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The distribution and diversity of woody vegetation are crucial for understanding the structure and ecology of urban forests. As urbanization accelerates, the construction and composition of urban forests vary significantly along the urban-rural gradient. Qingdao's urban forests offer an opportunity to test the relationship between the diversity of woody plants and the urban-rural gradient. We classified the urban-rural gradient using imperviousness and construction time, then investigated the diversity of woody plants in Qingdao's urban forests under different urban-rural gradients and tested the reasonableness of their allocation. Correlation analysis found that the diversity index of woody plants in urban forests was highly connected to the urban-rural gradient (by imperviousness: rMargalef Index = −0.589, rShannon-Wiener Index = -0.373, rPielou Index = −0.170, rSimpson Index = 0.272/by construction time: rMargalef Index = −0.530, rShannon-Wiener Index = −0.360, rPielou Index = −0.148, rSimpson Index = 0.272/0.174). With a decrease in urbanization density, the Margalef (H), Shannon-Wiener (H′), and Simpson (D) indices all decreased while the Pielou (E) index increased. The four diversity indices showed a substantial correlation with one another, but not with the Margalef and Pielou indices. The analysis utilizing the 10/20/30 rule of empirical demonstrates a clear irrationality in allocating shrub species in Qingdao's urban forests, and the distribution of tree species is reasonable. Based on the study results, strategies for optimizing and enhancing urban forests in Qingdao are proposed for different urban-rural gradients, respectively. This study can provide a scientific framework for urban biodiversity conservation and management in Qingdao and serve as a guide for urban forests and greening with comparable climates.

Abstract Platelets play a key role in physiological hemostasis and pathological thrombosis. Based on the limitations of current antiplatelet drugs, it's important to elucidate the mechanisms of regulating platelet activation. In addition to dissolving lipid nutrients, bile acids (BAs) can regulate platelet function. However, the specific mechanisms underlying BAs‐mediated effects on platelet activation and thrombotic diseases remain unknown. Therefore, the effects of BAs on platelets and intracellular regulatory mechanisms are explored. It is showed that the inhibitory effect of secondary BAs is more significant than that of primary BAs; lithocholic acid (LCA) shows the highest inhibitory effect. In the process of platelet activation, BAs suppress platelet activation via the spleen tyrosine kinase (SYK), protein kinase B (Akt), and extracellular signal‐regulated kinase1/2 (Erk1/2) pathways. Nck adaptor proteins (NCK1) deficiency significantly suppress the activity of platelets and arterial thrombosis. Phosphorylated proteomics reveal that LCA inhibited phosphorylation of syntaxin‐11 at S80/81 in platelets. Additional LCA supplementation attenuated atherosclerotic plaque development and reduced the inflammation in mice. In conclusion, BAs play key roles in platelet activation via Syk, Akt, ERK1/2, and syntaxin‐11 pathways, which are associated with NCK1. The anti‐platelet effects of BAs provide a theoretical basis for the prevention and therapy of thrombotic diseases.

Background: Patients with acute-on-chronic liver failure (ACLF) who take entecavir (ETV) and tenofovir disoproxil fumarate (TDF) experience a reduction in hepatic events and mortality. The effectiveness of tenofovir alafenamide (TAF) was not well investigated. This study was aim to compare the antiviral efficacy and mortality between TAF and ETV in patients with ACLF caused by the hepatitis B virus (HBV). Methods: One hundred and six patients with HBV-ACLF who received TAF (25 mg/day) and ETV (0.5 mg/day) for 12 weeks were analyzed. The primary endpoints were overall mortality and liver transplantation (LT) at week 12. Biochemical responses, virologic responses, mortality, drug safety, and side effects were evaluated. Results: At 4 and 12 weeks of TAF treatment, patients showed significantly higher HBV-DNA reduction ( P .05). Conclusions: This study showed that ACLF patients with chronic HBV infection treated with TAF had a rapid decline in HBV DNA, a higher rate of ALT reduction and improved CTP scores compared to the ETV group, thereby improving patient survival.

Under the constraints of low-carbon transformation goals, energy enterprises have significantly increased their debt default risk levels due to carbon price fluctuations. This article first analyzes the contagion mechanism of debt default risk among energy enterprises, and based on this, constructs a debt default risk contagion model among energy enterprises considering carbon price fluctuations, and then simulates and analyzes the evolution characteristics of debt default risk contagion among energy enterprises. The research results indicate that: (1) As the proportion of carbon emission cost increment and investor sentiment index increase, the stability of the debt network of energy enterprises strengthens. As the ratio of commercial credit among energy enterprises and influence of energy enterprises increase, the impact of debt risk gradually intensifies. (2) The investor sentiment index has a strengthening effect on the influence of energy enterprises, the proportion of commercial credit among energy enterprises, and the proportion of carbon emission cost increment. The commercial credit ratio between energy enterprises and its influence has a mutually reinforcing effect. (3) The investor sentiment index has suppressed debt default risk for various energy enterprises. The joint risk suppression effect of the proportion of carbon emission cost increment and the influence of energy enterprises in petroleum and petrochemical enterprises is more prominent. The joint risk constraint ability between the proportion of carbon emission cost increment and investor sentiment index in coal enterprises is stronger.

Wilderness has proven to provide a wide range of ecosystem services (ES). Wilderness have been shown to play an important role in preserving biodiversity and providing ES, which is indispensable to both nature and people. It is essential to integrate ES quantification into wilderness conservation and management. This study presents a method that combines the wilderness mapping and ecological indicators to measure ES of wilderness. The method was applied in 155,800 km2 of Shandong province in China, across 23 types of land use. First, relative wilderness value (RWV) and ecosystem service capability (ESC) were quantified according to Weighted Linear Combination (WLC). Then, spatial autocorrelation between RWV and ESC were tested and analyzed using GeoDa software. Finally, the Redundancy analysis was used to investigate the primary drivers of RWV and ESC in different landscape types. The findings showed that, there were 27,263 km2 of wilderness in Shandong province, of which 6,294 km2 were high-quality wilderness. The region with the highest RWV was the Yellow River Delta (RWV = 0.82), and the area with the highest ESC was Laoshan Mountain (ESC = 0.76). Spatial autocorrelation analysis showed a positive correlation between RWV and ESC (Pearson’s r = 0.637), both of which had significant spatial relevance (Moran’s I = 0.589, P

Abstract Background Abnormal platelet activation is a key factor in the occurrence and development of thrombotic diseases. However, the physiological mechanisms that underlie platelet homeostasis remain unclear. Oleic acid, one of the most abundant lipids in the human diet, has potential antithrombotic effects. This study aimed to investigate the effects of oleic acid on platelet activation and thrombosis. Methods Platelet aggregation, ATP release, and fibrinogen spread were evaluated to determine the role of oleic acid in platelet activation. A ferric chloride-induced carotid injury model was used to establish the effect of oleic acid on thrombus formation in vivo. Western blotting analysis and transfection experiments were performed to determine the mechanisms involved in this process. Results Oleic acid inhibited platelet aggregation, granule release, and calcium mobilization. Furthermore, it inhibited the spread of platelets on fibrinogen. We also found that oleic acid delayed arterial thrombosis in mice, as demonstrated in a murine model of ferric chloride-induced carotid artery thrombosis. The molecular mechanism of its inhibition of platelet activity may be through the Syk-PLCγ2 and CaMKKβ/AMPKα/VASP pathways. In addition, we demonstrated that the phosphorylation of AMPK at Ser496 was an important mechanism of platelet activation. Conclusions Our study showed that oleic acid inhibits platelet activation and reduces thrombogenesis by inhibiting the phosphorylation of multiple signaling molecules, offering new insights into the research and development of antiplatelet drugs. Video Abstract

In order to study the impact of risk aversion characteristics of enterprises on supply chain risk transmission, the risk aversion utility function is introduced, and the risk elasticity coefficient is used to construct a supplier-dominated low-carbon supply chain risk transmission model. Simulation analysis is conducted to investigate the transmission of emission reduction and revenue risks caused by internal and external contingent risk factors. The study reveals that under conditions of market demand uncertainty, the risk transmission effect is unaffected by the risk aversion characteristics of members in the low-carbon supply chain. While the risk-aversion characteristics of suppliers can decrease their own profit risk, they have a negative effect on the profit risk of manufacturers and the emission reduction risk of supply chain nodes. There exists a critical threshold for the impact of the risk-aversion degree of suppliers on their own emission reduction risk transmission effect. When this threshold is exceeded, the emission reduction risk decreases with increasing risk aversion intensity of suppliers, and vice versa. The risk aversion characteristics of manufacturers can weaken the negative effect of supplier risk aversion on the fluctuation risk of manufacturer profits, but they exacerbate the emission reduction risk transmission effect of manufacturers under asymmetric information influence. The findings have important theoretical and practical implications for supply chain risk management.

Salvia plebeia (Lamiaceae) is a valuable medicinal plant widely distributed across Asia and Oceania. However, the composition and accumulation patterns of its active ingredients in different organs during the growth and their biosynthetic mechanism remain unknown. Therefore, we conducted metabolite profiling, transcriptomic analysis, and biological functional verification to explore the distribution, accumulation, and biosynthesis mechanisms of flavonoids in S. plebeia. We identified 70 metabolites including 46 flavonoids, 16 phenolic acids, seven terpenoids, and one organic acid, of which 21 were previously unreported in S. plebeia. Combining metabolomic-transcriptomic analysis and biological functional verification, we identified the key genes involved in biosynthesis of its main active ingredients, hispidulin and homoplantaginin, including SpPAL, SpC4H, Sp4CL2, Sp4CL5, SpCHS1, SpCHI, SpFNS, SpF6H1, SpF6OMT1, SpF6OMT2, SpUGT1, SpUGT2, and SpUGT3. Using the identified genes, we reconstructed the hispidulin and homoplantaginin biosynthesis pathways in Escherichia coli, and obtained a yield of 5.33 and 3.86 mg/L for hispidulin and homoplantaginin, respectively. Our findings provide valuable insights into the changes in chemical components in different organs of S. plebeia during different growth and harvest stages and establishes a foundation for identifying and synthesizing its active components.

It is challenging for most Historical Preservation Areas (HPA) to improve thermal comfort, especially under the contradiction of urban preservation. The study selected the Badaguan District as the object, which is the most famous HPA in Qingdao. Simulation is conducted by ENVI-met based on field measurements. Taking the current situation (green space 46.6% and building density 17.8%) as the basic case, we modeled two cases (reducing the green space to 29.1% and increasing the building density to 29.9% respectively according to the local standard). The results show that: (1) There are significant differences in air temperature and relative humidity among different streets; (2) District parameters including sky view factor (SVF) and Aspect Ratio(H/W) have different impact on microclimate; (3) Reducing the percentage of the green space(GS) to 29.1% (Case Ⅰ)and increasing the percentage of the building density(BD) to 29.9% (Case Ⅱ) both make the microclimate deteriorate. (4) By comparing the thermal comfort calendars of three cases, the thermal environment of the basic case is the best, and thermal environment of Case II is the worst especially at 12:00. The study can inform policy makers and urban designers to discover the balance between preservation of HPA and thermal environment improvement.

In livestock, intramuscular adipose tissue is highly valued whereas adipose tissue in other depots is considered as waste. Thus, genetic factors that favor fat deposition in intramuscular compartments over that in other adipose depots are highly desirable in meat-producing animals. Fatty acid transport 1 (FATP1) has been demonstrated to promote cellular fatty acid uptake and metabolism; however, whether it also influences cellular lipid accumulation remains unclear. In the present study, we investigated the effects of FATP1 on the differentiation and proliferation of adipocytes in five types of cells derived from muscle and adipose tissue and estimated the effects of FATP1 on intramuscular fat (IMF) deposition. We showed that FATP1 is mainly expressed in heart and muscle tissue in buffaloes as well as cells undergoing adipogenic differentiation. Importantly, we found that FATP1 promoted the adipogenic differentiation of muscle-derived cells (buffalo myocytes and intramuscular preadipocytes and mouse C2C12 cells) but did not affect, or even inhibited, that of adipose-derived cells (buffalo subcutaneous preadipocytes and mouse 3T3-L1 cells, respectively). Correspondingly, our results further indicated that FATP1 promotes IMF deposition in mice in vivo. Meanwhile, FATP1 was found to enhance the proliferative activity of all the assessed cells, except murine 3T3-L1 cells. These results provide new insights into the potential effects of FATP1 on IMF deposition, especially regarding its positive effects on meat quality in buffaloes and other livestock.

The pathological processes of cancer are complex. Current methods used for chemotherapy have various limitations, such as cytotoxicity, multi-drug resistance, stem-like cells growth, and lack of specificity. Several types of nanomaterials are used for cancer treatment. Nanomaterials 1–100 nm in size have special optical, magnetic, and electrical characteristics. Nanomaterials have been fabricated for cancer treatments to overcome cytotoxicity and low specificity, and improve drug capacity and bioavailability. Despite the increasing number of related studies, few nanodrugs have been approved for clinical use. To improve translation of these materials, studies of targeted drug delivery using nanocarriers are needed. Cytotoxicity, enhanced permeability and retention effects, and the protective role of the protein corona remain to be addressed. This mini-review summarizes new nanomaterials manufactured in studies and in clinical use, analyses current barriers preventing their translation to clinical use, and describes the effective application of nanomaterials in cancer treatment.

Rapid urbanization has brought a range of urban environmental problems that could be harmful to human thermal comfort and health. Urban parks can improve outdoor thermal comfort significantly because of its cooling island effect. However, outdoor thermal comfort is difficult to predict because of its complex nature and there was rare research focused on human physiological thermal responses in different green spaces of urban parks. In this study, thermal comfort of 52 participants were evaluated based on questionnaire survey and physiological parameters measurements including skin temperature (SKT), oxygen saturation (SaO2), heart rate (HR), heart rate variability (HRV) under different green spaces in parks, simultaneously with microclimate measurements. According to the regression analysis, physiological parameters were found having high accuracy in predicting human outdoor thermal comfort, with R2 were 0.803 for SKT, 0.830 for HRV, 0.767 for HR, 0.711 for SaO2 respectively. Results demonstrated that these four physiological parameters were sensitive to microclimate changes and human outdoor comfort thermal state can be captured by monitoring them with reasonable accuracy. This research can provide reference to evaluate outdoor thermal comfort by incorporating the physiological parameters, which can also provide a design basis for creating thermal comfortable outdoor spaces in urban parks.

Fat deposition is a significant economic trait in livestock animals. Adipose tissues (ATs) developed in subcutaneous and visceral depots are considered waste whereas those within muscle are highly valued. In river buffaloes, lipogenesis is highly active in subcutaneous (especially in the sternum subcutaneous) and visceral depots but not in muscle tissue. Revealing the features and functions of ATs in different depots is significant for the regulation of their development. Here, we characterize the cell size, composition, and function of six AT depots in river buffaloes. Our data support that the subcutaneous AT depots have a larger cell size than visceral AT depots, and the subcutaneous AT depots, especially the sternum subcutaneous AT, are mainly associated with the extracellular matrix whereas the visceral AT depots are mainly associated with immunity. We found that sternum subcutaneous AT is significantly different from ATs in other depots, due to the high unsaturated fatty acid content and the significant association with metabolic protection. The perirenal AT is more active in FA oxidation for energy supply. In addition, the expression of HOX paralogs supports the variable origins of ATs in different depots, indicating that the development of ATs in different depots is mediated by their progenitor cells. The present study enhances our understanding of the cellular and molecular features, metabolism, and origin of AT depots in buffaloes, which is significant for the regulation of fat deposition and provides new insights into the features of AT depots in multiple discrete locations.

Macrophages play an important role in clearing necrotic myocardial tissues, myocardial ischemia–reperfusion injury, and ventricular remodeling after myocardial infarction. M1 macrophages not only participate in the inflammatory response in myocardial tissues after infarction, which causes heart damage, but also exert a protective effect on the heart during ischemia. In contrast, M2 macrophages exhibit anti-inflammatory and tissue repair properties by inducing the production of high levels of anti-inflammatory cytokines and fibro-progenitor cells. Interleukin (IL)-38, a new member of the IL-1 family, has been reported to modulate the IL-36 signaling pathway by playing a role similar to that of the IL-36 receptor antagonist, which also affects the production and secretion of macrophage-related inflammatory factors that play an anti-inflammatory role. IL-38 can relieve myocardial ischemia–reperfusion injury by promoting the differentiation of M1 macrophages into M2 macrophages, inhibit the activation of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome, and increase the secretion of anti-inflammatory cytokines, such as IL-10 and transforming growth factor-β. The intact recombinant IL-38 can also bind to interleukin 1 receptor accessory protein-like 1 (IL-1RAPL1) to activate the c-jun N-terminal kinase/activator protein 1 (JNK/AP1) pathway and increase the production of IL-6. In addition, IL-38 regulates dendritic cell-induced cardiac regulatory T cells, thereby regulating macrophage polarization and improving ventricular remodeling after myocardial infarction. Accordingly, we speculated that IL-38 and macrophage regulation may be therapeutic targets for ameliorating myocardial ischemic injury and ventricular remodeling after myocardial infarction. However, the specific mechanism of the IL-38 action warrants further investigation.

Abstract Background In China, although buffaloes are abundant, beef is mainly obtained from cattle, and this preference is mainly attributed to the low intramuscular fat (IMF) content of buffalo. Genetic factors are an important driver that affects IMF deposition. Results To reveal the intrinsic factors responsible for the low IMF content of buffalo, mRNA expression patterns in muscle and adipose tissue between buffalo and cattle were characterized by RNA sequencing analysis. The IMF content in Nanyang cattle was higher than that in Xinyang buffalo. A total of 1566 mRNAs expressed in adipose tissue showed differential expression between the longissimus dorsi muscles of buffalo and cattle. Functional annotation suggested a difference in the glycolysis/gluconeogenesis pathway between the two species. The results of RT-qPCR analysis and gain-of-function experiments confirmed the positive association between the IMF content and phosphoenolpyruvate carboxykinase 1 (PCK1) expression in buffalo. In both mouse C2C12 cells and cultured bovine myocytes, the activity of the PCK1 promoter in buffalo is lower than that in cattle. However, in mouse 3T3-L1 adipocytes and cultured bovine adipocytes, the activity of PCK1 in buffalo promoter is higher than that in cattle. Conclusions These results indicate the important role of PCK1 in buffalo IMF deposition and illustrate the differences between buffalo and cattle promoter activity that drive PCK1 expression. This research helps to establish a foundation for further studies investigating IMF deposition in buffalo.

Atherosclerosis, which is characterized by chronic inflammation in the arterial wall, is driven by immune cells and cytokines. Recent evidence indicated that interleukin (IL)-27 showed pleiotropic properties in immune diseases. However, precise mechanisms of IL-27, especially in atherosclerosis remains unknown. In our research, we examined the influence of the administration of IL-27 and an anti-IL-27p28 antibody (anti-IL-27p28-Ab) on both the initiation and the progression of atherosclerosis. In the groups (both the initiation and the progression) receiving recombinant IL-27 administration, the formation of atherosclerotic plaques was suspended, and the percentage of regulatory T cells (LAP+ or Foxp3+) in the spleen and peripheral blood was increased. Meanwhile, the number of T helper 1 (Th1) and T helper 17 (Th17) cells was decreased. In the peripheral blood plasma, TGF-β and IL-10 expression were increased, while the levels of IFN-γ and IL-17 were reduced. As for lesions, the mRNA expression of Foxp3, TGF-β, and IL-10 was increased, while that of IFN-γ and IL-17 was reduced. In the anti-IL-27p28 antibody groups, we obtained opposite results. We also observed that DCs treated with IL-27 display a tolerogenic phenotype and that IL-27–treated tolerogenic DCs (tDCs) are likely to play a protective role during atherosclerosis. Our study indicates that IL-27 or adoptive transfer of IL-27 loaded tDCs may be a new therapeutic approach in atherosclerosis.

There is an urgent need for the accurate analysis of heavy metal contamination in the field of ecology and environmental sciences, especially in the case of trace heavy metals, such as cadmium. Using doubly curved crystals (DCC) to achieve the monochromatic X-ray excitation of the sample to be measured and a silicon drift detector (SDD) to collect the fluorescence of the sample elements, combined with an algorithm analysis of the fundamental parameters (FP), the monochromatic energy-dispersive X-ray fluorescence (MED-XRF) system significantly improved the detection limits of the target elements. The detection limits, precision, and accuracy of the MED-XRF acquisition for 20 elements, including cadmium, lead, and arsenic, were evaluated and compared with the Determination of Inorganic Elements in Soil and Sediment Wavelength-Dispersive X-ray Fluorescence Spectrometry report and tested on the actual samples. The test results showed that the detection limit of the inorganic elements in soil and sediment determined by MED-XRF was mostly better than the industry standard, especially the detection limit of Cd, which was 0.04 mg/kg. The accuracy and correctness fully met the requirements for daily laboratory testing and, as a quality control tool, the actual sample testing and laboratory ICP-MS results were consistent. The research conducted in this project constituted a useful attempt to expand and improve the analytical methods for inorganic elements in soil and sediment, showing that MED-XRF is superior to conventional ED-XRF and WD-XRF and is the current new method of analysis for a low content of Cd in soil. MED-XRF offers a very important contribution to research on soil census, conservation, the rational use of agricultural land, and soil restoration and improvement, and provides strong support for field testing.

Fat deposition is one of the most important traits that are mediated by a set of complex regulatory factors in meat animals. Several researches have revealed the significant role of long non-coding RNAs (lncRNAs) in fat deposition while the precise regulatory mechanism is still largely elusive. In this study, we investigated the lncRNA profiles of adipose and muscle tissues in buffalo by using the Illumina HiSeq 3000 platform. In total, 43,809 lncRNAs were finally identified based on the computer algorithm. A comparison analysis revealed 241 lncRNAs that are differentially expressed (DE) in adipose and muscle tissues. We focused on lncSAMM50, a DE lncRNA that has a high expression in adipose tissue. Sequence alignment showed that lncSAMM50 is transcribed from the antisense strand of the upstream region of sorting and assembly machinery component 50 homolog (SAMM50), a gene involved in the function of mitochondrion and is subsequently demonstrated to inhibit the adipogenic differentiation of 3T3-L1 adipocyte cells in this study. lncSAMM50 is highly expressed in adipose tissue and upregulated in the mature adipocytes and mainly exists in the nucleus. Gain-of-function experiments demonstrated that lncSAMM50 promotes the adipogenic differentiation by upregulating adipogenic markers but with no effect on its host gene SAMM50 in buffalo adipocytes. These results indicate that lncSAMM50 enhances fat deposition in buffalo and provide a new factor for the regulatory network of adipogenesis.

In many plants, isoflavones are the main secondary metabolites that have various pharmacological activities, but the low water solubility of aglycones limits their usage. The O-glycosylation of (iso)flavones is a promising way to overcome this barrier. O-glycosyltransferases (UGTs) are key enzymes in the biosynthesis of (iso)flavonoid O-glycosides in plants. However, limited investigations on isoflavonoid O-UGTs have been reported, and they mainly focused on legumes. Iris domestica (L.) Goldblatt et Mabberley is a non-legume plant rich in various isoflavonoid glycosides. However, there are no reports regarding its glycosylation mechanism, despite the I. domestica transcriptome previously being annotated as having non-active isoflavone 7-O-UGTs. Our previous experiments indicated that isoflavonoid glycosides were induced by CuCl2 in I. domestica calli; therefore, we hypothesized that isoflavone O-UGTs may be induced by Cu2+. Thus, a comparative transcriptome analysis was performed using I. domestica seedlings treated with CuCl2, and eight new active BcUGTs were obtained. Biochemical analyses showed that most of the active BcUGTs had broad substrate spectra; however, substrates lacking 5-OH were rarely catalyzed. Real-time quantitative PCR results further indicated that the transcriptional levels of BcUGTs were remarkably induced by Cu2+. Our study increases the understanding of UGTs and isoflavone biosynthesis in non-legume plants.

With the acceleration of urbanization throughout the world, climate problems related to climate change including urban heat islands and global warming have become challenges to urban human settlements. Numerous studies have shown that greenways are beneficial to urban climate improvement and can provide leisure places for people. Taking the coastal greenway in Qingdao as the research object, mobile measurements of the microclimate of the greenway were conducted in order to put forward an evaluation method for the research of outdoor thermal comfort. The results showed that different vegetation coverage affected the PET (physiologically equivalent temperature), UTCI (Universal Thermal Climate Index) as well as thermal comfort voting. We found no significant correlation between activities, age, gender, and thermal comfort voting. Air temperature sensation and solar radiation sensation were the primary factors affecting the thermal comfort voting of all sections. Otherwise, within some sections, wind sensation and humidity sensation were correlated with thermal sensation voting and thermal comfort voting, respectively. Both PET and UTCI were found to have a negative correlation with the vegetation coverage on both sides of the greenway. However, the vegetation coverage had positive correlation (R = 0.072) for thermal sensation and significant positive correlation (R = 0.077*) for thermal comfort. The paved area cover was found to have a positive correlation with PET and UTCI, while having a negative correlation with thermal sensation (R = −0.049) and thermal comfort (R = −0.041). This study can provide scientific recommendations for the planning and design of greenway landscapes to improve thermal comfort.

It is no longer controversial that atherosclerosis is a vascular wall chronic inflammatory disease mediated by cells of innate and adaptive immunity. Galectin-9 (Gal-9) seems to be a crucial regulator of T-cell immunity by inducing apoptosis in specific T-cell subpopulations associated with autoimmunity and inflammatory disease. Accumulating evidence showed that galectin-9 signaling via T-cell immunoglobulin mucin 3 (TIM-3) is concerned with different regulatory functions in autoimmunity, including direct depletion of pro-inflammatory T-cells, expanding the number of regulatory T cells, altering macrophages to an anti-inflammatory state and the induction of repressive myeloid-derived suppressor cells. In addition, anti-Tim-3-Ab administration increased atherosclerotic plaque formation by blocking Tim-3–galectin-9 interaction. Hence, we hypothesize that galectin-9 may be a novel therapy for atherosclerotic disease. Further researches are needed to investigate the precise effect of galectin-9 in the process of atherosclerosis.

Background The coronavirus disease 2019 (COVID‐19) has developed into a global outbreak. Patients with cardiovascular disease (CVD) with COVID‐19 have different clinical characteristics and prognostic outcomes. This study aimed to summarize the clinical characteristics and laboratory indicators of patients with COVID‐19 with CVD, especially the critically ill patients. Methods and Results This study included 244 patients diagnosed with COVID‐19 and CVD (hypertension, coronary heart disease, or heart failure). The patients were categorized into critical (n=36) and noncritical (n=208) groups according to the interim guidance of China’s National Health Commission. Clinical, laboratory, and outcome data were collected from the patients’ medical records and compared between the 2 groups. The average body mass index of patients was significantly higher in the critical group than in the noncritical group. Neutrophil/lymphocyte ratio, and C‐reactive protein, procalcitonin, and fibrinogen, and d‐dimer levels at admission were significantly increased in the critical group. The all‐cause mortality rate among cases of COVID‐19 combined with CVD was 19.26%; the proportion of coronary heart disease and heart failure was significantly higher in deceased patients than in recovered patients. High body mass index, previous history of coronary heart disease, lactic acid accumulation, and a decrease in the partial pressure of oxygen were associated with death. Conclusions All‐cause mortality in patients with COVID‐19 with CVD in hospitals is high. The high neutrophil/lymphocyte ratio may be a predictor of critical patients. Overweight/obesity combined with coronary heart disease, severe hypoxia, and lactic acid accumulation resulting from respiratory failure are related to poor outcomes. Registration URL: https://www.chictr.org.cn; Unique identifier: ChiCTR2000029865.

Severe water deficits due to abnormal climatic conditions can be observed in hydrology and agriculture and can be assessed by various characteristics of the water system that showdifferent responses to climate variability. This paper comprehensively investigates the sensitivities of hydrological (i.e. streamflow and water storage) and agricultural (i.e. plant water availability) water deficits to climate variability at a global scale from a hydrological cycle perspective. The sensitivities of 77 large basins across the globe are quantified by both multiple linear regression (MLR) and the Budyko framework based on a newly released terrestrial water cycle dataset. We find that streamflow and water storage deficits are generally more sensitive to rainfall variation, while plant water availability is more responsive to variations of potential evapotranspiration. The climate sensitivities of the water deficit indices are shown to vary with the wetness index and are shaped by catchment surface properties like water storage capacity. The sensitivities of streamflow deficits to rainfall are higher in wetter regions, while the sensitivities of plant water availability to potential evapotranspiration are higher in drier regions. The findings about the divergent responses in water deficit indices can be conducive to developing region-dependent water resource management strategies to alleviate water deficits under a changing environment.

Background. Interleukin-37 (IL-37) acts as an inhibitor of innate and adaptive immunity. However, the exact role of IL-37 in the patients with acute coronary syndrome (ACS) remains to be elucidated. Methods. Patients were classified into 4 groups: normal coronary artery (NCA), stable angina (SA), unstable angina (UA), and acute myocardial infarction (AMI). The circulating Treg, Th1, and Th17 frequencies were measured. The effect of IL-37 on stimulated peripheral blood mononuclear cells (PBMCs) and the influence of IL-37 on DCs were explored. In addition, the role of IL-37-treated tDCs on Treg cell expansion and the stability of these tDCs were also tested. Results. Our results showed that the circulating Treg frequencies were decreased, while Th1 and Th17 frequencies were increased in ACS patients, and that IL-37 expanded Tregs but suppressed Th1 and Th17 cells in activated PBMCs derived from ACS patients. Of note, IL-37-treated human DCs obtained a tolerogenic phenotype, and such tDCs promoted expansion of Tregs and decreased the Th1 and Th17 populations when cocultured with CD4+ T cells. Interestingly, IL-37-treated DCs from patients with ACS are phenotypically and functionally comparable to IL-37-treated DCs from NCA patients, and tolerogenic properties of IL-37-treated DCs were highly stable. Conclusion. In conclusion, our results reveal a beneficial role of IL-37 in the patients with ACS and suggest that autologous IL-37-treated tDCs may be a novel therapeutic strategy for the patients with ACS.

Background: Accumulating evidence shows that the pathological autoreactive immune response is responsible for plaque rupture and the subsequent onset of acute coronary syndrome (ACS). Naturally occurring CD4+CD25+regulatory T cells (nTregs) are indispensable in suppressing the pathological autoreactive immune response and maintaining immune homeostasis. However, the number and the suppressive function of glycoprotein-A repetitions predominant (GARP) + CD4+ CD25+ activated nTregs were impaired in patients with ACS. Recent evidence suggests that heme oxygenase-1 (HO-1) can regulate the adaptive immune response by promoting the expression of Foxp3. We therefore hypothesized that HO-1 may enhance the function of GARP+ CD4+ CD25+Tregs in patients with ACS and thus regulate immune imbalance. Methods: T lymphocytes were isolated from healthy volunteers (control, n=30) and patients with stable angina (SA, n=40) or ACS (n=51). Half of these cells were treated with an HO-1 inducer (hemin) for 48 h, and the other half were incubated with complete RPMI-1640 medium. The frequencies of T-helper 1 (Th1), Th2, Th17 and latency-associated peptide (LAP) +CD4+ T cells and the expression of Foxp3 and GARP by CD4+CD25+T cells were then assessed by measuring flow cytometry after stimulation in vitro. The suppressive function of activated Tregs was measured by thymidine uptake. The levels of transforming growth factor-1 (TGF-β1) in the plasma were measured using enzyme-linked immunosorbent assay (ELISA). The expression levels of the genes encoding these proteins were analyzed by real-time polymerase chain reaction. Results: Patients with ACS exhibited an impaired number and suppressive function of GARP+ CD4+ CD25+Tregs and a mixed Th1/Th17-dominant T cell response when compared with the SA and control groups. The expression of LAP in T cells was also lower in patients with ACS compared to patients with SA and the control individuals. Treatment with an HO-1 inducer enhanced the biological activity of GARP+ CD4+ CD25+Tregs and resulted in increased expression of LAP and GARP by activated T cells. Conclusions: The reduced number and impaired suppressive function of GARP+ CD4+ CD25+Tregs result in excess effector T cell proliferation, leading to plaque instability and the onset of ACS. HO-1 can effectively restore impaired GARP+ CD4+ CD25+Tregs from patients with ACS by promoting LAP and GARP expression on activated T cells.

Hepatic encephalopathy (HE) is a neurological disease occurring in patients with hepatic insufficiency and/or portal-systemic blood shunting based on cirrhosis. The pathogenesis is not completely clear till now, but it is believed that hyperammonemia is the core of HE. Hyperammonemia caused by increased sources of ammonia and decreased metabolism further causes mental problems through the gut–liver–brain axis. The vagal pathway also plays a bidirectional role in the axis. Intestinal microorganisms play an important role in the pathogenesis of HE through the gut–liver–brain axis. With the progression of cirrhosis to HE, intestinal microbial composition changes gradually. It shows the decrease of potential beneficial taxa and the overgrowth of potential pathogenic taxa. Changes in gut microbiota may lead to a variety of effects, such as reduced production of short-chain fatty acids (SCFAs), reduced production of bile acids, increased intestinal barrier permeability, and bacterial translocation. The treatment aim of HE is to decrease intestinal ammonia production and intestinal absorption of ammonia. Prebiotics, probiotics, antibiotics, and fecal microbiota transplantation (FMT) can be used to manipulate the gut microbiome to improve hyperammonemia and endotoxemia. Especially the application of FMT, it has become a new treated approach to target microbial composition and function. Therefore, restoring intestinal microbial homeostasis can improve the cognitive impairment of HE, which is a potential treatment method. [ABSTRACT FROM AUTHOR]

BackgroundExcessive immune‐mediated inflammatory reactions play a deleterious role in postinfarction ventricular remodeling. Interleukin‐37 (IL‐37) emerges as an inhibitor of both innate and adaptive immunity. However, the exact role of IL‐37 and IL‐37 plus troponin I (TnI)–treated dendritic cells (DCs) in ventricular remodeling after myocardial infarction (MI) remains elusive. Methods and ResultsMI was induced by permanent ligation of the left anterior descending artery. Our results showed that treatment with recombinant human IL‐37 significantly ameliorated ventricular remodeling after MI, as demonstrated by decreased infarct size, better cardiac function, lower mortality, restricted inflammatory responses, decreased myocardial fibrosis, and inhibited cardiomyocyte apoptosis. In vitro, we examined the phenotype of IL‐37 plus TnI–conditioned DCs of male C57BL/6 mice and their capacity to influence the number of regulatory T cells. Our results revealed that IL‐37 plus TnI–conditioned DCs obtained the characteristics of tolerogenic DCs (tDCs) and expanded the number of regulatory T cells when co‐cultured with splenic CD4+ T cells. Interestingly, we also found that adoptive transfer of these antigen‐loaded tDCs markedly increased the number of regulatory T cells in the spleen, attenuated the infiltration of inflammatory cells in the infarct hearts, decreased myocardial fibrosis, and improved cardiac function. ConclusionsOur results reveal a beneficial role of IL‐37 or tDCs treated with IL‐37 plus TnI in post‐MI remodeling that is possibly mediated by reestablishing a tolerogenic immune response, indicating that IL‐37 or adoptive transfer of IL‐37 plus TnI–treated tDCs may be a novel therapeutic strategy for ventricular remodeling after MI.

Regulatory T cells play an important role in the progression of atherosclerosis. GARP is a newly biological membrane molecule existed on activated Tregs, which is related to the release of TGF-β. The antiatherosclerosis effects of statins partly depend on their multiple immune modulatory potencies. In this paper, we present that atorvastatin could upregulate the expression of GARP and TGF-β in CD4+ T cells and increase the numbers of CD4+LAP+ and CD4+Foxp3+ regulatory T cells in ApoE−/− mice. Also, we indicate that atorvastatin promotes the aggregation of GARP+ and Foxp3+ cells and secretory of the TGF-β1 in atherosclerotic plaques. Furthermore, we prove that atorvastatin could delay the procession of atherosclerosis and improve the stability of atherosclerotic plaques. Interestingly, we report that inhibition of GARP distinctly inhibits the anti-inflammatory effects of atorvastatin. We conclude that atorvastatin improves the inflammatory response in atherosclerosis partly by upregulating the expression of GARP on regulatory T cells.

Background. Recently, several studies suggest that galectin-9 (Gal-9) might play a pivotal role in the pathogenesis of autoimmune diseases. However, the exact role of Gal-9 in atherosclerosis remains to be elucidated. Methods. Serum Gal-9, high-sensitivity C-reactive protein (hs-CRP), interferon- (IFN-) γ, interleukin- (IL-) 4, IL-17, and transforming growth factor- (TGF-) β1 were measured. The effect of Gal-9 on peripheral blood mononuclear cells (PBMC) was investigated in patients with normal coronary artery (NCA). Results. The lowest level of Gal-9 was found in the ST-segment elevation myocardial infarction (STEMI) group, followed by the non-ST-segment elevation ACS (NSTEACS), the NCA, and the stable angina pectoris (SAP) groups, respectively. Additionally, Gal-9 was found to be independently associated with hs-CRP, lipoprotein(a), and creatinine. Notably, Gal-9 was also noted to be an independent predictor of the Gensini score. Moreover, Gal-9 suppressed T-helper 17 (Th17) and expanded regulatory T cells (Tregs), resulting in decreased IL-17 production and increased secretion of TGF-β1. Conclusions. Serum Gal-9 is associated with not only coronary artery disease (CAD), but also the severity of coronary arteries stenosis. Gal-9 can expand Tregs and suppress Th17 development in activated PBMC, implying that Gal-9 has the potential to dampen the development of atherosclerosis and may be a new therapy for CAD.