Ultra-stable hollow nanotube conjugated microporous polymer incorporating fluorenyl moieties for Co-capture of PM and CO2.

Conjugated microporous polymers have a highly delocalized π-π conjugated porous skeleton connected by covalent bonds, which can combine their excellent stability with high adsorption, in order to be applied to the study of co-capture of harmful particulate matter (PM) and carbon dioxide (CO2) under high temperature and high humidity conditions. In this paper, fluorene-based coupled conjugated microporous polymers (D-CMPs) with functionalized hollow nanotubes and abundant microporous structures were proposed. Through mechanism exploration and molecular electrostatic potential (MESP) calculation, the capture efficiency, adsorption capacity and selectivity of PM and CO2 in the waste gas stream of carbon-based combustion were analyzed. The results indicate that D-CMPs, with their rigid carbon-based π-conjugated framework, exhibit excellent tolerance under prolonged high-humidity conditions, with a capture efficiency exceeding 99.87% for PM0.3 and exceeding 99.99% for PM2.5. Meanwhile, based on its chemical/thermal stability, it can realize the recycling of adsorption-regeneration. On this basis, the "slip effect" induced by the open three-dimensional hierarchical porous structure of D-CMPs significantly enhances airflow dispersion and improves gas throughput (with a minimal permeation resistance of only 15 Pa). At a pressure of 1 bar and a temperature of 273.15 K, D-CMP-2 exhibited a CO2 adsorption capacity of up to 2.69 mmol g-1. The fitting results of three isothermal adsorption models demonstrate that D-CMPs exhibit an outstanding equilibrium selectivity towards CO2. Therefore, prior to the widespread adoption of low-carbon and clean energy technologies, porous solid materials exhibiting excellent structural stability, equilibrium selectivity, environmental tolerance, and high adsorption capacity emerge as optimal candidates for the treatment of industrial waste gases.

A meta-analysis of everolimus-eluting stents versus sirolimus-eluting stents and paclitaxel-eluting stents in diabetic patients.

OBJECTIVE: We performed this meta-analysis to determine which stent among everolimus eluting stents (EES), sirolimus eluting stents (SES) and paclitaxel eluting stents (PES) should be preferred for the treatment of DM patients. METHODS: A systematic search of publications about randomized controlled trials (RCTs) focused on diabetic patients received EES, SES or PES was conducted. We evaluated the following indicators: target vessel revascularization (TVR), target lesion revascularization (TLR), late luminal loss (LLL), stent thrombosis (ST), myocardial infarction (MI), all-cause mortality and cardiac mortality. RESULTS: EES showed obvious advantages over SES for DM patients, as it induced the lowest rate of target vessel revascularization and target lesion revascularization (TLR) (p = 0.04). In addition, EES induced lower in-segment LLL than PSE and SES and lower in-stent LLL than PES in DM patients (all p < 0.05). Moreover, EES effectively reduced all-cause mortality compared to SES (RR = 0.71, 95% CI: 0.52-0.99, p = 0.04) and MI rates compared to PES (RR = 0.44, 95% CI: 0.26-0.73, p = 0.0002). Furthermore, EES could reduce the ST rate compared with both SES (RR = 0.53, 95% CI: 0.28-0.98, p = 0.04) and PES (RR = 0.18, 95% CI: 0.07-0.51, p = 0.001). CONCLUSION: Among those three types of stents, EES should be the first recommended stent for DM patients.

Effects of ß2/aß2 on oxLDL-induced CD36 activation in THP-1 macrophages.

AIMS: ß2-glycoprotein I/anti-ß2-glycoprotein I antibody complex (ß2/aß2) could promote oxLDL-induced endothelial inflammation through Toll-like receptor 4 (TLR4), therefore accelerates atherosclerosis in patients with anti-phospholipid syndrome (APS). However, effects of ß2/aß2 and TLR4 on oxLDL-induced CD36 activation in macrophages remain to be elucidated and are currently under investigation. MATERIALS AND METHODS: THP-1 macrophages with or without the pre-treatment of TAK-242, a TLR4 inhibitor, were treated with RPMI 1640, oxLDL, oxLDL+ß2/aß2 or oxLDL + LPS.CD36 expression and subsequent intracellular lipid accumulation, cholesterol-transportation-related proteins (ACAT1, ABCG1 and ABCA1) expression, inflammatory cytokines (IL-1ß, TNF-α and IL-6) secretion, focal adhesion kinases (FAK) activation and matrix metalloproteinases (MMP-2 and MMP-9) expression by these THP-1 macrophages were evaluated. Moreover, effects of TLR4 on oxLDL+ß2/aß2-induced peroxisome proliferators-activated receptor-γ (PPAR-γ) expression and CD36 translocation have also been observed. KEY FINDINGS: Compared with oxLDL-treated ones, CD36 expression, intracellular lipid accumulation and FAK activation were inhibited, whereas the levels of inflammatory cytokines and MMPs were upregulated in THP-1 macrophages treated with oxLDL+ß2/aß2 (p < 0.05). Moreover, observed differences between oxLDL-treated and oxLDL+ß2/aß2-treated THP-1 macrophages could be reversed by TAK-242 pre-treatment (p < 0.05). Furthermore, oxLDL+ß2/aß2 promoted PPAR-γ expression and CD36 cytoplasmic translocation in THP-1 macrophages, these effects could also be attenuated by TAK-242 (p < 0.05). SIGNIFICANCE: Through a TLR4 dependent manner, ß2/aß2 inhibited oxLDL-induced CD36 expression, lipid accumulation and FAK activation, while promoted inflammatory cytokines and MMPs expression in THP-1 macrophages, indicating the novel dual roles played by ß2/aß2 in APS-related atherosclerosis.

Pro­atherogenic activation of A7r5 cells induced by the oxLDL/ß2GPI/anti­ß2GPI complex.

A previous study has revealed that oxidized low­density lipoprotein (oxLDL)/ß2­glycoprotein I (ß2GPI)/anti­ß2­glycoprotein I (anti­ß2GPI), an immune complex, is able to activate the Toll­like receptor 4 (TLR4)/nuclear factor κß (NF­κß) inflammatory signaling pathway in macrophages, and consequently enhance foam cell formation and the secretion of prothrombin activators. However, the effects of the oxLDL/ß2GPI/anti­ß2GPI complex on vascular smooth muscle cells have yet to be investigated. The present study investigated whether the oxLDL/ß2GPI/anti­ß2GPI complex was able to reinforce the pro­atherogenic activities of a rat thoracic aorta smooth muscle cell line (A7r5) and examined the underlying molecular mechanisms. The results revealed that the oxLDL/ß2GPI/anti­ß2GPI complex treatment significantly (P<0.05 vs. the media, oxLDL, oxLDL/ß2GPI and ß2GPI/anti­ß2GPI groups) enhanced the pro­atherogenic activation of A7r5 cells, including intracellular lipid loading, Acyl­coenzyme A cholesterol acyltransferase mRNA expression, migration, matrix metalloproteinase­9 and monocyte chemoattractant protein 1 secretion, all via TLR4. In addition, the expression of TLR4 and the phosphorylation of NF­κß p65, p38 and ERK1/2 were also upregulated in oxLDL/ß2GPI/anti­ß2GPI complex­treated A7r5 cells. Pre­treatment with TAK­242, a TLR4 inhibitor, was able to partly attenuate the oxLDL/ß2GPI/anti­ß2GPI complex­induced phosphorylation of NF­κß p65; however, it had no effect on the phosphorylation of extracellular regulated kinase 1/2 (ERK1/2) and p38. Meanwhile, the NF­κß p65 inhibitor ammonium pyrrolidinedithiocarbamate and the ERK1/2 inhibitor U0126, but not the p38 inhibitor SB203580, were able to block oxLDL/ß2GPI/anti­ß2GPI complex­induced foam cell formation and migration in A7r5 cells. Hence, it was demonstrated that the oxLDL/ß2GPI/anti­ß2GPI complex is able to enhance the lipid uptake, migration and active molecule secretion of A7r5 cells via TLR4, and finally deteriorate atherosclerosis plaques. Additionally, it was demonstrated that oxLDL/ß2GPI/anti­ß2GPI complex­induced foam cell formation and migration may be partly mediated by the TLR4/NF­κß signaling pathway and that ERK1/2 may also participate in the process.

[The mechanism of oxLDL/ß2GPI/anti-ß2GPI antibody complex promoting the expression of adhesion molecules in HUVECs].

Objective To investigate the effect of oxidative low-density lipoprotein/ß2 glycoprotein I/anti-ß2 glycoprotein I antibody (oxLDL/ß2GPI/anti-ß2GPI-Ab) complex on the expressions of adhesion molecules in human umbilical vein endothelial cells (HUVECs), and the role of Toll-like receptor 4 (TLR4) signaling pathway during this process. Methods HUVECs were stimulated with simple medium, oxLDL, oxLDL/ß2GPI complex, oxLDL/anti-ß2GPI-Ab complex, oxLDL/ß2GPI/anti-ß2GPI-Ab complex and LPS separately, and then the total mRNA and protein were collected. The mRNA and protein expressions of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and von Willebrand factor (vWF) were detected by real-time quantitative PCR and Western blotting, respectively. Pre-treatment method was applied to explore the influence of TLR4 antagonist TAK-242 (5 µmol/L) and p38MAPK antagonist SB203580 (10 µmol/L) on the expressions of adhesion molecules in HUVECs. THP-1 cell adhesion test was employed to evaluate the effect of oxLDL/ß2GPI/anti-ß2GPI-Ab complex on the ability of attracting monocytes of HUVECs. Results Compared with simple medium, oxLDL/ß2GPI/anti-ß2GPI-Ab complex obviously upregulated the expressions of ICAM-1, VCAM-1 and vWF in HUVECs and promoted the adhesion of THP-1 cells to HUVECs. In addition, these effects were inhibited by the pre-treatment of TAK-242 or SB203580. Conclusion OxLDL/ß2GPI/anti-ß2GPI-Ab complex could up-regulate the expressions of adhesion molecules in HUVECs and promote the adhesion of THP-1 cells to HUVECs, in which TLR4 and p38 MAPK were closely involved.

[The oxLDL/ß2GPI/ß2GPI-Ab complex promotes the migration and the expression of inflammatory cytokines in human umbilical vein endothelial cells].

Objective To study the effects of the complex of oxidized low density lipoprotein/ß2-glycoprotein I/ß2-glycoprotein I antibodies (oxLDL/ß2GPI/ß2GPI-Ab) on the migration of human umbilical vein endothelial cells (HUVECs) and the expression of inflammatory cytokines, and their underlying Toll-like receptor (TLR4) pathway. Methods HUVECs were treated with oxLDL, oxLDL/ß2GPI complex, oxLDL/ß2GPI-Ab complex, oxLDL/ß2GPI/ß2GPI-Ab complex, or lipopolysaccharide (LPS) for a period of time in their corresponding groups. The migration of HUVECs was observed by the wound-healing assay. The mRNA and protein levels of TLR4 in HUVECs were detected by real-time quantitative PCR (qRT-PCR) and Western blotting, respectively. The cells were pretreated with or without TAK-242 (the inhibitor of TLR4) 2 hours before stimulated by corresponding stimulus as described above. Then, the contents of monocyte chemotactic protein-1 (MCP-1), interleukin 1ß (IL-1ß) and IL-6 in cell culture supernatant were determined by ELISA, and their mRNAs were detected by qRT-PCR. Results The oxLDL/ß2GPI/ß2GPI-Ab complex promoted the migration of HUVECs effectively, and increased the expression of TLR4. The oxLDL/ß2GPI/ß2GPI-Ab complex increased the expressions of MCP-1, IL-1ß, and IL-6. TAK-242 could reduce the effects of oxLDL/ß2GPI/ß2GPI-Ab complex. Conclusion The oxLDL/ß2GPI/anti-ß2GPI-Ab complex can promote the migration of HUVECs and the expression of related inflammatory cytokines, and TLR4 may be involved in this process.

[Anti-ß2GPI antibody promotes release of inflammatory and pro-thrombosis molecules from arteries in apolipoprotein E-deficient mice].

Objective To investigate the roles of anti-beta 2 glycoprotein I antibodies (anti-ß2GPI Ab) in the expressions of atherosclerosis(AS)-related inflammatory factors and pro-thrombosis molecules in apolipoprotein E-deficient (ApoE-/-) mice. Methods ApoE-/- mice were randomly divided into normal saline (NS) group, 100 µg anti-ß2GPI Ab group, 100 µg homologous antibody (rabbit-IgG) group and 100 µg ß2GPI/anti-ß2GPI Ab complex group after silastic collars were placed around their carotid arteries by surgery. All mice were fed a high fat diet and corresponding stimuli were given through intraperitoneal injection at 7-day intervals. Six weeks later, the mice were executed. The blockage of carotid arteries of the operated side was observed by HE staining. The expressions of TLR4, tissue factor (TF) and von Willebrand factor (vWF) were detected by immunohistochemistry. The mRNA levels of interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) in aorta were tested by real-time quantitative PCR. Results HE staining showed that the blockage of carotid arteries in antibody group was the most obvious. The immunohistochemistry showed that the expressions of TLR4, TF and vWF in anti-ß2GPI Ab group increased remarkably. Furthermore, the mRNA levels of IL-1ß and TNF-α in anti-ß2GPI Ab group were higher than those in the other groups. Conclusion The anti-ß2GPI antibody promotes the formation of atherosclerotic plaques in mice by up-regulating the release of inflammatory cytokines IL-1ß, TNF-α and thrombosis-related molecules TF, vWF and TLR4, ultimately enhancing the development of AS.

[The oxLDL/ß2GPI/anti-ß2GPI antibody complex promotes A7r5 chemotaxis, migration and lipid accumulation].

Objective To explore the effect of the oxidized low-density lipoprotein/ß2 -glycoprotein I/ß2 glycoprotein I antibody (oxLDL/ß2GPI/ß2GPI-Ab) complex on the migration, chemotaxis and lipid accumulation of rat thoracic aortic smooth muscle A7r5 cell line, and unveil the role of Toll-like receptor 4 (TLR4) pathway during the process. Methods A7r5 cells were cultured in vitro with or without the pretreatment of TAK-242, a TLR4 inhibitor. Then the cells were stimulated by oxLDL, oxLDL/ß2GPI complex, ß2GPI, ß2GPI-Ab, ß2GPI/ß2GPI-Ab complex or oxLDL/ß2GPI/ß2GPI-Ab complex. Total RNA was extracted from the cells and the mRNA levels of monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9) and acetyl-CoA acetyltransferase 1 (ACAT1) were evaluated by real-time quantitative PCR. The cell supernatants were collected, and the protein levels of MCP-1 and MMP-9 were determined by ELISA. The migration of A7r5 was observed through wound-healing test. A7r5 cells pretreated with or without TAK-242 were stimulated by oxLDL or oxLDL/ß2GPI/ß2GPI-Ab complex, and the content of total cholesterol (TC) and free cholesterol (FC) in them were measured by corresponding test kits. Then the level of intracellular cholesterol ester (CE) was calculated. Results The oxLDL/ß2GPI/ß2GPI-Ab complex promoted the migration and cholesterol accumulation, and up-regulated the expressions of MCP-1, MMP-9 and ACAT1 in A7r5 cells. In addition, the application of TLR4 inhibitor, TAK-242, suppressed these effects. Conclusion oxLDL/ß2GPI/ß2GPI-Ab complex contributes to the process of atherosclerosis through promoting the migration, chemotaxis and lipid accumulation of a7r5 in a TLR4-dependent manner.