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Enterprise green innovation is committed to the coordinated development of regional economic growth and ecological environment protection. It is of great practical significance to explore the internal linkage between air pollution and enterprise green innovation in the era of double carbon policy. Based on the data of all A-share listed companies in China from 2014 to 2019, this paper studies the impact of air pollution on enterprise green innovation and the regulatory effect of enterprise credit level on air pollution and enterprise green innovation. The research finds that: first, air pollution will significantly promote enterprises to carry out green innovation, that is, increase the total number of green patent applications; Second, compared with the quality of green innovation, the promotion of air pollution on the number of green innovation is more obvious, that is, the number of green utility model patents is significantly increased; Third, the improvement of enterprise credit level will strengthen the negative effect between air pollution and enterprise green innovation. According to the research conclusion, this paper also puts forward rationalization suggestions for green innovation of enterprises and financial market problems.

Refereed/Peer-reviewed Despite a growing catalog of secreted factors critical for lymphatic network assembly, little is known about the mechanisms that modulate the expression level of these molecular cues in blood vascular endothelial cells (BECs). Here, we show that a BEC-specific transcription factor, SOX7, plays a crucial role in a non-cell-autonomous manner by modulating the transcription of angiocrine signals to pattern lymphatic vessels. While SOX7 is not expressed in lymphatic endothelial cells (LECs), the conditional loss of SOX7 function in mouse embryos causes a dysmorphic dermal lymphatic phenotype. We identify novel distant regulatory regions in mice and humans that contribute to directly repressing the transcription of a major lymphangiogenic growth factor (Vegfc) in a SOX7-dependent manner. Further, we show that SOX7 directly binds HEY1, a canonical repressor of the Notch pathway, suggesting that transcriptional repression may also be modulated by the recruitment of this protein partner at Vegfc genomic regulatory regions. Our work unveils a role for SOX7 in modulating downstream signaling events crucial for lymphatic patterning, at least in part via the transcriptional repression of VEGFC levels in the blood vascular endothelium.

Arteries and veins form in a stepwise process that combines vasculogenesis and sprouting angiogenesis. Despite extensive data on the mechanisms governing blood vessel assembly at the single-cell level, little is known about how collective cell migration contributes to the organization of the balanced distribution between arteries and veins. Here, we use an endothelial-specific zebrafish reporter, arteriobow, to label small cohorts of arterial cells and trace their progeny from early vasculogenesis throughout arteriovenous remodeling. We reveal that the genesis of arteries and veins relies on the coordination of 10 types of collective cell dynamics. Within these behavioral categories, we identify a heterogeneity of collective cell motion specific to either arterial or venous remodeling. Using pharmacological blockade, we further show that cell-intrinsic Notch signaling and cell-extrinsic blood flow act as regulators in maintaining the heterogeneity of collective endothelial cell behavior, which, in turn, instructs the future territory of arteriovenous remodeling.

During vascular development, arteries and veins form in a stepwise process that combines vasculogenesis and sprouting angiogenesis. Despite extensive data on the mechanisms governing blood vessel assembly at the single cell level, little is known about how cell populations migrate in a finely tuned and coordinated manner, and distribute precisely between arteries and veins. Here, we use an endothelial-specific zebrafish reporter,arteriobow, to label small cohorts of arterial cells and trace their progeny from the initial events of vasculogenesis through the process of arterio-venous remodeling. We reveal that the genesis of both arteries and veins relies on the coordination of ten types of collective cell behaviors originating from discrete endothelial cell clusters. Within these behavioral categories, we identify a heterogeneity of collective cell dynamics specific to either arterial or venous remodeling. Using pharmacological blockade, we further show that factors known to control vascular patterning such as cell-intrinsic Notch signaling and cell-extrinsic blood flow, potentially act as regulators by coordinating endothelial cohorts behavior, which in turn instructs the future territory of arterio-venous remodeling.

During vascular development, arteries and veins form in a stepwise process that combines vasculogenesis and sprouting angiogenesis. Despite extensive data on the mechanisms governing blood vessel assembly at the single cell level, little is known about how cell populations migrate in a finely tuned and coordinated manner, and distribute precisely between arteries and veins. Here, we use an endothelial-specific zebrafish reporter, arteriobow, to label small cohorts of arterial cells and trace their progeny from the initial events of vasculogenesis through the process of arterio-venous remodeling. We reveal that the genesis of both arteries and veins relies on the coordination of ten types of collective cell behaviors originating from discrete endothelial cell clusters. Within these behavioral categories, we identify a heterogeneity of collective cell dynamics specific to either arterial or venous remodeling. Using pharmacological blockade, we further show that factors known to control vascular patterning such as cell-intrinsic Notch signaling and cell-extrinsic blood flow, potentially act as regulators by coordinating endothelial cohorts behavior, which in turn instructs the future territory of arterio-venous remodeling.

Seismic response of RC moment frame structures (particularly, in low-rise buildings) is affected by the inelastic hysteretic response and energy dissipation of beam-column joints. In curren...

Hierarchical metals oxide nanostructure derived from annealing of metal–organic frameworks (MOFs) usually have large particle size and low specific surface area and, as a result their activities, become limited. In this work, we incorporated KMnO4 into Prussian blue (PB) microcubes and obtained Mn-doped α-Fe2O3 nanoboxes by annealing the complex. We found that KMnO4 stayed inside the pores of the PB framework and restricted the crystal growth of α-Fe2O3 during annealing. Consequently, the Mn-doped Fe2O3 nanoboxes have small particle size, large specific area (452 m2/g), and a significant amount of adsorbed oxygen in the form of OH– on the surface as determined by X-ray photoelectron spectroscopy. It could serve as an adsorbent to quickly remove the trace-level (40 mg/L) Pb2+ from water. Within 1 min, this nanoadsorbent (0.2 g/L) extracted >70% Pb2+ in the solution, and >91.6% in 15 min. Besides, it also selectively captures Pb2+ (40 mg/L) from a synthetic Pb/Zn mining wastewater containing Zn2+ (40 mg/L) ...

Key message Not only the first systematic characterization ofCAOgene in bamboo species, but also the first attempt to study the relationship betweenCAOgene expression and bamboo leaf color variation.

In angiosperms, NADPH: protochlorophyllide oxidoreductase (POR) catalyzes the photoreduction of protochlorophyllide (Pchlide) to chlorophyllide (Chlide), the only light-dependent step in chlorophyll biosynthesis. There is a wide variety of gene organization and light- and development-dependent regulatory mechanisms for the POR genes. In this study, a POR homologue, designated PjPORB, was isolated from Pseudosasa japonica cv. Akebonosuji, which is a cultivar of high ornamental value in landscape due to its unique green-white striped leaf phenotype. The full-length PjPORB cDNA was 1567 bp long with a 1185 bp ORF that encoded 394 amino acids. Multiple amino acid sequence alignment showed that the putative PjPORB shared a high similarity to POR homologues from other plant species, and that the cofactor (NADPH)-binding motif and active site motif in particular were highly conserved among all the PORs. Further, PjPORB was overexpressed in Arabidopsis thaliana; and the Pchlide contents of the genetically modified plants were reduced to a larger extent than that of wild type plants, thereby indicating its important role in Pchlide photoreduction. In real-time quantitative RT-PCR analysis, PjPORB was expressed at higher levels in leaf samples than in culms and roots, and showed a first increasing-then decreasing expression pattern during the development of white, stripe, and green leaf samples, thus indicating its essential role in leaf development. Although the mRNA levels for PjPORB did not differ considerably among white, stripe, and green leaf samples within the two almost same earlier developmental stages, its expression levels in the late leaf developmental stage fell into two distinct classes: high expression levels in strip and green leaf samples, and low expression levels in white leaf. Collectively, these expression data suggested that PjPORB may be involved in the leaf color variation for P. japonica cv. Akebonosuji.

Accurate gas turbine engine health status estimation is very important for engine applications and aircraft flight safety. Due to the fact that there are many to-be-estimated parameters, engine health status estimation is a very difficult optimization problem. Traditional gas path analysis (GPA) methods are based on the linearized thermodynamic engine performance model, and the estimation accuracy is not satisfactory on conditions that the nonlinearity of the engine model is significant. To solve this problem, a novel gas turbine engine health status estimation method has been developed. The method estimates degraded engine component parameters using quantum-behaved particle swarm optimization (QPSO) algorithm. And the engine health indices are calculated using these estimated component parameters. The new method was applied to turbine fan engine health status estimation and is compared with the other three representative methods. Results show that although the developed method is slower in computation speed than GPA methods it succeeds in estimating engine health status with the highest accuracy in all test cases and is proven to be a very suitable tool for off-line engine health status estimation.

A newly isolated Bacillus megaterium with epoxide hydrolase activity resolved racemic glycidyl (o, m, p)-methylphenyl ethers to give enantiopure epoxides in 84-99% enantiomeric excess and with 21-73 enantiomeric ratios. The (S)-enantiomer was obtained from rac-glycidyl (o or m)-methylphenyl ether while the (R)-epoxides was obtained from glycidyl p-methylphenyl ether. The observations are explained at the level by enzyme-substrate docking studies.

Epoxide hydrolase plays an important role in the detoxification of genotoxic compounds and in the control of physiological signaling molecules. Altered levels of epoxide hydrolase activity are associated with many diseases, such as emphysema, lung cancer, ovarian cancer, and laryngeal carcinoma. We designed and synthesized a resorufin-based fluorogenic probe, 7-(2-(oxiran-2-yl)ethoxy) resorufin, which was hydrolyzed by microsomal epoxide hydrolase to form the corresponding diol, which upon further treatment with sodium periodate released the strongly fluorescent resorufin. The probe exhibits good biological compatibility and photophysical properties, such as long wavelength excitation (571 nm) and emission (585 nm) and a wide working pH range (from 6.0 to 10.0), and thus facilitates the determination of the activity of microsomal epoxide hydrolase.

Angiostatin4.5 (AS4.5) is the product of plasmin autoproteolysis and consists of kringles 1 to 4 and ∼85% of kringle 5. In culture, cancer cell surface globular β-actin mediates plasmin autoproteolysis to AS4.5. We now show that plasminogen binds to prostate cancer cells and that the binding colocalizes with surface β-actin, but AS4.5 does not bind to the cell surface. Plasminogen and plasmin bind to immobilized β-actin similarly, with a Kd of ∼140 nmol/L. The binding is inhibited by ε-aminocaproic acid (εACA), indicating the requirement for a lysine-kringle domain interaction. Using a series of peptides derived from β-actin in competitive binding studies, we show that the domain necessary for plasminogen binding is within amino acids 55 to 69 (GDEAQSKRGILTLKY). Substitution of Lys61 or Lys68 with arginine results in the loss of the ability of the peptide to block plasminogen binding, indicating that Lys61 and Lys68 are essential for plasminogen binding. Other actin peptides, including peptides with lysine, did not inhibit the plasminogen-actin interaction. AS4.5 did not bind actin at concentrations up to 40 μmol/L. Plasminogen, plasmin, and AS4.5 all contain kringles 1 to 4; however, kringle 5 is truncated in AS4.5. Isolated kringle 5 binds to actin, suggesting intact kringle 5 is necessary for plasminogen and plasmin to bind to cell surface β-actin, and the truncated kringle 5 in AS4.5 results in its release from β-actin. These data may explain the mechanism by which AS4.5 is formed locally on cancer cell surfaces and yet acts on distant sites. (Cancer Res 2006; 66(14): 7211-5)

Purpose: Angiostatin4.5 (AS4.5), the endogenous human angiostatin, is derived from plasminogen in a two-step process. A plasminogen activator converts plasminogen to plasmin, then plasmin undergoes autoproteolysis to AS4.5. A free sulfhydryl donor can mediate plasmin autoproteolysis. To translate this process to human cancer therapy, we conducted a phase I trial of administration of a tissue plasminogen activator (tPA) with a free sulfhydryl donor (mesna). Patients and Methods: Fifteen patients with advanced solid tumors were treated. The dose of tPA was escalated (cohorts; 1, 2, 3, 5, and 7.5 mg/h for 6 hours). Mesna was administered as a 240 mg/m2 bolus followed by an infusion of 50 mg/h, concurrent with tPA. Both tPA and mesna were administered 3 consecutive days every 14 days. Results: No dose-limiting toxicity was observed. Two AS4.5 isoforms were generated, Lys-AS4.5 and Glu-AS4.5. Mean baseline Lys-AS4.5 level was 20.4 nmol/L (SE, 2.9). In the 5 mg/h tPA cohort, Lys-AS4.5 levels increased by an average of 143% or 24 nmol/L (SE, 4.9) above baseline. Glu-AS4.5 (Mr ∼ 62,000) was also generated (additional 77 amino acids at amino terminus compared with Lys-AS4.5). Glu-AS4.5 level at baseline was undetectable in four of five patients in the 5 mg/h tPA cohort, but at end of infusion, was ∼67 nmol/L (SE, 20). Two patients in the 5 mg/h tPA cohort experienced decreases in tumor markers with treatment, although no clinical objective responses were observed. Conclusion: This study shows that in vivo generation of AS4.5 is safe in humans and may provide a practical approach to achieve antiangiogenic therapy.

Angiostatin4.5 (AS4.5) is a naturally occurring human angiostatin isoform, consisting of plasminogen kringles 1–4 plus 85% of kringle 5 (amino acids Lys78 to Arg529). Prior studies indicate that plasminogen is converted to AS4.5 in a two-step reaction. First, plasminogen is activated to plasmin. Then plasmin undergoes autoproteolysis within the inner loop of kringle 5, which can be induced by a free sulfhydryl donor or an alkaline pH. We now demonstrate that plasminogen can be converted to AS4.5 in a cell membrane-dependent reaction. Actin was shown previously to be a surface receptor for plasmin(ogen). We now show that β-actin is present on the extracellular membranes of cancer cells (PC-3, HT1080, and MDA-MB231), and β-actin can mediate plasmin binding to the cell surface and autoproteolysis to AS4.5. In the presence of β-actin, no small molecule-free sulfhydryl donor is needed for generation of AS4.5. Antibodies to actin reduced membrane-dependent generation of AS4.5 by 70%. In a cell-free system, addition of actin to in vitro-generated plasmin resulted in stoichiometric conversion to AS4.5. Annexin II and α-enolase have been reported to be plasminogen receptors, but we did not demonstrate a role for these proteins in conversion of plasminogen to AS4.5. Our data indicate that membrane-associated β-actin, documented previously as a plasminogen receptor, is a key cell membrane receptor capable of mediating conversion of plasmin to AS4.5. This conversion may serve an important role in regulating tumor angiogenesis, invasion, and metastasis, and surface β-actin may also serve as a prognostic marker to predict tumor behavior.

During placentation, the concentration of fibrinous deposits on the surfaces of maternal vasculature plays a role in villous development and has been strongly implicated in the pathophysiology of human fetal growth restriction (FGR). Fibrinous deposits are conspicuous sites of platelet aggregation where there is local activation of the hemostatic cascade. During activation of the hemostatic cascade, a number of pro- and antiangiogenic agents may be generated at the cell surface, and an imbalance in these factors may contribute to the placental pathology characteristic of FGR. We tested the hypothesis that angiostatin(4.5) (AS(4.5)), a cleavage fragment of plasminogen liberated at the cell surface, is capable of causing FGR in mice. Increased maternal levels of AS(4.5) in vivo result in reproducible placental pathology, including an altered vascular compartment (both in decidual and labyrinthine layers) and increased apoptosis throughout the placenta. In addition, there is significant skeletal growth delay and conspicuous edema in fetuses from mothers that received AS(4.5). Maternally generated AS(4.5), therefore, can access maternal placental vasculature and have a severe effect on placental architecture and inhibit fetal development in vivo. These findings strongly support the hypothesis that maternal AS(4.5) levels can influence placental development, possibly by directly influencing trophoblast turnover in the placenta, and contribute to fetal growth delay in mice.

According to the characteristics of aero-engine's accelerating process, the control parameters and constraints are determined for the optimal acceleration control. A non-linear programming model is established to the optimal acceleration control for a certain turbofan engine, which high pressure rotor speed and high pressure turbine inlet temperature, are as the objective function of accelerating control. From two factors, increasing the diversity of particle swarm and accelerating the convergence speed, the particle swarm algorithm has been modified. By judging the particle properties, the particle swarm algorithm has be expanded from the feasible region to the entire solution space. The optimization simulation of control laws is performed using the modified particle swarm optimization for a turbofan engine's accelerating process. Results show that the algorithm has a strong border search capability and the engine's accelerating abilty has been enhanced.

At present, most of virtual-based equipment training systems are one-man and don't meet the need of remote and distributed equipment training. Besides, there are some disadvantages in integrating the old equipment material and building animations with user interactivity. In this paper, by combining internet/intranet with virtual reality, a web-based equipment training system with virtual reality is developed. The architecture, functions and implementation of system are introduced. Moreover, it is presented how to process 3D CAD equipment data and build the XML scenario. Finally, the operation of system is described.

To clone and identify the gene encoding human ubiquitin binding enzyme 2 and study its expression pattern.According to the sequence of human EST, which is highly homologous to the mouse ubiquitin binding/conjugating enzyme (E2), primers were synthesized to screen the human fetal brain cDNA library. The gene was analyzed by bioinformatics technique and its expression pattern was studied by using multiple-tissue Northern blot.Two cDNA clones encoding human ubiquitin conjugating enzyme have been isolated and identified. Both containing the ubiquitin conjugating domain, the 2 cDNA clones are 88% identical in amino acid sequences and splicing isoforms to each other only with an exon excised to form the short sequence. They belong to a highly conserved and widely expressed E2 enzyme family. Northern blot shows that they are expressed exclusively in adult human heart, placenta, and pancreas but no transcripts can be detected in brain, lung, liver, skeletal muscle or kidney.The gene encoding human ubiquitin binding enzyme is expressed under temporal control. As a key enzyme in the degradation of proteins, ubiquitin conjugating enzymes play a central role in the expression regulation on the level of post-translation.

Angiostatin4.5 (AS4.5), the naturally occurring human angiostatin isoform, is the product of plasmin autoproteolysis and consists of kringles 1 to 4 and ~85% of kringle 5. An important question related to tumor angiogenesis is the mechanism by which tumor cells convert plasminogen to angiostatin locally and yet the angiostatin acts systemically. We recently reported that cancer cell surface globular β-actin mediates plasmin autoproteolysis to AS4.5. We now characterize the binding of plasminogen, plasmin and AS4.5 to globular β-actin. Plasminogen and plasmin bind comparably to immobilized globular β-actin, with a KD of approximately 140 nM. The binding is inhibited by ε-aminocaproic acid (EACA), a lysine analog, indicating the requirement for a lysine-kringle domain interaction. Using a series of peptides derived from β-actin in competitive binding studies, we show that the actin domain necessary for binding of plasminogen is within “GDEAQSKRGILTLKY”, (amino acids 55 to 69), which includes lys61 and lys68. Substitution of lys61 or Lys68 with arginine results in the loss of the peptide’s ability to block plasminogen binding, indicating that lys61 and Lys68 are necessary for plasminogen binding. Other actin peptides, including peptides with other lysines, did not inhibit the plasminogen-actin interaction. While plasminogen and plasmin bind to actin efficiently, AS4.5 did not bind, even at high concentrations (500 nM). Plasminogen, plasmin, and AS4.5 all contain kringles 1–4, however, kringle 5 is truncated in AS4.5, suggesting that the kringle 5 is the domain by which plasminogen and plasmin bind to actin. We thus tested pure recombinant kringle 5 for its ability to specifically bind actin. Isolated kringle 5 was shown to bind to actin supporting the hypothesis that intact kringle 5 is necessary for plasminogen and plasmin to bind to cell surface β-actin, and the truncated kringle 5 in AS4.5 results in its release from β-actin. We propose the following paradigm: Plasminogen binds cell surface globular β-actin, where uPA mediates activation to plasmin which remains bound to actin. Actin then mediates plasmin autoproteolysis, with an intra-kringle 5 cleavage, resulting in AS4.5 formation. With the truncation of kringle 5, the AS4.5 dissociates from the surface actin and enters the systemic circulation. These data may help explain why AS4.5 is formed locally, on cancer cell surfaces, and yet acts systemically.