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Cardiovascular diseases have been identified as vital factors in global morbidity and mortality in recent years. The available evidence suggests that various cytokines and pathological proteins participate in these complicated and changeable diseases. The thrombospondin (TSP) family is a series of conserved, multidomain calcium-binding glycoproteins that cause cell-matrix and cell-cell effects via interactions with other extracellular matrix components and cell surface receptors. The TSP family has five members that can be divided into two groups (Group A and Group B) based on their different structures. TSP-1, TSP-2, and TSP-4 are the most studied proteins. Among recent studies and findings, we investigated the functions of several family members, especially TSP-5. We review the basic concepts of TSPs and summarize the relevant molecular mechanisms and cell interactions in the cardiovascular system. Targeting TSPs in CVD and other diseases has a remarkable therapeutic benefit.

Bone morphogenetic proteins (BMPs) are secretory proteins belonging to the transforming growth factor-β (TGF-β) superfamily. These proteins play important roles in embryogenesis, bone morphogenesis, blood vessel remodeling and the development of various organs. In recent years, as research has progressed, BMPs have been found to be closely related to cardiovascular diseases, especially atherosclerosis, vascular calcification, cardiac remodeling, pulmonary arterial hypertension (PAH) and hereditary hemorrhagic telangiectasia (HHT). In this review, we summarized the potential roles and related mechanisms of the BMP family in the cardiovascular system and focused on atherosclerosis and PAH.

BackgroundCardiac dysfunction is one of the most common complications of sepsis and is associated with the adverse outcomes and high mortality of sepsis patients. IL-12p40, the common subunit of IL-12 and IL-23, has been shown to be involved in a variety of inflammation-related diseases, such as psoriasis and inflammatory bowel disease. However, the role of IL-12p40 in lipopolysaccharide (LPS)-induced cardiac dysfunction remains obscure. This study aimed to explore the role of IL-12p40 in LPS-induced cardiac dysfunction and its potential mechanisms.MethodsIn this study, mice were treated with LPS and the cardiac expression of IL-12p40 was determined. Then, IL-12p40–/– mice were used to detect the role and mechanisms of IL-12p40 in LPS-induced cardiac injury. In addition, monocytes were adoptively transferred to IL-12p40–/– mice to explore their effects on LPS-induced cardiac dysfunction.ResultsThe results showed that cardiac IL-12p40 expression was significantly increased after treated with LPS. In addition, IL-12p40 deletion significantly aggravated LPS-induced cardiac dysfunction, evidenced by the increased serum levels of cardiomyocyte injury markers and heart injury scores, as well as by the deteriorated cardiac function. Moreover, IL-12p40 deletion increased LPS-induced monocyte accumulation and cardiac expression of inflammatory cytokines, as well as enhanced the activation of the NF-κB and MAPK pathways. Furthermore, adoptive transfer WT mouse monocytes to IL-12p40−/− mice alleviated LPS-induced cardiac dysfunction and decreased the phosphorylation of p65.ConclusionIL-12p40 deletion significantly aggravated LPS-induced cardiac injury and cardiac dysfunction in mice by regulating the NF-κB and MAPK signaling pathways, and this process was related to monocytes. Therefore, IL-12p40 show a protective role in SIC, and IL-12p40 deficiency or anti-IL-12p40 monoclonal antibodies may be detrimental to patients with SIC.

Technological innovation is a long-term activity with highly unpredictable returns on investment, which makes SMEs with information problems and lack of collateral value be vulnerable to financing constraints when engaging in innovation activities. This study incorporates financing and R&D activities into the evaluation of innovation efficiency and further considers the impact of financial regulation as an external factor in technology-based SMEs in China. This study puts forward a three-stage dynamic DDF-DEA model to explore the overall innovation efficiency as well as the efficiency of each stage in technology-based SMEs by dividing the innovation process into three stages, namely the financing stage, R&D stage and operating stage. The study reveals that the overall efficiency of innovation are higher in non-coastal areas of China than in coastal areas. Non-coastal regions have higher efficiency in the financing and operating stages, while coastal regions have higher efficiency in the R&D stage. Strengthening financial regulation could improve the financing and R&D efficiency both in coastal and non-coastal areas, but it has different effect on the operating efficiency in coastal and non-coastal areas. The results of this study could provide some reference for China and other emerging economies to formulate policies in improving the efficiency of financing and R&D. First published online 30 August 2022

Obesity is often accompanied by hypertension. Although a large number of studies have confirmed that NLRP3 inhibitors can improve cardiac remodeling in mice with a normal diet, it is still unclear whether NLRP3 inhibitors can improve heart failure (HF) induced by pressure overload in obese mice. The purpose of this study was to explore the role of MCC950, a selective NLRP3 inhibitor, on HF in obese mice and its metabolic mechanism. Obese mice induced with a 10-week high-fat diet (HFD) were used in this study. After 4 weeks of HFD, transverse aortic constriction (TAC) surgery was performed to induce a HF model. MCC950 (10 mg/kg, once/day) was injected intraperitoneally from 2 weeks after TAC and continued for 4 weeks. After echocardiography examination, we harvested left ventricle tissues and performed molecular experiments. The results suggest that in obese mice, MCC950 can significantly improve cardiac hypertrophy and fibrosis caused by pressure overload. MCC950 ameliorated cardiac inflammation after TAC surgery and promoted M2 macrophage infiltration in the cardiac tissue. MCC950 not only restored fatty acid uptake and utilization by regulating the expression of CD36 and CPT1β but also reduced glucose uptake and oxidation via regulating the expression of GLUT4 and p-PDH. In addition, MCC950 affected the phosphorylation of AKT and AMPK in obese mice with HF. In summary, MCC950 can alleviate HF induced by pressure overload in obese mice via improving cardiac metabolism, providing a basis for the clinical application of NLRP3 inhibitors in obese patients with HF.

Cardiovascular disease (CVD) is a class of diseases with high disability and mortality rates. In the elderly population, the incidence of cardiovascular disease is increasing annually. Between 1990 and 2016, the age-standardised prevalence of CVD in China significantly increased by 14.7%, and the number of cardiovascular disease deaths increased from 2.51 million to 3.97 million. Much research has indicated that cardiovascular disease is closely related to inflammation, immunity, injury and repair. Chemokines, which induce directed chemotaxis of reactive cells, are divided into four subfamilies: CXC, CC, CX3C, and XC. As cytokines, CXC chemokines are similarly involved in inflammation, immunity, injury, and repair and play a role in many cardiovascular diseases, such as atherosclerosis, myocardial infarction, cardiac ischaemia-reperfusion injury, hypertension, aortic aneurysm, cardiac fibrosis, postcardiac rejection, and atrial fibrillation. Here, we explored the relationship between the chemokine CXC subset and cardiovascular disease and its mechanism of action with the goal of further understanding the onset of cardiovascular disease.

Cardiovascular disease is one of the main causes of human mortality. Cytokines play crucial roles in the development of cardiovascular disease. Interleukin (IL)-6 family members are a series of cytokines, including IL-6, IL-11, IL-30, IL-31, OSM, LIF, CNTF, CT-1, CT-2, and CLC, that regulate multiple biological effects. Experimental and clinical evidence shows that IL-6 family members are closely related to cardiovascular diseases such as atherosclerosis, hypertension, aortic dissection, cardiac fibrosis, and cardiomyopathy. This review mainly discusses the role of IL-6 family members in cardiovascular disease for the sake of identifying possible intervention targets for cardiovascular disease prevention and treatment.

Wildlife is known to be a source of high-impact pathogens affecting people. However, the distribution, genetic diversity, and zoonotic potential of Cryptosporidium, Enterocytozoon bieneusi, and Giardia duodenalis in wildlife are poorly understood. Here, we conducted the first molecular epidemiological investigation of these three pathogens in wildlife in Zhejiang and Shanghai, China. Genomic DNAs were derived from 182 individual fecal samples from wildlife and then subjected to a nested polymerase chain reaction–based sequencing approach for detection and characterization. Altogether, 3 (1.6%), 21 (11.5%), and 48 (26.4%) specimens tested positive for Cryptosporidium species, E. bieneusi, and G. duodenalis, respectively. Sequence analyses revealed five known (BEB6, D, MJ13, SC02, and type IV) and two novel (designated SH_ch1 and SH_deer1) genotypes of E. bieneusi. Phylogenetically, novel E. bieneusi genotype SH_deer1 fell into group 6, and the other genotypes were assigned to group 1 with zoonotic potential. Three novel Cryptosporidium genotypes (Cryptosporidium avian genotype V-like and C. galli-like 1 and 2) were identified, C. galli-like 1 and 2 formed a clade that was distinct from Cryptosporidium species. The genetic distinctiveness of these two novel genotypes suggests that they represent a new species of Cryptosporidium. Zoonotic assemblage A (n = 36) and host-adapted assemblages C (n = 1) and E (n = 7) of G. duodenalis were characterized. The overall results suggest that wildlife act as host reservoirs carrying zoonotic E. bieneusi and G. duodenalis, potentially enabling transmission from wildlife to humans and other animals.

Cardiac dysfunction is a well-recognized complication of sepsis and is associated with the outcome and prognosis of septic patients. Evidence suggests that Il12a participates in the regulation of various cardiovascular diseases, including heart failure, hypertension and acute myocardial infarction. However, the effects of Il12a in sepsis-induced cardiac dysfunction remain unknown. In our study, lipopolysaccharide (LPS) and cecal ligation and puncture (CLP) model were used to mimic sepsis, and cardiac Il12a expression was assessed. In addition, Il12a knockout mice were used to detect the role of Il12a in sepsis-related cardiac dysfunction. We observed for the first time that Il12a expression is upregulated in mice after LPS treatment and macrophages were the main sources of Il12a. In addition, our findings demonstrated that Il12a deletion aggravates LPS-induced cardiac dysfunction and injury, as evidenced by the increased serum and cardiac levels of lactate dehydrogenase (LDH) and cardiac creatine kinase-myocardial band (CK-MB). Moreover, Il12a deletion enhances LPS-induced macrophage accumulation and drives macrophages toward the M1 phenotype in LPS-treated mice. Il12a deletion also downregulated the activity of AMP-activated protein kinase (AMPK) but increased the phosphorylation levels of p65 (p-p65) and NF-κB inhibitor alpha (p-IκBα). In addition, Il12a deletion aggravates CLP-induced cardiac dysfunction and injury. Treatment with the AMPK activator AICAR abolishes the deterioration effect of Il12a deletion on LPS-induced cardiac dysfunction. In conclusion, Il12a deletion aggravated LPS-induced cardiac dysfunction and injury by exacerbating the imbalance of M1 and M2 macrophages. Our data provide evidence that Il12a may represent an attractive target for sepsis-induced cardiac dysfunction.

Environment pollution was closely related to human health. The energy consumption is one of the important sources of environmental pollution in the development of economy. This paper used undesirable two-stage meta-frontier DDF (distance difference function) data envelopment analysis model to explore the impact of environment pollutants from energy consumption on the mortality of children and the aged, survival rate of 65 years old and health expenditure efficiency in 27 high income countries, 21 upper middle income countries, and 16 lower middle income countries from 2010 to 2014. High income countries had higher efficiency of energy and health than middle income countries in general. But whether in high income or middle income countries, the efficiency of non-renewable energy is higher than renewable energy. There was much room for both high income countries and middle income countries to improve renewable energy efficiency. Besides, middle income countries need to improve the efficiency of non-renewable energy and reduce pollutant emissions per unit of GDP. In terms of health efficiency, upper middle income countries performed worse than lower income countries. This phenomenon might indicate there was a U-shaped relationship between health efficiency and income level. Upper income countries should pay more attention to the environmental and health problems and cross the U-shaped turning point. The contribution of this article was to consider the heterogeneous performance of energy efficiency, environmental efficiency, and health efficiency under the influence of income level differences, and found that there might be a U-shaped relationship between health efficiency and income level.

Environmental protection and health issues have always been of great concern. This study employed modified Meta-Frontier Dynamic Network Data Envelopment Analysis to explore the environmental pollution effects from energy consumption on the mortality of children and adults, tuberculosis rate, survival rate, and health expenditure efficiencies in 15 old EU states and 13 new EU states from 2010 to 2014. We calculated the overall efficiency scores and technology gap ratios for each old EU and new EU states as well as the efficiencies of non-renewable energy, renewable energy, PM2.5, CO2, labor, GDP, tuberculosis, child mortality, adult mortality, health expenditure efficiency, and survival efficiency at the health stage. The average annual overall efficiencies of the old EU states are higher than that of the new EU states. Whether in terms of energy efficiencies or health efficiencies, the inputs and outputs of the old EU states are always higher than that of the new EU states. Overall, developing countries in Eastern Europe are lagging behind in terms of energy and health efficiencies. At the same time, the efficiency of child mortality is lower than that of adult mortality, and the efficiency of PM2.5 is higher than that of CO2 in both old and new EU states.

There is a close and important relationship between environmental pollution and public health, and environmental pollution has an important impact on the public health. This study employed the two-stage meta-frontier dynamic network data envelopment analysis (TMDN-DEA) model to explore the environment pollution effects from energy consumption on the mortality of children and adult, tuberculosis rate, survival rate and health expenditure efficiencies in 28 EU countries and 53 non-EU countries from 2010 to 2014. We calculated the overall efficiency scores and the technology gap ratios of each EU and non-EU countries and the efficiencies of input and output variables in the production and health stage. The average overall efficiencies each year in EU countries are higher than in the non-EU countries. But EU countries have higher energy efficiency than non-EU countries, and non-EU countries have higher health efficiency than EU countries. The health expenditure efficiencies in the EU countries are obviously lower than those in non-EU countries. The renewable energy efficiencies are obviously higher than the non-renewable energy efficiencies; PM2.5 efficiencies are obviously higher than the CO2 efficiencies and the children’s mortality rate efficiencies are higher than the adult’s mortality rate efficiencies for EU countries and non-EU countries. The government management in the EU and non-EU countries should be strengthened to reduce the air pollutant and carbon dioxide emissions and raise energy transformation to the clean energy in renewable energy and improve health efficiencies in medical and health care field.

This paper examines the impact of institutions on regional financial development using a panel data model of 11 East Asian countries during 1996-2017. It divides the institutional factors into six economic factors and six legalpolitical factors. The analysis demonstrates that the legalpolitical institutional factors have a stronger impact on financial development than the economic institutional factors in East Asia. Improvement in institutional quality such as fiscal freedom, business freedom, control of corruption, government effectiveness, regulatory quality and rule of law can promote financial development. Improvements of these institutional factors facilitate the ability of enterprises to allocate resources and improve the strength of business operations, thereby reducing transaction costs and making the financial operating environment fairer and more efficient. With the improvement of institutional factors, financial development will have more opportunities to develop better. Institutional impacts are more pronounced in the financial development in Malaysia, Indonesia, the Philippines and Myanmar than in the other countries such as China, Japan, Korea and Singapore. [ABSTRACT FROM AUTHOR]