CO2 utilization for methanol production: a review on the safety concerns and countermeasures.

The catalytic conversion of carbon dioxide is one of the important ways to achieve the goal of carbon neutralization, which can be further divided into electrocatalysis, thermal catalysis, and photocatalysis. Although photocatalysis and electrocatalysis have the advantages of mild reaction conditions and low energy consumption, the thermal catalytic conversion of CO2 has larger processing capacity, better reduction effect, and more complete industrial foundation, which is a promising technology in the future. During the development of new technology from laboratory to industrial application, ensuring the safety of production process is essential. In this work, safety optimization design of equipment, safety performance of catalysts, accident types, and their countermeasures in the industrial applications of CO2 to methanol are reviewed and discussed in depth. Based on that, future research demands for industrial process safety of CO2 to methanol were proposed, which provide guidance for the large-scale application of CO2 thermal catalytic conversion technology.

Bergenin alleviates proliferative arterial diseases by modulating glucose metabolism in vascular smooth muscle cells.

BACKGROUND: Vascular smooth muscle cell (VSMC) proliferation and phenotypic switching are key mechanisms in the development of proliferative arterial diseases. Notably, reprogramming of the glucose metabolism pattern in VSMCs plays an important role in this process. PURPOSE: The aim of this study is to investigate the therapeutic potential and the mechanism underlying the effect of bergenin, an active compound found in Bergenia, in proliferative arterial diseases. METHODS: The effect of bergenin on proliferative arterial disease was evaluated using platelet-derived growth factor (PDGF)-stimulated VSMCs and a mouse model of carotid artery ligation. VSMC proliferation and phenotypic switching were evaluated in vitro using cell counting kit-8, 5-ethynyl-2-deoxyuridine incorporation, scratch, and transwell assays. Carotid artery neointimal hyperplasia was evaluated in vivo using hematoxylin and eosin staining and immunofluorescence. The expression of proliferation and VSMC contractile phenotype markers was evaluated using PCR and western blotting. RESULTS: Bergenin treatment inhibited PDGF-induced VSMC proliferation and phenotypic switching and reduced neointimal hyperplasia in the carotid artery ligation model. Additionally, bergenin partially reversed the PDGF-induced Warburg-like glucose metabolism pattern in VSMCs. RNA-sequencing data revealed that bergenin treatment significantly upregulated Ndufs2, an essential subunit of mitochondrial complex I. Ndufs2 knockdown attenuated the inhibitory effect of bergenin on PDGF-induced VSMC proliferation and phenotypic switching, and suppressed neointimal hyperplasia in vivo. Conversely, Ndufs2 overexpression enhanced the protective effect of bergenin. Moreover, Ndufs2 knockdown abrogated the effects of bergenin on the regulation of glucose metabolism in VSMCs. CONCLUSION: These findings suggest that bergenin is effective in alleviating proliferative arterial diseases. The reversal of the Warburg-like glucose metabolism pattern in VSMCs during proliferation and phenotypic switching may underlie this therapeutic mechanism.

CTRP3 alleviates mitochondrial dysfunction and oxidative stress injury in pathological cardiac hypertrophy by activating UPRmt via the SIRT1/ATF5 axis.

Pathological cardiac hypertrophy is an independent risk factor for heart failure. Disruption of mitochondrial protein homeostasis plays a key role in pathological cardiac hypertrophy; however, the mechanism of maintaining mitochondrial homeostasis in pathological cardiac hypertrophy remains unclear. In this study, we investigated the regulatory mechanisms of mitochondrial protein homeostasis in pathological cardiac hypertrophy. Wildtype (WT) mice, knockout mice, and mice transfected with lentivirus overexpressing mouse C1q-tumor necrosis factor-related protein-3 (CTRP3) underwent transverse aortic constriction or sham surgery. After 4 weeks, cardiac function, mitochondrial function, and oxidative stress injury were examined. For mechanistic studies, neonatal rat cardiomyocytes were treated with small interfering RNA or overexpression plasmids for the relevant genes. CTRP3 overexpression attenuated transverse aortic constriction (TAC) induced pathological cardiac hypertrophy, mitochondrial dysfunction, and oxidative stress injury compared to that in WT mice. TAC or Ang II resulted in compensatory activation of UPRmt, but this was not sufficient to counteract pathologic cardiac hypertrophy. CTRP3 overexpression further induced activation of UPRmt during pathologic cardiac hypertrophy and thereby alleviated pathologic cardiac hypertrophy, whereas CTRP3 knockout or knockdown inhibited UPRmt. ATF5 was a key regulatory molecule of UPRmt, as ATF5 knockout prevented the cardioprotective effect of CTRP3 in TAC mice. In vitro, SIRT1 was identified as a possible downstream CTRP3 effector molecule, and SIRT1 knockout blocked the cardioprotective effects of CTRP3. Our results also suggest that ATF5 may be regulated by SIRT1. Our study demonstrates that CTRP3 activates UPRmt via the SIRT1/ATF5 axis under pathological myocardial hypertrophy, thus attenuating mitochondrial dysfunction and oxidative stress injury.

Effect of Jet Velocity on the Formation of Moderate or Intense Low-Oxygen Dilution Combustion of Pulverized Coal.

Moderate or intense low-oxygen dilution (MILD) combustion of pulverized coal is regarded as a new combustion technology with great potential due to its advantages of reducing NO x emission and improving the uniformity of heat flux in the furnace. Increasing the jet velocity has been proved to be an important technical means to achieve MILD oxy-coal combustion, especially without a high level of preheat, but the transition mechanism of coal combustion modes with the increase of jet velocity is not clear enough. In this work, a high-velocity coal-laden jet combustion system on the basis of a flat-flame burner was designed to study the effect of jet velocity on the formation of MILD combustion of pulverized coal. The combustion mode transition of the pulverized coal jet is revealed by analyzing the flame structure, temperature, radiation, and reaction intensity through a variety of optical measurement methods. Theoretical criteria for combustion mode were applied to predict the formation of MILD combustion and were validated by the experimental data. In the environment with an ambient temperature of 1600 °C, the transition velocity of the coal jet into the MILD combustion regime is about 50 m/s and about 100 m/s at 5 and 15% O2 molar fraction, respectively. The dilution effect, jet entrainment, and turbulent mixing in the high-velocity jet, as the key factors to achieve an MILD combustion regime, were analyzed theoretically and experimentally. The dilution effect inherent in the jet significantly reduces the reactant concentration and ultimately reduces the reaction intensity and flame brightness while the entrainment of the jet promotes the radial dispersion of particles and the flame uniformity, which is dominant at lower jet velocities. Strong turbulent mixing promotes the ignition and volatile combustion, which is dominant at higher jet velocities.

Primary membranous nephrotic syndrome with chylothorax as first presentation: A case report and literature review.

BACKGROUND: Primary membranous nephrotic syndrome with chylothorax as the first manifestation is an unusual condition. To date, only a few cases have been reported in clinical practice. CASE SUMMARY: The clinical data of a 48-year-old man with primary nephrotic syndrome combined with chylothorax admitted to the Department of Respiratory and Critical Care Medicine of Shaanxi Provincial People's Hospital were retrospectively analysed. The patient was admitted to the hospital for 12 d due to shortness of breath. Imaging showed pleural effusion, laboratory tests confirmed true chylothorax, and renal biopsy revealed membranous nephropathy. After primary disease treatment and early active symptom treatment, the prognosis of the patient was good. This case suggests that chylothorax is a rare complication of primary membranous nephrotic syndrome in adults, and early lymphangiography and renal biopsy can assist in the diagnosis when there are no contraindications. CONCLUSION: Primary membranous nephrotic syndrome combined with chylothorax is rare in clinical practice. We report a relevant case to provide case information for clinicians and to improve diagnosis and treatment.

The Effect of Temperature on Molecular Structure of Medium-Rank Coal via Fourier Transform Infrared Spectroscopy.

Fourier transform infrared spectroscopy (FTIR) was used to study the molecular structure of four medium- and low-temperature heat-treated medium-rank coals. The FTIR spectral parameters, which consist of CH2/CH3, aromaticity (fa), aromatic carbon rate (fC), aromatic hydrogen rate (fH), oxygen-containing (C-O) rate (IR), organic matter maturity (M), and the degree of aromatic condensation (Dc), indicate different characteristics, including changes in the aromatic hydrocarbon structure, fatty hydrocarbon structure, hydroxyl structure, and oxygen-containing functional groups of medium-rank coal. The results show that with the increase in heat treatment temperature, the sulfur content in coal gradually decreases, but the C/H ratio gradually increases. Meanwhile, the content of kaolinite and pyrite in coal gradually decreases, whereas the content of dolomite and hematite gradually increases. With the increase in heat treatment temperature, the relative content of ether oxygen hydroxyl groups in the hydroxyl structure significantly decreases, but the relative content of self-associated hydroxyl groups increases. The relative content of alkyl ether (C-O) in oxygen-containing functional groups gradually increases, whereas the relative content of aromatic nucleus C=C vibration presents a trend of first increasing and then decreasing. In addition, -CH2- is the majority in the structure of fatty hydrocarbons, and the absorption peak intensity of asymmetric -CH3 stretching vibration increases with the increase in heat-treated temperature. The structure of aromatic hydrocarbons mainly consists of four substituted benzene rings (except for R-303.15 K), in which the relative content of the trisubstituted benzene ring decreases with the increase in heat treatment temperature. With the increase in the heat-treated temperature of medium-rank coal, Dc, fH, fC, and fa show a trend of first increasing and then decreasing, M and IR reveal a trend of first decreasing and then increasing, and CH2/CH3 present a gradually decreasing trend. In conclusion, during the increase in the heat treatment temperature of medium-rank coal, the length of the fatty side chains in the fatty hydrocarbon structure becomes shorter, the number of branch chains continuously increases, and the maturity and condensation degree of organic matter first increases and then decreases. On this basis, further research on the effect of coal gasification suggests combining various technologies such as 13C NMR, XRD, and TG-MS to obtain semi-quantitative structural information of molecules in coal from different perspectives.

Influence Factors and Feasibility Evaluation on Geological Sequestration of CO2 in Coal Seams: A Review.

The geological sequestration of CO2 in coal seams holds significant implications for coalbed methane development and greenhouse gas mitigation. This paper examines the principles, influencing factors, and evaluation methods for geological CO2 sequestration in coal seams by analyzing relevant domestic and international findings. Suitable geological conditions for CO2 sequestration include burial depths between 300 and 1300 m, permeability greater than 0.01 × 10-3 µm2, caprock and floor strata with water isolation capabilities, and high-rank bituminous coal or anthracite with low ash yield. Geological structures, shallow freshwater layers, and complex hydrological conditions should be avoided. Additionally, the engineering conditions of temperature, pressure, and storage time for CO2 sequestration should be given special attention. The feasibility evaluation of CO2 geological storage in coal seams necessitates a comprehensive understanding of coalfield geological factors. By integrating the evaluation principles of site selection feasibility, injection controllability, sequestration security, and development economy, various mathematical models and "one vote veto" power can optimize the sequestration area and provide recommendations for rational CO2 geological storage layout.

GLUT4 mediates the protective function of gastrodin against pressure overload-induced cardiac hypertrophy.

Gastrodia elata exhibits extensive pharmacological activity; its extract gastrodin (GAS) has been used clinically to treat cardiovascular diseases. In the present study, we examined the effect of GAS in a mice model of pathological cardiac hypertrophy, which was induced using transverse aortic constriction (TAC). Male C57BL/6 J mice underwent either TAC or sham surgery. GAS was administered post-surgically for 6 weeks and significantly improved the deterioration of cardiac contractile function caused by pressure overload, cardiac hypertrophy, and fibrosis in mice. Treatment with GAS for 6 weeks upregulated myosin heavy chain α and down-regulated myosin heavy chain ß and atrial natriuretic peptide, while insulin increased the effects of GAS against cardiac hypertrophy. In vitro studies showed that GAS could also protect phenylephrine-induced cardiomyocyte hypertrophy, and these effects were attenuated by BAY-876, and increased by insulin. Taken together, our results suggest that the anti-hypertrophic effect of gastrodin depends on its entry into cardiomyocytes through GLUT4.

Epicardial adipose tissue, metabolic disorders, and cardiovascular diseases: recent advances classified by research methodologies.

Epicardial adipose tissue (EAT) is located between the myocardium and visceral pericardium. The unique anatomy and physiology of the EAT determines its great potential in locally influencing adjacent tissues such as the myocardium and coronary arteries. Classified by research methodologies, this study reviews the latest research progress on the role of EAT in cardiovascular diseases (CVDs), particularly in patients with metabolic disorders. Studies based on imaging techniques demonstrated that increased EAT amount in patients with metabolic disorders is associated with higher risk of CVDs and increased mortality. Then, in-depth profiling studies indicate that remodeled EAT may serve as a local mediator of the deleterious effects of cardiometabolic conditions and plays a crucial role in CVDs. Further, in vitro coculture studies provided preliminary evidence that the paracrine effect of remodeled EAT on adjacent cardiomyocytes can promote the occurrence and progression of CVDs. Considering the important role of EAT in CVDs, targeting EAT might be a potential strategy to reduce cardiovascular risks. Several interventions have been proved effective in reducing EAT amount. Our review provides valuable insights of the relationship between EAT, metabolic disorders, and CVDs, as well as an overview of the methodological constructs of EAT-related studies.

Low-dose exercise protects the heart against established myocardial infarction via IGF-1-upregulated CTRP9 in male mice.

Regular exercise is recommended as an important component of therapy for cardiovascular diseases in clinical practice. However, there are still major challenges in prescribing an optimized exercise regimen to individual patients with established cardiac disease. Here, we tested the effects of different exercise doses on cardiac function in mice with established myocardial infarction (MI). Exercise was introduced to mice with MI after 4 weeks of surgery. Low-dose exercise (15 min/day for 8 weeks) improved mortality and cardiac function by increasing 44.39% of ejection fractions while inhibiting fibrosis by decreasing 37.74% of distant region. Unlike higher doses of exercise, low-dose exercise consecutively upregulated cardiac expression of C1q complement/tumor necrosis factor-associated protein 9 (CTRP9) during exercise (>1.5-fold). Cardiac-specific knockdown of CTRP9 abolished the protective effects of low-dose exercise against established MI, while cardiac-specific overexpression of CTRP9 protected the heart against established MI. Mechanistically, low-dose exercise upregulated the transcription factor nuclear receptor subfamily 2 group F member 2 by increasing circulating insulin-like growth factor 1 (IGF-1), therefore, upregulating cardiac CTRP9 expression. These results suggest that low-dose exercise protects the heart against established MI via IGF-1-upregulated CTRP9 and may contribute to the development of optimized exercise prescriptions for patients with MI.

Development and Application of an In Vitro Method to Evaluate Anthracnose Resistance in Soybean Germplasm.

Anthracnose caused by Colletotrichum truncatum is a major fungal disease of soybean, especially vegetable soybean (edamame). Studies of this disease have mainly focused on resistance evaluation, but the primary methods used-in vivo inoculation of pods or plants under greenhouse or field conditions-have limitations with respect to accuracy, stability, scale, and environmental safety. In this study, we developed a method for inoculating pods in vitro by soaking in a mycelial suspension. We optimized the crucial components, including the mycelial suspension concentration (40 to 60 mg mL-1), the maturity of the sampled pods (15 days after flowering), and the post-inoculation incubation period (5 days). Application of the mycelial suspension by soaking rather than spraying improved the efficiency of inoculation and made large-scale evaluation possible. Using this method, we evaluated 589 soybean germplasm resources (275 cultivars, 233 landraces, and 81 wild accessions). We identified 25 highly resistant cultivars, 11 highly resistant landraces, but only one highly resistant wild accession. Our results will aid future research on soybean anthracnose resistance, including gene discovery, the elucidation of molecular mechanisms, and the breeding of resistant cultivars.

Identification of Genes Linking Natural Killer Cells to Apoptosis in Acute Myocardial Infarction and Ischemic Stroke.

Natural killer (NK) cells are a type of innate lymphoid cell that are involved in the progression of acute myocardial infarction and ischemic stroke. Although multiple forms of programmed cell death are known to play important roles in these diseases, the correlation between NK cells and apoptosis-related genes during acute myocardial infarction and ischemic stroke remains unclear. In this study, we explored the distinct patterns of NK cell infiltration and apoptosis during the pathological progression of acute myocardial infarction and ischemic stroke using mRNA expression microarrays from the Gene Expression Omnibus database. Since the abundance of NK cells correlated positively with apoptosis in both diseases, we further examined the correlation between NK cell abundance and the expression of apoptosis-related genes. Interestingly, APAF1 and IRAK3 expression correlated negatively with NK cell abundance in both acute myocardial infarction and ischemic stroke, whereas ATM, CAPN1, IL1B, IL1R1, PRKACA, PRKACB, and TNFRSF1A correlated negatively with NK cell abundance in acute myocardial infarction. Together, these findings suggest that these apoptosis-related genes may play important roles in the mechanisms underlying the patterns of NK cell abundance and apoptosis in acute myocardial infarction and ischemic stroke. Our study, therefore, provides novel insights for the further elucidation of the pathogenic mechanism of ischemic injury in both the heart and the brain, as well as potential useful therapeutic targets.

Mitochondrial Quality Control in the Maintenance of Cardiovascular Homeostasis: The Roles and Interregulation of UPS, Mitochondrial Dynamics and Mitophagy.

Maintenance of normal function of mitochondria is vital to the fate and health of cardiomyocytes. Mitochondrial quality control (MQC) mechanisms are essential in governing mitochondrial integrity and function. The ubiquitin-proteasome system (UPS), mitochondrial dynamics, and mitophagy are three major components of MQC. With the progress of research, our understanding of MQC mechanisms continues to deepen. Gradually, we realize that the three MQC mechanisms are not independent of each other. To the contrary, there are crosstalk among the mechanisms, which can make them interact with each other and cooperate well, forming a triangle interplay. Briefly, the UPS system can regulate the level of mitochondrial dynamic proteins and mitophagy receptors. In the process of Parkin-dependent mitophagy, the UPS is also widely activated, performing critical roles. Mitochondrial dynamics have a profound influence on mitophagy. In this review, we provide new processes of the three major MQC mechanisms in the background of cardiomyocytes and delve into the relationship between them.

Melatonin suppresses ER stress-dependent proapoptotic effects via AMPK in bone mesenchymal stem cells during mitochondrial oxidative damage.

BACKGROUND: Bone marrow mesenchymal stem cells (BMSCs) have been used as important cell-based tools for clinical applications. Oxidative stress-induced apoptosis causes a low survival rate after transplantation, and the underlying mechanisms remain unknown. The endoplasmic reticulum (ER) and mitochondria are vital organelles regulated by adenosine monophosphate (AMP)-activated protein kinase (AMPK), especially during oxidative stress injury. Melatonin exerts an antioxidant effect by scavenging free radicals. Here, we aimed to explore whether cytoprotective melatonin relieves ER stress-mediated mitochondrial dysfunction through AMPK in BMSCs after oxidative stress injury. METHODS: Mouse BMSCs were isolated and exposed to H2O2 in the absence or presence of melatonin. Thereafter, cell damage, oxidative stress levels, mitochondrial function, AMPK activity, ER stress-related proteins, and apoptotic markers were measured. Additionally, the involvement of AMPK and ER stress in the melatonin-mediated protection of BMSCs against H2O2-induced injury was investigated using pharmacologic agonists and inhibitors. RESULTS: Melatonin improved cell survival and restored mitochondrial function. Moreover, melatonin intimately regulated the phosphorylation of AMPK and molecules associated with ER stress pathways. AMPK activation and ER stress inhibition following melatonin administration improved the mitochondrial membrane potential (MMP), reduced mitochondria-initiated oxidative damage, and ultimately suppressed apoptotic signaling pathways in BMSCs. Cotreatment with N-acetyl-L-cysteine (NAC) significantly enhanced the antioxidant effect of melatonin. Importantly, pharmacological AMPK activation/ER stress inhibition promoted melatonin-induced cytoprotection, while pharmacological AMPK inactivation/ER stress induction conferred resistance to the effect of melatonin against H2O2 insult. CONCLUSIONS: Our data also reveal a new, potentially therapeutic mechanism by which melatonin protects BMSCs from oxidative stress-mediated mitochondrial apoptosis, possibly by regulating the AMPK-ER stress pathway.