Efficient photodegradation of phenol assisted by persulfate under visible light irradiation via a nitrogen-doped titanium-carbon composite

To realize the utilization of visible light and improve the photocatalytic efficiency of organic pollutant degradation in wastewater, a nitrogen-doped titanium-carbon composite (N-TiO₂/AC) prepared by sol-gel methods was applied in the photodegradation of phenol assisted by persulfate under visible light irradiation (named N-TiO₂/AC/PS/VIS). The results show that a synergistic effect exists between visible-light photocatalysis and persulfate activation. Compared with TiO₂/PS/VIS, the phenol degradation rate was found to be observably improved by 65% in the N-TiO₂/AC/PS/VIS system. This significant increase in degradation rate was mainly attributed to the following two factors: 1) The N and C doping can change the crystal structure of TiO₂, which extends the TiO₂ absorption wavelength range to the visible light region. 2) As an electron acceptor, PS can not only prevent electrons and holes from recombining with each other but can also generate strong oxidizing radicals such as ∙SO₄^– and ∙OH to accelerate the reaction dynamics. The process of phenol degradation was found to be consistent with the Langmuir pseudo-first-order kinetic model with an apparent rate constant k of 1.73 min^–1. The N-TiO₂/AC/PS/VIS process was proven to be a facile method for pollutant degradation with high pH adaptability, excellent visible-light utilization and good application prospects.     

改进的永磁同步电机双矢量模型预测转矩控制

针对永磁同步电机（PMSM）传统模型预测转矩控制（MPTC）权重系数设置复杂、转矩和磁通脉动大的问题,提出了一种改进的PMSM双矢量MPTC方法。该方法扩展虚拟矢量以增加候选电压矢量,结合电压矢量作用于转矩和磁链的原则,减少选择候选矢量的计算量。同时,针对转矩无差拍和磁通无差拍,运用候选矢量的转矩占空比和磁通占空比构造了优化规则代替传统预测转矩控制中的代价函数,避免权重系数的整定问题。仿真结果表明,所提改进方法不仅提高稳态性能,而且能保持MPTC动态响应迅速的特点。     

同轴电纺法TiO2/g-C3N4的制备及光催化性能研究

传统的静电纺丝法使用单一的毛细管状喷头喷丝,通常用于制备实心且表面光滑单一组分的纳米纤维,无法得到具有多种功能性结构的复合材料,应用范围较窄。以酞酸丁酯和尿素为原料,采用同轴静电纺丝法成功制备了TiO₂/g-C₃N₄复合材料,并用X射线衍射（XRD）、傅里叶变换红外光谱（FTIR）、紫外可见漫反射光谱（UV-vis DRS）、场发射扫描电子显微镜（SEM）和Brunauer-Emmett-Teller （BET）分析对样品进行了表征,通过光催化降解亚甲基蓝溶液（MB）研究了不同g-C₃N₄添加量对TiO₂/g-C₃N₄复合材料光催化性能的影响。实验结果表明,采用同轴静电纺丝法结合500℃煅烧工艺成功制备了大比表面积及高光催化性能的TiO₂/g-C₃N₄复合材料。当g-C₃N₄添加量为0.15 g时,TiO₂/g-C₃N₄复合材料对亚甲基蓝溶液（MB）的光催化降解效率可达93.8%,且经过5次重复实验后降解率仍可达80%以上。     

A panoramic view of Li7P3S11 solid electrolytes synthesis,structural aspects and practical challenges for all-solid-state lithium batteries

The development of an inorganic electrochemical stable solid-state electrolyte is essentially responsible for future state-of-the-art all-solid-state lithium batteries (ASSLBs). Because of their advantages in safety, working temperature, high energy density, and packaging, ASSLBs can develop an ideal energy storage system for modern electric vehicles (EVs). A solid electrolyte (SE) model must have an economical synthesis approach, exhibit electrochemical and chemical stability, high ionic conductivity, and low interfacial resistance. Owing to its highest conductivity of 17 mS·cm^-1, and deformability, the sulfide-based Li₇P₃S₁₁ solid electrolyte is a promising contender for the high-performance bulk type of ASSLBs. Herein, we present a current glimpse of the progress of synthetic procedures, structural aspects, and ionic conductivity improvement strategies. Structural elucidation and mechanistic approaches have been extensively discussed by using various characterization techniques. The chemical stability of Li₇P₃S₁₁ could be enhanced via oxide doping, and hard and soft acid/base (HSAB) concepts are also discussed. The issues to be undertaken for designing the ideal solid electrolytes, interfacial challenges, and high energy density have been discoursed. This review aims to provide a bird's eye view of the recent development of Li₇P₃S₁₁-based solid-state electrolyte applications and explore the strategies for designing new solid electrolytes with a target-oriented approach to enhance the efficiency of high energy density all-solid-state lithium batteries.     

Ru/CN催化对苯二甲酸二甲酯加氢制备1,4-环己烷二甲酸二甲酯

通过超声辅助NaBH4还原法制备了3%Ru/CN催化剂（Ru的质量分数）,该催化剂用于对苯二甲酸二甲酯（DMT）加氢制备1,4-环己烷二甲酸二甲酯（DMCD）。采用Raman、SEM、TEM、N2吸脱附、XRD、XPS等对载体和催化剂的组成、表面性质进行表征,结果表明,氮元素成功掺入碳骨架中且氮掺杂碳材料为介孔结构。研究了催化剂的用量、反应温度、H2 压力、反应时间等对催化剂加氢性能的影响。结果表明,当反应物用量为1.00 g,催化剂（含载体）用量为0.05 g,反应温度140 ℃,反应压力5.0 MPa,反应时间1 h时,DMT转化率为100%,DMCD选择性为99.3%。3%Ru/CN-1000催化剂循环使用5次后,催化剂催化性能未见明显下降,DMT转化率为98.8%,DMCD选择性为99.7%。     

Evidence for a Negative Correlation between Human Reactive Enamine-Imine Intermediate Deaminase A (RIDA) Activity and Cell Proliferation Rate: Role of Lysine Succinylation of RIDA

Reactive intermediate deaminase (Rid) proteins are enzymes conserved in all domains of life. UK114, a mammalian member of RidA subfamily, has been firstly identified as a component of liver perchloric acid-soluble proteins (L-PSP). Although still poorly defined, several functions have been attributed to the mammalian protein UK114/RIDA, including the reactive intermediate deamination activity. The expression of UK114/RIDA has been observed in some tumors, arousing interest in this protein as an evaluable tumor marker. However, other studies reported a negative correlation between UK114/RIDA expression, tumor differentiation degree and cell proliferation. This work addressed the question of UK114/RIDA expression in human non-tumor HEK293 cell lines and in some human tumor cell lines. Here we reported that human RIDA (hRIDA) was expressed in all the analyzed cell line and subjected to lysine (K-)succinylation. In HEK293, hRIDA K-succinylation was negatively correlated to the cell proliferation rate and was under the control of SIRT5. Moreover, K-succinylation clearly altered hRIDA quantification by immunoblotting, explaining, at least in part, some discrepancies about RIDA expression reported in previous studies. We found that hRIDA was able to deaminate reactive enamine-imine intermediates and that K-succinylation drastically reduced deaminase activity. As predicted by in silico analysis, the observed reduction of deaminase activity has been related to the drastic alterations of hRIDA structure inferred by K-succinylation. The role of hRIDA and the importance of its K-succinylation in cell metabolism, especially in cancer biology, have been discussed.     

Nicotinamide Phosphoribosyltransferase as a Key Molecule of the Aging/Senescence Process

Aging is a phenomenon underlined by complex molecular and biochemical changes that occur over time. One of the metabolites that is gaining strong research interest is nicotinamide adenine dinucleotide, NAD⁺, whose cellular level has been shown to decrease with age in various tissues of model animals and humans. Administration of NAD⁺ precursors, nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR), to supplement NAD⁺ production through the NAD⁺ salvage pathway has been demonstrated to slow down aging processes in mice. Therefore, NAD⁺ is a critical metabolite now understood to mitigate age-related tissue function decline and prevent age-related diseases in aging animals. In human clinical trials, administration of NAD⁺ precursors to the elderly is being used to address systemic age-associated physiological decline. Among NAD⁺ biosynthesis pathways in mammals, the NAD⁺ salvage pathway is the dominant pathway in most of tissues, and NAMPT is the rate limiting enzyme of this pathway. However, only a few activators of NAMPT, which are supposed to increase NAD⁺, have been developed so far. In this review, we will focus on the importance of NAD⁺ and the possible application of an activator of NAMPT to promote successive aging.     

Bone Marrow-Mesenchymal Stromal Cell Secretome as Conditioned Medium Relieves Experimental Skeletal Muscle Damage Induced by Ex Vivo Eccentric Contraction

Bone marrow-mesenchymal stem/stromal cells (MSCs) may offer promise for skeletal muscle repair/regeneration. Growing evidence suggests that the mechanisms underpinning the beneficial effects of such cells in muscle tissue reside in their ability to secrete bioactive molecules (secretome) with multiple actions. Hence, we examined the effects of MSC secretome as conditioned medium (MSC-CM) on ex vivo murine extensor digitorum longus muscle injured by forced eccentric contraction (EC). By combining morphological (light and confocal laser scanning microscopies) and electrophysiological analyses we demonstrated the capability of MSC-CM to attenuate EC-induced tissue structural damages and sarcolemnic functional properties’ modifications. MSC-CM was effective in protecting myofibers from apoptosis, as suggested by a reduced expression of pro-apoptotic markers, cytochrome c and activated caspase-3, along with an increase in the expression of pro-survival AKT factor. Notably, MSC-CM also reduced the EC-induced tissue redistribution and extension of telocytes/CD34⁺ stromal cells, distinctive cells proposed to play a “nursing” role for the muscle resident myogenic satellite cells (SCs), regarded as the main players of regeneration. Moreover, it affected SC functionality likely contributing to replenishment of the SC reservoir. This study provides the necessary groundwork for further investigation of the effects of MSC secretome in the setting of skeletal muscle injury and regenerative medicine.     

Cardiac Oxidative Signaling and Physiological Hypertrophy in the Na/K-ATPase α1s/sα2s/s Mouse Model of High Affinity for Cardiotonic Steroids

The Na/K-ATPase is the specific receptor for cardiotonic steroids (CTS) such as ouabain and digoxin. At pharmacological concentrations used in the treatment of cardiac conditions, CTS inhibit the ion-pumping function of Na/K-ATPase. At much lower concentrations, in the range of those reported for endogenous CTS in the blood, they stimulate hypertrophic growth of cultured cardiac myocytes through initiation of a Na/K-ATPase-mediated and reactive oxygen species (ROS)-dependent signaling. To examine a possible effect of endogenous concentrations of CTS on cardiac structure and function in vivo, we compared mice expressing the naturally resistant Na/K-ATPase α1 and age-matched mice genetically engineered to express a mutated Na/K-ATPase α1 with high affinity for CTS. In this model, total cardiac Na/K-ATPase activity, α1, α2, and β1 protein content remained unchanged, and the cardiac Na/K-ATPase dose–response curve to ouabain shifted to the left as expected. In males aged 3–6 months, increased α1 sensitivity to CTS resulted in a significant increase in cardiac carbonylated protein content, suggesting that ROS production was elevated. A moderate but significant increase of about 15% of the heart-weight-to-tibia-length ratio accompanied by an increase in the myocyte cross-sectional area was detected. Echocardiographic analyses did not reveal any change in cardiac function, and there was no fibrosis or re-expression of the fetal gene program. RNA sequencing analysis indicated that pathways related to energy metabolism were upregulated, while those related to extracellular matrix organization were downregulated. Consistent with a functional role of the latter, an angiotensin-II challenge that triggered fibrosis in the α1^r/rα2^s/s mouse failed to do so in the α1^s/sα2^s/s. Taken together, these results are indicative of a link between circulating CTS, Na/K-ATPase α1, ROS, and physiological cardiac hypertrophy in mice under baseline laboratory conditions.