Can low-carbon city construction reduce carbon intensity？Empirical evidence from low-carbon city pilot policy in China.

Low-carbon city pilot policy (LCCP) is an innovative initiative for promoting low-carbon transformation and green development in China, which is of great practical significance for realizing China's vision of "double carbon" on schedule. In this study, LCCP implementation is treated as a "quasi-natural experiment," and the spatial difference-in-differences approach is used to quantitatively examine the carbon reduction effects and impact mechanisms of LCCP using panel data of 283 cities in China from 2006 to 2017. The results show that since 2011, LCCP has significantly reduced the carbon intensity of the pilot cities by 0.13%, resulting from the effects of urban environmental governance, industrial structure optimization, and urban innovation level improvement. Meanwhile, there is a significant spatial spillover effect which results in a 0.9% reduction in carbon intensity of neighboring cities. The spatial spillover range of the reduction effect is about 500 km, which decays with distance. Moreover, the carbon reduction effect of the policy is spatially and temporally heterogeneous, and the reduction effect is more significant for resource-based cities, and different for resource-based cities in different development stages. The above findings provide useful policy insights for constructing low-carbon cities under China's "dual carbon goals" and help to realize the win-win path of green development and carbon reduction transition.

Amine-Functionalized Natural Halloysite Nanotubes Supported Metallic (Pd, Au, Ag) Nanoparticles and Their Catalytic Performance for Dehydrogenation of Formic Acid.

In today's age of resource scarcity, the low-cost development and utilization of renewable energy, e.g., hydrogen energy, have attracted much attention in the world. In this work, cheap natural halloysite nanotubes (HNTs) were modified with γ-aminopropyltriethoxysilane (APTES), and the functionalized HNTs were used as to support metal (Pd, Au, Ag) catalysts for dehydrogenation of formic acid (DFA). The supports and fabricated catalysts were characterized with ICP, FT-IR, XRD, XPS and TEM. The functional groups facilitate the anchoring of metal particles to the supports, which brings about the high dispersion of metallic particles in catalysts. The catalysts show high activity against DFA and exhibit selectivity of 100% toward H2 at room temperature or less. The interactions between active centers and supports were investigated by evaluation and comparison of the catalytic performances of Pd/NH2-HNTs, PdAg/NH2-HNTs and PdAu/NH2-HNTs for DFA.

Engineered Exosomes with Independent Module/Cascading Function for Therapy of Parkinson's Disease by Multistep Targeting and Multistage Intervention Method.

Current exosome engineering methods usually lead to the damage of exosome morphology and membrane, which cannot meet the complex needs of disease treatment. Herein, the concept of an "independent module/cascading function" is proposed to construct an engineered exosome nanotherapy platform including an independent artificial module and a natural module. The artificial module with movement/chemotaxis function is first synthesized, and then it is controllably combined with the natural exosome module with "one by one" mode through a "differentiated" modification method. The whole process can not only maintain the activity of the natural exosome module, but also endows it with motion ability, so as to realize the purpose of "cascading function" in the process of disease treatment. The above engineered exosomes are used in the treatment of Parkinson's disease (PD). Moreover, the multistep targeting strategy of "disease microenvironment-damaged cells-diseased mitochondria" and the multistage intervention concept of "inhibiting deterioration and promoting repair" are proposed, so as to break through the bottleneck of the existing treatment of PD.

Nitric oxide-driven nanomotors with bowl-shaped mesoporous silica for targeted thrombolysis.

Vein thrombosis is one of the most serious types of cardiovascular disease. During the traditional treatment, due to the excessive blood flow rate, the drug utilization rate at the thrombus site is low and the thrombolysis efficiency is poor. In this study, bowl-shaped silica nanomotors driven by nitric oxide (NO) are designed to target the thrombus surface by modifying arginine-glycine-aspartic acid (RGD) polypeptide, and simultaneously loading l-arginine (LA) and thrombolytic drug urokinase (UK) in its mesopore structure. LA can react with excessive reactive oxygen species (ROS) in the thrombus microenvironment to produce NO, thus promoting the movement of nanomotors to improve the retention efficiency and utilization rate of drugs in the thrombus site, and at the same time achieve the effect of eliminating ROS and reducing the oxidative stress of inflammatory endothelial cells. The loaded UK can dissolve thrombus quickly. It is worth mentioning that NO can not only be used as a power source of nanomotors, but also can be used as a therapeutic agent to stimulate the growth of endothelial cells and reduce vascular injury. This therapeutic agent based on nanomotor technology is expected to provide support for future research on thrombus treatment.

Multi-Pathway Microenvironment Regulation for Atherosclerosis Therapy Based on Beta-Cyclodextrin/L-Arginine/Au Nanomotors with Dual-Mode Propulsion.

Most of the current non-pharmacological treatment strategies for atherosclerosis (AS) suffer from poor penetration into the plaque and only aim at a certain factor in its formation process, resulting in limited therapeutic effect. Herein, a kind of nanomotor with dual-mode propulsion is constructed, which is sensitive to higher reactive oxygen species (ROS) at the AS site and near-infrared (NIR) laser by the covalent binding and self-assembly of ß-cyclodextrin (ß-CD) and L-arginine (LA) with immobilization of Au nanoparticles. NIR laser irradiation can be used as a driving force and to ablate inflammatory macrophages through the photothermal effect. The nitric oxide (NO) released by the nanomotors can be used as another driving force and a therapeutic agent to promote endothelial repair in the plaque site. LA can eliminate ROS in the inflammatory site, and ß-CD can promote the removal of cholesterol from foam cells. In particular, the two driving modes of nanomotors synergistically promote their aggregation and penetration in the plaque. This kind of nanomotor can regulate the microenvironment of AS in multiple ways, including combination therapy for endothelial repair, lipid clearance, and reducing ROS, which is expected to become a potential non-pharmacological strategy in the treatment of AS.

Applying machine learning to balance performance and stability of high energy density materials.

The long-standing performance-stability contradiction issue of high energy density materials (HEDMs) is of extremely complex and multi-parameter nature. Herein, machine learning was employed to handle 28 feature descriptors and 5 properties of detonation and stability of 153 HEDMs, wherein all 21,648 data used were obtained through high-throughput crystal-level quantum mechanics calculations on supercomputers. Among five models, namely, extreme gradient boosting regression tree (XGBoost), adaptive boosting, random forest, multi-layer perceptron, and kernel ridge regression, were respectively trained and evaluated by stratified sampling and 5-fold cross-validation method. Among them, XGBoost model produced the best scoring metrics in predicting the detonation velocity, detonation pressure, heat of explosion, decomposition temperature, and lattice energy of HEDMs, and XGBoost predictions agreed best with the 1,383 experimental data collected from massive literatures. Feature importance analysis was conducted to obtain data-driven insight into the causality of the performance-stability contradiction and delivered the optimal range of key features for more efficient rational design of advanced HEDMs.

Molecular polarizabilities of some energetic compounds.

The dependence of sensitivity of an explosive on its molecular structure may be mainly attributed to the molecular deformability, which can be expressed by some characteristic parameters, resonance energy for aromatic an explosive, strain energy for a strained-ring or strained-cage explosive, large π-π separation energy for a large π-π linked-explosive, bond rotational energy barriers of C-NO2, N-NO2, O-NO2 for C-NO2, N-NO2, O-NO2 bond-based explosives, and so on. Molecular polarizability of an explosive is also an important molecular deformability index, which can be effectively used to compare impact sensitivities of explosive's isomers, isoelectronic species, and similar structures. Interestingly, comparing the molecular polarizabilities under external electric fields with different energy levels of isomeric N20(Ih) and N20(D3d) clusters and the Mo2N20 and Re2N20 complex compounds, it is found that there are different energy thresholds of significant molecular expansion.

Myeloid-specific deletion of thrombospondin 1 protects against inflammation and insulin resistance in long-term diet-induced obese male mice.

Thrombospondin 1 (TSP1) is a multifunctional matricellular protein. Recent studies demonstrate that TSP1 is highly expressed in adipose tissue (AT) and positively associated with AT inflammation and insulin resistance (IR). In this study, the contribution of different cellular sources of TSP1 to obesity-induced metabolic complications is determined by using mice with either adipocyte or myeloid/macrophage-specific deletion of TSP1 in a diet-induced obese model. The results demonstrated that neither adipocyte nor myeloid/macrophage-specific deletion of TSP1 affected the development of long-term high-fat diet-induced obesity. Adipocyte-specific deletion of TSP1 did not protect mice from obesity-induced inflammation and IR. On the contrary, obese mice with myeloid/macrophage loss of TSP1 had reduced macrophage accumulation in AT, which was accompanied with reduced inflammation and improved glucose tolerance and insulin sensitivity compared with obese control mice. Reduced macrophage-derived-TGF-ß1 signaling and adipose tissue fibrosis were also observed in long-term high-fat-fed mice with myeloid/macrophage-specific TSP1 deletion. Moreover, in vitro experiments demonstrated an autocrine effect of TSP1-mediated TGF-ß activation in macrophages in obesity. Collectively this study highlights the critical contribution of myeloid/macrophage-derived TSP1 to obesity-associated chronic inflammation and IR, which may serve as a new therapeutic target for metabolic disease.