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This study exhibits potential prospects in thermal management fields and promising alternatives for the thermal harvesting of renewable energy.

This study aims to evaluate the effect of purinergic ligand-gated ion channel 7 receptor (P2X7R) antagonist A438079 in kidneys of children with primary nephrotic syndrome (PNS). In vitro, human podocytes were respectively stimulated with oxLDL (80 µg/ml), A438079 (10 µmol/L), or the compound oxLDL and A438079 together. CXC chemokine ligand 16 (CXCL16) and P2X7R expression levels were detected by Western blot and immunofluorescence assay, respectively. Immunofluorescence assay was used to detect Dil-oxLDL, and a Colorimetric Cholesterol Detection Kit was used for quantitative determination. Our results demonstrated that CXCL16 and P2X7R expression levels were remarkably increased in the renal tissue from children with PNS, particularly in the same location. Furthermore, in contrast to children with minimal change disease, the expressions of P2X7R and CXCL16 in renal tissue of children with focal segmental glomerulosclerosis were more obvious. In vitro, CXCL16 and P2X7R expression levels in human podocytes stimulated with oxLDL were markedly elevated accompanying higher intracellular lipid accumulation compared with the normal control group. In addition, pretreatment of human podocytes with A438079 before the start of oxLDL stimulation causes a significant reduction in CXCL16 expression and a decrease in lipid accumulation. Overall, CXCL16 and P2X7R may participate in the progression of PNS. The lipid accumulation reduction caused by A438079 may be through deregulating the CXCL16 pathway, suggesting that there is a potential role for P2X7R antagonists to remedy PNS.

Retinal neovascularization (RNV), a pathological process shared among diabetic retinopathy, retinopathy of prematurity and other retinopathies, has been widely studied, but the mechanism remains unclear. In this study, the mechanism by which the interleukin (IL)‐23/IL‐17 axis regulates RNV in oxygen‐induced retinopathy (OIR) model mice and in cell experiments in vitro was characterized. In the retinas of OIR mice, IL‐23/IL‐17 axis activation was increased and regulated RNV formation, and this effect was accompanied by increased macrophage recruitment and nucleotide‐binding domain leucine‐rich repeat and pyrin domain containing receptor 3 (NLRP3) inflammasome activation. Moreover, inhibiting the IL‐23/IL‐17 axis reduced the number of macrophage and the expression and activation of NLRP3 inflammasome. On the other hand, recombinant (r) IL‐23p19 and rIL‐17A promoted the expression and activation of NLRP3 inflammasome, and the proliferation and migration of macrophages. Furthermore, macrophage elimination decreased the activation of IL‐23/IL‐17 axis and the expression and activation of NLRP3 inflammasome. In summary, our experiments showed that the IL‐23/IL‐17 axis promoted the formation of RNV by activating the NLRP3 inflammasome in retinal macrophages of an OIR mouse model.

Diazepam binding inhibitor (DBI)-translocator protein (18kDa) (TSPO) signaling in the retina was reported to possess coordinated macroglia-microglia interactions. We investigated DBI-TSPO signaling and its correlation with vascular endothelial growth factor (VEGF), neurotrophic or inflammatory cytokines in neovascular retinopathy, and under hypoxic conditions. The vitreous expression of DBI, VEGF, nerve growth factor (NGF), and interleukin-1beta (IL-1β) were examined in proliferative diabetic retinopathy (PDR) patients with or without anti-VEGF therapy and nondiabetic controls. Retinal DBI-TSPO signaling and the effect of the anti-VEGF agent were evaluated in a mouse model of oxygen-induced retinopathy (OIR). Interactions between Müller cell-derived VEGF and DBI, as well as cocultured microglial cells under hypoxic conditions, were studied, using Western blot, real-time RT-PCR, enzyme-linked immunosorbent assay (ELISA), flow cytometry, and immunofluorescent labeling. Results showed that vitreous levels of DBI, VEGF, NGF, and IL-1β were significantly higher in PDR patients compared with controls, which further changed after anti-VEGF therapy. A statistical association was found between vitreous DBI and VEGF, NGF, IL-1β, and age. The application of the anti-VEGF agent in the OIR model induced retinal expression of DBI and NGF, and attenuated inflammation and microglial cell activation. Inhibition of Müller cell-derived VEGF could increase its DBI expression under hypoxic conditions, while the DBI-TSPO signaling pathway is essential for anti-VEGF agents exerting anti-inflammatory and neuroprotective effects, as well as limiting inflammatory magnitude, promoting its neurotrophin production and anti-inflammatory (M2) polarization in microglial cells. These findings suggest the beneficial effect of anti-VEGF therapy on inflammation and neurotrophy of retinal glial cells through modulation of the DBI-TSPO signaling pathway.

The composites with high thermal conductivity (TC) have attracted extensive attention in thermal management fields. Incorporating a three dimensional (3D) thermal transport framework in polymer is one of the most effective ways to improve the TC of composites. However, most micro-zone of those 3D thermal transport framework is filled with polymers with very low TC, leading to limited TC improvement of polymer composites. Herein we presented a novel 3D boron nitride (BN)/nickel foam (NF)/epoxy (EP) composite with high TC. Results indicated that as a good reinforced filler with high TC, BN was homogeneously dispersed in epoxy and fully filled into 3D NF micro-zone to get obvious TC increase of the BN/NF/EP composites. With the micro-zone enhancement strategy, the prepared BN/NF/EP-50 composite demonstrated excellent thermal conductive property. The obtained TC (5.14 W m−1 K−1) is approximately 24 and 5 times higher than that of epoxy and NF/EP composite, respectively. This research potentially provides a unique way to design and fabricate high TC 3D materials with the micro-zone enhancement strategy.

CeO2 was used as the only oxidant for aniline polymerization, and polyaniline (PANI) was grown on CeO2 surface to form CeO2@PANI nanocomposites. SEM and TEM showed that the CeO2@PANI composites were nanorods in a core-shell structure. XPS indicated that CeO2-core was reduced by aniline into Ce3+, which was then captured by the PANI-shell. Then the passive ability of CeO2@PANI coating on steels was explored. EIS showed that the impedance modulus of the CeO2@PANI coating exceeded 108 Ω·cm2 after accelerated immersion. The SVET and XPS confirmed that PANI polarized the anodic reaction, Ce3+ suppressed the cathodic reaction, and PO43- formed complex precipitation. Some high-valent metal oxides can directly oxidize the aniline polymerization to form MO@PANI hybrid particles. The cations obtained by the metal oxide reduction can be captured by PANI and participate in passivation together with dopants. This study provides a new kind of nanocomposite fillers that can effectively passivate steel substrates within epoxy coatings for long-time protection.

Nephrotic syndrome (NS) is one of the most common causes of chronic kidney disease in the pediatric population. Hyperlipidemia is one of the main features of NS. The present study investigated the role of CXC motif chemokine ligand 16 (CXCL16) and ADAM metallopeptidase domain 10 (ADAM10) in oxidized low‑density lipoprotein (oxLDL)‑stimualted podocytes and the underlying mechanisms. CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting. Cell migration assays were conducted to assess the migration of oxLDL‑treated podocytes. CXCL16 or ADAM10 overexpression and knockdown assays were conducted. The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group. Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups. By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups. The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton. Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.

Primary nephrotic syndrome (PNS) is the commonest glomerular disease affecting children. Previous studies have confirmed that CXC motif chemokine ligand 16 (CXCL16) is involved in the pathogenesis of PNS. However, the exact mechanisms underlying the pathogenesis of PNS remain to be elucidated. Thus, the present study aimed to elucidate the role of CXCL16 in PNS. It was found that the expression of CXCL16 and extracellular signal‑regulated kinases 1 and 2 (ERK1/2) were significantly increased in clinical PNS renal tissues using reverse transcription‑quantitative PCR, western blot analysis and immunohistochemistry. Lentivirus overexpression or short hairpin RNA vector was used to induce the overexpression or knockdown of CXCL16 in podocytes, respectively. Overexpression of CXCL16 in podocytes could decrease the cell proliferation and increase the migration and apoptosis, whereas CXCL16 knockdown increased cell proliferation and decreased cell migration and apoptosis. Results of the present study further demonstrated that ERK2 protein expression was regulated by CXCL16. The knockdown of ERK2 expression reversed the effects of CXCL16 on the proliferation, apoptosis, migration and epithelial mesenchymal transition (EMT) of podocytes. Collectively, the findings of the present study highlighted that the CXCL16/ERK1/2 pathway regulates the growth, migration, apoptosis and EMT of human podocytes.

Background: The current study was done to identify key genes associated with Kawasaki disease (KD). Methods: Three datasets were collected from Gene Expression Omnibus (GEO) database. Then, differentially expressed genes (DEGs) analysis, gene ontology (GO) annotation, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were performed. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression levels of DEGs in KD. Receiver operating characteristic (ROC) analysis was performed to assess the diagnostic value of DEGs. Results: In total, 2923 DEGs (1239 up- and 1684 down-regulated genes) were detected in KD. Ribosome, Leishmaniasis, and Tuberculosis significantly enriched KEGG pathways of DEGs. Six DEGs, including ADM, S100A12, ZNF438, MYD88, FCGR2A, and FCGR3B, were selected for qRT-PCR validation. Except for MYD88, the qRT-PCR results displayed similar expression patterns with that in our integrated analysis. ROC analysis revealed the diagnostic value of the six DEGs. Conclusions: Our study was expected to provide clues toward understanding the pathophysiology of KD inflammation.

Improving the heat dissipation efficiency of electronic products is the key to the design of many modern electronic and mechanical systems. Herein, we combined the 3D network fabricating with the way of micron-nano reinforcement to prepare high thermal conductivity and excellent thermal stability composites. Epoxy resin was used as the matrix, while the silicon carbide foam (f-SiC) as skeleton and the BN/nano-SiC as thermally conductive fillers. The thermal conductivity of the EP/f-SiC/BN/nano-SiC composite reaches 3.5 W·m− 1·K− 1, which is about 16.6 times higher than that of pure epoxy resin. The characterization results of TC and infrared thermography images indicate that the EP/f-SiC/BN/nano-SiC composite possess superior heat transport performance. Meantime, the EP/f-SiC/BN/nano-SiC composite have excellent thermal stability, the THRI of EP/f-SiC/BN/nano-SiC reaches 195.8℃, which is 21.3℃ higher than that of pure EP. This work would provide a new strategy for improving the TC of polymers by using other 3D skeletons and micron-nano fillers, and is conducive to the development of high thermal conductivity and excellent thermal stability materials.

Single-stage oil/water separation membranes usually suffer from weak chemical stability, susceptible mechanical damage and relatively low permeating flux, and the sophisticated preparation processes also limit their massive utilization. In this work, Cu(OH)2 nanoneedles coated copper mesh (CM) is prepared by simple and eco-friendly anodic oxidation at a current density of 4 mA/cm2 for 6 min, which is the most efficient route reported so far. The mesh exhibits outstanding superhydrophilicity and underwater superoleophobicity towards various oils with contact angles up to 164.9°, achieving superior oil/water separation efficiency of above 99.5% and ultrahigh permeating flux of 191 160 L·m−2h−1 solely driven by gravity. Impressively, the Cu(OH)2/CM demonstrates excellent chemical stability and anti-fouling performance when exposed to acidic and strongly alkaline solutions, saturated NaCl solution and various organic solvents. High durability to withstand mechanical challenges, e.g. high-power sonication and sand abrasion, is experimentally confirmed owing to strong cohesional strength of Cu(OH)2 nanoneedles on CM surface. Importantly, the Cu(OH)2/CM exhibits favorable long-term recyclability with stable microstructure morphologies even after 50 cycles. These distinct advantages endow the Cu(OH)2/CM to be an ideal candidate to efficiently separate oil pollutants from water. The oil/water separation mechanisms are proposed based on the concept of intrusion pressure.

Superhydrophobic surfaces with special wettability have a promising potential for self-cleaning, anti-fouling, and anti-corrosion applications. However, the practical applications of superhydrophobic coatings are currently limited by their poor mechanical strength and hydrophobic durability. Here, we report a superhydrophobic epoxy (EP) composite coating with improved durability, achieved by a dual interfacial enhancement. First, melt extrusion technology was used to enhance the bonding force between EP and polytetrafluorethylene (PTFE). Then, combining dopamine self-polymerization and sol-gel approaches, the interfacial strength between graphene-polydopamine (GP) and SiO2 was enhanced by in-situ growth of SiO2 on the GP surface. After modification with 1H,1H,2H,2H-perfluorooctyltriethoxysilane (POTS), the superhydrophobic EP-PTFE/GP-SiO2-POTS coating (WCA = 156.3 ± 1.5°, WSA = 3.5 ± 0.5°) was successfully prepared on a steel surface by electrostatic spraying. With the enhanced interfacial strength, the prepared composite coating demonstrated excellent mechanical performance, and could withstand 105 abrasion cycles with only 54.4 mg weight loss. Moreover, due to the induction effect of graphene, a special multilayered nano-micro-nano structure was formed by the evenly distributed nano-SiO2 particles on the coating surface, which is beneficial to extend its superhydrophobic duration. The prepared coating can maintain its superhydrophobicity even after being scratched or immersed in 3.5 wt% NaCl solution for 60 days. Therefore, the prepared superhydrophobic coating demonstrates great potential for application in anti-fouling, drag reduction, and other fields.

Nonresponse is a very common phenomenon in survey sampling. Nonignorable nonresponse – that is, a response mechanism that depends on the values of the variable having nonresponse – is the m...

In this paper, a versatile low-cost and simple spraying process was reported for fabricating epoxy resin (EP)/fluorinated ethylene propylene (FEP)/modified ZnO (m-ZnO) superhydrophobic coating (EP/FEP/m-ZnO). The ZnO nanoparticles were modified by the low surface-energy material of stearic acid, and the pore-forming agent (NH4HCO3) was used to build micro/nano-structures. Results showed that the composite coating with 32 wt.% of m-ZnO, 5 wt.% of NH4HCO3 exhibits the optimum superhydrophobicity, with water contact angle (WCA) of 160° and sliding angle of 2°. More importantly, the WCA of the as-prepared composite coating still maintains more than 130° under strong acid or 3.5 wt.% NaCl aqueous solution for 270 h immersion, which demonstrates the excellent anti-corrosive performance of EP/FEP/m-ZnO superhydrophobic coating. The WCA of the EP/FEP/m-ZnO coating still kept 136° and only gained weight loss of 1.04% after being rubbed with 300 cycles, and the weight loss of EP/FEP coating is 18.85% under the same condition. All the above aspects are the direct evidences for the highest wear resistance of EP/FEP/m-ZnO superhydrophobic coating. Furthermore, the adhesive ability of the EP/FEP/m-ZnO composite coating was satisfied with the requirements of Grade 1, that standing for strong adhesion between the coating and substrate. Simultaneously, the soil and fly ash could be easily cleaned from the surface of superhydrophobic coating with flowing droplets, that showing unique self-cleaning property. Furthermore, the EP/FEP/m-ZnO superhydrophobic coating has excellent anti-corrosion performance. It is believed that the nano/micro structure formed by the inorganic filler m-ZnO and pore-forming agent of NH4HCO3 plays an important role. The suitable magnitude of pores has a positive meaning on fabricating the EP/FEP/m-ZnO superhydrophobic coating. The multifunctional coating has a high application value in condition of wear resistance, self-cleaning and anticorrosion, this facile and economic method may offer an effective strategy for surface and interface science and even industrial production.

A multifunctional super-hydrophobic polyethersulfone (PES)/1H, 1H, 2H, 2H-perfluorooctyltriethoxysilane (POTS)/MoS2–polydopamine (PDA)–TiO2 coating was fabricated by a simple spraying method that involved two consecutive steps of dopamine (DA) self-polymerization on MoS2 sheet surface and in situ growth of TiO2 nano-particles. The coating possessed super-hydrophobicity with the water contact angle (WCA) of 159 ± 2° and excellent self-cleaning property. Remarkable mechanical stability was obtained with original super-hydrophobicity even after 10,000 abrasion cycles of damage under the load of 50 KPa. It also retained high WCA of 150° after exposure to strong acids (HCl, pH = 1) and bases (NaOH, pH = 14) for at least 30 h. Compared with the uncoated aluminum substrate, the corrosion resistance of the coating was significantly enhanced with lower corrosion current density of 2.7 × 10−9 A/cm2 and higher corrosion potential of −41 mV after immersion in a 3.5 wt% NaCl solution for 15 days. All these results suggest the super-hydrophobic PES/POTS/MoS2–PDA–TiO2 coating exhibits great potential as a functional surface in a wide range of practical applications.

The purpose of our research is to elucidate whether oxLDL activates P2X7R in cultured human podocytes and if the activation of P2X7R leads to podocyte apoptosis. Additionally, we explore the underlying mechanism involved in podocyte apoptosis. Immortalized human podocytes were incubated with oxLDL (80 µg/ml), P2X7R antagonist A438079 (10 µM), or the compound of A438079 and oxLDL for 48 h, respectively. Cellular apoptosis and ROS were evaluated using flow cytometer. P2X7R, Bax, and Caspase-3 protein expression were detected by western blot and immunofluorescence analysis.The expression of P2X7R, ROS, Bax, and Caspase-3 in human podocytes incubated with oxLDL was significantly up-regulated and was found to have higher intracellular lipid accumulation and podocyte apoptosis compared with the NC group. However, co-administration with A438079, ROS, Bax, and Caspase-3 expression both significantly down-regulate as well as lower lipid accumulation and cellular apoptosis in the oxLDL-induced podocyte group. We revealed that P2X7R is involved in the regulation of oxLDL-treated podocytes. Additionally, we found that the anti-apoptotic effect of A438079 is correlated with ROS, Bax, and Caspase-3 expression down-regulated.

Carbon nanotubes (CNTs), as a carrier of diethylenetriaminepenta(methylphosphonic acid) (DTPMPA), combining with flake zinc and PVDF powders, were used to fabricate a novel organosilicon epoxy resin-based (EP) composite coating (EP/iDCNTs/Zn/PVDF) for antiscaling and anti-corrosion purposes. Compared with EP coating, the EP/iDCNTs/Zn/PVDF composite coating exhibited unique antiscaling properties with the CaCO3 deposition on the coating surface decreased by 81.6%. It was mainly because the coating surface contains DTPMPA, and Zn2+released by corrosion of Zn powder, which jointly inhibited the deposition behavior of CaCO3. Meanwhile, the fabricated composite coating hardly adhered by CaCO3 crystals which was due to its higher hydrophobicity. Moreover, anti-corrosion tests proved that the prepared composite coating's impedance modulus was about 2 orders higher than that of the EP coating. This was ascribed to the improving shielding effect of fillers and high hydrophobicity of coating, preventing the water and oxygen molecules from penetrating into the composite coating.

Ionic liquids (ILs) are promising high-performance lubricants with remarkable lubrication and antiwear capabilities in tribology. In this article, first solid-state (at room temperature) IL-incorpo...

As one of the most promising methods for H2O2 production, H2O2 electroproduction has received increasingly more attention. In this study, a spherical particle polydopamine (pDA) modified carbon felt (noted as ht-pDA/ACF) for H2O2 production was fabricated. At a constant potential of 2.0 V and pH of 1.0, the H2O2 production of the ht-pDA/ACF cathode reached 220 mg/L after 6 h of electrolyzing, compared to the 30 mg/L H2O2 production of raw carbon felt. Firstly, the spherical pDA exposes more active sites that are favorable to the 2e− ORR compared to pDA film. Secondly, the ring cleavage and re-cyclization of indole structure in the pDA during electrolyzing could form the radicals that act as the intermediate to the H2O2 formation. This research exhibits a low-cost method to modify carbon materials for effective H2O2 electroproduction. The ht-pDA/ACF cathode is promising for green H2O2 production and wastewater treatment.

Polymer-based composites with efficient thermal energy dissipation performance can be prospectively applied in electronics and military industry. However, significantly improving the thermal conductivity (TC) of polymer-based composites is still challenging. Herein, 3D sulfanilamide-modified expanded graphite/epoxy (EG-SA/EP) composites with interconnected filler network were successfully prepared by a pre-filling and hot-pressing method. Benefiting from the interconnected network, the composite with 70 wt% EG-SA demonstrated ultrahigh bulk TC of 98 W/m·K (which exceeds some commercially-used metals) and up to 44,445% TC enhancement efficiency. Meanwhile, the EG-SA/EP composites exhibited excellent electromagnetic interference shielding performance of 85 dB (which is sufficient to block 99.9999997% of incident radiation), high electric conductivity of 7153 S/m and excellent thermal infrared response capability (the time to raise surface temperature from 19 to 82 °C is only 3 s). As for the mechanism of heat transfer, the 3D structure of EG-SA maintained through epoxy pre-filling in EG-SA is the main reason for the significantly improved TC. This is because the new method enables EG-SA to build a unique dense interconnected network in composites in the subsequent hot-pressing process, but the traditional direct mixing method easily destroys the inherent micro-3D structure of EG. The above excellent performances endow the EG-SA/EP composites with huge potential application value.

Activation of the purinergic P2X7 receptor (P2X7R) has been associated with the development of experimental nephritis. Therefore, the current study aimed to explore the mechanism of P2X7R in renal injured mice with adriamycin (ADR) nephropathy. The protective effect of a P2X7R antagonist on the kidneys of mice with ADR nephropathy was also evaluated. Nephropathy was induced by a single intravenous injection of ADR (10.5 mg/kg). A total of 6 h before the model was established, the P2X7R antagonist A438079 (100, 200 and 300 µmol/kg) was injected into the mice, which was subsequently administered daily for 1 week by intraperitoneal injection. Subsequently, all mice were sacrificed, after which blood, 24 h-urine and the kidneys were collected. The levels of albumin (ALB) and total cholesterol (TC) in the serum, along with urine protein content at 24 h were determined using an automatic biochemical analyzer. The levels of IL-1β and IL-18 were additionally detected in the renal tissues by ELISA. Moreover, the expression of P2X7R, oxidized (ox)-low density lipoprotein (LDL), C-X-C motif chemokine ligand 16 (CXCL16), Bax, caspase-3 and NLRP3 in renal tissues was detected by immunohistochemistry. Apoptosis in the renal tissues was observed using the TUNEL assay. The results demonstrated that compared with the control group, decreased weight, increased proteinuria, decreased serum ALB and increased serum TC was observed in the ADR group. The expression of IL-1β, IL-18, P2X7R, ox-LDL, CXCL16, Bax, caspase-3 and NLRP3, as well as cellular apoptosis in the renal tissues of the ADR group, was significantly increased in the ADR group compared with the control. However, compared with the ADR group, the changes in all indices in the ADR + A438079 groups were attenuated. Overall, P2X7R, ox-LDL and CXCL16 may be associated with ADR nephropathy, while inhibition of P2X7R may reduce the expression of ox-LDL by downregulating the CXCL16 pathway to alleviate kidney injury in mice with ADR nephropathy. Furthermore, activated P2X7R may promote the release of inflammatory cytokines IL-1β and IL-18 through the downstream P2X7R/NLRP3 pathway and upregulate the expression of Bax and caspase-3 to promote apoptosis, which participates in the process of ADR nephropathy. Inhibiting P2X7R may also reduce the release of IL-1β and IL-18 by downregulating the P2X7R/NLRP3 pathway, downregulating the expression of Bax and caspase-3, and reducing apoptosis, thereby alleviating kidney injury in mice with ADR nephropathy.

Background To investigate the difference in retinal nerve fiber layer (RNFL) thickness, choroidal thickness (CT) and superficial retinal vessels between thyroid-associated ophthalmopathy (TAO) patients and healthy controls. To identify the potential influencing factors for these parameters and evaluate their diagnostic abilities in TAO. Methods Twenty active TAO patients, 33 inactive TAO patients and 29 healthy participants were enrolled. TAO patients were divided according to the clinical activity score (CAS). RNFL thickness and CT were measured by HD-OCT, while foveal avascular zone (FAZ), vascular density and perfusion density were measured by optical coherence tomography angiography (OCTA). SPSS software was used for statistical analysis. Results Active TAO patients had thinner RNFL thickness than the other two groups (P P P P = 0.045, P = 0.001). The inactive TAO group had significantly higher vascular density than the other two groups (all P P = 0.045, P = 0.001), as well as the average values (P = 0.032). The FAZ area was positively correlated with intraocular pressure (r = 0.274, P = 0.013), while it was negatively correlated with axial length (r = − 0.344, P = 0.002). The vascular density and perfusion density were not significantly correlated with different clinical variables (all P > 0.05). The AUC analysis indicated these parameters also exhibited a significant discriminatory power in TAO diagnosis. Conclusions TAO patients had significant variations in RNFL thickness, choroidal thickness, FAZ area and superficial retinal vessels. These parameters appeared to be potential adjuncts in the evaluation of TAO patients.

The formation of retinal neovascularization (RNV) is the primary pathological process underlying retinopathy of prematurity (ROP). Previous studies have shown that inflammatory factors are related to the formation of RNV. Tumor necrosis factor-α (TNF-α), as an important factor in the inflammatory response, is involved in the regulation of RNV formation. However, the mechanism through which TNF-α inhibition reduces RNV formation is not fully clarified. Therefore, the purpose of this study was to explore the effect of etanercept, an inhibitor of TNF-α, on RNV, and its possible mechanism. In vivo, an oxygen-induced retinopathy (OIR) mouse model was used to determine the effect of etanercept on the formation of RNV by performing immunostaining. The effect of etanercept on tumor necrosis factor receptor-associated factor 2 (TRAF2), pro-angiogenic-related factors, and pro/anti-inflammatory factors in OIR mice was assessed by real-time PCR and Western blotting. In vitro, the effect of etanercept on TNF-α-induced human retinal microvascular endothelial cell tube formation was evaluated by tube formation assays, and the potential mechanism of etanercept was explored by Western blotting. In vivo, etanercept reduced the area of RNV and decreased the expression of TRAF2 in the OIR mouse model. Etanercept also suppressed the expression of several pro-angiogenic factors and regulated the pro/anti-inflammatory factors. In vitro, etanercept reduced endothelial cell tube formation by inhibiting activation of the NF-κB signaling pathway. Etanercept can regulate pro/anti-inflammatory factors and reduce the expression of pro-angiogenic factors by inhibiting NF-κB phosphorylation, thereby reducing RNV formation.