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In order to regulate the surface properties of calcined kaolinite for the purpose of achieving uniform distribution within various polar dispersion media, 3-aminopropyltriethoxysilane and phenyl glycidyl ether were employed to chemically modify calcined kaolinite. The grafting rate, surface properties, and dispersion properties of calcined kaolinite particles in different polar organic media were changed by varying the dosage of the modifiers. FT-IR analysis confirmed successful surface modification, while thermogravimetric analysis indicated a maximum graft coverage of 18.44 μmol/m2 for the modified particles. Contact angle measurements and particle size distribution analyses demonstrated the effective adjustment of surface characteristics by the modifiers. Specifically, at a mass ratio of 1.0 of modifier to kaolinite particles, the modified particles exhibited a contact angle of around 125°, achieving uniform dispersion in different polarity media. Particle size distribution ranged from 1600 nm to 2100 nm in cyclohexane and petroleum ether, and from 900 nm to 1200 nm in dioxane, ethyl acetate, and DMF, showcasing a significant improvement in dispersion performance compared to unmodified particles. Concurrently, to improve the mechanical properties of PBAT, modified particles were incorporated into the PBAT matrix, and the effect of modified particle addition on the tensile strength and fracture tensile rate of the composites was investigated. The optimal amount of modified particles is 6 wt.%~8 wt.%. This article aims at synthesizing modifier molecules containing different hydrophilic and hydrophobic groups to chemically graft onto the surface of calcined kaolinite. The hydrophilic and hydrophobic groups on the modified particles can adapt to dispersed systems of different polarities and achieve good distribution within them. The modified particles are added to PBAT to achieve good compatibility and enhance the mechanical properties of the composite material. [ABSTRACT FROM AUTHOR]

The desulfurization capacity of top slag in the process of pre-desulfurization of hot metal containing vanadium and titanium was researched. The top slag system of CaO-SiO2-MgO-Al2O3-TiO2-VOx that was formed by blast furnace slag and a CaO desulfurization agent reduced the sulfur in hot metal from 0.08 wt.% to 0.02 wt.%. It was found that the resulfurization of the slag happened in the later periods of the desulfurization process. The vanadium–titanium oxides were both acidic in the desulfurization slag. TiO2 and VOx reacted with the basic oxides to form CaTiO3 and MgV2O4 at 1623 K, which reduced free CaO and was not conducive to top slag desulfurization. The results of calculation showed that the top slag desulfurization accounted for 15% of the total desulfurization. Using the ionic and molecule coexistence theory of slag structure, it is shown that the desulfurization efficiency could be enhanced by adjusting both the amount of desulfurization agent and the composition of the blast furnace slag before pre-desulfurization. [ABSTRACT FROM AUTHOR]

This paper studies the process mineralogy, mechanism, and kinetics of column leaching behavior of low-grade high-calcium–magnesium copper ore. The effect of sulfuric acid concentration, leach solution spraying intensity, and material particle size on column leaching kinetics is discussed. The kinetic analysis of column leaching of copper indicates that sulfuric acid concentration has a significant impact. As sulfuric acid concentration increases, the limiting step of reaction shifts from chemical reaction control to a combination of chemical reaction and diffusion mixing control. Spraying intensity also affects copper column leaching; increasing intensity shifts the limiting step from diffusion control to mixing control, thereby mitigating the effects of diffusion control. Regarding other elements, it is found that iron leaching is primarily controlled by chemical reaction, while calcium leaching is mainly controlled by chemical reaction. As sulfuric acid concentration increases from 10 g/L to 20 g/L, the limiting step for calcium leaching shifts from chemical reaction control to chemical reaction and diffusion-mixing control. [ABSTRACT FROM AUTHOR]

Responsive feeding serves as an important protective factor for infant growth and overall health development. This study based on self‐determination theory (SDT) aimed to assess the effects of a responsive breastfeeding (RBF) intervention programme on maternal breastfeeding and infant growth and development. A total of 110 mother–infant pairs were recruited and randomly divided into an intervention group (n = 55) and a control group (n = 55). The primary outcomes were breastfeeding motivation score, breastfeeding self‐efficacy (BSE) and exclusive breastfeeding rate; the secondary outcomes were infant physical development at 6 weeks and 3 months. A repeated measures ANOVA indicated that the intervention group had significantly higher Enjoyment scores compared to the control group at three time points: at discharge (MD: 5.28; 95% CI: 3.68 to 6.89; p < 0.001), 6 weeks post‐partum (MD: 5.06; 95% CI: 3.80 to 6.31; p < 0.001) and 3 months post‐partum (MD: 5.24; 95% CI: 4.12 to 6.35; p < 0.001). Similarly, the intervention group reported significantly higher connection and mother's self‐perception scores at discharge (MD: 4.31; 95% CI: 3.07 to 5.56; p < 0.001), 6 weeks post‐partum (MD: 4.69; 95% CI: 3.71 to 5.68; p < 0.001) and 3 months post‐partum (MD: 4.93; 95% CI: 4.14 to 5.72; p < 0.001), compared to the control group. In contrast, the pressure from significant others scores were higher in the control group relative to the intervention group at discharge (MD: −2.09; 95% CI: −2.88 to −1.31; p < 0.001), 6 weeks post‐partum (MD: −4.35; 95% CI: −5.20 to −3.49; p < 0.001) and 3 months (MD: −4.89; 95% CI: −5.70 to −4.08; p < 0.001). Finally, the intervention group also reported higher Instrumental Needs scores at all three time points: at discharge (MD: 1.96; 95% CI: 1.35 to 2.58; p < 0.001), 6 weeks post‐partum (MD: 3.58; 95% CI: 3.05 to 4.11; p < 0.001) and 3 months post‐partum (MD: 1.18; 95% CI: 0.68 to 1.69; p < 0.001). BSE scores were significantly higher in the intervention group compared to the control group at discharge (MD: 14.29; 95% CI: 10.38 to 18.21; p < 0.001), 6 weeks post‐partum (MD: 14.04; 95% CI: 11.05 to 17.02; p < 0.001) and 3 months post‐partum (MD: 6.80; 95% CI: 4.66 to 8.94; p < 0.001). The rates of exclusive breastfeeding were higher in the intervention group than in the control group at each stage of the intervention (p < 0.01). At 6 weeks post‐partum, the intervention group's infants showed slower weight (t = −0.90, p = 0.371) and length (t = −0.69, p = 0.495) growth compared to the control group, though not significantly. By 3 months post‐partum, there was a significant difference in both weight (t = −3.46, p = 0.001) and length (t = −2.95, p = 0.004) between the groups. The findings in this study suggest that the RBF intervention programme based on SDT may be effective in improving mothers' motivation to breastfeed, building breastfeeding self‐confidence and increasing the rate of exclusive breastfeeding. The effects of the intervention on infant physical development will need to be verified with longer follow‐up in future research. Key messages: This study validated the application of responsive breastfeeding (RBF) intervention during the exclusive breastfeeding phase of Chinese infants.The RBF intervention may help to increase mothers' level of autonomous motivation for breastfeeding, enhance breastfeeding self‐efficacy and increase exclusive breastfeedingrates. The intervention had no significant effect on the weight and length of 6 week old infants but significantly impacted 3monthold infants, with slower growth observed in the intervention group compared to the control group.Future intervention programmes shouldinclude extended follow‐up periods to investigate the long‐term effects of RBF on infant growth and development. [ABSTRACT FROM AUTHOR]

Tissue infiltration by circulating leukocytes via directed migration (also referred to as chemotaxis) is a common pathogenic mechanism of inflammatory diseases. G protein–coupled receptors (GPCRs) are essential for sensing chemokine gradients and directing the movement of leukocytes during immune responses. The tumor necrosis factor α-induced protein 8-like (TIPE or TNFAIP8L) family of proteins are newly described pilot proteins that control directed migration of murine leukocytes. However, how leukocytes integrate site-specific directional cues, such as chemokine gradients, and utilize GPCR and TIPE proteins to make directional decisions are not well understood. Using both gene knockdown and biochemical methods, we demonstrated here that 2 human TIPE family members, TNFAIP8 and TIPE2, were essential for directed migration of human CD4+ T cells. T cells deficient in both of these proteins completely lost their directionality. TNFAIP8 interacted with the Gαi subunit of heterotrimeric (α, β, γ) G proteins, whereas TIPE2 bound to PIP2 and PIP3 to spatiotemporally control immune cell migration. Using deletion and site-directed mutagenesis, we established that Gαi interacted with TNFAIP8 through its C-terminal amino acids, and that TIPE2 protein interacted with PIP2 and PIP3 through its positively charged amino acids on the α0 helix and at the grip-like entrance. We also discovered that TIPE protein membrane translocation (i.e. crucial for sensing chemokine gradients) was dependent on PIP2. Collectively, our work describes a new mechanistic paradigm for how human T cells integrate GPCR and phospholipid signaling pathways to control directed migration. These findings have implications for therapeutically targeting TIPE proteins in human inflammatory and autoimmune diseases. [ABSTRACT FROM AUTHOR]

A man diagnosed as TAFRO syndrome was successfully responded to a novel immunosuppressive regimen containing methylprednisolone and mycophenolate mofetil. Blood cells firstly recovered, followed by the general situation and complete recover 1 month later, highlighting the danger of TAFRO syndrome and the importance of immunosuppressive agents in reversing pathological course. [ABSTRACT FROM AUTHOR]

Myeloid‐derived suppressor cells (MDSCs) are a heterogeneous population of leukocytes that are important for tumorigenesis and tumor immunotherapy. They comprise up to 10% of leukocytes in the blood of tumor patients and their depletion may be required for successful tumor immunotherapy. However, the identity of MDSCs remains obscure, primarily due to their heterogeneity and lack of a known lineage‐specific transcription factor specifying their differentiation. Using single‐cell transcriptomics and gene knockout approaches, we now describe a subset of murine and human myeloid suppressor cells, named rel‐dependent monocytes (rMos), which are programmed by the transcription factor c‐Rel of the NF‐κB family. Unlike MDSCs described previously, the c‐Rel‐dependent monocytes expressed a high amount of the proinflammatory cytokine IL‐1β together with a low level of suppressive molecule arginase 1. Both in vitro and in tumor‐bearing mice, these c‐Rel+IL‐1βhiArg1− monocytes promoted tumor growth by potently suppressing T cell function and showed a strong migratory phenotype, all of which were impaired by c‐Rel deficiency or inhibition. Mechanistic studies revealed that c‐Rel controlled the expression of monocyte signature genes through a unique transcriptional complex called the c‐Rel enhanceosome, and IL‐1β‐CCL2 crosstalk between tumor cells and the rel‐dependent monocytes maintained the suppressive tumor microenvironment. Thus, c‐Rel specifies the development of a suppressive monocyte population and could be selectively targeted for treating cancer. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 44-year-old man presented to our hospital with both acute left occipital pulsating headache that had lasted for 5 days and swelling of the left eyelid that persisted for 12 h following an upper respiratory infection. The article discusses that the results of computed tomography (CT), magnetic resonance imaging (MRI), and magnetic resonance angiography scans of the brain as well as of cerebrospinal fluid (CSF) tests were normal.

Introduction: The TNF‐α‐induced protein‐8 (TNFAIP8, also known as TIPE) family of molecules comprises four members: TNFAIP8 and TIPEs1‐3. Since the first description of these proteins, their roles in fine‐tuning inflammation and in directing leukocyte migration have been described in several organ systems. However, their relationship with intervertebral disc (IVD) is unknown. Materials and methods: Here, we describe the expression of TNFAIP8 family genes in the nucleus pulposus (NP) and annulus fibrosus (AF) of the normal adult murine IVD. We further describe the expression of these genes in the injured male and female murine IVD. Results: Tnfaip8 gene expression was decreased, and Tipe1 gene expression was essentially unchanged, in response to injury. Tipe2 and Tipe3 gene expression was markedly elevated in response to IVD injury, along with those encoding known inflammatory markers (ie, Tnfa, Il6, Cxcl1, and Adam8). Additionally, sex‐related differences were also observed for some of these genes in intact and injured mouse IVDs. Future studies include examining tissue distribution of TNFAIP8 family proteins and identifying cells that produce them. In addition, examining mice that are deficient in TNFAIP8 molecules, in relation to gene expression, tissue morphology and mouse behavior, may further delineate the roles of these molecules in IVD inflammation and degeneration. [ABSTRACT FROM AUTHOR]

The Al-containing particles in ODS alloys with Al addition usually exhibit relatively large size, and inevitably result in a limited improvement in mechanical properties. In this paper, W-Al-Y 2 O 3 alloy was prepared by a two-step sintering process to refine the Al-containing particles. Microstructure evolution of dispersoid particles was characterized by scanning electron microscope (SEM), electron probe microanalysis (EPMA) and transmission electron microscopy (TEM). During the first holding step at 1000 °C, the dissolved Al precipitated directly from W matrix, where the formed γ-Al 2 O 3 particles were nano-sized and developed a coherent relationship with W matrix. This coherent relationship hindered transformation of γ-Al 2 O 3 into submicron-sized α-Al 2 O 3. Moreover, the nano-sized γ-Al 2 O 3 contributed to formation of fine Y 3 Al 5 O 12 dispersoid particles with the sintering temperature further increased to 1600 °C. 71% of the dispersoid particles were distributed within grains and most of them were nano-sized γ-Al 2 O 3 and Y 3 Al 5 O 12 , giving a fine grain size of 0.49 μm. Due to the refined microstructure, the compressive strength and microhardness of W-Al-Y 2 O 3 alloy reached 2545.9 MPa and 787.8 HV, respectively. • W-Al-Y 2 O 3 alloy was prepared by two-step SPS to refine Al-containing dispersoids. • Nano-sized γ-Al 2 O 3 precipitated from W matrix during first holding step at 1000 °C. • Nano-sized γ-Al 2 O 3 exhibited coherent relationship with W matrix. • Nano-sized γ-Al 2 O 3 also contributed to formation of fine Y 3 Al 5 O 12 dispersoids. • Compressive strength and microhardness reached 2545.9 MPa and 787.8 HV, respectively. [ABSTRACT FROM AUTHOR]

Summary: Immune homeostasis is essential for the normal functioning of the immune system, and its breakdown leads to fatal inflammatory diseases. We report here the identification of a member of the tumor necrosis factor-α-induced protein-8 (TNFAIP8) family, designated TIPE2, that is required for maintaining immune homeostasis. TIPE2 is preferentially expressed in lymphoid tissues, and its deletion in mice leads to multiorgan inflammation, splenomegaly, and premature death. TIPE2-deficient animals are hypersensitive to septic shock, and TIPE2-deficient cells are hyper-responsive to Toll-like receptor (TLR) and T cell receptor (TCR) activation. Importantly, TIPE2 binds to caspase-8 and inhibits activating protein-1 and nuclear factor-κB activation while promoting Fas-induced apoptosis. Inhibiting caspase-8 significantly blocks the hyper-responsiveness of TIPE2-deficient cells. These results establish that TIPE2 is an essential negative regulator of TLR and TCR function, and its selective expression in the immune system prevents hyperresponsiveness and maintains immune homeostasis. [Copyright &y& Elsevier]

The surface of calcined kaolinite particles underwent chemical modification using Vinyltriethoxysilane (VTMS) and 3-mercaptopropionic acid (3-MPA). The grafting ratio of VTMS on the calcined kaolinite surface was adjusted by varying its quantity. FT-IR analysis revealed the initial grafting of VTMS onto the kaolinite surface, resulting in the formation of a C=C reactive site on the surface. Subsequently, an olefin click reaction with 3-MPA occurred, leading to the effective grafting of 3-MPA onto the kaolinite surface and the formation of an efficient coating. Thermal analysis indicated that the optimal grafting level was achieved at a modifier content V:K ratio of 0.5. The estimated grafting ratio of the modifier on the kaolinite surface was approximately 40% when V:K was 0.5. Water contact angle and dispersion experiments demonstrated that the surface properties of kaolinite were effectively controlled by this modification approach. At V:K = 0.3, the modified kaolinite particles exhibited good dispersion in both polar and non-polar solvents. In polar solvents, the average particle size of modified kaolinite was below 1100 nm, while in non-polar solvents, it did not exceed 5000 nm. Considering all aspects, a V:K ratio of 0.3 is recommended. Further investigation into the impact of adding 3-MPA on the surface properties of modified kaolinite particles based on V:K = 0.3 revealed that the hydrophilicity of the modified particles could be enhanced. However, it is advised to keep the maximum M:V ratio (3-MPA to kaolinite) at 1.0. [ABSTRACT FROM AUTHOR]

Abstract Polyamide membranes based on trimesoyl chloride (TMC) have captured the majority of the market share for desalination in water treatment. The TMC based membrane is prone to form calcium bridges with the organic foulants due to the relatively strong deprotonation ability of the benzoic acid generated from the incomplete reaction of the acyl chloride monomers. The foulants are thus rapidly deposited on the surface of the TMC based membrane, which results in the deterioration of water production and decrease of membrane lifespan. Herein, we have fabricated a polyamide membrane based on novel trimesoyl-[4,4-dimethyl-5(4H)-azlactone] (TMDMA) monomer instead of TMC monomer. Since the carboxylic groups of the prepared TMDMA polyamide nanofilm are not directly connected to the phenyl ring, the acidity coefficient (p K a ) value is higher and, consequently, deprotonation ability is expected to be weaker. To confirm this theory, we have conducted the fouling experiment on TMDMA based membrane using alginate as a model foulant and compared that with TMC based polyamide membranes. A lower flux decline (33%) and higher cleaning efficiency (90.72%) are observed for the TMDMA polyamide membrane, while the flux decline and cleaning efficiency for the TMC based polyamide membrane are 52% and 49.52% respectively. Furthermore, the average Ca2+ density of the TMDMA polyamide membrane surface before and after cleaning are 81.52 mg m−2 and 21.61 mg m−2 respectively, which are lower than that of the TMC based polyamide membrane surface. Thus, it is clearly showing that the surface of the TMDMA polyamide membrane is not prone to form calcium bridges with foulants due to the weaker complexation between Ca2+ and the carboxylic acid groups. Graphical abstract Image 1 Highlights • Novel non-trimesoyl chloride based polyamide were fabricated by interfacial polymerization. • The novel membrane showed lower flux decline and higher cleaning efficiency than that of TMC based polyamide membranes. • Significantly reduced Ca2+ deposition density was observed on the surface of the novel membrane. [ABSTRACT FROM AUTHOR]

Oxide dispersion strengthened tungsten (ODS-W) alloys are promising plasma facing material in future fusion reactors. In this study, composite powders of W-Er 2 O 3 were prepared by co-deposition method and hydrogen reduction, and then consolidated by spark plasma sintering (SPS). Microstructure evolution during co-deposition process was investigated using X-ray diffraction (XRD), scanning electron microscope (SEM), transmission electron microscope (TEM) and Fourier transform infrared spectrometer (FTIR). Also, simulation using DMol3 module in Materials Studio was carried out to understand the co-deposition mechanism. The results showed that H+ of W-OH bond in white tungstic acid was replaced by Er3+ due to coordination reaction during co-deposition process, leading to formation of ring-like chelate of (WO) n Er. This indicates that doping of Er3+ was achieved at a molecular level. Consequently, Er 2 O 3 particles were relatively uniformly distributed in W-Er 2 O 3 alloy, and the hardness and compressive strength reached 627 ± 19 HV and 1640 ± 40 MPa, respectively. • Thermodynamic diagram of W-H 2 O was calculated to optimize co-deposition process. • Co-deposition mechanism was analyzed by simulation and experimental methods. • W-Er 2 O 3 alloy was prepared by co-deposition method and two-step SPS. • Er 2 O 3 particles were relatively uniformly distributed in alloy. • Hardness and compressive strength reached 627 HV and 1640 MPa, respectively. [ABSTRACT FROM AUTHOR]

The interplay between inflammation and metabolism is widely recognized, yet the underlying molecular mechanisms remain poorly characterized. Using experimental database mining and genome-wide gene expression profiling methods, we found that in contrast to other TNFAIP8 family members, TNFAIP8L2 (TIPE2) was preferentially expressed in human myeloid cell types. In addition, Tnfaip8l2 expression drastically decreased in lipopolysaccharide (LPS)-stimulated macrophages. Consequently, Tnfaip8l2 deficiency led to heightened expression of genes that were enriched for leukocyte activation and lipid biosynthesis pathways. Furthermore, mitochondrial respiration rate was increased in Tnfaip8l2-deficient macrophages, as measured by Seahorse metabolic analyzer. Taken together, these results indicate that Tnfaip8l2 serves as a “brake” for immunometabolism, which needs to be released for optimized metabolic reprogramming as well as mounting effective inflammatory responses. The unique anti-inflammatory and metabolic-modulatory function of TNFAIP8L2 renders it a novel therapeutic target for cardiovascular diseases and cancer. [ABSTRACT FROM AUTHOR]

Summary More than half of human cancers have aberrantly upregulated phosphoinositide signals; yet how phospholipid signals are controlled during tumorigenesis is not fully understood. We report here that TIPE3 (TNFAIP8L3) is the transfer protein of phosphoinositide second messengers that promote cancer. High-resolution crystal structure of TIPE3 shows a large hydrophobic cavity that is occupied by a phospholipid-like molecule. TIPE3 preferentially captures and shuttles two lipid second messengers, i.e., phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 3,4,5-trisphosphate, and increases their levels in the plasma membrane. Notably, human cancers have markedly upregulated TIPE3 expression. Knocking out TIPE3 diminishes tumorigenesis, whereas enforced TIPE3 expression enhances it in vivo. Thus, the function and metabolism of phosphoinositide second messengers are controlled by a specific transfer protein during tumorigenesis. [ABSTRACT FROM AUTHOR]

Summary: The connection between cancer and inflammation is widely recognized, yet the underlying molecular mechanisms are poorly understood. We report here that TIPE2 provides a molecular bridge from inflammation to cancer by targeting the Ras signaling pathway. TIPE2 binds the Ras-interacting domain of the RalGDS family of proteins, which are essential effectors of activated Ras. This binding prevented Ras from forming an active complex, thereby inhibiting the activation of the downstream signaling molecules Ral and AKT. Consequently, TIPE2 deficiency led to heightened activation of Ral and AKT, resistance to cell death, increased migration, and dysregulation of exocyst complex formation. Conversely, TIPE2 overexpression induced cell death and significantly inhibited Ras-induced tumorigenesis in mice. Importantly, TIPE2 expression was either completely lost or significantly downregulated in human hepatic cancer. Thus, TIPE2 is an inhibitor of both inflammation and cancer, and a potential drug target for inflammatory and neoplastic diseases. [ABSTRACT FROM AUTHOR]

Abstract: A novel acetylene black-PTFE cathode for electrogeneration of hydrogen peroxide (H2O2) was fabricated using acetylene black powder (ABP) as catalyst, PTFE as binder. The effect of mass ratio of ABP to PTFE, solution pH (3–11), applied current density (5–20mAcm−2) and surface hydrophobic property on the activity and useful life of cathode was investigated using a two-electrode undivided cell fed with air at 2Lmin−1 in Na2SO4 solution of 0.05M, and the characteristics of cathode were examined by FTIR spectra, BET measurement, SEM image and CV study. The experimental results showed that: (1) so far the activity of cathode is the highest for the electrogeneration of H2O2 with air feed, at pH 3 and the current density of 20mAcm−2 the average H2O2 generation rate reaching 58.9mgL−1 h−1 cm−2 during 150min of electrolysis and the current efficiency being 92.7%; (2) a proper and stable surface hydrophobic property could significantly increase the useful life of cathode; (3) the cathode had a remarkable restoration and regeneration performance. [Copyright &y& Elsevier]

Myeloid-derived suppressor cells (MDSCs) are "polarized" myeloid cells that effectively promote tumorigenesis by inhibiting antitumor immunity. How myeloid cells acquire the protumoral properties during tumorigenesis is poorly understood. We report here that the polarity protein TIPE2 (tumor necrosis factor-α-induced protein 8-like 2) mediates the functional polarization of murine and human MDSCs by specifying their pro- and antitumoral properties. Tumor cells induced the expression of TIPE2 in Gr1+CD11b+ cells through reactive oxygen species (ROS). TIPE2 in turn increased the expression of protumoral mediators such as CCAAT/enhancer-binding protein-β while inhibiting the expression of antitumoral mediators. Consequently, tumor growth in TIPE2-deficient mice was significantly diminished, and TIPE2-deficient MDSCs markedly inhibited tumor growth upon adoptive transfer. Pharmaceutical blockade of ROS inhibited TIPE2 expression in MDSCs and reduced tumor growth in mice. These findings indicate that TIPE2 plays a key role in the functional polarization of MDSCs and represents a new therapeutic target for cancer immunotherapy., (© 2019 Yan et al.)

Poly(piperazine-amide)-based nanofiltration membranes exhibit a smooth surface and superior antifouling properties but often have lower Ca 2+ and Mg 2+ rejection due to their larger inner micropore and thus cannot be extensively used in water-softening applications. To decrease the pore size of poly(piperazine-amide) membranes, we designed and synthesized a novel monomer, 1,2,3,4-cyclobutane tetracarboxylic acid chloride (BTC), which possesses a smaller molecular conformation than trimesoyl chloride (TMC). The thickness of the prepared BTC-piperazine (PIP) polyamide nanofilm via interfacial polymerization is as thin as 15 nm, significantly lower than the 50 nm thickness of the TMC-PIP nanofilm. The surface characterization reveals that the BTC-PIP polyamide membrane exhibits an enhanced hydrophilicity, a smooth surface, and a decreased surface-negative charge. The desalination performance (both rejection and water flux) of these membranes in terms of Ca 2+ and Mg 2+ exceeds that of the current commercial water-softening membranes. In addition, the BTC-PIP polyamide membrane also exhibits superior antifouling properties compared to the TMC-based polyamide membrane. More importantly, molecular simulations show that the BTC-PIP membrane has a lower average pore size than that of the TMC-PIP membrane, which demonstrates an enhanced steric hindrance effect, as confirmed by desalination performance. Our results demonstrate that in the household and industrial water-softening market, BTC-PIP membrane with decreased porosity, enhanced hydrophilicity, and smooth surface is preferred alternative to the conventional TMC-based polyamide membranes.

The polarization of leukocytes toward chemoattractants is essential for the directed migration (chemotaxis) of leukocytes. How leukocytes acquire polarity after encountering chemical gradients is not well understood. We found here that leukocyte polarity was generated by TIPE2 (TNFAIP8L2), a transfer protein for phosphoinositide second messengers. TIPE2 functioned as a local enhancer of phosphoinositide-dependent signaling and cytoskeleton remodeling, which promoted leading-edge formation. Conversely, TIPE2 acted as an inhibitor of the GTPase Rac, which promoted trailing-edge polarization. Consequently, TIPE2-deficient leukocytes were defective in polarization and chemotaxis, and TIPE2-deficient mice were resistant to leukocyte-mediated neural inflammation. Thus, the leukocyte polarizer is a dual-role phosphoinositide-transfer protein and represents a potential therapeutic target for the treatment of inflammatory diseases.

The TNF-α-induced protein 8 (TNFAIP8 or TIPE) is a risk factor for cancer and bacterial infection, and its expression is upregulated in a number of human cancers. However, its physiologic and pathologic functions are unclear. In this study, we describe the generation of TIPE-deficient mice and their increased sensitivity to colonic inflammation. TIPE-deficient mice were generated by germ line gene targeting and were born without noticeable developmental abnormalities. Their major organs, including lymphoid organs and intestines, were macroscopically and microscopically normal. However, after drinking dextran sodium sulfate-containing water, TIPE-deficient mice developed more severe colitis than wild type mice did, as demonstrated by decreased survival rates, increased body weight loss, and enhanced leukocyte infiltration, bacterial invasion, and inflammatory cytokine production in the colon. Bone marrow chimeric experiments revealed that TIPE deficiency in nonhematopoietic cells was responsible for the exacerbated colitis in TIPE-deficient mice. Consistent with this result, TIPE-deficient intestinal epithelial cells had increased rate of cell death and decreased rate of proliferation as compared with wild type controls. These findings indicate that TIPE plays an important role in maintaining colon homeostasis and in protecting against colitis., (Copyright © 2015 by The American Association of Immunologists, Inc.)

TNF-α-induced protein 8 (TNFAIP8 or TIPE) is a newly described regulator of cancer and infection. However, its precise roles and mechanisms of actions are not well understood. We report in this article that TNFAIP8 regulates Listeria monocytogenes infection by controlling pathogen invasion and host cell apoptosis in a RAC1 GTPase-dependent manner. TNFAIP8-knockout mice were resistant to lethal L. monocytogenes infection and had reduced bacterial load in the liver and spleen. TNFAIP8 knockdown in murine liver HEPA1-6 cells increased apoptosis, reduced bacterial invasion into cells, and resulted in dysregulated RAC1 activation. TNFAIP8 could translocate to plasma membrane and preferentially associate with activated RAC1-GTP. The combined effect of reduced bacterial invasion and increased sensitivity to TNF-α-induced clearance likely protected the TNFAIP8-knockout mice from lethal listeriosis. Thus, by controlling bacterial invasion and the death of infected cells through RAC1, TNFAIP8 regulates the pathogenesis of L. monocytogenes infection., (Copyright © 2015 by The American Association of Immunologists, Inc.)

Both commensal bacteria and infiltrating inflammatory cells play essential roles in the pathogenesis of inflammatory bowel disease. The molecular mechanisms whereby these pathogenic factors are regulated during the disease are not fully understood. We report in this article that a member of the TNF-α-induced protein 8 (TNFAIP8) family called TIPE2 (TNFAIP8-like 2) plays a crucial role in regulating commensal bacteria dissemination and inflammatory cell function in experimental colitis induced by dextran sodium sulfate (DSS). Following DSS treatment, TIPE2-deficient mice, or chimeric mice that are deficient in TIPE2 only in their hematopoietic cells, lost less body weight and survived longer than wild-type controls. Consistent with this clinical observation, TIPE2-deficient mice exhibited significantly less severe colitis and colonic damage. This was associated with a marked reduction in the colonic expression of inflammatory cytokines, such as TNF-α, IL-6, and IL-12. Importantly, the ameliorated DSS-induced colitis in TIPE2(-/-) mice also was associated with reduced local dissemination of commensal bacteria and a weaker systemic inflammatory response. Combined with our previous report that TIPE2 is a negative regulator of antibacterial immunity, these results indicate that TIPE2 promotes colitis by inhibiting mucosal immunity to commensal bacteria., (Copyright © 2014 by The American Association of Immunologists, Inc.)