Explore the vast range of titles available.

In freeform surface grid structures, quadrilateral meshes offer high visual transparency and simple joint connections, but their structural stability is relatively limited. To enhance stability, designers often introduce additional structural elements along the diagonals of the quadrilateral mesh, forming double-layer quadrilateral grid systems such as cable-braced gridshells. However, current design methodologies do not support the simultaneous optimization of both layers. As a result, the two layers are often designed independently in practical applications, leading to complex joint detailing that compromises construction efficiency, architectural aesthetics, and overall structural performance. To address these challenges, this study presents a weighted multi-objective geometry optimization framework based on a Guided-Projection algorithm. The proposed method integrates half-edge data structure and multiple geometric and structural constraints, enabling the simultaneous optimization of quadrilateral mesh planarity (i.e., panels lying on flat planes) and the orthogonality (i.e., angles approaching 90°) of diagonal cable layouts. Through multiple case studies, the method demonstrates significant improvements in panel planarity and cable orthogonality. The results also highlight the algorithm’s rapid convergence and high computational efficiency. Finite element analysis further validates the structural benefits of the optimized configurations, including reduced peak axial forces in cables, more uniform cable force distribution, and enhanced overall stiffness and buckling resistance. In conclusion, the method improves structural stability, constructability, and design efficiency, offering a practical tool for optimizing freeform cable-braced gridshells.

Consider the revenue-maximizing problem in which a single seller wants to sell k different items to a single buyer, who has independently distributed values for the items with additive valuation. The [Formula] case was completely resolved by Myerson’s classical work in 1981, whereas for larger k the problem has been the subject of much research efforts ever since. Recently, Hart and Nisan analyzed two simple mechanisms: selling the items separately, or selling them as a single bundle. They showed that selling separately guarantees at least a [Formula] fraction of the optimal revenue; and for identically distributed items, bundling yields at least a [Formula] fraction of the optimal revenue. In this paper, we prove that selling separately guarantees at least [Formula] fraction of the optimal revenue, whereas for identically distributed items, bundling yields at least a constant fraction of the optimal revenue. These bounds are tight (up to a constant factor), settling the open questions raised by Hart and Nisan. The results are valid for arbitrary probability distributions without restrictions. Our results also have implications on other interesting issues, such as monotonicity and randomization of selling mechanisms.

Traditional monitoring methods cannot obtain the overall thermal information for power transformers. To solve this problem, a distributed fiber optic sensor (DFOS) was creatively applied inside an operating 35 kV power transformer by highly integrating with the electromagnetic wires. Then, the transformer prototype with totally global sensing capability was successfully developed and it was qualified for power grid application through the strict ex-factory tests. The as designed optical fiber sensor works stably all the time with a temperature accuracy of ±0.2 °C and spatial positioning accuracy of 0.8 m. Based on the obtained internal temperature distribution, Gaussian convolution was further applied for the signal processing and hereby, the hotspots for all the windings and iron cores could be accurately traced. The hottest points were located at 89.1% (55 °C) of the high voltage winding height and 89.7% (77.5 °C) of the low voltage winding height. The actual precise hotspot location corrected the traditional cognition on the transformer windings and it would serve as an essential reference for the manufactures. This new nondestructive internal sensing and condition monitoring method also exhibits a promising future for the DFOS applying in the high-voltage electrical apparatus industry.

Cardiovascular disease (CVD) is the leading cause of death worldwide, especially in developed countries, and atherosclerosis (AS) is the common pathological basis of many cardiovascular diseases (CVDs) such as coronary heart disease (CHD). The role of the gut microbiota in AS has begun to be appreciated in recent years. Trimethylamine N-oxide (TMAO), an important gut microbe-dependent metabolite, is generated from dietary choline, betaine, and L-carnitine. Multiple studies have suggested a correlation between plasma TMAO levels and the risk of AS. However, the mechanism underlying this relationship is still unclear. In this review, we discuss the TMAO-involved mechanisms of atherosclerotic CVD from the perspective of inflammation, inflammation-related immunity, cholesterol metabolism, and atherothrombosis. We also summarize available clinical studies on the role of TMAO in predicting prognostic outcomes, including major adverse cardiovascular events (MACE), in patients presenting with AS. Finally, since TMAO may be a novel therapeutic target for AS, several therapeutic strategies including drugs, dietary, etc. to lower TMAO levels that are currently being explored are also discussed.Cardiovascular disease (CVD) is the leading cause of death worldwide, especially in developed countries, and atherosclerosis (AS) is the common pathological basis of many cardiovascular diseases (CVDs) such as coronary heart disease (CHD). The role of the gut microbiota in AS has begun to be appreciated in recent years. Trimethylamine N-oxide (TMAO), an important gut microbe-dependent metabolite, is generated from dietary choline, betaine, and L-carnitine. Multiple studies have suggested a correlation between plasma TMAO levels and the risk of AS. However, the mechanism underlying this relationship is still unclear. In this review, we discuss the TMAO-involved mechanisms of atherosclerotic CVD from the perspective of inflammation, inflammation-related immunity, cholesterol metabolism, and atherothrombosis. We also summarize available clinical studies on the role of TMAO in predicting prognostic outcomes, including major adverse cardiovascular events (MACE), in patients presenting with AS. Finally, since TMAO may be a novel therapeutic target for AS, several therapeutic strategies including drugs, dietary, etc. to lower TMAO levels that are currently being explored are also discussed.

Atherosclerosis and its associated cardiovascular diseases (CVDs) are serious threats to human health and have been reported to be associated with the gut microbiota. Recently, the role of berberine (BBR) in atherosclerosis and gut microbiota has begun to be appreciated. The purposes of this study were to observe the effects of high or low doses of BBR on atherosclerosis and gut microbiota modulation, and to explore their correlation in ApoE mice fed a high-fat diet. A significant decrease in atherosclerotic lesions was observed after treatment with BBR, with the effect of the high dose being more obvious. Both BBR treatments significantly reduced total cholesterol, APOB100, and very low-density lipoprotein cholesterol levels but levels of high/low-density lipoprotein cholesterol and lipoprotein (a) were only reduced by high-dose BBR. Decreased pro-inflammatory cytokines tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6 and increased anti-inflammatory IL-10 and adiponectin levels were observed in the high-dose BBR group, but no decrease in IL-6 or increase in IL-10 was evident using the low-dose of BBR. 16S rRNA sequencing showed that BBR significantly altered the community compositional structure of gut microbiota. Specifically, BBR enriched the abundance of , , , , and , and changed the abundance of . These microbiota displayed good anti-inflammatory effects related to the production of short-chain fatty acids (SCFAs) and were related to glucolipid metabolism. and were significantly enriched in high-dose BBR group while and were more enriched in low-dose, and was enriched in both BBR doses. Metagenomic analysis further showed an elevated potential for lipid and glycan metabolism and synthesis of SCFAs, as well as reduced potential of TMAO production after BBR treatment. The findings demonstrate that both high and low-dose BBR can improve serum lipid and systemic inflammation levels, and alleviate atherosclerosis induced by high-fat diet in ApoE mice. The effects are more pronounced for the high dose. This anti-atherosclerotic effect of BBR may be partly attributed to changes in composition and functions of gut microbiota which may be associated with anti-inflammatory and metabolism of glucose and lipid. Notably, gut microbiota alterations showed different sensitivity to BBR dose.

Ischemia-reperfusion (I/R) is a pathological process that occurs in many organs and diseases. Reperfusion, recovery of blood flow, and reoxygenation often lead to reperfusion injury. Drug therapy and early reperfusion therapy can reduce tissue injury and cell necrosis caused by ischemia, leading to irreversible I/R injury. Ferroptosis was clearly defined in 2012 as a newly discovered iron-dependent, peroxide-driven, nonapoptotic form of regulated cell death. Ferroptosis is considered the cause of reperfusion injury. This discovery provides new avenues for the recognition and treatment of diseases. Ferroptosis is a key factor that leads to I/R injury and organ failure. Given the important role of ferroptosis in I/R injury, there is considerable interest in the potential role of ferroptosis as a targeted treatment for a wide range of I/R injury-related diseases. Recently, substantial progress has been made in applying ferroptosis to I/R injury in various organs and diseases. The development of ferroptosis regulators is expected to provide new opportunities for the treatment of I/R injury. Herein, we analytically review the pathological mechanism and targeted treatment of ferroptosis in I/R and related diseases from the perspectives of myocardial I/R injury, cerebral I/R injury, and ischemic renal injury.

Recent advances in image super-resolution (SR) explore the power of deep learning to achieve a better reconstruction performance. The deep reconstruction methods mostly reconstruct the super-resolution image based on a large amount of external data training. In order to make full use of the internal features of the image, we propose a novel network for SR called super-resolution network by fusing internal and external features (SRNIF). Specifically, we use the self-similar image itself as the prior knowledge and propose a fully convolutional deep neural network (called Internal Feature Enhancement module, IFE) to extract the internal features of the image so as to obtain detailed texture of the inputted image. Then, the detailed features extracted by the internal feature enhancement module are embedded into the residual network, and the spatial feature transform (SFT) module is used to form the residual module. A deep residual network based on the fusion of internal and external features is built. The proposed method comes with a strong early reconstruction ability and can create the final high-resolution image step by step. Experimental results show that the method has enhanced the texture characteristics and quality of the reconstructed image, and the visual effect and peak signal-to-noise ratio (PSNR) has been improved.

Preeclampsia (PE) is a severe complication of unclear pathogenesis associated with pregnancy. This research aimed to elucidate the properties of immune cell infiltration and potential biomarkers of PE based on bioinformatics analysis. Two PE datasets were imported from the Gene ExpressioOmnibus (GEO) and screened to identify differentially expressed genes (DEGs). Significant module genes were identified by weighted gene co-expression network analysis (WGCNA). DEGs that interacted with key module genes (GLu-DEGs) were analyzed further by Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses. The diagnostic value of the genes was assessed using receiver operating characteristic (ROC) curves and protein-protein interaction (PPI) networks were constructed using GeneMANIA, and GSVA analysis was performed using the MSigDB database. Immune cell infiltration was analyzed using the TISIDB database, and StarBase and Cytoscape were used to construct an RBP-mRNA network. The identified hub genes were validated in two independent datasets. For further confirmation, placental tissue from healthy pregnant women and women with PE were collected and analyzed using both RT-qPCR and immunohistochemistry. A total of seven GLu-DEGs were obtained and were found to be involved in pathways associated with the transport of sulfur compounds, PPAR signaling, and energy metabolism, shown by GO and KEGG analyses. GSVA indicated significant increases in adipocytokine signaling. Furthermore, single-sample Gene Set Enrichment Analysis (ssGSEA) indicated that the levels of activated B cells and T follicular helper cells were significantly increased in the PE group and were negatively correlated with GLu-DEGs, suggesting their potential importance. In summary, the results showed a correlation between glutamine metabolism and immune cells, providing new insights into the understandingPE pathogenesis and furnishing evidence for future advances in the treatment of this disease.

Background Cardiac injury is now a common complication of coronavirus disease (COVID-19), but it remains unclear whether cardiac injury-related biomarkers can be independent predictors of mortality and severe disease development or intensive care unit (ICU) admission. Methods Two investigators searched the PubMed, EMBASE, Cochrane Library, MEDLINE, Chinese National Knowledge Infrastructure (CNKI), Wanfang, MedRxiv, and ChinaXiv databases for articles published through March 30, 2020. Retrospective studies assessing the relationship between the prognosis of COVID-19 patients and levels of troponin I (TnI) and other cardiac injury biomarkers (creatine kinase [CK], CK myocardial band [CK-MB], lactate dehydrogenase [LDH], and interleukin-6 [IL-6]) were included. The data were extracted independently by two investigators. Results The analysis included 23 studies with 4631 total individuals. The proportions of severe disease, ICU admission, or death among patients with non-elevated TnI (or troponin T [TnT]), and those with elevated TnI (or TnT) were 12.0% and 64.5%, 11.8% and 56.0%, and 8.2% and. 59.3%, respectively. Patients with elevated TnI levels had significantly higher risks of severe disease, ICU admission, and death (RR 5.57, 95% CI 3.04 to 10.22, P  < 0.001; RR 6.20, 95% CI 2.52 to 15.29, P  < 0.001; RR 5.64, 95% CI 2.69 to 11.83, P  < 0.001). Patients with an elevated CK level were at significantly increased risk of severe disease or ICU admission (RR 1.98, 95% CI 1.50 to 2.61, P  < 0.001). Patients with elevated CK-MB levels were at a higher risk of developing severe disease or requiring ICU admission (RR 3.24, 95% CI 1.66 to 6.34, P  = 0.001). Patients with newly occurring arrhythmias were at higher risk of developing severe disease or requiring ICU admission (RR 13.09, 95% CI 7.00 to 24.47, P  < 0.001). An elevated IL-6 level was associated with a higher risk of developing severe disease, requiring ICU admission, or death. Conclusions COVID-19 patients with elevated TnI levels are at significantly higher risk of severe disease, ICU admission, and death. Elevated CK, CK-MB, LDH, and IL-6 levels and emerging arrhythmia are associated with the development of severe disease and need for ICU admission, and the mortality is significantly higher in patients with elevated LDH and IL-6 levels. Graphical abstract

The nod-like receptor family pyrin domain containing 3 (NLRP3) is currently the most widely studied inflammasome and has become a hot topic of recent research. As a macromolecular complex, the NLRP3 inflammasome is activated to produce downstream factors, including caspase-1, IL-1β, and IL-18, which then promote local inflammatory responses and induce pyroptosis, leading to unfavorable effects. A growing number of studies have examined the relationship between the NLRP3 inflammasome and cardiovascular diseases (CVDs). However, some studies have shown that the NLRP3 inflammasome is not involved in the occurrence of certain diseases. Therefore, identifying the mechanism of action of the NLRP3 inflammasome and its potential involvement in the pathological process of disease progression is of utmost importance. This review discusses the mechanisms of NLRP3 inflammasome activation and the relationship between the inflammasome and CVDs, including coronary atherosclerosis, myocardial ischemia/reperfusion, cardiomyopathies, and arrhythmia, as well as CVD-related treatments.