Emergent charge order in pressurized kagome superconductor CsV3Sb5.

The discovery of several electronic orders in kagome superconductors AV3Sb5 (A means K, Rb, Cs) provides a promising platform for exploring unprecedented emergent physics1-9. Under moderate pressure (<2.2 GPa), the triple-Q charge density wave (CDW) order is monotonically suppressed by pressure, while the superconductivity shows a two-dome-like behaviour, suggesting an unusual interplay between superconductivity and CDW order10,11. Given that time-reversal symmetry breaking and electronic nematicity have been revealed inside the triple-Q CDW phase8,9,12,13, understanding this CDW order and its interplay with superconductivity becomes one of the core questions in AV3Sb5 (refs. 3,5,6). Here, we report the evolution of CDW and superconductivity with pressure in CsV3Sb5 by 51V nuclear magnetic resonance measurements. An emergent CDW phase, ascribed to a possible stripe-like CDW order with a unidirectional 4a0 modulation, is observed between Pc1 ≅ 0.58 GPa and Pc2 ≅ 2.0 GPa, which explains the two-dome-like superconducting behaviour under pressure. Furthermore, the nuclear spin-lattice relaxation measurement reveals evidence for pressure-independent charge fluctuations above the CDW transition temperature and unconventional superconducting pairing above Pc2. Our results not only shed new light on the interplay of superconductivity and CDW, but also reveal new electronic correlation effects in kagome superconductors AV3Sb5.

Charge-density-wave-driven electronic nematicity in a kagome superconductor.

Electronic nematicity, in which rotational symmetry is spontaneously broken by electronic degrees of freedom, has been demonstrated as a ubiquitous phenomenon in correlated quantum fluids including high-temperature superconductors and quantum Hall systems1,2. Notably, the electronic nematicity in high-temperature superconductors exhibits an intriguing entanglement with superconductivity, generating complicated superconducting pairing and intertwined electronic orders. Recently, an unusual competition between superconductivity and a charge-density-wave (CDW) order has been found in the AV3Sb5 (A = K, Rb, Cs) family with two-dimensional vanadium kagome nets3-8. Whether these phenomena involve electronic nematicity is still unknown. Here we report evidence for the existence of electronic nematicity in CsV3Sb5, using a combination of elastoresistance measurements, nuclear magnetic resonance (NMR) and scanning tunnelling microscopy/spectroscopy (STM/S). The temperature-dependent elastoresistance coefficient (m11 minus m12) and NMR spectra demonstrate that, besides a C2 structural distortion of the 2a0 × 2a0 supercell owing to out-of-plane modulation, considerable nematic fluctuations emerge immediately below the CDW transition (approximately 94 kelvin) and finally a nematic transition occurs below about 35 kelvin. The STM experiment directly visualizes the C2-structure-pinned long-range nematic order below the nematic transition temperature, suggesting a novel nematicity described by a three-state Potts model. Our findings indicate an intrinsic electronic nematicity in the normal state of CsV3Sb5, which sets a new paradigm for revealing the role of electronic nematicity on pairing mechanism in unconventional superconductors.

Target practice: modeling tumors with stem cells.

A variant neoplastic line of human pluripotent stem cell (hPSC) displays unique tumorigenic properties, including enhanced self-renewal and survival, and aberrant blockade in differentiation. Sachlos et al. adopted a neoplastic hPSC differentiation platform to screen small molecules that selectively induce differentiation of cancer stem cells.

Graph-pMHC: graph neural network approach to MHC class II peptide presentation and antibody immunogenicity.

Antigen presentation on MHC class II (pMHCII presentation) plays an essential role in the adaptive immune response to extracellular pathogens and cancerous cells. But it can also reduce the efficacy of large-molecule drugs by triggering an anti-drug response. Significant progress has been made in pMHCII presentation modeling due to the collection of large-scale pMHC mass spectrometry datasets (ligandomes) and advances in machine learning. Here, we develop graph-pMHC, a graph neural network approach to predict pMHCII presentation. We derive adjacency matrices for pMHCII using Alphafold2-multimer and address the peptide-MHC binding groove alignment problem with a simple graph enumeration strategy. We demonstrate that graph-pMHC dramatically outperforms methods with suboptimal inductive biases, such as the multilayer-perceptron-based NetMHCIIpan-4.0 (+20.17% absolute average precision). Finally, we create an antibody drug immunogenicity dataset from clinical trial data and develop a method for measuring anti-antibody immunogenicity risk using pMHCII presentation models. Our model increases receiver operating characteristic curve (ROC)-area under the ROC curve (AUC) by 2.57% compared to just filtering peptides by hits in OASis alone for predicting antibody drug immunogenicity.

Extracellular Matrix Disorganization Caused by ADAMTS16 Deficiency Leads to Bicuspid Aortic Valve With Raphe Formation.

BACKGROUND: A better understanding of the molecular mechanism of aortic valve development and bicuspid aortic valve (BAV) formation would significantly improve and optimize the therapeutic strategy for BAV treatment. Over the past decade, the genes involved in aortic valve development and BAV formation have been increasingly recognized. On the other hand, ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) gene family members have been reported to be able to modulate cardiovascular development and diseases. The present study aimed to further investigate the roles of ADAMTS family members in aortic valve development and BAV formation. METHODS: Morpholino-based ADAMTS family gene-targeted screening for zebrafish heart outflow tract phenotypes combined with DNA sequencing in a 304 cohort BAV patient registry study was initially carried out to identify potentially related genes. Both ADAMTS gene-specific fluorescence in situ hybridization assay and genetic tracing experiments were performed to evaluate the expression pattern in the aortic valve. Accordingly, related genetic mouse models (both knockout and knockin) were generated using the CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/clustered regularly interspaced short palindromic repeat-associated 9) method to further study the roles of ADAMTS family genes. The lineage-tracing technique was used again to evaluate how the cellular activity of specific progenitor cells was regulated by ADAMTS genes. Bulk RNA sequencing was used to investigate the signaling pathways involved. Inducible pluripotent stem cells derived from both BAV patients and genetic mouse tissue were used to study the molecular mechanism of ADAMTS. Immunohistochemistry was performed to examine the phenotype of cardiac valve anomalies, especially in the extracellular matrix components. RESULTS: ADAMTS genes targeting and phenotype screening in zebrafish and targeted DNA sequencing on a cohort of patients with BAV identified ADAMTS16 (a disintegrin and metalloproteinase with thrombospondin motifs 16) as a BAV-causing gene and found the ADAMTS16 p. H357Q variant in an inherited BAV family. Both in situ hybridization and genetic tracing studies described a unique spatiotemporal pattern of ADAMTS16 expression during aortic valve development. Adamts16+/- and Adamts16+/H355Q mouse models both exhibited a right coronary cusp-noncoronary cusp fusion-type BAV phenotype, with progressive aortic valve thickening associated with raphe formation (fusion of the commissure). Further, ADAMTS16 deficiency in Tie2 lineage cells recapitulated the BAV phenotype. This was confirmed in lineage-tracing mouse models in which Adamts16 deficiency affected endothelial and second heart field cells, not the neural crest cells. Accordingly, the changes were mainly detected in the noncoronary and right coronary leaflets. Bulk RNA sequencing using inducible pluripotent stem cells-derived endothelial cells and genetic mouse embryonic heart tissue unveiled enhanced FAK (focal adhesion kinase) signaling, which was accompanied by elevated fibronectin levels. Both in vitro inducible pluripotent stem cells-derived endothelial cells culture and ex vivo embryonic outflow tract explant studies validated the altered FAK signaling. CONCLUSIONS: Our present study identified a novel BAV-causing ADAMTS16 p. H357Q variant. ADAMTS16 deficiency led to BAV formation.

The role of HPV11 E7 in modulating STING-dependent interferon ß response in recurrent respiratory papillomatosis.

Recurrent respiratory papillomatosis (RRP) is a rare benign tumor caused mainly by the infection of the respiratory tract epithelial cells by the human papillomavirus (HPV) type 6/11. However, the specific mechanisms underlying the inhibition of the host's innate immune response by HPV remain unclear. For this purpose, we employed single-cell RNA sequencing to analyze the states of various immune cells in RRP samples post-HPV infection and utilized a cellular model of HPV infection to elucidate the mechanisms by which HPV evades the innate immune system in RRP. The results revealed distinct immune cell heterogeneity in RRP and demonstrated that HPV11 E7 can inhibit the phosphorylation of the stimulator of interferon genes protein, thereby circumventing the body's antiviral response. In vitro co-culture experiments demonstrated that stimulation of macrophages to produce interferon-beta induced the death of HPV-infected epithelial cells, also reducing HPV viral levels. In summary, our study preliminarily identifies the potential mechanisms by which HPV evades the host's antiviral immune response, as well as the latent antiviral functions exhibited by activated macrophages. This research serves as an initial exploration of antiviral immune evasion in RRP, laying a solid foundation for investigating immunotherapeutic approaches for the disease.IMPORTANCESurgical tumor reduction is the most common treatment for recurrent respiratory papillomatosis (RRP). One of the characteristics of RRP is its persistent recurrence, and multiple surgeries are usually required to control the symptoms. Recently, some adjuvant therapies have shown effectiveness, but none of them can completely clear human papillomavirus (HPV) infection, and thus, a localized antiviral immune response is significant for disease control; after all, HPV infection is limited to the epithelium. Inhibition of interferon-beta (IFN-ß) secretion by HPV11 E7 viral proteins in epithelial cells by affecting stimulator of interferon genes phosphorylation may account for the persistence of low-risk HPV replication in the RRP. Moreover, suppression of the IFN-I pathway in RRP cell types might provide clues regarding the hyporeactive function of local immune cells. However, activation of macrophage groups to produce IFN-ß can still destroy HPV-infected cells.

RSK1 promotes mammalian axon regeneration by inducing the synthesis of regeneration-related proteins.

In contrast to the adult mammalian central nervous system (CNS), the neurons in the peripheral nervous system (PNS) can regenerate their axons. However, the underlying mechanism dictating the regeneration program after PNS injuries remains poorly understood. Combining chemical inhibitor screening with gain- and loss-of-function analyses, we identified p90 ribosomal S6 kinase 1 (RSK1) as a crucial regulator of axon regeneration in dorsal root ganglion (DRG) neurons after sciatic nerve injury (SNI). Mechanistically, RSK1 was found to preferentially regulate the synthesis of regeneration-related proteins using ribosomal profiling. Interestingly, RSK1 expression was up-regulated in injured DRG neurons, but not retinal ganglion cells (RGCs). Additionally, RSK1 overexpression enhanced phosphatase and tensin homolog (PTEN) deletion-induced axon regeneration in RGCs in the adult CNS. Our findings reveal a critical mechanism in inducing protein synthesis that promotes axon regeneration and further suggest RSK1 as a possible therapeutic target for neuronal injury repair.

Mitophagy Controls the Activities of Tumor Suppressor p53 to Regulate Hepatic Cancer Stem Cells.

Autophagy is required for benign hepatic tumors to progress into malignant hepatocellular carcinoma. However, the mechanism is unclear. Here, we report that mitophagy, the selective removal of mitochondria by autophagy, positively regulates hepatic cancer stem cells (CSCs) by suppressing the tumor suppressor p53. When mitophagy is enhanced, p53 co-localizes with mitochondria and is removed by a mitophagy-dependent manner. However, when mitophagy is inhibited, p53 is phosphorylated at serine-392 by PINK1, a kinase associated with mitophagy, on mitochondria and translocated into the nucleus, where it binds to the NANOG promoter to prevent OCT4 and SOX2 transcription factors from activating the expression of NANOG, a transcription factor critical for maintaining the stemness and the self-renewal ability of CSCs, resulting in the reduction of hepatic CSC populations. These results demonstrate that mitophagy controls the activities of p53 to maintain hepatic CSCs and provide an explanation as to why autophagy is required to promote hepatocarcinogenesis.

nCoVDock2: a docking server to predict the binding modes between COVID-19 targets and its potential ligands.

The rapid emergence of SARS-CoV-2 variants with multi-sites mutations is considered as a major obstacle for the development of drugs and vaccines. Although most of the functional proteins essential for SARS-CoV-2 have been determined, the understanding of the COVID-19 target-ligand interactions remains a key challenge. The old version of this COVID-19 docking server was built in 2020, and free and open to all users. Here, we present nCoVDock2, a new docking server to predict the binding modes for targets from SARS-CoV-2. First, the new server supports more targets. We replaced the modeled structures with newly resolved structures and added more potential targets of COVID-19, especially for the variants. Second, for small molecule docking, Autodock Vina was upgraded to the latest version 1.2.0, and a new scoring function was added for peptide or antibody docking. Third, the input interface and molecular visualization were updated for a better user experience. The web server, together with an extensive help and tutorial, are freely available at: https://ncovdock2.schanglab.org.cn.

Differential genetic mutations and immune cell infiltration in high- and low-risk STAD: Implications for prognosis and immunotherapy efficacy.

This study investigates genetic mutations and immune cell dynamics in stomach adenocarcinoma (STAD), focusing on identifying prognostic markers and therapeutic targets. Analysis of TCGA-STAD samples revealed C > A as the most common single nucleotide variant (SNV) in both high and low-risk groups. Key mutated driver genes included TTN, TP53 and MUC16, with frame-shift mutations more prevalent in the low-risk group and missense mutations in the high-risk group. Interaction analysis of hub genes such as C1QA and CD68 showed significant correlations, impacting immune cell infiltration patterns. Using ssGSEA, we found higher immune cell infiltration (B cells, CD4+ T cells, CD8+ T cells, DC cells, NK cells) in the high-risk group, correlated with increased risk scores. xCell algorithm results indicated distinct immune infiltration levels between the groups. The study's risk scoring model proved effective in prognosis prediction and immunotherapy efficacy assessment. Key molecules like CD28, CD27 and SLAMF7 correlated significantly with risk scores, suggesting potential targets for high-risk STAD patients. Drug sensitivity analysis showed a negative correlation between risk scores and sensitivity to certain treatments, indicating potential therapeutic options for high-risk STAD patients. We also validated the carcinogenic role of RPL14 in gastric cancer through phenotypic experiments, demonstrating its influence on cancer cell proliferation, invasion and migration. Overall, this research provides crucial insights into the genetic and immune aspects of STAD, highlighting the importance of a risk scoring model for personalized treatment strategies and clinical decision-making in gastric cancer management.

Species sensitivities to artificial light at night: A phylogenetically controlled multilevel meta-analysis on melatonin suppression.

The rapid urbanization of our world has led to a surge in artificial lighting at night (ALAN), with profound effects on wildlife. Previous research on wildlife's melatonin, a crucial mechanistic indicator and mediator, has yielded inconclusive evidence due to a lack of comparative analysis. We compiled and analysed an evidence base including 127 experiments with 437 observations across 31 wild vertebrates using phylogenetically controlled multilevel meta-analytic models. The evidence comes mainly from the effects of white light on melatonin suppression in birds and mammals. We show a 36% average decrease in melatonin secretion in response to ALAN across a diverse range of species. This effect was observed for central and peripheral melatonin, diurnal and nocturnal species, and captive and free-living populations. We also reveal intensity-, wavelength-, and timing-dependent patterns of ALAN effects. Exposure to ALAN led to a 23% rise in inter-individual variability in melatonin suppression, with important implications for natural selection in wild vertebrates, as some individuals may display higher tolerance to ALAN. The cross-species evidence has strong implications for conservation of wild populations that are subject to natural selection of ALAN. We recommend measures to mitigate harmful impacts of ALAN, such as using 'smart' lighting systems to tune the spectra to less harmful compositions.

Precision Synthesis of Polysarcosine via Controlled Ring-Opening Polymerization of N-Carboxyanhydride: Fast Kinetics, Ultrahigh Molecular Weight, and Mechanistic Insights.

The rapid and controlled synthesis of high-molecular-weight (HMW) polysarcosine (pSar), a potential polyethylene glycol (PEG) alternative, via the ring-opening polymerization (ROP) of N-carboxyanhydride (NCA) is rare and challenging. Here, we report the well-controlled ROP of sarcosine NCA (Sar-NCA) that is catalyzed by various carboxylic acids, which accelerate the polymerization rate up to 50 times, and enables the robust synthesis of pSar with an unprecedented ultrahigh molecular weight (UHMW) up to 586 kDa (DP ∼ 8200) and exceptionally narrow dispersity (D̵) below 1.05. Mechanistic experiments and density functional theory calculations together elucidate the role of carboxylic acid as a bifunctional catalyst that significantly facilitates proton transfer processes and avoids charge separation and suggest the ring opening of NCA, rather than decarboxylation, as the rate-determining step. UHMW pSar demonstrates improved thermal and mechanical properties over the low-molecular-weight counterparts. This work provides a simple yet highly efficient approach to UHMW pSar and generates a new fundamental understanding useful not only for the ROP of Sar-NCA but also for other NCAs.

Long-term follow-up of haploidentical haematopoietic stem cell transplantation in paediatric patients with high-risk acute myeloid leukaemia: Report from a single centre.

Data from 200 children with high-risk acute myeloid leukaemia who underwent their first haploidentical haematopoietic stem cell transplantation (haplo-HSCT) between 2015 and 2021 at our institution were analysed. The 4-year overall survival (OS), event-free survival (EFS) and cumulative incidence of relapse (CIR) were 71.9%, 62.3% and 32.4% respectively. The 100-day cumulative incidences of grade II-IV and III-IV acute graft-versus-host disease (aGVHD) were 41.1% and 9.5% respectively. The 4-year cumulative incidence of chronic GVHD (cGVHD) was 56.1%, and that of moderate-to-severe cGVHD was 27.3%. Minimal residual disease (MRD)-positive (MRD+) status pre-HSCT was significantly associated with lower survival and a higher risk of relapse. The 4-year OS, EFS and CIR differed significantly between patients with MRD+ pre-HSCT (n = 97; 63.4%, 51.4% and 41.0% respectively) and those with MRD-negative (MRD-) pre-HSCT (n = 103; 80.5%, 73.3% and 23.8% respectively). Multivariate analysis also revealed that acute megakaryoblastic leukaemia without Down syndrome (non-DS-AMKL) was associated with extremely poor outcomes (hazard ratios and 95% CIs for OS, EFS and CIR: 3.110 (1.430-6.763), 3.145 (1.628-6.074) and 3.250 (1.529-6.910) respectively; p-values were 0.004, 0.001 and 0.002 respectively). Thus, haplo-HSCT can be a therapy option for these patients, and MRD status pre-HSCT significantly affects the outcomes. As patients with non-DS-AMKL have extremely poor outcomes, even with haplo-HSCT, a combination of novel therapies is urgently needed.

In Situ Electrospinning MOF-Derived Highly Dispersed α-Cobalt Confined in Nitrogen-Doped Carbon Nanofibers Nanozyme for Biomolecule Monitoring.

Designing a metal-organic framework (MOF)-derived nanozyme with highly dispersed active sites and high catalytic activity as well as robust structure for colorimetric biosensing of diverse biomolecules remains a substantial challenge. Here, an MOF-derived highly dispersed and pure α-cobalt confined in a nitrogen-doped carbon nanofiber (α-Co@NCNF) nanozyme with superior glucose oxidase (GOD)- and peroxidase (POD)-like activities was constructed for colorimetric assay of multiple biomolecules. Specifically, the α-Co@NCNF nanozyme was synthesized, utilizing in situ electrospinning Co-MOFs into polyacrylonitrile nanofiber (PAN) followed by a pyrolysis process. Taking advantage of the in situ electrospinning strategy, the α-Co nanoparticles were confined in continuous porous NCNF to restrict the growth and prevent the aggregation and oxidation during the pyrolysis process. The resulting special structure considerably improved the enzyme-like performance. A series of experiments validate that the enzyme-like activity of the α-Co@NCNF nanozyme was superior to that of Co@CoO@NCNF (derivatives from Co-MOFs grown on the surface of PAN nanofiber) and nature enzymes. Furthermore, α-Co@NCNF nanozyme-based colorimetric biosensing was developed for monitoring glucose, hydrogen peroxide (H2O2), and glutathione (GSH) and the corresponding linear ranges are 0.1-50 and 50-900 µM and 5-55 and 0.1-20 µM accompanied by the corresponding low detection of 0.03, 1.66, and 0.03 µM. The proposed method for the construction of α-Co@NCNF nanozyme with dual enzyme-like properties provides a new insight for designing novel nanozymes and has prospects for application in colorimetric biosensing.

Mini-dose methotrexate combined with methylprednisolone for the initial treatment of acute GVHD: a multicentre, randomized trial.

BACKGROUND: There is an urgent unmet need for effective initial treatment for acute graft-versus-host disease (aGVHD) adding to the standard first-line therapy with corticosteroids after allogeneic haematopoietic stem cell transplantation (allo-HSCT). METHODS: We performed a multicentre, open-label, randomized, phase 3 study. Eligible patients (aged 15 years or older, had received allo-HSCT for a haematological malignancy, developed aGVHD, and received no previous therapies for aGVHD) were randomly assigned (1:1) to receive either 5 mg/m2 MTX on Days 1, 3, or 8 and then combined with corticosteroids or corticosteroids alone weekly. RESULTS: The primary endpoint was the overall response rate (ORR) on Day 10. A total of 157 patients were randomly assigned to receive either MTX plus corticosteroids (n = 78; MTX group) or corticosteroids alone (n = 79; control group). The Day 10 ORR was 97% for the MTX group and 81% for the control group (p = .005). Among patients with mild aGVHD, the Day 10 ORR was 100% for the MTX group and 86% for the control group (p = .001). The 1-year estimated failure-free survival was 69% for the MTX group and 41% for the control group (p = .002). There were no differences in treatment-related adverse events between the two groups. CONCLUSIONS: In conclusion, mini-dose MTX combined with corticosteroids can significantly improve the ORR in patients with aGVHD and is well tolerated, although it did not achieve the prespecified 20% improvement with the addition of MTX. TRIAL REGISTRATION: The trial was registered with clinicaltrials.gov (NCT04960644).

Decoding the "Fingerprint" of Implant Materials: Insights into the Foreign Body Reaction.

Foreign body reaction (FBR) is a prevalent yet often overlooked pathological phenomenon, particularly within the field of biomedical implantation. The presence of FBR poses a heavy burden on both the medical and socioeconomic systems. This review seeks to elucidate the protein "fingerprint" of implant materials, which is generated by the physiochemical properties of the implant materials themselves. In this review, the activity of macrophages, the formation of foreign body giant cells (FBGCs), and the development of fibrosis capsules in the context of FBR are introduced. Additionally, the relationship between various implant materials and FBR is elucidated in detail, as is an overview of the existing approaches and technologies employed to alleviate FBR. Finally, the significance of implant components (metallic materials and non-metallic materials), surface CHEMISTRY (charge and wettability), and physical characteristics (topography, roughness, and stiffness) in establishing the protein "fingerprint" of implant materials is also well documented. In conclusion, this review aims to emphasize the importance of FBR on implant materials and provides the current perspectives and approaches in developing implant materials with anti-FBR properties.

High-Performance 2D Ambipolar MoTe2 Lateral Memristors by Mild Oxidation.

2D transition metal dichalcogenides (TMDCs) have been intensively explored in memristors for brain-inspired computing. Oxidation, which is usually unavoidable and harmful in 2D TMDCs, could also be used to enhance their memristive performances. However, it is still unclear how oxidation affects the resistive switching behaviors of 2D ambipolar TMDCs. In this work, a mild oxidation strategy is developed to greatly enhance the resistive switching ratio of ambipolar 2H-MoTe2 lateral memristors by more than 10 times. Such an enhancement results from the amplified doping due to O2 and H2O adsorption and the optimization of effective gate voltage distribution by mild oxidation. Moreover, the ambipolarity of 2H-MoTe2 also enables a change of resistive switching direction, which is uncommon in 2D memristors. Consequently, as an artificial synapse, the MoTe2 device exhibits a large dynamic range (≈200) and a good linearity (1.01) in long-term potentiation and depression, as well as a high-accuracy handwritten digit recognition (>96%). This work not only provides a feasible and effective way to enhance the memristive performance of 2D ambipolar materials, but also deepens the understanding of hidden mechanisms for RS behaviors in oxidized 2D materials.

Thermally Enhanced Phosphorescent Carbon Nanodots for Monitoring Cold-Chain Logistics.

Room-temperature phosphorescent materials, renowned for their long luminescence lifetimes, have garnered significant attention in the field of optical materials. However, the challenges posed by thermally induced quenching have significantly hindered the advancement of luminescence efficiency and stability. In this study, thermally enhanced phosphorescent carbon nanodots (CND) are developed by incorporating them into fiber matrices. Remarkably, the phosphorescence lifetime of the thermally enhanced CND exhibits a twofold enhancement, increasing from 326 to 753 ms, while the phosphorescence intensity experienced a tenfold enhancement, increasing from 25 to 245 as the temperature increased to 373 K. Rigid fiber matrices can effectively suppress the non-radiative transition rate of triplet excitons, while high temperatures can desorb oxygen adsorbed on the surface of the CND, disrupting the interaction between the CND and oxygen. Consequently, a thermally enhanced phosphorescence is obtained. In addition, benefiting from the thermally enhanced phosphorescence property of CND, a warning indicator with an anti-counterfeiting function for monitoring cold-chain logistics is demonstrated based on CND.

Comprehensive profiling of epigenetic modifications in fast-growing Moso bamboo shoots.

The fast growth of Moso bamboo (Phyllostachys edulis) shoots is caused by the rapid elongation of each internode. However, the key underlying cellular processes and epigenetic mechanisms remain largely unexplored. We used microscopy and multi-omics approaches to investigate two regions (bottom and middle) of the 18th internode from shoots of two different heights (2 and 4 m). We observed that internode cells become longer, and that lignin biosynthesis and glycosyltransferase family 43 (GT43) genes are substantially upregulated with shoot height. Nanopore direct RNA sequencing (DRS) revealed a higher N6-methyladenine (m6A) modification rate in 2-m shoots than in 4-m shoots. In addition, different specific m6A modification sites were enriched at different growth stages. Global DNA methylation profiling indicated that DNA methylation levels are higher in 4-m shoots than in 2-m shoots. We also detected shorter poly(A) tail lengths (PALs) in 4-m shoots compared with 2-m shoots. Genes showing differential PAL were mainly enriched in the functional terms of protein translation and vesicle fusion. An association analysis between PALs and DNA methylation strongly suggested that gene body CG methylation levels are positively associated with PAL. This study provides valuable information to better understand post-transcriptional regulations responsible for fast-growing shoots in Moso bamboo.

Biomimetic Structural Proteins: Modular Assembly and High Mechanical Performance.

Protein-based biomaterials attract growing interests due to their encoded and programmable robust mechanical properties, superelasticity, plasticity, shape adaptability, excellent interfacial behavior, etc., derived from sequence-guided backbone structures, particularly compared to chemically synthetic counterparts in materials science and biomedical engineering. For example, protein materials have been successfully fabricated as (1) artificial implants (man-made tendons, cartilages, or dental tissues), due to programmable chemistry and biocompatibility; (2) smart biodevices with temperature/light-response and self-healing effects; and (3) impact resistance materials having great mechanical performance due to biomimetics. However, the existing method of regenerating protein materials from natural sources has two critical issues, low yield and structural damage, making it unable to meet demands. Therefore, it is crucial to develop an alternative strategy for fabricating protein materials. Heterologous expression of natural proteins with a modular assembly approach is an effective strategy for material preparation. Standardized, easy-to-assemble protein modules with specific structures and functions are developed through experimental and computational tools based on natural functional protein sequences. Through recombination and heterologous expression, these artificial protein modules become keys to material fabrication. Undergoing an assembly process similar to supramolecular self-assembly of proteins in cells, biomimetic modules can be fabricated for formation of macroscopic materials such as fibers and adhesives. This strategy inspired by synthetic biology and supramolecular chemistry is important for improving target protein yields and assembly integrity. It also preserves and optimizes the mechanical functions of structural proteins, accelerating the design and fabrication of artificial protein materials.In this Account, we overview recent studies on fabricating biomimetic protein materials to elucidate the concept of modular assembly. We discuss the design of biomimetic structural proteins at the molecular level, providing a wealth of details determining the bulk properties of materials. Additinally, we describe the modular self-assembly and assembly driven by inducing molecules, and mechanical properties and applications of resulting fibers. We used these strategies to develop fiber materials with high tensile strength, high toughness, and properties such as anti-icing and high-temperature resistance. We also extended this approach to design protein-based adhesives with ultra-strong adhesion, biocompatibility, and biodegradability for surgical applications such as wound sealing and healing. Other protein materials, including films and hydrogels, have been developed through chemical assembly routes. Finally, we describe exploiting synthetic biology and chemistry to overcome bottlenecks in structural protein modular design, biosynthesis, and material assembly and our perspectives for future development in structural biomaterials.