Direct Ink Writing of Low-Concentration MXene/Aramid Nanofiber Inks for Tunable Electromagnetic Shielding and Infrared Anticounterfeiting Applications.

MXene inks offer a promising avenue for the scalable production and customization of printing electronics. However, simultaneously achieving a low solid content and printability of MXene inks, as well as mechanical flexibility and environmental stability of printed objects, remains a challenge. In this study, we overcame these challenges by employing high-viscosity aramid nanofibers (ANFs) to optimize the rheology of low-concentration MXene inks. The abundant entangled networks and hydrogen bonds formed between MXene and ANF significantly increase the viscosity and yield stress up to 103 Pa·s and 200 Pa, respectively. This optimization allows the use of MXene/ANF (MA) inks at low concentrations in direct ink writing and other high-viscosity processing techniques. The printable MXene/ANF inks with a high conductivity of 883.5 S/cm were used to print shields with customized structures, achieving a tunable electromagnetic interference shielding effectiveness (EMI SE) in the 0.2-48.2 dB range. Furthermore, the MA inks exhibited adjustable infrared (IR) emissivity by changing the ANF ratio combined with printing design, demonstrating the application for infrared anticounterfeiting. Notably, the printed MXene/ANF objects possess outstanding mechanical flexibility and environmental stability, which are attributed to the reinforcement and protection of ANF. Therefore, these findings have significant practical implications as versatile MXene/ANF inks can be used for customizable, scalable, and cost-effective production of flexible printed electronics.

Iron(I) Complex Bearing an Open-Shell Diazenido Ligand.

Low-valent transition-metal diazenido species are important intermediates in transition-metal-mediated dinitrogen reduction reactions. Isolable complexes of the type unanimously feature closed-shell diazenido ligands. Those bearing open-shell diazenido ligands have remained elusive. Herein, we report the synthesis, characterization, and reactivity of a d7 iron(I) complex featuring an open-shell silyldiazenido ligand, [(ICy)Fe(NNSiiPr3)(η2:η2-dvtms)] (1, ICy = 1,3-dicyclohexylimidazole-2-ylidene, dvtms = divinyltetramethyldisiloxane). Complex 1 is prepared in good yield by silylation of the iron(-I)-N2 complex [K(18-crown-6)][(ICy)Fe(N2)(η2:η2-dvtms)] with iPr3SiOTf and has been fully characterized by various spectroscopic methods. Theoretical studies, in combination with characterization data, established an S = 1/2 ground spin-state for 1 that can best be described as a quartet iron(I) center featuring an antiferromagnetically coupled triplet silyldiazenido ligand. The diazenido and alkene ligands in 1 are labile, as indicated by the facile disproportionation reaction of 1 at ambient temperature to transform into the iron(II) bis(diazenido) species [(ICy)(NNSiiPr3)2Fe(dvtms)Fe(NNSiiPr3)2(ICy)] (2) and the iron(0) species [(ICy)Fe(η2:η2-dvtms)] and also the alkene-exchange reaction of 1 with PhCH═CHBC8H14 to form [(ICy)Fe(NNSiiPr3)(η2-trans-PhCH═CHBC8H14)] (3). Complex 1 is light-sensitive. Upon photolysis, it undergoes a SiiPr3 radical-transfer reaction to yield [(ICy)Fe(σ:η2-MeCHSiMe2OSiMe2CH═CHSiiPr3)] (4) and N2. The reactions of 1 with the trityl radical and organic bromides yield iron(II) complexes, which indicates its reducing nature. Moreover, 1 is a weak hydrogen-atom abstractor, as indicated by its inertness toward HSi(SiMe3)3 and cyclohexa-1,4-diene and the low calculated N-H bond dissociation energy (48 kcal/mol) of its corresponding iron(II) iso-hydrazenido species.

Mitochondrial ferritin alleviates ferroptosis in a kainic acid-induced mouse epilepsy model by regulating iron homeostasis: Involvement of nuclear factor erythroid 2-related factor 2.

BACKGROUND: Epilepsy is a widespread and chronic disease of the central nervous system caused by a variety of factors. Mitochondrial ferritin (FtMt) refers to ferritin located within the mitochondria that may protect neurons against oxidative stress by binding excess free iron ions in the cytoplasm. However, the potential role of FtMt in epilepsy remains unclear. We aimed to investigate whether FtMt and its related mechanisms can regulate epilepsy by modulating ferroptosis. METHODS: Three weeks after injection of adeno-associated virus (AAV) in the skull of adult male C57BL/6 mice, kainic acid (KA) was injected into the hippocampus to induce seizures. Primary hippocampal neurons were transfected with siRNA using a glutamate-mediated epilepsy model. After specific treatments, Western blot analysis, immunofluorescence, EEG recording, transmission electron microscopy, iron staining, silver staining, and Nissl staining were performed. RESULTS: At different time points after KA injection, the expression of FtMt protein in the hippocampus of mice showed varying degrees of increase. Knockdown of the FtMt gene by AAV resulted in an increase in intracellular free iron levels and a decrease in the function of iron transport-related proteins, promoting neuronal ferroptosis and exacerbating epileptic brain activity in the hippocampus of seizure mice. Additionally, increasing the expression level of FtMt protein was achieved by AAV-mediated upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) gene in the hippocampus of seizure mice. CONCLUSIONS: In epilepsy, Nrf2 modulates ferroptosis by involving the expression of FtMt and may be a potential therapeutic mechanism of neuronal injury after epilepsy. Targeting this relevant process for treatment may be a therapeutic strategy to prevent epilepsy.

Transthoracic Ultrasound Improves Cardiac Function in Mice.

Cardiac dysfunction is a severe complication that is associated with an increased risk of mortality in multiple diseases. Cardioprotection solution that has been researched is the electrical stimulation of the vagus nerve to exert cardio protection. This method has been shown to reduce the systemic inflammatory response and maintain the immune homeostasis of the heart. However, the invasive procedure of electrode implantation poses a risk of nerve or fiber damage. Here, we propose transthoracic ultrasound stimulation (US) of the vagus nerve to alleviate cardiac dysfunction caused by lipopolysaccharide (LPS). We developed a noninvasive transthoracic US system and exposed anesthetized mice to ultrasound protocol or sham stimulation 24 h after LPS treatment. Results showed that daily heart targeting US for 4 days significantly increased left ventricular systolic function ( p = 0.01) and improved ejection fraction ( p = 0.03) and shortening fraction ( p = 0.04). Furthermore, US significantly reduced inflammation cytokines, including IL-6 ( p = 0.03) and IL- 1ß ( p = 0.04). In addition, cervical vagotomy abrogated the effect of US, suggesting the involvement of the vagus nerve's anti-inflammatory effect. Finally, the same ultrasound treatment but for a longer period (14 days) also significantly increased cardiac function in naturally aged mice. Collectively, these findings suggest the potential of transthoracic US as a possible novel noninvasive approach in the context of cardiac dysfunction with reduced systolic function and provide new targets for rehabilitation of peripheral organ function.

Development and Comprehensive Benchmark of a High-Quality AMBER-Consistent Small Molecule Force Field with Broad Chemical Space Coverage for Molecular Modeling and Free Energy Calculation.

Biomolecular simulations have become an essential tool in contemporary drug discovery, and molecular mechanics force fields (FFs) constitute its cornerstone. Developing a high quality and broad coverage general FF is a significant undertaking that requires substantial expert knowledge and computing resources, which is beyond the scope of general practitioners. Existing FFs originate from only a limited number of groups and organizations, and they either suffer from limited numbers of training sets, lower than desired quality because of oversimplified representations, or are costly for the molecular modeling community to access. To address these issues, in this work, we developed an AMBER-consistent small molecule FF with extensive chemical space coverage, and we provide Open Access parameters for the entire modeling community. To validate our FF, we carried out benchmarks of quantum mechanics (QM)/molecular mechanics conformer comparison and free energy perturbation calculations on several benchmark data sets. Our FF achieves a higher level of performance at reproducing QM energies and geometries than two popular open-source FFs, OpenFF2 and GAFF2. In relative binding free energy calculations for 31 protein-ligand data sets, comprising 1079 pairs of ligands, the new FF achieves an overall root-mean-square error of 1.19 kcal/mol for ΔΔG and 0.92 kcal/mol for ΔG on a subset of 463 ligands without bespoke fitting to the data sets. The results are on par with those of the leading commercial series of OPLS FFs.

Breeding maize of ideal plant architecture for high-density planting tolerance through modulating shade avoidance response and beyond.

Maize is a major staple crop widely used as food, animal feed, and raw materials in industrial production. High-density planting is a major factor contributing to the continuous increase of maize yield. However, high planting density usually triggers a shade avoidance response and causes increased plant height and ear height, resulting in lodging and yield loss. Reduced plant height and ear height, more erect leaf angle, reduced tassel branch number, earlier flowering, and strong root system architecture are five key morphological traits required for maize adaption to high-density planting. In this review, we summarize recent advances in deciphering the genetic and molecular mechanisms of maize involved in response to high-density planting. We also discuss some strategies for breeding advanced maize cultivars with superior performance under high-density planting conditions.

Biomimetic submicromotor with NIR light triggered motion and cargo release inspired by cuttlefish.

Biomimetic design is very helpful and significant for the smart construction of micro/nanomotors with artificial intelligence. In this work, inspired by cuttlefish, who can rapidly eject poisonous ink and are also capable of fast movement to escape, we designed and fabricated a biomimetic submicromotor with the ability of simultaneous quick movement and a temperature threshold caused explosive cargo release triggered by near infra-red (NIR) light irradiation, which was approximately equivalent to the action of cuttlefish when encountering a predator. The yolk@shell structured polydopamine@mesoporous silica (PDA@MS60) with immovable and asymmetric yolk distribution was employed as a platform, and this was followed by the simultaneous encapsulation of phase change materials (PCM) and cargo molecules. The NIR light irradiation could not only propel the direct motion of the submicromotor, but also caused the explosive release of the cargo loaded in the submicromotor when the temperature exceeded the melting point of the PCM.

Corrigendum: CREB5 hypermethylation involved in the ganglioside GM1 therapy of Parkinson's disease.

[This corrects the article DOI: 10.3389/fnagi.2023.1122647.].

Lysine vitcylation is a novel vitamin C-derived protein modification that enhances STAT1-mediated immune response.

Vitamin C (vitC) is a vital nutrient for health and also used as a therapeutic agent in diseases such as cancer. However, the mechanisms underlying vitC's effects remain elusive. Here we report that vitC directly modifies lysine without enzymes to form vitcyl-lysine, termed "vitcylation", in a dose-, pH-, and sequence-dependent manner across diverse proteins in cells. We further discover that vitC vitcylates K298 site of STAT1, which impairs its interaction with the phosphatase PTPN2, preventing STAT1 Y701 dephosphorylation and leading to increased STAT1-mediated IFN pathway activation in tumor cells. As a result, these cells have increased MHC/HLA class-I expression and activate immune cells in co-cultures. Tumors collected from vitC-treated tumor-bearing mice have enhanced vitcylation, STAT1 phosphorylation and antigen presentation. The identification of vitcylation as a novel PTM and the characterization of its effect in tumor cells opens a new avenue for understanding vitC in cellular processes, disease mechanisms, and therapeutics.

Low molecular weight fucoidan modified nanoliposomes for the targeted delivery of the anti-inflammation natural product berberine.

The inflammatory response is the basis of many diseases, such as atherosclerosis and ulcerative colitis. Inhibiting inflammatory response is the key to treating these diseases. Berberine hydrochloride (BBR), a natural product, has shown effective inflammation inhibitory activity. However, its distribution throughout the body results in a variety of serious side effects. Currently, there is a lack of targeted delivery systems for BBR to inflammatory sites. In view of the fact that the recruitment of inflammatory cells by activated vascular endothelial cells is a key step in inflammation development. Here, we design a system that can specifically deliver berberine to activated vascular endothelial cells. Low molecular weight fucoidan (LMWF), which can specifically bind to P-selectin, was coupled to PEGylated liposomes (LMWF-Lip), and BBR is encapsulated into LMWF-Lip (LMWF-Lip/BBR). In vitro, LMWF-Lip significantly increases the uptake by activated human umbilical vein endothelial cells (HUVEC). Injection of LMWF-Lip into the tail vein of rats can effectively accumulate in the swollen part of the foot, where it is internalized by the characteristics of activated vascular endothelial cells. LMWF-Lip/BBR can effectively inhibit the expression of P-selectin in activated vascular endothelial cells, and reduce the degree of foot edema and inflammatory response. In addition, compared with free BBR, the toxicity of BBR in LMWF-Lip/BBR to main organs was significantly reduced. These results suggest that wrapping BBR in LMWF-Lip can improve efficacy and reduce its systemic toxicity as a potential treatment for various diseases caused by inflammatory responses.

CREB5 hypermethylation involved in the ganglioside GM1 therapy of Parkinson's disease.

Introduction: The treatment with monosialotetrahexosylganglioside (GM1) improves the symptoms of Parkinson's disease (PD). The alteration of DNA methylation in the blood was examined to investigate epigenetic modification by GM1 treatment. Methods: After a 28-day continuous intravenous infusion of GM1 (100mg), the motor and non-motor symptoms were evaluated by UPDRS III, Mini-mental state examination (MMSE) scores, FS-14, SCOPA-AUT, and PDQ-8. Moreover, blood samples were collected and PBMC was isolated. Genome-wide DNA methylation was performed by an 850K BeadChip. RNA levels and apoptosis were examined by RT-PCR and flow cytometry in rotenone-based cell models. The CREB5 plasmid was transfected by electroporation into SH-SY5Y cells. We also identified 235 methylation variable positions achieving genome-wide significance in 717558 differentially methylated positions (DMPs) (P = 0.0003) in comparison of pre-treatment with post-treatment measurements (statistical analysis paired-samples t-test). Results: By searching the Gene Expression Omnibus (GEO) dataset and GWAS, 23 methylation variable positions were screened. Moreover, there are 7 hypomethylated methylation variable positions correlated with the scores of motor symptoms (UPDRS III scale). According to KEGG pathways enrichment analysis, the methylated genes CACNA1B (hypomethylated), CREB5 (hypermethylated), GNB4 (hypomethylated), and PPP2R5A (hypomethylated) were enriched in the dopaminergic synapse pathway. Pretreated with GM1 (80 µM) for 1 h, cell apoptosis and impaired neurite outgrowth were inhibited in rotenone-induced PD cell models. The RNA expression of CREB5 was increased in rotenone-treated SH-SY5Y cells. GM1 treatment decreased rotenone-induced CREB5 gene expression. The enhancement of CREB5 gene expression suppressed the protective role of GM1 in rotenone-induced cell apoptosis. Discussion: The application of GM1 improves the motor and non-motor symptoms of PD associated with the decreased CREB5 expression and the hypermethylation of CREB5. Clinical trial registration: https://www.chictr.org.cn/showproj.html?proj=120582t, identifier ChiCTR2100042537.

Engineered MOF-Enzyme Nanocomposites for Tumor Microenvironment-Activated Photodynamic Therapy with Self-Luminescence and Oxygen Self-Supply.

Photodynamic therapy (PDT) is a promising strategy for cancer treatment. However, its efficiency is hindered by three key parameters, namely, limited penetration depth of external light, tumor hypoxia, and self-aggregation of photosensitizers. Herein, we fabricated a novel "all-in-one" chemiluminescence-PDT nanosystem through the integration of an oxygen-supplying protein (hemoglobin, Hb) and a luminescent donor (luminol, Lum) in hierarchically engineered mesoporous porphyrinic metal-organic framework (MOF) nanoparticles. Mechanistically, the in situ chemiluminescence of Lum is activated by the high concentration of H2O2 in 4T1 cancer cells and further catalyzed by Hb and then absorbed by the porphyrin ligands in MOF nanoparticles through chemiluminescence resonance energy transfer. The excited porphyrins then sensitize oxygen supplied by Hb to produce sufficient reactive oxygen species that kill cancer cells. The MOF-based nanocomposite demonstrates excellent anticancer activity both in vitro and in vivo, with eventually a 68.1% tumor inhibition rate after intravenous injections without external light irradiation. This self-illuminating, oxygen-self-supplying nanosystem integrates all essential components of PDT into one simple nanoplatform, demonstrating great potential for the selective phototherapy of deep-seated cancer.

Molecular Characterization and Efficacy Evaluation of Transgenic Maize Harboring cry2Ab-vip3A-cp4epsps for Insect Resistance and Herbicide Tolerance.

Insect infestation and weed interference have a seriously negative impact on the growth, yield, and grain quality of maize. In this study, transgenic maize plants harboring three exogenous genes, cry2Ab, vip3A, and cp4epsps, that were constructed into a single T-DNA were developed for protection against insects and weeds. The transgene integration sites on the chromosomes in two transgenic maize events, CVC-1 and CVC-2, were determined using whole genome sequencing and specific PCR detection. As revealed by laboratory insect bioassays, these two transgenic events exhibited strong insecticidal toxicity against three major species of Lepidoptera insects, including Mythimna separata, Helicoverpa armigera, and Spodoptera frugiperda, with mortality rates exceeding 96%, 100%, and 100%, respectively, after six days of infestation. In addition, CVC-1 exhibited a high tolerance to glyphosate under field conditions. The successful expressions of cry2Ab, vip3A, and cp4epsps in various tissues at different developmental stages of CVC-1 were validated at the transcriptional and translational levels using quantitative real-time reverse transcription PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. These findings demonstrated that the transgenic maize CVC-1 developed using this triple gene construct has excellent insect resistance and herbicide tolerance, which may provide a valuable germplasm resource and data support for future maize breeding of insect and weed control.

Manipulation of the Buried Interface for Robust Formamidinium-based Sn-Pb Perovskite Solar Cells with NiOx Hole-Transport Layers.

Low band gap tin-lead perovskite solar cells (Sn-Pb PSCs) are expected to achieve higher efficiencies than Pb-PSCs and regarded as key components of tandem PSCs. However, the realization of high efficiency is challenged by the instability of Sn2+ and the imperfections at the charge transfer interfaces. Here, we demonstrate an efficient ideal band gap formamidinium (FA)-based Sn-Pb (FAPb0.5 Sn0.5 I3 ) PSC, by manipulating the buried NiOx /perovskite interface with 4-hydroxyphenethyl ammonium halide (OH-PEAX, X=Cl- , Br- , or I- ) interlayer, which exhibits fascinating functions of reducing the surface defects of the NiOx hole transport layer (HTL), enhancing the perovskite film quality, and improving both the energy level matching and physical contact at the interface. The effects of different halide anions have been elaborated and a 20.53 % efficiency is obtained with OH-PEABr, which is the highest one for FA-based Sn-Pb PSCs using NiOx HTLs. Moreover, the device stability is also boosted.

Regulating the Interplay at the Buried Interface for Efficient and Stable Carbon-Based CsPbI2Br Perovskite Solar Cells.

Buried interface modification is promising for preparing high-performance perovskite solar cells (PSCs) by improving the film quality and adjusting the interfacial energy level alignment. In this work, multifunctional ethylenediaminetetraacetic acid diammonium (EAD)-modulated ZnO is employed as an effective buried interface to regulate the interplay between SnO2 and CsPbI2Br in carbon-based inorganic PSCs (C-IPSCs). The burying of EAD into the ZnO interlayer not only enhances the photoelectric properties of ZnO by passivating oxygen defects but also adjusts the energy level alignment of the buried interface. More importantly, the perovskite quality is optimized and the buried interface defects are passivated due to the formation of coordination and hydrogen bondings. Benefiting from such a robust and efficient charge transfer configuration, a maximum power conversion efficiency of 14.58% is achieved in the optimized device, which represents the highest performance reported among those of low-temperature CsPbI2Br C-IPSCs. In addition, the unencapsulated device demonstrates better long-term and thermal stability.

Resveratrol alleviated neuroinflammation induced by pseudorabies virus infection through regulating microglial M1/M2 polarization.

BACKGROUND: Pseudorabies virus (PRV) infections in susceptible non-porcine species trigger uncontrolled inflammations and eventually fatal encephalitis. Resveratrol (Res) has broad pharmacological functions including anti-virus, anti-inflammation, and neuroprotective. PURPOSE: We attempted to investigate the potential of Res in ameliorating PRV infection pathology in mice and decipher the mechanism of Res in treating PRV. METHODS: The mice were infected by PRV to investigate the protective effect of Res. Blood-brain barrier (BBB) permeability, H&E/Nissl/TUNEL staining, Real-time PCR and ELISA analyses were performed. Primary microglia and neuron were isolated from mice and cultured. The co-culture model of microglia and neuron was established by transwell. Immunofluorescence assay and flow cytometry were used. RESULTS: In this study, we showed that Res ameliorated brain damage by reducing BBB permeability in PRV-infected mice, and diminished the expressions of MMP-2, MMP-9 and ZO-1 in the cortex. Pathological changes of neurons by H&E/Nissl/TUNEL staining suggested that Res could alleviate neuronal lesions. Moreover, Res inhibited the expressions of pro-inflammatory factors (IL-6, TNF-α) and chemokines (CCL3, CXCL10, MCP-1), but increased the expressions of anti-inflammatory factors (IL-4, IL-10) and neurotrophic factor (TGF-ß, NGF and GDNF) in brain. In vitro cultured microglia cells, Res could suppress M1 microglia polarization and activate M2 microglia polarization. Co-culture of PRV-infected microglia with neuron cells by transwell system indicated that Res alleviated inflammatory response and neuronal apoptosis. CONCLUSION: This study provided evidence that Res could protect mice from PRV-induced encephalitis through regulation of microglia polarization and neuronal apoptosis suggesting the potential for treatment of viral encephalitis.

Rapid and label-free histological imaging of unprocessed surgical tissues via dark-field reflectance ultraviolet microscopy.

Routine examination for intraoperative histopathologic assessment is lengthy and laborious. Here, we present the dark-field reflectance ultraviolet microscopy (DRUM) that enables label-free imaging of unprocessed and thick tissues with subcellular resolution and a high signal-to-background ratio. To the best of our knowledge, DRUM provides image results for pathological assessment with the shortest turnaround time (2-3 min in total from sample preparation to tissue imaging). We also proposed a virtual staining process to convert DRUM images into pseudo-colorized images and enhance the image familiarity of pathologists. By imaging various tissues, we found DRUM can resolve cell nuclei and some extranuclear features, which are comparable to standard H&E images. Furthermore, the essential diagnostic features of intraoperatively excised tumor tissues also can be revealed by DRUM, demonstrating its potential as an additional aid for intraoperative histopathology.

Accelerating Electrochemical Water Oxidation Activity by Tailoring Morphology and Electronic Structure of Nickel Organic Framework Nanoarrays with a Fe Etching Effect.

Fe-mediated nickel organic framework nanoarrays (NiFe-MOFs NAs) on carbon cloth were successfully constructed from ultrathin nanosheets via an etching effect. This strategy also combined the dissolution and coordination effect of acidic ligand (2,6-naphthalenedicarboxylic acid, NDC) to a self-sacrificial template of Ni(OH)2 NAs. Benefiting from the strong Fe etching effect, dense and thick brick-like Ni-NDC nanoplates were tailored into loose and ultrathin NiFe-NDC nanosheets with abundant squamous nanostructures, which were still tightly attached to carbon cloth. As a consequence, more coordinatively unsaturated metal sites (CUMSs) that served as active centers were exposed to accelerate oxygen production. Meanwhile, the electronic structure of active Ni centers was modulated by the incorporation of Fe atoms. The charge density redistribution between Ni and Fe ultimately optimized the energy barrier of the adsorption/desorption of oxygenated intermediates, promoting the kinetics for water oxidation.

Enhanced Electromagnetic Shielding and Thermal Management Properties in MXene/Aramid Nanofiber Films Fabricated by Intermittent Filtration.

High-efficiency electromagnetic interference (EMI) shielding and heat dissipation synergy materials with flexible, robust, and environmental stability are urgently demanded in next-generation integration electronic devices. In this work, we report the lamellar MXene/Aramid nanofiber (ANF) composite films, which establish a nacre-like structure for EMI shielding and heat dissipation by using the intermittent filtration strategy. The MXene/ANF composite film filled with 50 wt % MXene demonstrates enhanced mechanical properties with a strength of 230.5 MPa, an elongation at break of 6.2%, and a toughness of 11.8 MJ·m3 (50 wt % MXene). These remarkable properties are attributed to the hydrogen bonding and highly oriented structure. Furthermore, due to the formation of the MXene conductive network, the MXene/ANF composite film shows an outstanding conductivity of 624.6 S/cm, an EMI shielding effectiveness (EMI SE) of 44.0 dB, and a superior specific SE value (SSE/t) of 18847.6 dB·cm2/g, which is better than the vacuum filtration film. Moreover, the MXene/ANF composite film also shows a great thermal conductivity of 0.43 W/m·K. The multifunctional MXene/ANF composite films with high-performance EMI shielding, heat dissipation, and joule heating show great potential in the field of aerospace, military, microelectronics, microcircuit, and smart wearable electronics.

Interleukin-29 Accelerates Vascular Calcification via JAK2/STAT3/BMP2 Signaling.

Background Vascular calcification (VC), associated with enhanced cardiovascular morbidity and mortality, is characterized by the osteogenic transdifferentiation of vascular smooth muscle cells. Inflammation promotes VC initiation and progression. Interleukin (IL)-29, a newly discovered member of type III interferon, has recently been implicated in the pathogenesis of autoimmune diseases. Here we evaluated the role of IL-29 in the VC process and underlying inflammatory mechanisms. Methods and Results The mRNA expression of IL-29 was significantly increased and positively associated with an increase in BMP2 (bone morphogenetic protein 2) mRNA level in calcified carotid arteries from patients with coronary artery disease or chronic kidney disease. IL-29 and BMP2 proteins are colocalized in human calcified arteries. IL-29 binding to its specific receptor IL-28Rα (IL-28 receptor α) (IL-29/IL-28Rα) inhibited the proliferation of rat vascular smooth muscle cells without altering cell apoptosis or migration. IL-29 promoted the calcification of rat vascular smooth muscle cells and their osteogenic transdifferentiation in vitro as well as the rat aortic ring calcification ex vivo, induced by the calcification medium or osteogenic medium. The procalcification effect of IL-29 was reduced by pharmacological inhibition of IL-29/IL-28Rα binding as well as suppression of janus kinase 2/signal transducer and activator of transcription pathway activation, accompanied by decreased BMP2 expression in the cultured rat vascular smooth muscle cells. Conclusions These results suggest an important role of IL-29 in VC development, at least partly, via activating the janus kinase 2/signal transducer and activator of transcription 3 signaling. Inhibition of IL-29 or its specific receptor, IL-28Rα, may provide a novel strategy to reduce VC in patients with vascular diseases.