiotas. We also found that the expression of REGs may be regulated by gut Lactobacillus through LRRC19-mediated activation of NF-κB. Therefore, our study establishes a regulatory axis of LRRC19, REGs, altered microbiotas, and chemokines for the recruitment of immune cells and the regulation of intestinal inflammation.

Gut microbiota may not only affect composition of local immune cells but also affect systemic immune cells. However, it is not completely clear how gut microbiota modulate these immune systems. Here, we found that there exist expanded macrophage pools in huREG3γtgIEC mice. REG3γ-associated Lactobacillus, which is homology to Lactobacillus Taiwanese, could enlarge macrophage pools not only in the small intestinal lamina propria but also in the spleen and adipose tissues. STAT3-mediated signal(s) was a critical factor in the Lactobacillus-mediated anti-inflammatory macrophages. We also offered evidence for critical cellular links among REG3γ-associated Lactobacillus, tissue macrophages, and obesity diseases. Anti-inflammatory macrophages in the lamina propria, which are induced by REG3γ-associated Lactobacillus, may migrate into adipose tissues and are involved in resistance against high-fat diet-mediated obesity. Thus, REG3γ-associated Lactobacillus-induced anti-inflammatory macrophages in gut tissues may play a role in adipose tissue homeostasis.

Hippo signalling plays key role in tissue growth and homeostasis, and its dysregulation is implicated in various human diseases. Expanded (Ex) is an important upstream activator of Hippo signalling; however, how Ex activates Hippo signalling is still poorly understood. Here, we demonstrate that Ex forms a homodimer via C-terminal interaction, and that the ExC2 region (912-1164 aa) is sufficient and essential for Ex dimerization. Functional analysis shows that ExC2 is required for Ex to promote the phosphorylation and inactivation of Yki in Drosophila cells. Further in vivo analysis shows that ExC2 is important for Ex to control Drosophila tissue growth. Our study, thus, uncovers a novel mechanism whereby Ex homodimerization mediates its full activation to promote Hippo signalling in growth control. [ABSTRACT FROM AUTHOR]

Although all murine MDSCs are defined as Gr1+CD11b+, their true immunophenotype remains elusive. In this study, we found murine Gr1+CD11b+ cells can be divided into two subsets: Gr1+CD11b+B220- and Gr1+CD11b+B220+, especially in the spleen tissues. Unlike the dominant B220- subset, the B220+ sub-population was not induced by tumor in vivo. Moreover, Gr1+CD11b+B220+ cells from tumor-bearing mice spleens were unable to induce arginase 1 and inducible nitric oxide synthase expression, inhibit T cell proliferation, or promote tumor growth in primary tumor site. Nevertheless, these cells suppressed tumor metastasis in vivo and reduced cancer cell motility in vitro, while Gr1+CD11b+B220- cells from tumor-bearing mice spleens promoted tumor metastasis and enhanced cancer cell motility. Furthermore, both the polymorphonuclear (PMN-MDSCs) and monocytic MDSCs (Mo-MDSCs) could be further divided into B220- and B220+ subsets; interestingly, tumor only induced the expansion of B220- PMN-MDSCs and B220- Mo-MDSCs, but not the B220+ counterparts. Compared with B220- PMN-MDSCs and B220- Mo-MDSCs, the Ly6G+Ly6C-CD11b+B220+ and Ly6G-Ly6C+CD11b+B220+ cells from tumor-bearing mice spleens exhibited a more mature phenotype without immunosuppressive activity. Additionally, IL-6 deficiency attenuated the tumor-induced accumulation of MDSCs, B220- MDSCs and B220- PMN-MDSCs but increased the percentages of Gr1+CD11b+B220+, Ly6G+Ly6C-CD11b+B220+, and Ly6G-Ly6C+CD11b+B220+ cells, indicating the opposing roles of the IL-6 signaling pathway in the expansion of B220- MDSCs and their B220+ counterparts. Taken together, our findings indicate that the B220+ subset is a distinct subset of Gr1+CD11b+ cells functionally different from the B220- subpopulation during tumorigenesis and induction of MDSCs to B220+ cells may be helpful for cancer therapy. [ABSTRACT FROM AUTHOR]

Mixed-lineage leukemia 1 (MLL1), which exerts its H3K4 methyltransferase activity by interacting with WDR5, ASH2L, and RBBP5, plays a pivotal role in regulating hematopoietic stem cell homeostasis. Disrupting the integrity of MLL1-complex has been reported to be associated with acute leukemia. However, the exact role of MLL1-complex in myeloid cells is unknown. In this study, microarray analysis revealed that the core components of the Mll1-complex, Wdr5, Ash2l, and Mll1, were concurrently downregulated by tumor-secreted factors as well as GM-CSF + IL-6 during the accumulation and activation of murine myeloidderived suppressor cells (MDSCs). These changes were further validated by quantitative RT-PCR and Western blotting both in vitro and in vivo. The expression levels of WDR5 and ASH2L were also significantly decreased in bone marrow MDSCs of lung cancer patients compared with that of healthy controls. Functionally, ectopic expression of Wdr5, Ash2l, and Mll1 (C terminus) reversed the accumulation and function of GM-CSF + IL-6-induced as well as tumor-cocultured polymorphonuclear MDSCs (PMN-MDSCs) by promoting them to differentiate into mature neutrophil-like cells. Mechanistically, GM-CSF + IL-6-activated Stat3 and Cebpb synergistically induced the expression of miR-21a, miR-21b, and miR-181b, and thus inhibited the expression of Wdr5, Ash2l, and Mll1 by targeting to their 39 untranslated regions, respectively. Furthermore, knockdown of these microRNAs also suppressed the expansion and function of GM-CSF + IL-6-induced PMN-MDSCs. Taken together, our findings indicate that the Stat3/Cebpb-miR-21a/b/181b-Mll1-complex axis may play a critical role in PMN-MDSC expansion, activation, and differentiation, and this axis may provide an effectively immunological therapeutic approach for patients with cancer or other immunological diseases. [ABSTRACT FROM AUTHOR]