Effects of SO2 on selective catalytic reduction of NO with NH3 over a TiO2 photocatalyst

The effect of SO₂ gas was investigated on the activity of the photo-assisted selective catalytic reduction of nitrogen monoxide (NO) with ammonia (NH₃) over a TiO₂ photocatalyst in the presence of excess oxygen (photo-SCR). The introduction of SO₂ (300 ppm) greatly decreased the activity of the photo-SCR at 373 K. The increment of the reaction temperature enhanced the resistance to SO₂ gas, and at 553 K the conversion of NO was stable for at least 300 min of the reaction. X-ray diffraction, FTIR spectroscopy, thermogravimetry and differential thermal analysis, x-ray photoelectron spectroscopy (XPS), elemental analysis and N₂ adsorption measurement revealed that the ammonium sulfate species were generated after the reaction. There was a strong negative correlation between the deposition amount of the ammonium sulfate species and the specific surface area. Based on the above relationship, we concluded that the deposition of the ammonium sulfate species decreased the specific surface area by plugging the pore structure of the catalyst, and the decrease of the specific surface area resulted in the deactivation of the catalyst.     

Control of the particle microstructure during the synthesis of bulk-polymerized transparent methacrylate-acrylonitrile-butadiene-styrene resin

A series of methacrylate-acrylonitrile-butadiene-styrene (MABS) resins was prepared using bulk polymerization. The polarity of the continuous phase and the compatibility of two phases were changed by adjusting the methyl methacrylate (MMA) content, choosing values that were close to styrene-butadiene rubber solubility value. The possibility of controlling the microstructure of the MABS resin by changing the polarity of the components and the compatibility of two phases was assessed. The dynamic mechanical analysis shows that the compatibility of two phases varies with the MMA content. The morphological analysis shows that increasing MMA contents results in a gradual decrease in the sub-inclusion structure with a network skeleton of rubber particles, and that all the particles become solid rubber when the MMA content reaches 75%. The sub-inclusion structure reappears but does not have a network skeleton when the MMA content is 90%. The impact strength and morphological analysis indicate that the solid rubber particles and the sub-inclusion structure with a network skeleton provide excellent toughness, while the sub-inclusion structure without a network skeleton does not. In contrast, the transmittance of the ABS resin first increased and then decreased with increasing MMA content.     

Current Status on Stem Cells and Cancers of the Gastric Epithelium

Gastric cancer is still a leading cause of cancer-related mortality worldwide in spite of declining incidence. Gastric cancers are, essentially, adenocarcinomas and one of the strongest risk factors is still infection with Helicobacter pylori. Within the last years, it became clear that gastric self-renewal and carcinogenesis are intimately linked, particularly during chronic inflammatory conditions. Generally, gastric cancer is now regarded as a disease resulting from dysregulated differentiation of stem and progenitor cells, mainly due to an inflammatory environment. However, the situation in the stomach is rather complex, consisting of two types of gastric units which show bidirectional self-renewal from an unexpectedly large variety of progenitor/stem cell populations. As in many other tumors, cancer stem cells have also been characterized for gastric cancer. This review focuses on the various gastric epithelial stem cells, how they contribute to self-renewal and which routes are known to gastric adenocarcinomas, including their stem cells.     

Direct Injection of CRISPR/Cas9-Related mRNA into Cytoplasm of Parthenogenetically Activated Porcine Oocytes Causes Frequent Mosaicism for Indel Mutations

Some reports demonstrated successful genome editing in pigs by one-step zygote microinjection of mRNA of CRISPR/Cas9-related components. Given the relatively long gestation periods and the high cost of housing, the establishment of a single blastocyst-based assay for rapid optimization of the above system is required. As a proof-of-concept, we attempted to disrupt a gene (GGTA1) encoding the α-1,3-galactosyltransferase that synthesizes the α-Gal epitope using parthenogenetically activated porcine oocytes. The lack of α-Gal epitope expression can be monitored by staining with fluorescently labeled isolectin BS-I-B₄ (IB4), which binds specifically to the α-Gal epitope. When oocytes were injected with guide RNA specific to GGTA1 together with enhanced green fluorescent protein (EGFP) and human Cas9 mRNAs, 65% (24/37) of the developing blastocysts exhibited green fluorescence, although almost all (96%, 23/24) showed a mosaic fluorescent pattern. Staining with IB4 revealed that the green fluorescent area often had a reduced binding activity to IB4. Of the 16 samples tested, six (five fluorescent and one non-fluorescent blastocysts) had indel mutations, suggesting a correlation between EGFP expression and mutation induction. Furthermore, it is suggested that zygote microinjection of mRNAs might lead to the production of piglets with cells harboring various mutation types.     

Glibenclamide for the Treatment of Ischemic and Hemorrhagic Stroke

Ischemic and hemorrhagic strokes are associated with severe functional disability and high mortality. Except for recombinant tissue plasminogen activator, therapies targeting the underlying pathophysiology of central nervous system (CNS) ischemia and hemorrhage are strikingly lacking. Sur1-regulated channels play essential roles in necrotic cell death and cerebral edema following ischemic insults, and in neuroinflammation after hemorrhagic injuries. Inhibiting endothelial, neuronal, astrocytic and oligodendroglial sulfonylurea receptor 1–transient receptor potential melastatin 4 (Sur1–Trpm4) channels and, in some cases, microglial K_ATP (Sur1–Kir6.2) channels, with glibenclamide is protective in a variety of contexts. Robust preclinical studies have shown that glibenclamide and other sulfonylurea agents reduce infarct volumes, edema and hemorrhagic conversion, and improve outcomes in rodent models of ischemic stroke. Retrospective studies suggest that diabetic patients on sulfonylurea drugs at stroke presentation fare better if they continue on drug. Additional laboratory investigations have implicated Sur1 in the pathophysiology of hemorrhagic CNS insults. In clinically relevant models of subarachnoid hemorrhage, glibenclamide reduces adverse neuroinflammatory and behavioral outcomes. Here, we provide an overview of the preclinical studies of glibenclamide therapy for CNS ischemia and hemorrhage, discuss the available data from clinical investigations, and conclude with promising preclinical results that suggest glibenclamide may be an effective therapeutic option for ischemic and hemorrhagic stroke.     

非连续采空区矿柱力学分析的数值模拟

为探讨非连续采空区矿柱力学原理，通过FLAC3D数值模拟技术，对下向水平分层进路式胶结充填采矿法开采形成的非连续采空区中矿柱的受力状态进行了分析。研究表明，非连续采空区中矿柱所受的力主要为覆岩的自重应力，水平应力对其影响不大；随着埋深的增加矿柱承受的垂直方向的力近似呈直线增加；随着非连续采空区跨度的增加（进路数量增加），非连续采空区受垂直方向的应力逐渐由围岩两侧向矿柱中间过渡。     

某铁矿隔水护顶矿柱厚度计算及安全影响预测

科学合理地确定矿山隔水护顶矿柱安全厚度是矿山安全生产的前提条件，为保障某铁矿地表民房、道路等建（构）筑物安全，防止矿山开采过程中产生的导水裂隙带贯通第四系含水层，采用荷载传递交汇线法、K.B.鲁别涅依他估算法和冒落带、导水裂隙带高度估算法3种理论分析方法对隔水护顶矿柱厚度进行计算，并利用数值模拟手段对留设隔水护顶矿柱后的开采过程安全影响进行了分析，对理论计算结果进行了验证。3种理论计算方法得出的隔水护顶矿柱厚度分别为14.3～17.3 m、17.5～31.4 m和41.8～57.4 m，推荐隔水护顶矿柱留设厚度为60 m。通过数值模拟分析得出，在留设60 m厚的隔水护顶矿柱的基础上，开采区域和隔水护顶矿柱位置产生的最大拉应力约0.47 MPa，矿山开采不会对隔水护顶矿柱造成破坏；地表产生的最大水平位移约5.8 cm，最大垂直位移约26.5 cm，最大倾斜为1.70 mm/m，最大曲率为0.20 mm/m2，最大水平变形值为0.70 mm/m，满足相关规范要求，预测矿山开采不会造成地表建（构）筑物破坏。     

The Interplay of Modulus,Strength, and Ductility in Adhesive Design Using Biomimetic Polymer Chemistry

High‐performance adhesives require mechanical properties tuned to demands of the surroundings. A mismatch in stiffness between substrate and adhesive leads to stress concentrations and fracture when the bonding is subjected to mechanical load. Balancing material strength versus ductility, as well as considering the relationship between adhesive modulus and substrate modulus, creates stronger joints. However, a detailed understanding of how these properties interplay is lacking. Here, a biomimetic terpolymer is altered systematically to identify regions of optimal bonding. Mechanical properties of these terpolymers are tailored by controlling the amount of a methyl methacrylate stiff monomer versus a similar monomer containing flexible poly(ethylene glycol) chains. Dopamine methacrylamide, the cross‐linking monomer, is a catechol moiety analogous to 3,4‐dihydroxyphenylalanine, a key component in the adhesive proteins of marine mussels. Bulk adhesion of this family of terpolymers is tested on metal and plastic substrates. Incorporating higher amounts of poly(ethylene glycol) into the terpolymer introduces flexibility and ductility. By taking a systematic approach to polymer design, the region in which material strength and ductility are balanced in relation to the substrate modulus is found, thereby yielding the most robust joints.     

Interleukin-1β Modulation of the Mechanobiology of Primary Human Pulmonary Fibroblasts: Potential Implications in Lung Repair

Pro-inflammatory cytokines like interleukin-1β (IL-1β) are upregulated during early responses to tissue damage and are expected to transiently compromise the mechanical microenvironment. Fibroblasts are key regulators of tissue mechanics in the lungs and other organs. However, the effects of IL-1β on fibroblast mechanics and functions remain unclear. Here we treated human pulmonary fibroblasts from control donors with IL-1β and used Atomic Force Microscopy to unveil that IL-1β significantly reduces the stiffness of fibroblasts concomitantly with a downregulation of filamentous actin (F-actin) and alpha-smooth muscle (α-SMA). Likewise, COL1A1 mRNA was reduced, whereas that of collagenases MMP1 and MMP2 were upregulated, favoring a reduction of type-I collagen. These mechanobiology changes were functionally associated with reduced proliferation and enhanced migration upon IL-1β stimulation, which could facilitate lung repair by drawing fibroblasts to sites of tissue damage. Our observations reveal that IL-1β may reduce local tissue rigidity by acting both intracellularly and extracellularly through the downregulation of fibroblast contractility and type I collagen deposition, respectively. These IL-1β-dependent mechanical effects may enhance lung repair further by locally increasing pulmonary tissue compliance to preserve normal lung distension and function. Moreover, our results support that IL-1β provides innate anti-fibrotic protection that may be relevant during the early stages of lung repair.