Search Results (296)

This review covers the current state, challenges, and future directions of catalytic combustion technologies for mitigating fugitive methane emissions from the fossil fuel industry. Methane, a potent greenhouse gas, is released from diverse sources, including natural gas production, oil operations, coal mining, and natural gas engines. The paper details the primary emission sources, and addresses the technical difficulties associated with dilute and variable methane streams such as ventilation air methane (VAM) from underground coal mines and low-concentration leaks from oil and gas infrastructure. Catalytic combustion is a useful abatement solution due to its ability to destruct methane in lean and challenging conditions at lower temperatures than conventional combustion, thereby minimizing secondary pollutant formation such as NO_X. The review surveys the key catalyst classes, including precious metals, transition metal oxides, hexa-aluminates, and perovskites, and underscores the crucial role of reactor internals, comparing packed beds, monoliths, and open-cell foams in terms of activity, mass transfer, and pressure drop. The paper discusses advanced reactor designs, including flow-reversal and other recuperative systems, modelling approaches, and the promise of advanced manufacturing for next-generation catalytic devices. The review highlights the research needs for catalyst durability, reactor integration, and real-world deployment to enable reliable methane abatement. Full article

Atherosclerosis (AS), a major contributor to cardiovascular disease, hypertension, and stroke, is associated with significant morbidity and mortality. Antimicrobial peptides (AMPs) 3-13, W3R6, and chensinin-1b were engineered based on the sequence of chensinin-1, originally isolated from the skin secretion of Rana chensinensis. This study investigated their therapeutic potential in ApoE^-/- AS mice and THP-1-derived foam cells, focusing on the regulation of cholesterol metabolism. AMP 3-13 markedly reduced body weight gain, aortic root plaque formation, and plasma cholesterol levels in ApoE^-/- mice. Transcriptomic analysis revealed that AMP 3-13 significantly altered gene expression related to cholesterol metabolism and the PPAR signaling pathway. Specifically, AMP 3-13 upregulated PPARγ, ABCA1, and ABCG1, while downregulating CD36 in aortic root plaques. In THP-1-derived foam cells, AMP 3-13 and its analogs activated the PPARγ–ABCA1/ABCG1 axis, enhancing cholesterol efflux. Concurrently, they inhibited CD36 expression by competing with PPARγ for promoter binding, thereby reducing ox-LDL uptake. These findings suggested that AMP 3-13 and its analogs represented promising therapeutic agents for AS through their ability to reduce cholesterol accumulation in foam cell. Full article

Endothelial hyperpermeability is a hallmark of diverse inflammatory and vascular pathologies, including sepsis, acute respiratory distress syndrome (ARDS), ischemia–reperfusion injury, and atherosclerosis. Traditionally considered a passive return to baseline following stimulus withdrawal, barrier recovery is now recognized as an active, endothelial-driven process. Earlier work identified individual components of this restorative phase, such as cyclic adenosine monophosphate (cAMP)/exchange protein directly activated by cAMP 1 (Epac1) signaling, Rap1/Rac1 activation, vasodilator-stimulated phosphoprotein (VASP) phosphorylation, and targeted cytoskeletal remodeling, as well as kinase pathways involving PKA, PKG, and Src. However, these were often regarded as discrete events lacking a unifying framework. Recent integrative analyses, combining mechanistic insights from multiple groups, reveal that nitric oxide (NO) generated early during hyperpermeability can initiate a delayed cAMP/Epac1 cascade. This axis coordinates Rap1/Rac1-mediated cortical actin polymerization, VASP-driven junctional anchoring, retro-translocation of endothelial nitric oxide synthase (eNOS) to caveolar domains, PP2A-dependent suppression of actomyosin tension, and Krüppel-like factor 2 (KLF2)-driven transcriptional programs that sustain endothelial quiescence. Together, these pathways form a temporally orchestrated, multi-tiered “inactivation” program capable of restoring barrier integrity even in the continued presence of inflammatory stimuli. This conceptual shift reframes NO from solely a barrier-disruptive mediator to the initiating trigger of a coordinated, pro-resolution mechanism. The unified framework integrates cytoskeletal dynamics, junctional reassembly, focal adhesion turnover, and redox/transcriptional control, providing multiple potential intervention points. Therapeutically, Epac1 activation, Rap1/Rac1 enhancement, RhoA/ROCK inhibition, PP2A activation, and KLF2 induction represent strategies to accelerate endothelial sealing in acute microvascular syndromes. Moreover, applying these mechanisms to arterial endothelium could limit low-density lipoprotein (LDL) entry and foam cell formation, offering a novel adjunctive approach for atherosclerosis prevention. In this review, we will discuss both the current understanding of endothelial hyperpermeability mechanisms and the emerging pathways of its active inactivation, integrating molecular, structural, and translational perspectives. Full article

Atherosclerosis (AS), the leading cause of cardiovascular disease (CVD), is the thickening and stiffening of arterial walls, mainly of coronary arteries, the aorta, and the internal carotid artery. Blood flow is restricted by the deposit of lipid-rich macrophages (foam cells), calcium, fibrin, and cellular debris into plaques on the inner lining (tunica intima) of arterial walls. Damaged endothelia become inflamed and accumulate macrophages, monocytes, granulocytes, and dendritic cells, which intensifies plaque formation and increases the risk of myocardial infarction (MI) and thrombosis. Many of the anatomical and physiological abnormalities in arterial walls can be linked to colonic bacteria that produce inflammation-inducing metabolites, e.g., succinate, fumarate, fatty acids (FAs), reactive oxygen species (ROS), lipopolysaccharides (LPS), and trimethylamine-N-oxide (TMAO). TMAO triggers platelet formation, inhibits the synthesis of bile acids (BAs), accelerates the formation of aortic lesions, and upregulates the expression of membrane glycoprotein CD36 (also known as platelet glycoprotein 4) on the surface of platelets and epithelial cells. The ability of internal mammary arteries (IMAs) to produce higher levels of apolipoprotein C-III (apo-CIII) and paraoxonase (PON), compared to coronary arteries, prevents plaque buildup. The tunica intima of IMAs is rich in heparin sulfate and endothelial nitric oxide synthase (eNOS). Increased production of NO relaxes VSMCs and suppresses GTP cyclohydrolase (GTPCH), which lowers blood pressure. Higher levels of prostacyclin (PG12) produced by IMAs inhibit platelet aggregation. IMAs are structurally different from coronary arteries by having a thinner, non-fenestrated, tunica intima without a prominent internal elastic lamina. These characteristics render IMAs ideal conduits in coronary artery bypass graft (CABG) surgery. This review provides information that may explain why IMAs are less affected by inflammatory reactions and more resilient to plaque formation. Full article

Atherosclerosis is a chronic vascular disease characterized by lipid accumulation, endothelial dysfunction, and persistent inflammation, which can ultimately lead to life-threatening complications, such as myocardial infarction and stroke. Current therapies primarily focus on lowering cholesterol levels or preventing blood clot formation. However, the multifactorial and dynamic nature of atherosclerotic progression is not addressed. We designed a therapeutic platform based on onion-derived extracellular vesicles (Onex), nanovesicles originating from onions with excellent biocompatibility and strong anti-inflammatory effects. Onex was engineered with the VHPK peptide, to construct V-Onex, specifically targeting vascular cell adhesion molecule-1 (VCAM-1), which is strongly upregulated in inflamed endothelial cells during atherosclerosis. Engineered V-Onex exhibited excellent biocompatibility and stability without inducing cytotoxicity in human umbilical vein endothelial cells (HUVECs) and THP-1 cells. V-Onex selectively accumulated in inflamed endothelial cells and significantly reduced the expression of inflammatory markers in HUVECs and THP-1 cells. It also suppresses the migration of endothelial cells and reduces their interaction with monocytes, both of which contribute to plaque formation. In THP-1 cells, V-Onex inhibited the uptake of oxidized low-density lipoprotein and reduced foam cell formation. Collectively, V-Onex is a promising modular targeted nanovesicle platform capable of modulating multiple pathological processes associated with atherosclerosis. Full article

This study examines the toxicological effects of carbon nanotubes (CNTs) of different diameters—single-walled CNTs (SWCNT, 2 nm) and multi-walled CNTs (MWCNT, 74 nm)—on two macrophage cell lines, rat alveolar NR8383 cells and human differentiated THP-1. Using standardized exposure conditions and employing an integrated omics approach (transcriptomic and proteomic analyses), both CNT types were found to induce cellular stress responses and inflammation, especially in NR8383 cells, with notable involvement of the Sirtuin signaling pathway. After 24 h, MWCNTs uniquely disrupted lipid metabolism in NR8383 cells, resulting in foam cell formation and syncytia. While SWCNTs were less disruptive to metabolic pathways, they significantly altered gene regulation, particularly RNA splicing mechanisms. The dispersion medium—fetal bovine serum (FBS) versus human surfactant—also modulated the observed toxicological responses, highlighting the critical role of the protein corona in influencing CNT-cell interactions. These findings demonstrate that CNT diameter significantly affects cytotoxicity and cellular response pathways in a cell-type-specific manner. Full article

This study investigates the feasibility of incorporating chemically recycled polyol (glycolysate), derived from semi-rigid polyurethane waste from the building industry, into rigid PUF formulations intended for thermal insulation applications. Glycolysis was performed using a diethylene glycol–glycerol mixture (4:1) at 185 °C in the presence of a dibutyltin dilaurate (DBTDL) catalyst. The resulting glycolysate was characterized by a hydroxyl number of 590 mg KOH/g. Foams containing 5–50% recycled polyol were prepared and described in terms of foaming kinetics, cellular structure, thermal conductivity, apparent density, mechanical performance, dimensional stability, flammability, and volatile organic compound (VOC) emissions. The incorporation of glycolysate accelerated the foaming process, with the gel time reduced from 44 s to 16 s in the sample containing 40% recycled polyol, enabling a reduction in catalyst content. The substitution of up to 40% virgin polyol with recycled polyol maintained a high closed-cell content (up to 87.7%), low thermal conductivity (λ₁₀ = 26.3 mW/(m·K)), and dimensional stability below 1%. Additionally, compressive strength improvements of up to 30% were observed compared to the reference foam (294 kPa versus 208 kPa for the reference sample). Flammability testing confirmed compliance with the B2 classification (DIN 4102), while preliminary qualitative VOC screening indicated no formation of additional harmful volatile compounds in glycolysate-containing samples compared to the reference. The results demonstrate that glycolysate can be effectively utilized in high-performance insulation materials, contributing to improved resource efficiency and a reduced carbon footprint. Full article

Atherosclerosis (AS) is directly linked to the aging and damage of endothelial cells (ECs). As ECs and vascular smooth muscle cells (VSMCs) age, more autocrine and paracrine signals are released, extending a vicious cycle of tissue aging and physiological dysfunction. The recruitment of immune cells to inflamed arteries, including coronary arteries, and an increase in the uptake of oxidised low-density lipoprotein (ox-LDL) by macrophages (foam cells) onto the tunica intima (intima) of coronary arteries restrict blood flow. The inability of aging and damaged ECs to accommodate vast changes in signalling molecules, many produced by gut microbiota, leads to a range of anatomical and physiological arterial anomalies. These include degradation of cardiovascular membranes, fibrosis, calcification, plaque formation, and an increasingly dysfunctional immune system. Changes in the gut microbiome of the elderly have a direct effect on the immune response, as the signalling molecules produced by gut microbiota target specific receptors on inflamed arteries. This review summarizes the anatomical and physiological changes associated with the aging of coronary arteries and emphasizes the conditions leading to AS. The importance of butyrate-producing gut microbiota in preventing AS, especially in the elderly, is discussed. Full article

The internal mammary arteries (IMAs) and coronary arteries share many common characteristics. The inner layer (tunica intima, or intima) of both arteries is lined with a smooth, longitudinally orientated monolayer of endothelial cells (ECs), connective tissue, and an internal elastic lamina that separates the tunica intima from the tunica media (middle layer). The intima of IMAs is lined with an additional protective layer, the neointima, containing vascular smooth muscle cells (VSMCs). The neointima, located between the intima and internal elastic lamina, protects IMAs from damage by assisting in the remodeling of VSMCs. Coarse longitudinal folds in the internal elastic lamina of IMAs partially prevent the infiltration of VSMCs into damaged IMAs, and intimal thickening is thus less likely to occur. Inflamed IMAs resist the migration of monocytes across the endothelial layer and prevent the formation of lipid-rich macrophages (foam cells) within the subintimal or medial layers of arteries. IMAs are thus less likely to form plaques and develop atherosclerosis (AS). Higher levels of prostacyclin (PGI2) in IMAs prevent blood clotting. The anti-thrombotic agents, and production of tumor necrosis factor α (TNF-α), interferon-γ (INF-γ), and visfatin render IMAs more resistant to inflammation. An increase in the production of nitric oxide (NO) by ECs of IMAs may be due to small ubiquitin-like modifier (SUMO) proteins that alter the nuclear factor kappa B (NF-κB) and TLR pathways. The production of reactive oxygen species (ROS) in IMAs is suppressed due to the inhibition of NADPH oxidase (NOX) by a pigment epithelium-derived factor (PEDF), which is a serine protease inhibitor (SERPIN). In this review, a comparison is drawn between the anatomy of IMAs and coronary arteries, with an emphasis on how ECs of IMAs react to immunological changes, rendering them more suited for coronary artery bypass grafts (CABGs). This narrative review covers the most recent findings published in PubMed and Crossref databases. Full article

Type 2 diabetes mellitus (T2DM) affects 90% of diabetes cases and worsens cardiovascular health by causing oxidative stress, which leads to oxidized LDL (oxLDL) and foam cell formation, contributing to atherosclerosis. This study examined the relationship between CD36 gene variants, soluble CD36 (sCD36), oxLDL, and MDA-LDL in T2DM and ST-segment elevation myocardial infarction (STE-T2DM) patients in western Mexico. The analysis included 400 T2DM patients, 400 STE-T2DM patients, and 400 healthy controls. Results showed that STE-T2DM patients were older, mainly male, and had higher rates of smoking, sedentarism, and hypertension. Both diabetic groups exhibited elevated triacylglycerols and low HDL, with significantly higher C-reactive protein in STE-T2DM (p < 0.0001). No significant differences in CD36 gene variant frequencies were found, but sCD36 levels were elevated in STE-T2DM, with associations to specific genotypes. oxLDL was higher in STE-T2DM compared to controls (p = 0.0268). Binary logistic regression analysis identified male sex, younger age, sedentarism, and rs3173798 T/T genotype as independent risk factors for myocardial infarction (AUC: 0.9267, p < 0.0001). Elevated sCD36 levels may reflect atherosclerosis progression in diabetes, indicating the need for further studies to clarify CD36’s role in cardiometabolic dysfunction. These findings highlight CD36’s involvement in oxidative stress responses through its interaction with oxLDL and MDA-LDL, suggesting its potential role as a molecular target in antioxidant defense mechanisms. Full article

Atherosclerosis is a multifactorial, chronic inflammatory disorder characterized by the progressive accumulation of plaque within the arterial wall. Recent research has highlighted the pivotal role of bioactive peptides in modulating vascular homeostasis and inflammation. Among these, salusin-α and salusin-β have emerged as critical regulators of atherogenesis. These peptides are generated via differential proteolytic processing of preprosalusin: an amino acid precursor encoded by the torsin family 2 member A gene. Despite their common origin, salusin-α and salusin-β exhibit divergent biological activities. Salusin-β promotes vascular inflammation by enhancing oxidative stress, activating the nuclear factor kappa B signaling pathway, and upregulating proinflammatory cytokines as well as adhesion molecules, and it also facilitates foam cell formation by increasing the expression of acyl-CoA/cholesterol acyltransferase 1 and scavenger receptors, thereby contributing to plaque progression. In contrast, salusin-α appears to exert protective, anti-inflammatory, and anti-atherogenic effects by increasing the expression of the interleukin-1 receptor antagonist and inhibiting key proinflammatory mediators. Additionally, these peptides modulate the proliferation of vascular smooth muscle cells and fibroblasts, with salusin-β promoting cellular proliferation and fibrosis via calcium and 3′,5′-cyclic adenosine monophosphate-mediated pathways, while the role of salusin-α in these processes is less well defined. Altered plasma levels of salusins have been correlated with the presence and severity of atherosclerotic lesions, suggesting their potential as diagnostic biomarkers and therapeutic targets. This review provides a comprehensive overview of biosynthesis, tissue distribution, and dual roles of salusins in vascular inflammation and remodeling, emphasizing their significance in the pathogenesis and early detection of atherosclerotic cardiovascular disease. Full article

Atherosclerosis (AS) is a complex pathological process characterized by the pivotal involvement of foam cells in its pathogenesis. As the primary cellular components of arterial plaques, foam cells critically determine plaque stability. Foam cells derive mainly from macrophages, and their formation is driven by dysregulated lipid metabolism within these immune cells. Macrophage cholesterol metabolism is a highly regulated process comprising four key phases: uptake, esterification, hydrolysis, and efflux. Under physiological conditions, these four phases maintain a delicate balance. However, disruption of cholesterol homeostasis results in the excessive accumulation of intracellular lipid, promoting the formation of foam cell and inflammasome activation, thereby accelerating the atherosclerotic progression. Therefore, targeting macrophage cholesterol metabolism has emerged as a promising therapeutic approach for AS. This review summarizes the mechanisms underlying macrophage cholesterol metabolism and highlights recent progress in identifying bioactive components of traditional Chinese medicines (TCMs) that mitigate AS through the modulation of macrophage cholesterol homeostasis. These findings may offer novel insights into the development of clinically effective therapies for the prevention of AS. Full article

Systemic lupus erythematosus (SLE) is characterized by autoimmune dysregulation, elevated autoantibody production, and persistent inflammation, predisposing patients to atherosclerosis (AS). Atherogenesis is dependent on lipid homeostasis and inflammatory processes, with the formation of lipid-laden, macrophage-derived foam cells (MDFC) essential for atherosclerotic lesion progression. Elevated cholesterol levels within lipid rafts trigger heightened pro-inflammatory responses in macrophages via Toll-like receptor 9 (TLR9). Artesunate (ART), an artemisinin derivative sourced from Artemisia annua, exhibits therapeutic potential in modulating inflammation and autoimmune conditions. Nonetheless, its impact and mechanisms in SLE-associated AS (SLE-AS) remain largely unexplored. Our investigation demonstrated that ART could effectively ameliorate lupus-like symptoms and atherosclerotic plaque development in SLE-AS mice. Moreover, ART enhanced cholesterol efflux from MDFC by upregulating ABCA1, ABCG1, and SR-B1 both in vivo and in vitro. Moreover, ART reduced cholesterol accumulation in bone marrow-derived macrophages (BMDMs), thereby diminishing TLR9 recruitment to lipid rafts. ART also suppressed TLR9 expression and its downstream effectors in the kidney and aorta of SLE-AS mice, attenuating the TLR9-mediated inflammatory cascade in CPG2395 (ODN2395)-stimulated macrophages. Through bioinformatics analysis and experimental validation, PPARγ was identified as a pivotal downstream mediator of ART in macrophages. Depleting PPARγ levels reduced the expression of ABCA1, ABCG1, and SR-B1 in macrophages, consequently impeding cholesterol efflux. In conclusion, these findings suggest that ART ameliorates SLE-AS by restoring cholesterol homeostasis through the PPARγ-ABCA1/ABCG1/SR-B1 pathway and suppressing lipid raft-driven TLR9/MyD88 inflammation. Full article

This study proposes a continuous preparation strategy for poly (l-lactic acid) (PLLA) scaffolds with oriented hierarchical microporous structures for bone repair. A PLLA-oriented multi-stage microporous bone repair scaffold (hereafter referred to as the oriented multi-stage microporous scaffold) was designed using a novel extrusion foaming technology that integrates fused deposition modeling (FDM) 3D printing with supercritical carbon dioxide (SC-CO₂) microcellular foaming technology. The influence of the 3D-printed structure on the microcellular morphology of the oriented multi-stage microporous scaffold was investigated and optimized. The combination of FDM and SC-CO₂ foaming technology enables a continuous extrusion foaming process for preparing oriented multi-stage microporous scaffolds. The mechanical strength of the scaffold reached 15.27 MPa, meeting the requirements for bone repair in a low-load environment. Notably, the formation of open pores on the surface of the oriented multi-stage microporous scaffold positively affected cell proliferation, differentiation, and activity, as well as the expression of anti-inflammatory and pro-inflammatory factors. In vitro cell experiments (such as CCK-8) showed that the cell proliferation rate in the oriented multi-stage microporous scaffold reached 100–300% after many days of cultivation. This work provides a strategy for the design and manufacture of PLLA scaffolds with hierarchical microcellular structures and biocompatibility for bone repair. Full article

Atherosclerosis (AS), a progressive inflammatory disease of coronary arteries, the aorta, and the internal carotid artery, is considered one of the main contributors to cardiovascular disorders. Blood flow is restricted by accumulating lipid-rich macrophages (foam cells), calcium, fibrin, and cellular debris into plaques on the intima of arterial walls. Butyrate maintains gut barrier integrity and modulates immune responses. Butyrate regulates G-protein-coupled receptor (GPCR) signaling and activates nuclear factor kappa-B (NF-κB), activator protein-1 (AP-1), and interferon regulatory factors (IFRs) involved in the production of proinflammatory cytokines. Depending on the inflammatory stimuli, butyrate may also inactivate NF-κB, resulting in the suppression of proinflammatory cytokines and the stimulation of anti-inflammatory cytokines. Butyrate modulates mitogen-activated protein kinase (MAPK) to promote or suppress macrophage inflammation, muscle cell growth, apoptosis, and the uptake of oxidized low-density lipoprotein (ox-LDL) in macrophages. Activation of the peroxisome proliferator-activated receptor γ (PPARγ) pathway plays a role in lipid metabolism, inflammation, and cell differentiation. Butyrate inhibits interferon γ (IFN-γ) signaling and suppresses NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) involved in inflammation and scar tissue formation. The dual role of butyrate in AS is discussed by addressing the interactions between butyrate, intestinal epithelial cells (IECs), endothelial cells (ECs) of the main arteries, and immune cells. Signals generated from these interactions may be applied in the diagnosis and intervention of AS. Reporters to detect early AS is suggested. This narrative review covers the most recent findings published in PubMed and Crossref databases. Full article