Graphene-Reinforced Biodegradable Resin Composites for Stereolithographic 3D Printing of Bone Structure Scaffolds

A biodegradable UV-cured resin has been fabricated via stereolithography apparatus (SLA). The formulation consists of a commercial polyurethane resin as an oligomer, trimethylolpropane trimethacrylate (TEGDMA) as a reactive diluent and phenylbis (2, 4, 6-trimethylbenzoyl)-phosphine oxide (Irgacure 819) as a photoinitiator. The tensile strength of the three-dimensional (3D) printed specimens is 68 MPa, 62% higher than that of the reference specimens (produced by direct casting). The flexural strength and modulus can reach 115 MPa and 5.8 GPa, respectively. A solvent-free method is applied to fabricate graphene-reinforced nanocomposite. Porous bone structures (a jawbone with a square architecture and a sternum with a round architecture) and gyroid scaffold of graphene-reinforced nanocomposite for bone tissue engineering have been 3D printed via SLA. The UV-crosslinkable graphene-reinforced biodegradable nanocomposite using SLA 3D printing technology can potentially remove important cost barriers for personalized biological tissue engineering as compared to the traditional mould-based multistep methods

Modified Ni-carbonate interfaces for enhanced CO₂ methanation activity: tuned reaction pathway and reconstructed surface carbonates

A Ni/Zr-La2O2CO3 catalyst with interfaces between Ni metal and Zr-modified carbonate support was used for atmospheric CO2 methanation reaction, exhibiting 81% conversion and 99.6% CH4 selectivity at 300 °C. The Zr4+ ions incorporated in La2O2CO3 lattices properly strengthened the Ni-carbonate interaction for enhancing the Ni dispersion and hydrogen activation ability of the catalyst. The Zr-modification could also tune the surface basic property for promoting the adsorptive dissociation of CO2. In-situ DRIFT spectra demonstrated that only the hydrogenation reaction pathway of formate intermediates was proceeded in Ni/La2O2CO3-catalyzed CO2 methanation. As a contrast, the hydrogenation pathways of CO and formate intermediates with relatively high activity were co-existed at the modified Ni-Zr-La2O2CO3 interfaces. Furthermore, the isotopic data evidenced that dynamic reconstruction and interconversion of the surface carbonate species occurred in the reaction, which might contribute to the key steps of CO2 dissociation and intermediates transformation.We thank National Natural Science Foundation of China (22178161) and National Key R&D Program of China (2018YFE0122600) for financial support

Table2_Functional analysis of differently expressed ferroptosis-related genes in patients with mitral valve prolapse.XLSX

Background: The prevalence of mitral valve prolapse (MVP) in heart valvular diseases is globally increasing. However, the understanding of its etiology and pathogenesis is limited. So far, the relationship between ferroptosis-related genes and long non-coding RNAs (lncRNAs) in MVP remains unexplored. This study investigates the potential pathogenesis of ferroptosis-related genes in MVP and provides a therapeutic target for the disease.Methods: Blood samples from patients with MVP and healthy volunteers were collected for transcriptomic sequencing to analyze the expression of ferroptosis-related differentially expressed genes (DEGs) and differentially expressed long non-coding RNAs (DElncRNAs Co-expression network of ferroptosis-related DEGs and DElncRNAs. Furthermore, this work conducted GO and KEGG enrichment analyses.Results:CDKN2A, SLC1A4, ATF3, and other core genes related to the mitral valve prolapse were screened out. CDKN2A, SLC1A4, and ATF3 genes were at the core position of the network, regulated by numerous lncRNAs. Notably, these genes are primarily involved in the extracellular region and p53 signaling pathway.Conclusion: In summary, CDKN2A, SLC1A4, and ATF3 regulate the pathophysiological process of MVP and are potential therapeutic targets.</p

Table_6_Genome-wide analysis of RNA-binding proteins co-expression with alternative splicing events in mitral valve prolapse.xlsx

ObjectivesWe investigated the role and molecular mechanisms of RNA-binding proteins (RBPs) and their regulated alternative splicing events (RASEs) in the pathogenesis of mitral valve prolapse (MVP). MethodsFor RNA extraction, we obtained peripheral blood mononuclear cells (PBMCs) from five patients with MVP, with or without chordae tendineae rupture, and five healthy individuals. High-throughput sequencing was used for RNA sequencing (RNA-seq). Differentially expressed genes (DEGs) analysis, alternative splicing (AS) analysis, functional enrichment analysis, co-expression of RBPs, and alternative splicing events (ASEs) analysis were conducted.ResultsThe MVP patients exhibited 306 up-regulated genes and 198 down-regulated genes. All down- and up-regulated genes were enriched in both Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Furthermore, MVP was closely associated with the top 10 enriched terms and pathways. In MVP patients, 2,288 RASEs were found to be significantly different, and four suitable RASEs (CARD11 A3ss, RBM5 ES, NCF1 A5SS, and DAXX A3ss) were tested. We identified 13 RNA-binding proteins (RBPs) from the DEGs and screened out four RBPs (ZFP36, HSPA1A, TRIM21, and P2RX7). We selected four RASEs based on the co-expression analyses of RBPs and RASEs, including exon skipping (ES) of DEDD2, alternative 3′ splice site (A3SS) of ETV6, mutually exclusive 3′UTRs (3pMXE) of TNFAIP8L2, and A3SS of HLA-B. Furthermore, the selected four RBPs and four RASEs were validated by reverse transcription–quantitative polymerase chain reaction (RT-qPCR) and showed high consistency with RNA sequencing (RNA-seq).ConclusionDysregulated RBPs and their associated RASEs may play regulatory roles in MVP development and may therefore be used as therapeutic targets in the future.</p

Table6_Functional analysis of differently expressed ferroptosis-related genes in patients with mitral valve prolapse.XLSX

Background: The prevalence of mitral valve prolapse (MVP) in heart valvular diseases is globally increasing. However, the understanding of its etiology and pathogenesis is limited. So far, the relationship between ferroptosis-related genes and long non-coding RNAs (lncRNAs) in MVP remains unexplored. This study investigates the potential pathogenesis of ferroptosis-related genes in MVP and provides a therapeutic target for the disease.Methods: Blood samples from patients with MVP and healthy volunteers were collected for transcriptomic sequencing to analyze the expression of ferroptosis-related differentially expressed genes (DEGs) and differentially expressed long non-coding RNAs (DElncRNAs Co-expression network of ferroptosis-related DEGs and DElncRNAs. Furthermore, this work conducted GO and KEGG enrichment analyses.Results:CDKN2A, SLC1A4, ATF3, and other core genes related to the mitral valve prolapse were screened out. CDKN2A, SLC1A4, and ATF3 genes were at the core position of the network, regulated by numerous lncRNAs. Notably, these genes are primarily involved in the extracellular region and p53 signaling pathway.Conclusion: In summary, CDKN2A, SLC1A4, and ATF3 regulate the pathophysiological process of MVP and are potential therapeutic targets.</p

Table1_Functional analysis of differently expressed ferroptosis-related genes in patients with mitral valve prolapse.XLSX

Background: The prevalence of mitral valve prolapse (MVP) in heart valvular diseases is globally increasing. However, the understanding of its etiology and pathogenesis is limited. So far, the relationship between ferroptosis-related genes and long non-coding RNAs (lncRNAs) in MVP remains unexplored. This study investigates the potential pathogenesis of ferroptosis-related genes in MVP and provides a therapeutic target for the disease.Methods: Blood samples from patients with MVP and healthy volunteers were collected for transcriptomic sequencing to analyze the expression of ferroptosis-related differentially expressed genes (DEGs) and differentially expressed long non-coding RNAs (DElncRNAs Co-expression network of ferroptosis-related DEGs and DElncRNAs. Furthermore, this work conducted GO and KEGG enrichment analyses.Results:CDKN2A, SLC1A4, ATF3, and other core genes related to the mitral valve prolapse were screened out. CDKN2A, SLC1A4, and ATF3 genes were at the core position of the network, regulated by numerous lncRNAs. Notably, these genes are primarily involved in the extracellular region and p53 signaling pathway.Conclusion: In summary, CDKN2A, SLC1A4, and ATF3 regulate the pathophysiological process of MVP and are potential therapeutic targets.</p

Table_4_Genome-wide analysis of RNA-binding proteins co-expression with alternative splicing events in mitral valve prolapse.xlsx

ObjectivesWe investigated the role and molecular mechanisms of RNA-binding proteins (RBPs) and their regulated alternative splicing events (RASEs) in the pathogenesis of mitral valve prolapse (MVP). MethodsFor RNA extraction, we obtained peripheral blood mononuclear cells (PBMCs) from five patients with MVP, with or without chordae tendineae rupture, and five healthy individuals. High-throughput sequencing was used for RNA sequencing (RNA-seq). Differentially expressed genes (DEGs) analysis, alternative splicing (AS) analysis, functional enrichment analysis, co-expression of RBPs, and alternative splicing events (ASEs) analysis were conducted.ResultsThe MVP patients exhibited 306 up-regulated genes and 198 down-regulated genes. All down- and up-regulated genes were enriched in both Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Furthermore, MVP was closely associated with the top 10 enriched terms and pathways. In MVP patients, 2,288 RASEs were found to be significantly different, and four suitable RASEs (CARD11 A3ss, RBM5 ES, NCF1 A5SS, and DAXX A3ss) were tested. We identified 13 RNA-binding proteins (RBPs) from the DEGs and screened out four RBPs (ZFP36, HSPA1A, TRIM21, and P2RX7). We selected four RASEs based on the co-expression analyses of RBPs and RASEs, including exon skipping (ES) of DEDD2, alternative 3′ splice site (A3SS) of ETV6, mutually exclusive 3′UTRs (3pMXE) of TNFAIP8L2, and A3SS of HLA-B. Furthermore, the selected four RBPs and four RASEs were validated by reverse transcription–quantitative polymerase chain reaction (RT-qPCR) and showed high consistency with RNA sequencing (RNA-seq).ConclusionDysregulated RBPs and their associated RASEs may play regulatory roles in MVP development and may therefore be used as therapeutic targets in the future.</p