非晶态固体的结构可以决定性能吗?

晶态固体的力学性能与塑性变形主要由结构缺陷,比如位错的运动决定.而在非晶态固体中结构如何决定性能,仍然是固体力学、材料学和凝聚态物理学共同关心但尚未解决的核心问题之一.传统材料学研究的经典范式为"结构决定性能".遵循这一信条,已经有大量的实验表征与理论、模拟研究,尝试将非晶态固体的某种结构特征与性能建立一一对应关系.但是,科学界对于非晶固体结构-性能关系成立与否,以及背后隐藏的规律知之甚少.本文针对非晶态固体的变形机制以及其微结构特征,基于分子动力学模拟,定量评估短程简单结构与中长程复杂结构在决定非晶态固体动力学性能方面的效用.通过海量抽样每种具体玻璃结构的激活能(标识激发难易程度),尝试将结构参数与激活能建立定量关系,从而揭示出非晶态固体结构-性能关系的隐藏主控因素为结构的空间关联,受限比几何结构本身更关键.只有某种结构在空间上呈现亚纳米级的空间关联长度,这种完备结构才有可能有效地决定非晶态固体的力学性能,而短程简单结构则无效.进一步,给出了评价非晶态固体结构预测性能有效性的普适定量方法,为建立广义无序物质的结构-性能关系提供了筛选准则.     

A NEW ALGORITHM FOR COMPUTING THE INVERSE AND GENERALIZED INVERSE OF THE SCALED FACTOR CIRCULANT MATRIX

A new algorithm for finding the inverse of a nonsingular scaled factor circulant matrix is presented by the Euclid＇s algorithm. Extension is made to compute the group inverse and the Moore-Penrose inverse of the singular scaled factor circulant matrix. Numerical examples are presented to demonstrate the implementation of the proposed algorithm.     

A Novel Ternary Composite of Polyurethane/Polyaniline/Nanosilica with Antistatic Property and Excellent Mechanical Strength: Preparation and Mechanism

Chinese Journal of Polymer Science - Antistatic and strength properties are of vital importance for polyurethane rubber used in moving parts of many industrial instruments. Herein, polyurethane was...     

Crystal Structure of Human CD47 in Complex with Engineered SIRPα.D1(N80A)

Background: Targeting the CD47/SIRPα signaling pathway represents a novel approach to enhance anti-tumor immunity. However, the crystal structure of the CD47/SIRPα has not been fully studied. This study aims to analyze the structure interface of the complex of CD47 and IMM01, a novel recombinant SIRPα-Fc fusion protein. Methods: IMM01-Fab/CD47 complex was crystalized, and diffraction images were collected. The complex structure was determined by molecular replacement using the program PHASER with the CD47-SIRPαv2 structure (PDB code 2JJT) as a search model. The model was manually built using the COOT program and refined using TLS parameters in REFMAC from the CCP4 program suite. Results: Crystallization and structure determination analysis of the interface of IMM01/CD47 structure demonstrated CD47 surface buried by IMM01. Comparison with the literature structure (PDB ID 2JJT) showed that the interactions of IMM01/CD47 structure are the same. All the hydrogen bonds that appear in the literature structure are also present in the IMM01/CD47 structure. These common hydrogen bonds are stable under different crystal packing styles, suggesting that these hydrogen bonds are important for protein binding. In the structure of human CD47 in complex with human SIRPα, except SER66, the amino acids that form hydrogen bonds are all conserved. Furthermore, comparing with the structure of PDB ID 2JJT, the salt bridge interaction from IMM01/CD47 structure are very similar, except the salt bridge bond between LYS53 in IMM01 and GLU106 in CD47, which only occurs between the B and D chains. However, as the side chain conformation of LYS53 in chain A is slightly different, the salt bridge bond is absent between the A and C chains. At this site between chain A and chain C, there are a salt bridge bond between LYS53 (A) and GLU104 (C) and a salt bridge bond between HIS56 (A) and GLU106 (C) instead. According to the sequence alignment results of SIRPα, SIRPβ and SIRPγ in the literature of PDB ID 2JJT, except ASP100, the amino acids that form common salt bridge bonds are all conserved. Conclusion: Our data demonstrated crystal structure of the IMM01/CD47 complex and provides a structural basis for the structural binding interface and future clinical applications.     

Mitochondrial citrate accumulation drives alveolar epithelial cell necroptosis in lipopolysaccharide-induced acute lung injury

Necroptosis is the major cause of death in alveolar epithelial cells (AECs) during acute lung injury (ALI). Here, we report a previously unrecognized mechanism for necroptosis. We found an accumulation of mitochondrial citrate (citrate^mt) in lipopolysaccharide (LPS)-treated AECs because of the downregulation of Idh3α and citrate carrier (CIC, also known as Slc25a1). shRNA- or inhibitor–mediated inhibition of Idh3α and Slc25a1 induced citrate^mt accumulation and necroptosis in vitro. Mice with AEC-specific Idh3α and Slc25a1 deficiency exhibited exacerbated lung injury and AEC necroptosis. Interestingly, the overexpression of Idh3α and Slc25a1 decreased citrate^mt levels and rescued AECs from necroptosis. Mechanistically, citrate^mt accumulation induced mitochondrial fission and excessive mitophagy in AECs. Furthermore, citrate^mt directly interacted with FUN14 domain-containing protein 1 (FUNDC1) and promoted the interaction of FUNDC1 with dynamin-related protein 1 (DRP1), leading to excessive mitophagy-mediated necroptosis and thereby initiating and promoting ALI. Importantly, necroptosis induced by citrate^mt accumulation was inhibited in FUNDC1-knockout AECs. We show that citrate^mt accumulation is a novel target for protection against ALI involving necroptosis.Subject terms: Infection, Respiratory tract diseases     

Activating SIRT3 in peritoneal mesothelial cells alleviates postsurgical peritoneal adhesion formation by decreasing oxidative stress and inhibiting the NLRP3 inflammasome

Peritoneal adhesions (PAs) are a serious complication of abdominal surgery and negatively affect the quality of life of millions of people worldwide. However, a clear molecular mechanism and a standard therapeutic strategy for PAs have not been established. Here, we developed a standardized method to mimic the pathological changes in PAs and found that sirtuin 3 (SIRT3) expression was severely decreased in adhesion tissues, which was consistent with our bioinformatics analysis and patient adhesion tissue analysis. Thus, we hypothesized that activating SIRT3 could alleviate postsurgical PAs. Sirt3-deficient (Sirt3^−/−) mice exhibited many more PAs after standardized abdominal surgery. Furthermore, compared with wild-type (Sirt3^+/+) mice, Sirt3-deficient (Sirt3^−/−) mice showed more prominent reactive oxygen species (ROS) accumulation, increased levels of inflammatory factors, and exacerbated mitochondrial damage and fragmentation. In addition, we observed NLRP3 inflammasome activation in the adhesion tissues of Sirt3^−/− but, not Sirt3^+/+ mice. Furthermore, mesothelial cells sorted from Sirt3^−/− mice exhibited impaired mitochondrial bioenergetics and redox homeostasis. Honokiol (HKL), a natural compound found in several species of the genus Magnolia, could activate SIRT3 in vitro. Then, we demonstrated that treatment with HKL could reduce oxidative stress and the levels of inflammatory factors and suppress NLRP3 activation in vivo, reducing the occurrence of postsurgical PAs. In vitro treatment with HKL also restored mitochondrial bioenergetics and promoted mesothelial cell viability under oxidative stress conditions. Taken together, our findings show that the rescue of SIRT3 by HKL may be a new therapeutic strategy to alleviate and block postsurgical PA formation.Subject terms: Trauma, Molecularly targeted therapy, Acute inflammation     

Identification of Protosappanoside D from Caesalpinia decapetala and Evaluation of Its Pharmacokinetic,Metabolism and Pharmacological Activity

Protosappanoside D (PTD) is a new component isolated from the extract of Caesalpinia decapetala for the first time. Its structure was identified as protosappanin B-3-O-β-D-glucoside by ¹H-NMR, ¹³C-NMR, 2D-NMR and MS techniques. To date, the pharmacological activities, metabolism or pharmacokinetics of PTD has not been reported. Therefore, this research to study the anti-inflammatory activity of PTD was investigated via the LPS-induced RAW264.7 cells model. At the same time, we also used the UHPLC/Q Exactive Plus MS and UPLC-MS/MS methods to study the metabolites and pharmacokinetics of PTD, to calculate its bioavailability for the first time. The results showed that PTD could downregulate secretion of the pro-inflammatory cytokines. In the metabolic study, four metabolites were identified, and the primary degradative pathways in vivo involved the desaturation, oxidation, methylation, alkylation, dehydration, degradation and desugarization. In the pharmacokinetic study, PTD and its main metabolite protosappanin B (PTB) were measured after oral and intravenous administration. After oral administration of PTD, its T_max was 0.49 h, t_1/2z and MRT_(0–t) were 3.47 ± 0.78 h and 3.06 ± 0.63 h, respectively. It shows that PTD was quickly absorbed into plasma and it may be eliminated quickly in the body, and its bioavailability is about 0.65%.     

Fabrication of Orange Fluorescent Boron-Doped Graphene Quantum Dots for Al3+ Ion Detection

Aluminum is a kind of metal that we often encounter. It can also be absorbed by the human body invisibly and will affect our bodies to a certain extent, e.g., by causing symptoms associated with Alzheimer’s disease. Therefore, the detection of aluminum is particularly important. The methods to detect metal ions include precipitation methods and electrochemical methods, which are cumbersome and costly. Fluorescence detection is a fast and sensitive method with a low cost and non-toxicity. Traditional fluorescent nanomaterials have a high cost, high toxicity, and cause harm to the human body. Graphene quantum dots are a new type of fluorescent nanomaterials with a low cost and non-toxicity that can compensate for the defects of traditional fluorescent nanomaterials. In this paper, c-GQDs and o-GQDs with good performance were prepared by a bottom-up hydrothermal method using o-phenylenediamine as a precursor and citric acid or boric acid as modulators. They have very good optical properties: o-GQDs exhibit orange fluorescence under UV irradiation, while c-GQDs exhibits cyan fluorescence. Then, different metal ions were used for ion detection, and it was found that Al³⁺ had a good quenching effect on the fluorescence of the o-GQDs. The reason for this phenomenon may be related to the strong binding of Al³⁺ ions to the N and O functional groups of the o-GQDs and the rapid chelation kinetics. During the chelation process, the separation of o-GQDs’ photoexcited electron hole pairs leads to their rapid electron transfer to Al³⁺, in turn leading to the occurrence of a fluorescence-quenching phenomenon. In addition, there was a good linear relationship between the concentration of the Al³⁺ ions and the fluorescence intensity, and the correlation coefficient of the linear regression equation was 0.9937. This illustrates the potential for the wide application of GQDs in sensing systems, while also demonstrating that Al³⁺ sensors can be used to detect Al³⁺ ions.