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Covalent organic frameworks have recently gained increasing attention in photocatalytic hydrogen generation from water. However, their structure-property-activity relationship, which should be beneficial for the structural design, is still far-away explored. Herein, we report the designed synthesis of four isostructural porphyrinic two-dimensional covalent organic frameworks (MPor-DETH-COF, M = H 2 , Co, Ni, Zn) and their photocatalytic activity in hydrogen generation. Our results clearly show that all four covalent organic frameworks adopt AA stacking structures, with high crystallinity and large surface area. Interestingly, the incorporation of different transition metals into the porphyrin rings can rationally tune the photocatalytic hydrogen evolution rate of corresponding covalent organic frameworks, with the order of CoPor-DETH-COF < H 2 Por-DETH-COF < NiPor-DETH-COF < ZnPor-DETH-COF. Based on the detailed experiments and calculations, this tunable performance can be mainly explained by their tailored charge-carrier dynamics via molecular engineering. This study not only represents a simple and effective way for efficient tuning of the photocatalytic hydrogen evolution activities of covalent organic frameworks at molecular level, but also provides valuable insight on the structure design of covalent organic frameworks for better photocatalysis. Covalent organic frameworks (COFs) present well-defined materials for constructing structure-property-activity relationships. Herein, authors explore isostructural porphyrinic two-dimensional COFs with tunable of photocatalytic H 2 production rates arising from tailored charge-carrier dynamics.

The outbreak of the coronavirus disease 2019 (COVID-19), caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become an evolving global health crisis. Currently, a number of risk factors have been identified to have a potential impact on increasing the morbidity of COVID-19 in adults, including old age, male sex, pre-existing comorbidities, and racial/ethnic disparities. In addition to these factors, changes in laboratory indices and pro-inflammatory cytokines, as well as possible complications, could indicate the progression of COVID-19 into a severe and critical stage. Children predominantly suffer from mild illnesses due to COVID-19. Similar to adults, the main risk factors in pediatric patients include age and pre-existing comorbidities. In contrast, supplementation with a healthy diet and sufficient nutrition, COVID-19 vaccination, and atopic conditions may act as protective factors against the infection of SARS-CoV-2. COVID-19 vaccination not only protects vulnerable individuals from SARS-CoV-2 infection, more importantly, it may also reduce the development of severe disease and death due to COVID-19. Currently used therapies for COVID-19 are off-label and empiric, and their impacts on the severity and mortality of COVID-19 are still unclear. The interaction between asthma and COVID-19 may be bidirectional and needs to be clarified in more studies. In this review, we highlight the clinical evidence supporting the rationale for the risk and protective factors for the morbidity, severity, and mortality of COVID-19.

Climatic impacts of historical volcanism are principally tied to the eruption size, while observation versus model discrepancies have been commonly attributed to the uncertainties in paleo‐reconstruction or malpresentation of volcanic aerosols in models. Here we present convergent evidence for significant compensation effect of ocean latent heat (LH) in balancing the tropical volcanic‐induced heat loss, by introducing an effective perturbation ratio which is found to decrease with increasing eruption magnitude. Four LH compensation hot spots overlapping with the trade wind regions are identified, together with three western boundary currents regions with intensified LH loss. Comparison between the 1258 Samalas and 1452 Unidentified eruptions suggests considerable modulation of the concurring El Nino‐Southern Oscillation on LH anomaly, which is further verified by CESM large ensemble sensitivity experiments. This study depicts how the interplay between the ocean and the atmosphere could contribute to the overall resilience of the climate system in the face of volcanic disturbances. Plain Language Summary Large volcanic eruptions drive significant climate perturbation and the resulting cooling generally decreases with increasing eruption size, especially over the surface and upper ocean. In this study we introduce an effective volcanic perturbation ratio, defined as the ratio between the surface net flux anomaly and the volcanic‐induced shortwave flux anomaly, and analyze its relationship with the eruption magnitude. Our results, based on tree‐ring reconstructions and the CESM‐LME simulations, suggest that the effective ratio gradually decreases with the increasing shortwave perturbation, and the reduction of latent heat (LH) flux from ocean to atmosphere balances a significant portion of the volcanic‐induced net surface heat loss. LH varies with wind speeds and vertical specific humidity gradient. We identify four LH compensation effect hot spots which highly overlap with the trade wind regions, and three western boundary currents regions with intensified ocean latent heat loss. We run sensitivity experiments using the 1815 eruption of Mount Tambora as a test case, and find that the ENSO responses accompanying the eruption could modify the LH compensation effect. Key Points Volcanic‐induced temperature responses do not scale linearly with the eruption sizes in both reconstruction and model simulations with same aerosol ‐ radiative treatment Ocean latent heat (LH) flux plays an important role in compensating volcanic‐induced radiative heat loss which enhance with growing eruption size Internal climate variability such as ENSO inserts significant influence on LH's compensation role through the wind‐evaporation‐SST feedback

With the development of economic globalization, urban agglomerations have become growth poles and core areas of economic development. By building knowledge innovation networks in urban agglomerations, we can effectively improve the strength of inter-city knowledge innovation links and better realize the integrated and synergistic development of the region. This study selected core cities in the Yangtze River Delta urban agglomeration as the study area, constructed the knowledge innovation network based on inter-city dissertation cooperation data from 2010 to 2020, and analyzed the characteristics and evolution of its knowledge network by combining social network analysis and geospatial analysis. The research results show that: (1) with changes in policies and investment in scientific research and innovation, intra-regional thesis cooperation in the Yangtze River Delta urban agglomeration has been increasing and the scale of the knowledge innovation cooperation network is growing; (2) in addition to the core cities radiating innovation resources outward to drive the development of other node cities, other cities are continuously improving their own innovation capabilities, taking the initiative to strengthen knowledge innovation cooperation with core cities and enhancing their own position in the network; (3) there are no longer isolated cities within the Yangtze River Delta urban agglomeration, and a multi-core knowledge network structure centered on Shanghai, Nanjing, Hangzhou, and Suzhou has initially formed, but the network is still spatially heterogeneous; (4) there are still problems within the Yangtze River Delta urban agglomeration such as uneven development of knowledge innovation and low participation of peripheral cities, which need to be addressed jointly by all regions. The article concludes with some suggestions for countermeasures to provide a reference for the Yangtze River Delta urban agglomeration to continuously strengthen intra-regional knowledge cooperation in the future, enhance regional competitiveness, and ultimately achieve synergistic development among cities.

Earthquakes that rupture several faults occur frequently within the shallow lithosphere but are rarely observed for intermediate‐depth events (70–300 km). On 29 November 2007, the Mw7.4 Martinique earthquake struck the Lesser Antilles Island Arc near the deep end of the Wadati‐Benioff‐Zone. The sparse regional seismic network of 2007 previously hampered a detailed examination of this unusually complex event. Here, we combine seismic data from different studies with regional moment tensor inversion results and 3D full‐waveform modeling. We show that the earthquake is a doublet consisting of dip‐slip and strike‐slip motion along two oblique structures, both activated under extensional stress along the strike of the slab. Comparison with tectonic reconstructions suggests that the earthquake ruptured along a re‐activated ridge‐transform segment of the subducted Proto‐Caribbean spreading ridge. The unprecedented resolution of the source process highlights the influence of pre‐existing structures on localizing slab deformation also at intermediate‐depth. Plain Language Summary Some earthquakes in continents and near the ocean floor are known to break multiple, differently oriented, faults. Such compound earthquakes are rarely observed in subducted plates in the intermediate‐depth region between 70 and 300 km. Intermediate‐depth earthquake mechanics and stress state are possibly different from shallower earthquakes, and maybe they hinder complex events. On 29 November 2007, the Mw7.4 Martinique earthquake occurred at a depth of ∼150 km, near the deep end of the regional seismic zone below the Lesser Antilles Arc. The regional seismic network in 2007 was relatively sparse; it revealed the earthquake had a complex mechanism but did not previously allow for an in‐depth study. In this study, we combine different types of data and methods, including full waveform information, based on a recently derived 3D regional velocity model. Our analyses shows that the Martinique earthquake consisted of at least two distinct sub‐events on perpendicular faults in the subducted plate—a source doublet. By comparing the orientations of the doublet faults with plate tectonic reconstructions, we infer that this intermediate‐depth earthquake broke along a fossil plate‐boundary. This indicates that such structures remain structural weaknesses even after subduction. Key Points Moment tensor solutions, aftershock activity, back‐projection, and source‐time function suggest a complex rupture of the 29 November 2007, Mw7.4 Martinique earthquake Regional Moment Tensor modeling and aftershock cross‐correlation identified the event as a source doublet Earthquake likely re‐activated a fossil ridge‐transform structure associated with the subducted Proto‐Caribbean spreading ridge

Nonalcoholic fatty liver disease (NAFLD) is the most frequent cause of chronic liver diseases worldwide. At present, there are no effective pharmacological therapies for NAFLD except lifestyle intervention-mediated weight loss. Atractylenolide III (ATL III), the major bioactive component found in Atractylode smacrocephala Koidz, has been shown to exert anti-oxidant, anti-tumor, anti-allergic response, anti-bacterial effects and cognitive protection. Here we investigate the therapeutic potential and underlying mechanisms of ATL III for the treatment of NAFLD. Male C57BL/6J mice were fed a high-fat diet (HFD) and treated with ATL III. Lipid accumulation was analyzed by Oil Red O staining in liver tissues and free fatty acids (FFAs)-treated hepatocytes. AMP-activated protein (AMPK) and sirtuin 1(SIRT1) signaling pathways were inhibited by Compound C and EX527 , respectively. Small-interfering RNA (siRNA) was used to knockdown adiponectin receptor 1 (AdipoR1) expression in HepG2 cells. ATL III treatment ameliorated liver injury and hepatic lipid accumulation in the HFD-induced NAFLD mouse model as demonstrated by that ATL III administration significantly reduced serum levels of alanine aminotransferase, glutamic oxaloacetic transaminase, triglycerides, total cholesterol and low-density lipoprotein. Furthermore, treatment with ATL III alleviated hepatic oxidative stress, inflammation and fibrosis in the HFD feeding model. To study the underlying mechanisms, we performed Computer Aided Design assay and found that open-formed AdipoR1 and adiponectin receptor 2 were the potential receptors targeted by ATL III. Interestingly, HFD feeding or FFAs treatment only reduced hepatic AdipoR1 expression, while such reduction was abolished by ATL III administration. In addition, treatment with ATL III activated the AdipoR1 downstream AMPK /SIRT1 signaling pathway and reduced lipid deposition in HepG2 cells, which was diminished by silencing AdipoR1. Finally, inhibition of AMPK or SIRT1, the AdipoR1 downstream signaling, abolished the protective effects of ATL III on lipid deposition and oxidative stress in FFAs-treated HepG2 cells. Our findings suggest that ATL III is a therapeutic drug for the treatment of NAFLD and such protective effect is mediated by activating hepatic AdipoR1-mediated AMPK/SIRT1 signaling pathway.

In the marketing of multinational enterprises, cultural differences have a complex impact on international marketing strategies. On one hand, taking advantage of cultural differences can diversify the corporate culture. On the other hand, cultural differences make management difficult, and there will be conflicts in mutual exchanges. This paper mainly summarizes the past literature, and connects the problems raised in some earlier studies and the situations solved in subsequent studies in series to make the logic chain more complete. At the same time, new problems are raised on this basis. After reviewing the literature, this work concludes that the multicultural environment is becoming more complex, and managers need to have a deeper understanding of different cultures while calculating the gains and losses, so as to integrate culture. Therefore, the research significance of this paper is to make a complete summary of the existing research results, sort out the unresolved problems, and provide ideas for subsequent related research.

This paper investigates the robust model reference tracking control problem for high‐order descriptor linear systems (HODLS) subject to norm‐bounded parameter uncertainties. The problem is divided into two subproblems: a robust proportional plus derivative state feedback stabilization (RPPDSFS) problem and a robust feed‐forward compensation (RFFC) problem. In the presence of uncertainties, by using the controller consisting of RPPDSFS part and RFFC part, all the signals of the closed‐loop system are bounded. The latter is equivalent to seeking three coefficient matrices such that a series of linear matrix equations are satisfied, and simultaneously the effect caused by uncertainties is minimized. Based on the right coprime factorization, the RFFC problem is further converted into a minimization problem with a quadratic performance index and some linear constraints. Thereafter, a linear matrix equation that determines the optimal solution is achieved. The restrictive condition that the coefficient matrix of the augmented reference system is non‐defective is relaxed, which reduces the conservativeness. A numerical example and the application of a three‐axis dynamic flight motion simulator manifest the effectiveness and the practicability of the proposed algorithm. This paper focuses on the robust model reference tracking control problem for high‐order descriptor linear systems subject to parameter uncertainties. The new robust feed‐forward compensation algorithm is proposed for high‐order descriptor linear systems, which take the first‐ or second‐order descriptor linear systems and high‐order linear systems as special cases and have a wide perspective of applications. The restrictive condition that the coefficient matrix of the augmented reference system is non‐defective is relaxed, which reduces the conservativeness.

Autophagy is primarily considered a non‐selective degradation process induced by starvation. Nutrient‐independent basal autophagy, in contrast, imposes intracellular QC by selective disposal of aberrant protein aggregates and damaged organelles, a process critical for suppressing neurodegenerative diseases. The molecular mechanism that distinguishes these two fundamental autophagic responses, however, remains mysterious. Here, we identify the ubiquitin‐binding deacetylase, histone deacetylase‐6 (HDAC6), as a central component of basal autophagy that targets protein aggregates and damaged mitochondria. Surprisingly, HDAC6 is not required for autophagy activation; rather, it controls the fusion of autophagosomes to lysosomes. HDAC6 promotes autophagy by recruiting a cortactin‐dependent, actin‐remodelling machinery, which in turn assembles an F‐actin network that stimulates autophagosome–lysosome fusion and substrate degradation. Indeed, HDAC6 deficiency leads to autophagosome maturation failure, protein aggregate build‐up, and neurodegeneration. Remarkably, HDAC6 and F‐actin assembly are completely dispensable for starvation‐induced autophagy, uncovering the fundamental difference of these autophagic modes. Our study identifies HDAC6 and the actin cytoskeleton as critical components that define QC autophagy and uncovers a novel regulation of autophagy at the level of autophagosome–lysosome fusion.

This study investigated associations between cardiometabolic diseases, frailty, and healthcare utilization and expenditure among Chinese older adults. The participants were 5204 community-dwelling adults aged at least 60 years from the China Health and Retirement Longitudinal Study. Five cardiometabolic diseases were assessed including hypertension, dyslipidemia, diabetes, cardiac diseases and stroke. Frailty status was based on five criteria: slowness, weakness, exhaustion, inactivity, and shrinking. Participants were deemed frailty if they met at least three criteria. As the number of cardiometabolic diseases increased, so did the prevalence of frailty, and the proportion of healthcare utilization, including outpatient visit and inpatient visit. Moreover, the total healthcare expenditure and the odds of catastrophic health expenditure were increased with the number of cardiometabolic disorders. After adjusting for covariates, cardiometabolic diseases were positively associated with higher odds of frailty, incurring outpatient and inpatient visit. And individuals with 2 or more cardiometabolic diseases had a higher odds of catastrophic health expenditure than persons with non-cardiometabolic disease. Participants who were frailty were more likely to report higher odds of healthcare utilization. These findings suggest that both cardiometabolic diseases and frailty assessment may improve identification of older adults likely to require costly, extensive healthcare.