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Traditional pressure-sensitive microcapsules used in textiles face challenges of insufficient environmental friendliness in the production process and uncontrollable fragrance release. To address this issue, this study utilized quaternary ammonium chitosan and silica as wall materials to develop a magnetic aromatic microcapsule. The microstructure of the microcapsules was controlled by magnetic field induction, and its evolution pattern was investigated. After magnetic field induction, the microcapsules exhibited a trend of evolving from spherical to asymmetrical shapes, accompanied by significant changes in mechanical properties. Asymmetrical microcapsules showed higher adhesion and lower stiffness. When applied to cotton textiles, the cotton textiles treated with asymmetrical microcapsules released 63.40 % of lavender essential oil after 200 friction cycles, representing an 11.3 % improvement in release efficiency compared to regular microcapsules, indicating better mechanical stimulus responsiveness. Additionally, in antibacterial tests, aromatic cotton exhibited a 96.52 % inhibition ratio against Escherichia coli. In summary, this study explores methods to adjust the mechanical properties of microcapsules and the relationship between mechanical properties and microstructure, providing a new approach for functional textiles.
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Antibacterianos , Cápsulas , Quitosano , Escherichia coli , Compuestos de Amonio Cuaternario , Quitosano/química , Compuestos de Amonio Cuaternario/química , Escherichia coli/efectos de los fármacos , Antibacterianos/química , Antibacterianos/farmacología , Campos Magnéticos , Aceites Volátiles/química , Aceites Volátiles/farmacología , Odorantes/análisis , Textiles , Dióxido de Silicio/química , Fibra de AlgodónRESUMEN
Maternal obesity has long-term effects on offspring metabolic health. Among the potential mechanisms, prior research has indicated potential disruptions in circadian rhythms and gut microbiota in the offspring. To challenge this hypothesis, we implemented a maternal high fat diet regimen before and during pregnancy, followed by a standard diet after birth. Our findings confirm that maternal obesity impacts offspring birth weight and glucose and lipid metabolisms. However, we found minimal impact on circadian rhythms and microbiota that are predominantly driven by the feeding/fasting cycle. Notably, maternal obesity altered rhythmic liver gene expression, affecting mitochondrial function and inflammatory response without disrupting the hepatic circadian clock. These changes could be explained by a masculinization of liver gene expression similar to the changes observed in polycystic ovarian syndrome. Intriguingly, such alterations seem to provide the first-generation offspring with a degree of protection against obesity when exposed to a high fat diet.
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Familial Partial Lipodystrophy 3 (FPLD3) is a rare genetic disorder caused by loss-of-function mutations in the PPARG gene, characterized by a selective absence of subcutaneous fat and associated metabolic complications. However, the molecular mechanisms of FPLD3 remain unclear. In this study, we recruited a 17-year-old Chinese female with FPLD3 and her family, identifying a novel PPARG frameshift mutation (exon 4: c.418dup: p.R140Kfs*7) that truncates the PPARγ protein at the 7th amino acid, significantly expanding the genetic landscape of FPLD3. By performing next generation sequencing of circular RNAs (circRNAs), microRNAs (miRNAs), and mRNAs in plasma exosomes, we discovered 59 circRNAs, 57 miRNAs, and 299 mRNAs were significantly altered in the mutation carriers in the comparison of healthy controls. Integration analysis highlighted that the circ_0001597-miR-671-5p pair and 18 mRNAs might be incorporated into the metabolic regulatory networks of the FPLD3 induced by the novel PPARG mutation. Functional annotation suggested that these genes were significantly enriched in glucose and lipid metabolism related pathways. Among the circRNA-miRNA-mRNA network, we identified two critical regulators, EGR1, a key transcription factor known for its role in insulin signaling pathways and lipid metabolism, and AGPAT3, which gets involved in the biosynthesis of triglycerides and lipolysis. Circ_0001597 regulates the expression of these genes through miR-671-5p, potentially contributing to the pathophysiology of FPLD3. Overall, this study clarified a circulating exosomal circRNA-miRNA-mRNA network in a FPLD3 family with a novel PPARG mutation, providing evidence for exploring promising biomarkers and developing novel therapeutic strategies for this rare genetic disorder.
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Developing a general method that leads to the formation of different classes of chiral bioactive compounds and their stereoisomers is an attractive but challenging research topic in organic synthesis. Furthermore, despite the great value of asymmetric transfer hydrogenation (ATH) in both organic synthesis and the pharmaceutical industry, the monohydrogenation of unsymmetrical 1,2-diketones remains underdeveloped. Here, we report the aryloxy group-assisted highly regio-, diastereo-, and enantioselective ATH of racemic 1,2-diketones. The work produces a myriad of enantioenriched dihydroxy ketones, and further transformations furnish all eight stereoisomers of diaryl triols, polyphenol, emblirol, and glycerol-type natural products. Mechanistic studies and calculations reveal two working modes of the aryloxy group in switching the regioselectivity from a more reactive carbonyl to a less reactive one, and the potential of ATH on 1,2-diketones in solving challenging synthetic issues has been clearly demonstrated.
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OBJECTIVE: Nonalcoholic fatty liver disease (NAFLD) is considered an independent risk factor for cardiovascular disease (CVD). The overall morbidity and mortality of CVD increase with higher fibrosis stage in NAFLD. Carotid atherosclerosis (CAS) is an important predictor of cardiovascular events. However, the relationship between liver fibrosis degree and the risk of CAS in NAFLD patients remains uncertain. We aimed to investigate the relationship between noninvasive liver fibrosis markers and CAS risk in patients with NAFLD. MATERIALS AND METHODS: This study included 3,302 participants with NAFLD. Participants were divided into a CAS group and a non-CAS group based on carotid artery ultrasound results. They were then stratified into quartiles using various noninvasive liver fibrosis markers (fibrosis-4 (FIB-4), modified FIB-4 (mFIB-4), aminotransferase to platelet ratio index (APRI), aminotransferase to alanine aminotransferase ratio (AAR), AAR-to-platelet ratio index (AARPRI), and Forns index) to assess the associations between these markers and the risk of CAS. RESULTS: In the NAFLD population, individuals with CAS exhibited elevated levels of blood pressure, glucose, lipids, and noninvasive liver fibrosis markers (p < 0.001). The higher quartiles of noninvasive liver fibrosis markers, including FIB-4, mFIB-4, AAR, AARPRI, and Forns index, were significantly associated with increased risks of CAS, even after adjusting for multiple CVD risk factors. CONCLUSIONS: In individuals with NAFLD, increased noninvasive liver fibrosis markers were independently associated with elevated CAS risk, which may be beneficial in assessing the risk of CVD in individuals with NAFLD.
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Biomarcadores , Enfermedades de las Arterias Carótidas , Cirrosis Hepática , Enfermedad del Hígado Graso no Alcohólico , Humanos , Enfermedad del Hígado Graso no Alcohólico/complicaciones , Enfermedad del Hígado Graso no Alcohólico/sangre , Masculino , Femenino , Persona de Mediana Edad , Enfermedades de las Arterias Carótidas/sangre , Enfermedades de las Arterias Carótidas/diagnóstico por imagen , Cirrosis Hepática/sangre , Cirrosis Hepática/complicaciones , Biomarcadores/sangre , Factores de Riesgo , Adulto , Anciano , Alanina Transaminasa/sangre , Ultrasonografía , Recuento de Plaquetas , Modelos LogísticosRESUMEN
Volatile chemical products (VCPs) are increasingly recognized as significant sources of volatile organic compounds (VOCs) in urban atmospheres, potentially serving as key precursors for secondary organic aerosol (SOA) formation. This study investigates the formation and physicochemical transformations of VCP-derived SOA, produced through ozonolysis of VOCs evaporated from a representative room deodorant air freshener, focusing on the effects of aerosol evaporation on its molecular composition, light absorption properties, and reactive oxygen species (ROS) generation. Following aerosol evaporation, solutes become concentrated, accelerating reactions within the aerosol matrix that lead to a 42% reduction in peroxide content and noticeable browning of the SOA. This process occurs most effectively at moderate relative humidity (â¼40%), reaching a maximum solute concentration before aerosol solidification. Molecular characterization reveals that evaporating VCP-derived SOA produces highly conjugated nitrogen-containing products from interactions between existing or transformed carbonyl compounds and reduced nitrogen species, likely acting as chromophores responsible for the observed brownish coloration. Additionally, the reactivity of VCP-derived SOA was elucidated through heterogeneous oxidation of sulfur dioxide (SO2), which revealed enhanced photosensitized sulfate production upon drying. Direct measurements of ROS, including singlet oxygen (1O2), superoxide (O2â¢-), and hydroxyl radicals (â¢OH), showed higher abundances in dried versus undried SOA samples under light exposure. Our findings underscore that drying significantly alters the physicochemical properties of VCP-derived SOA, impacting their roles in atmospheric chemistry and radiative balance.
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Aerosoles , Compuestos Orgánicos Volátiles , Compuestos Orgánicos Volátiles/química , Oxidación-Reducción , Contaminantes Atmosféricos/química , Especies Reactivas de Oxígeno/química , Atmósfera/químicaRESUMEN
OBJECTIVE: Endometrial cancer (EC) is a prevalent gynecologic malignancy. The critical role of PTPN18 in EC has been reported, while its role in the aerobic glycolysis of EC cells remains unclear. Our current study focused on the mechanism of PTPN18 in the regulation of aerobic glycolysis in EC. METHODS: PTPN18 expression levels in endometrial stromal cells (KC02-44D) and EC cells (KLE, HEC-1-A, HEC-1B, and HEC-50) were determined. Following transfection of sh-PTPN18 in HEC-1-A cells, the changes in cell migratory and invasive abilities were assessed by the Transwell assay, and the changes in glucose consumption, lactic acid secretion, and ATP levels were detected using kits. The expression levels of glycolysis-related proteins HIF-1α, PKM2, and LDHA and the activation of the MYC/PI3K/AKT pathway were detected by Western blot. Additionally, sh-PTPN18 and pcDNA3.1-MYC were transfected into HEC-1-A cells to further explore their roles in the changes in aerobic glycolysis, migration, and invasion ability of EC cells. RESULTS: Expression of PTPN18 in EC cells was up-regulated (HEC-1-A>HEC-1B>HEC-50>KLE). PTPN18 knockdown suppressed EC cell migration and invasion. Additionally, PTPN18 knockdown reduced glucose consumption, lactate production, ATP levels, and glycolysis-related protein levels (HIF-1α, PKM2, LDHA). PTPN18 knockdown inhibited the activation of the MYC/PI3K/AKT pathway in EC cells. MYC overexpression partially annulled the inhibitory effects of PTPN18 knockdown on aerobic glycolysis, migration, and invasion of EC cells. CONCLUSION: Our present study provided evidence that the knockdown of PTPN18 inhibited the aerobic glycolysis, migration, and invasion of EC cells by suppressing the MYC/PI3K/AKT pathway.
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BACKGROUND: The incidence of spontaneous abortion (SA), which affects approximately 15-20% of pregnancies, is the most common complication of early pregnancy. Pathogenic copy number variations (CNVs) are recognized as potential genetic causes of SA. However, CNVs of variants of uncertain significance (VOUS) have been identified in products of conceptions (POCs), and their correlation with SA remains uncertain. RESULTS: Of 189 spontaneous abortion cases, trisomy 16 was the most common numerical chromosome abnormality, followed by monosomy X. CNVs most often occurred on chromosomes 4 and 8. Gene Ontology and signaling pathway analysis revealed significant enrichment of genes related to nervous system development, transmembrane transport, cell adhesion, and structural components of chromatin. Furthermore, genes within the VOUS CNVs were screened by integrating human placental expression profiles, PhyloP scores, and Residual Variance Intolerance Score (RVIS) percentiles to identify potential candidate genes associated with spontaneous abortion. Fourteen potential candidate genes (LZTR1, TSHZ1, AMIGO2, H1-4, H2BC4, H2AC7, H3C8, H4C3, H3C6, PHKG2, PRR14, RNF40, SRCAP, ZNF629) were identified. Variations in LZTR1, TSHZ1, and H4C3 may contribute to embryonic lethality. CONCLUSIONS: CNV sequencing (CNV-seq) analysis is an effective technique for detecting chromosomal abnormalities in POCs and identifying potential candidate genes for SA.
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Background: Circular RNAs (circRNAs) exhibit unique patterns of expression and high levels of stability in patient plasma samples such that they represent ideal non-invasive biomarkers that can be leveraged to detect a wide array of diseases including endometrial cancer (EC). This study was designed to identify circRNAs with potential diagnostic utility in serum samples from EC patients while also evaluating the utility of macrophage migration inhibitory factor (MIF) as a biomarker when screening for this form of cancer in the clinic. Methods: Levels of circEPSTI1 and MIF were assessed in the plasma of EC patients and healthy subjects (n=186 each) through qPCR and ELISAs. The diagnostic utility of these biomarkers was assessed with receiver operating characteristic curve (ROC) analyses. Results: Relative to healthy subjects, EC patient serum contained significantly elevated circEPSTI1 and MIF. An association was noted between circEPSTI1 expression in stages, histologic grade, and residual tumor. ROC curves confirmed that serum circEPSTI1 levels distinguished between controls and patients with EC with an Area of 0.835 and serum MIF levels distinguished between controls and patients with EC with an Area of 0.6646. When instead diagnosing patients based on the combination of MIF and circEPSTI1, the Area further rose to 0.8604. Conclusion: Assessing the combination of circEPSTI1 and MIF may be a viable approach to reliably diagnosing EC.
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Therapeutic strategies are the hot-spot issues in treating patients with advanced oral squamous cell carcinoma (OSCC). Mounting studies have proved that triggering ferroptosis is one of the promising targets for OSCC management. In this study, we performed a first attempt to collect the current evidence on the proposed roles of ferroptosis in OSCC through a comprehensive review. Based on clinical data from the relevant studies within this topic, we found that ferroptosis-associated tumor microenvironment, ferroptosis-related genes (FRGs), and ferroptosis-related lncRNAs exhibited a potent prognostic value for OSCC patients. Mechanistically, experimental data revealed that the proliferation and tumorigenesis of OSCC might be associated with the inhibition of cellular ferroptosis through the activation of glutathione peroxidase 4 (GPX4) and adipocyte enhancer-binding protein 1 (AEBP1), suppression of glutathione (GSH) and Period 1 (PER1) expression, and modulation of specific non-coding RNAs (i.e., miR-520d-5p, miR-34c-3p, and miR-125b-5p) and their targeted proteins. Several specific interventions (i.e., Quisinostat, Carnosic acid, hyperbaric oxygen, melatonin, aqueous-soluble sporoderm-removed G. lucidum spore powder, and disulfiram/copper complex) were found to dramatically induce ferroptosis cell death of OSCC via multiple mechanisms. This review highlighted the pivotal role of ferroptosis in the pathogenesis and prognosis of OSCC. Future anticancer therapeutic strategies targeting ferroptosis and its associated molecules might provide a new insight for OSCC treatment.
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Carcinoma de Células Escamosas , Ferroptosis , Neoplasias de la Boca , Ferroptosis/genética , Humanos , Neoplasias de la Boca/patología , Neoplasias de la Boca/genética , Neoplasias de la Boca/metabolismo , Pronóstico , Carcinoma de Células Escamosas/patología , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/genética , Regulación Neoplásica de la Expresión Génica , Microambiente TumoralRESUMEN
Quercetin is a representative flavonoid that is widely present in fruits, herbs, and vegetables. It is also an important active core component in traditional Chinese medicines. As an important flavonoid, quercetin has various properties and exerts antioxidant, anti-inflammatory, and cardioprotective effects. The public interest in quercetin is increasing, and quercetin has been used to prevent or treat numerous of diseases, such as polycystic ovary syndrome (PCOS), cancer, autoimmune diseases and chronic cardiovascular diseases, in clinical experiments and animal studies due to its powerful antioxidant properties and minimal side effects. Quercetin exerts marked pharmacological effects on gynecological disorders; however, there have been no reviews about the potential health benefits of quercetin in the context of gynecological disorders, including PCOS, premature ovary failure (POF), endometriosis (EM), ovarian cancer (OC), cervical cancer (CC) and endometrial carcinoma (EC). Thus, this review aimed to summarize the biological effects of quercetin on gynecological disorders and its mechanisms.
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Síndrome del Ovario Poliquístico , Quercetina , Humanos , Animales , Femenino , Quercetina/farmacología , Quercetina/uso terapéutico , Síndrome del Ovario Poliquístico/tratamiento farmacológico , Antioxidantes/farmacología , Antioxidantes/uso terapéutico , Flavonoides/uso terapéuticoRESUMEN
DNA methylation, an epigenetic mechanism that alters gene expression without changing DNA sequence, is essential for organism development and key biological processes like genomic imprinting and X-chromosome inactivation. Despite tremendous efforts in DNA methylation research, accurate quantification of cytosine methylation remains a challenge. Here, a single-base methylation quantification approach is introduced by weighting methylation of consecutive CpG sites (Wemics) in genomic regions. Wemics quantification of DNA methylation better predicts its regulatory impact on gene transcription and identifies differentially methylated regions (DMRs) with more biological relevance. Most Wemics-quantified DMRs in lung cancer are epigenetically conserved and recurrently occurred in other primary cancers from The Cancer Genome Atlas (TCGA), and their aberrant alterations can serve as promising pan-cancer diagnostic markers. It is further revealed that these detected DMRs are enriched in transcription factor (TF) binding motifs, and methylation of these TF binding motifs and TF expression synergistically regulate target gene expression. Using Wemics on epigenomic-transcriptomic data from the large lung cancer cohort, a dozen novel genes with oncogenic potential are discovered that are upregulated by hypomethylation but overlooked by other quantification methods. These findings increase the understanding of the epigenetic mechanism by which DNA methylation regulates gene expression.
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Metilación de ADN , Epigénesis Genética , Neoplasias Pulmonares , Metilación de ADN/genética , Epigénesis Genética/genética , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Islas de CpG/genéticaRESUMEN
[Retraction to: BMB Rep. 2022 June 30; 55(6): 299-304.] Retraction: "Inhibition of ClC-5 suppresses proliferation and induces apoptosis in cholangiocarcinoma cells through the Wnt/ß-catenin signaling pathway," by Zhe Shi, Liyuan Zhou, Yan Zhou, Xiaoyan Jia, Xiangjun Yu, Xiaohong An and Yanzhen Han, BMB Rep. 2022; 55(6) 299-304: The above article, published online on 30 June 2022 in BMB Reports https://doi.org/10.5483/ BMBRep.2022.55.6.044), has been retracted by agreement between the authors and the journal's Editor in Chief. The authors unable to replicate certain results presented in the article and have therefore made the difficult decision to withdraw it. Editorial Board, BMB Reports.
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BACKGROUND: Time in range (TIR), as an important glycemic variability (GV) index, is clearly associated with disease complications in type 1 diabetes (T1D). Metabolic dysregulation is also involved in the risks of T1D complications. However, the relationship between metabolites and TIR remains poorly understood. We used metabolomics to investigate metabolic profile changes in T1D patients with different TIR. METHODS: This study included 85 T1D patients and 81 healthy controls. GV indices, including TIR, were collected from continuous glucose monitoring system. The patients were compared within two subgroups: TIR-L (TIR < 50%, n = 21) and TIR-H (TIR > 70%, n = 14). To screen for differentially abundant metabolites and metabolic pathways, serum and urine samples were obtained for untargeted metabolomics by ultra-performance liquid chromatographyâmass spectrometry. Correlation analysis was conducted with GV metrics and screened biomarkers. RESULTS: Metabolites were significantly altered in T1D and subgroups. Compared with healthy controls, T1D patients had higher serum levels of 5-hydroxy-L-tryptophan, 5-methoxyindoleacetate, 4-(2-aminophenyl)-2,4-dioxobutanoate, and 4-pyridoxic acid and higher urine levels of thromboxane B3 but lower urine levels of hypoxanthine. Compared with TIR-H group, The TIR-L subgroup had lower serum levels of 5-hydroxy-L-tryptophan and mevalonolactone and lower urine levels of thromboxane B3 and phenylbutyrylglutamine. Dysregulation of pathways, such as tryptophan, vitamin B6 and purine metabolism, may be involved in the mechanism of diabetic complications related to glycemic homeostasis. Mevalonolactone, hypoxanthine and phenylbutyrylglutamine showed close correlation with TIR. CONCLUSIONS: We identified altered metabolic profiles in T1D individuals with different TIR. These findings provide new insights and merit further exploration of the underlying molecular pathways relating to diabetic complications.
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Despite the immense success of immune checkpoint blockade (ICB) in cancer treatment, many tumors, including melanoma, exhibit innate or adaptive resistance. Tumor-intrinsic T-cell deficiency and T-cell dysfunction have been identified as essential factors in the emergence of ICB resistance. Here, we found that protein arginine methyltransferase 1 (PRMT1) expression was inversely correlated with the number and activity of CD8+ T cells within melanoma specimen. PRMT1 deficiency or inhibition with DCPT1061 significantly restrained refractory melanoma growth and increased intratumoral CD8+ T cells in vivo. Moreover, PRMT1 deletion in melanoma cells facilitated formation of double-stranded RNA derived from endogenous retroviral elements (ERV) and stimulated an intracellular interferon response. Mechanistically, PRMT1 deficiency repressed the expression of DNA methyltransferase 1 (DNMT1) by attenuating modification of H4R3me2a and H3K27ac at enhancer regions of Dnmt1, and DNMT1 downregulation consequently activated ERV transcription and the interferon signaling. Importantly, PRMT1 inhibition with DCPT1061 synergized with PD-1 blockade to suppress tumor progression and increase the proportion of CD8+ T cells as well as IFNγ+CD8+ T cells in vivo. Together, these results reveal an unrecognized role and mechanism of PRMT1 in regulating antitumor T-cell immunity, suggesting PRMT1 inhibition as a potent strategy to increase the efficacy of ICB. SIGNIFICANCE: Targeting PRMT1 stimulates interferon signaling by increasing expression of endogenous retroviral elements and double-stranded RNA through repression of DNMT1, which induces antitumor immunity and synergizes with immunotherapy to suppress tumor progression.
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Interferones , Melanoma , Humanos , Melanoma/metabolismo , ARN Bicatenario , Linfocitos T CD8-positivos , Metiltransferasas/metabolismo , Proteína-Arginina N-Metiltransferasas/metabolismo , Proteínas Represoras/genética , Proteínas Represoras/metabolismoRESUMEN
By increasing the content of Ni3+, the catalytic activity of nickel-based catalysts for the oxygen evolution reaction (OER), which is still problematic with current synthesis routes, can be increased. Herein, a Ni3+-rich of Ni3S4/FeS on FeNi Foam (Ni3S4/FeS@FNF) via anodic electrodeposition to direct obtain high valence metal ions for OER catalyst is presented. XPS showed that the introduction of Fe not only further increased the Ni3+ concentration in Ni3S4/FeS to 95.02%, but also inhibited the dissolution of NiOOH by up to seven times. Furthermore, the OER kinetics is enhanced by the combination of the inner Ni3S4/FeS heterostructures and the electrochemically induced surface layers of oxides/hydroxides. Ni3S4/FeS@FNF shows the most excellent OER activity with a low Tafel slope of 11.2 mV dec-1 and overpotentials of 196 and 445 mV at current densities of 10 and 1400 mA cm-2, respectively. Furthermore, the Ni3S4/FeS@FNF catalyst can be operated stably at 1500 mA cm-2 for 200 h without significant performance degradation. In conclusion, this work has significantly increased the high activity Ni3+ content in nickel-based OER electrocatalysts through an anodic electrodeposition strategy. The preparation process is time-saving and mature, which is expected to be applied in large-scale industrialization.
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Transfer RNA-derived fragments (tRFs) are a class of small non-coding regulatory RNAs that are involved in the pathophysiology of many diseases. However, the role of tRFs in cancer progression remains largely elusive. Here, we demonstrate that a pan-cancer 3'-tRF, CAT1 (cancer associated tRF 1), is ubiquitously upregulated in tumors and associated with poor prognosis of a variety of cancers, including lung cancer. The upregulated CAT1 in cancer cells binds to RNA-binding protein with multiple splicing (RBPMS) and displaces NOTCH2 association from RBPMS, thereby inhibiting the subsequent CCR4-NOT deadenylation-complex-mediated NOTCH2 mRNA decay. The CAT1-enhanced NOTCH2 expression promotes lung cancer cell proliferation and metastasis in vitro and in vivo. In addition, plasma CAT1 levels are substantially increased in patients with lung cancer compared to non-cancer control subjects. Our findings reveal an intrinsic connection between cancer-specific upregulation of CAT1 and cancer progression, show the regulation of NOTCH signaling in cancer by a 3'-tRF, and highlight its great clinical potential.
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Neoplasias Pulmonares , ARN de Transferencia , Humanos , ARN Mensajero/genética , ARN de Transferencia/metabolismo , Transformación Celular Neoplásica , Neoplasias Pulmonares/genética , Proteínas de Unión al ARN , Receptor Notch2/genética , Receptor Notch2/metabolismoRESUMEN
Employing metal anodes can greatly increase the volumetric/gravimetric energy density versus a conventional ion-insertion anode. However, metal anodes are plagued by dendrites, corrosion, and interfacial side reaction issues. Herein, a continuous and flexible amorphous MOF layer was successfully synthesized and used as a protective layer on metal anodes. Compared with the crystalline MOF layer, the continuous amorphous MOF layer can inhibit dendrite growth at the grain boundary and eliminate ion migration near the grain boundary, showing high interfacial adhesion and a large ion migration number (tZn2+ = 0.75). In addition, the continuous amorphous MOF layer can effectively solve several key challenges, e.g., corrosion of the zinc anode, hydrogen evolution reaction, and dendrite growth on the zinc surface. The prepared Zn anode with the continuous amorphous MOF (A-MOF) layer exhibited an ultralong cycling life (around one year, more than 7900 h) and a low overpotential (<40 mV), which is 12 times higher than that of the crystalline MOF protective layer. Even at 10 mA cm-2, it still showed high stability for more than 5500 cycles (1200 h). The enhanced performance is realized for full cells paired with a MnO2 cathode. In addition, a flexible symmetrical battery with the Zn@A-ZIF-8 anode exhibited good cyclability under different bending angles (0°, 90°, and 180°). More importantly, various metal substrates were successfully coated with compact A-ZIF-8. The A-ZIF-8 layer can obviously improve the stability of other metal anodes, including those of Mg and Al. These results not only demonstrate the high potential of amorphous MOF-decorated Zn anodes for AZIBs but also propose a type of protective layer for metal anodes.
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The relationship between vitamin D deficiency and sensitivity to thyroid hormones was unclear. We aimed to explore the association of 25-hydroxyvitamin D (25(OH)D) levels with thyroid hormone sensitivity in euthyroid adults. A total of 3143 subjects were included. The serum 25(OH)D, free thyroxine (FT3), free thyrotropin (FT4), thyroid-stimulating hormone (TSH), and other clinical variables were measured. Vitamin D deficiency was defined as 25(OH)D < 20 ng/mL. Thyroid feedback quantile-based index (TFQI), parametric thyroid feedback quantile-based index (PTFQI), thyroid-stimulating hormone index (TSHI), thyrotrophic thyroxine resistance index (TT4RI), and FT3/FT4 were calculated to assess thyroid hormone sensitivity. Results showed that 58.8% of the participants had vitamin D deficiency. They had significantly higher levels of triglyceride, insulin, FT3, FT4, TSH, TFQI, PTFQI, TSHI, and TT4RI and lower levels of high-density lipoprotein cholesterol than those with sufficient vitamin D (all p < 0.05). Logistic regression analysis showed that the risk of impaired sensitivity to thyroid hormones evaluated by TFIQ, PTFQI, TSHI, and TT4RI increased by 68% (OR: 1.68; 95%CI: 1.45-1.95; and p < 0.001), 70% (OR: 1.70; 95%CI: 1.46-1.97; and p < 0.001), 66% (OR: 1.66; 95%CI: 1.43-1.92; and p < 0.001), and 50% (OR: 1.50; 95%CI: 1.30-1.74; and p < 0.001), respectively, in participants with vitamin D deficiency compared with those with sufficient vitamin D after adjusting for multiple confounders. In conclusion, in euthyroid populations, vitamin D deficiency was associated with impaired sensitivity to thyroid hormones.