RESUMEN
BACKGROUND: Acute Kidney Injury (AKI), a prevalent complication of Liver Transplantation (LT) that occurs during the perioperative period has been established to profoundly impact the prognosis of transplant recipients. This study aimed to investigate the mechanism of the hepatic IRI-induced AKI and to identify potential therapeutic targets for treating this condition and improving the prognosis of LT patients. METHODS: An integrated transcriptomics and proteomics approach was employed to investigate transcriptional and proteomic alterations in hepatic IRI-induced AKI and the hypoxia-reoxygenation (H/R) model using TCMK-1 cells and the hepatic IRI-induced AKI mouse model using male C57BL/6 J mice were employed to elucidate the underlying mechanisms. Hematoxylin-eosin staining, reverse transcription quantitative polymerase chain reaction, enzyme-linked immunosorbent assay and Western blot were used to assess the effect of Rosiglitazone (RGZ) on hepatic IRI-induced AKI in vitro and in vivo. RESULTS: According to the results, 322 genes and 128 proteins were differentially expressed between the sham and AKI groups. Furthermore, Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomics (KEGG) pathway analyses revealed significant enrichment in pathways related to amino acid and lipid metabolism. Additionally, the Protein-Protein Interaction (PPI) network analysis of the kidney tissues obtained from a hepatic IRI-induced AKI mouse model highlighted arachidonic acid metabolism as the most prominent pathway. Animal and cellular analyses further revealed that RGZ, a PPAR-γ agonist, could inhibit the expression of the PPAR-γ/NF-κB signaling pathway-associated proteins in in vitro and in vivo. CONCLUSIONS: These findings collectively suggest that RGZ ameliorates hepatic IRI-induced AKI via PPAR-γ/NF-κB signaling pathway modulation, highlighting PPAR-γ as a crucial therapeutic target for AKI prevention post-LT.
RESUMEN
Brain lipidic peroxidation is closely associated with the pathophysiology of various psychiatric diseases including depression. Malondialdehyde (MDA), a reactive aldehyde produced in lipid region, serves as a crucial biomarker for lipid peroxidation. However, techniques enabling real-time detection of MDA are still lacking due to the inherent trade-off between recognition dynamics and robustness. Inspired by the structure of phospholipid bilayers, amphiphilic carbon dots named as CG-CDs targeted to cell membrane are designed for real-time monitoring of MDA fluctuations. The design principle relies on the synergy of dynamic hydrogen bonding recognition and cell membrane targetability. The latter facilitates the insertion of CG-CDs into lipid regions and provides a hydrophobic environment to stabilize the labile hydrogen bonding between CG-CDs and MDA. As a result, recognition robustness and dynamics are simultaneously achieved for CG-CDs/MDA, allowing for in situ visualization of MDA kinetics in cell membrane due to the instant response (<5 s), high sensitivity (9-fold fluorescence enhancement), intrinsic reversibility (fluorescence on/off), and superior selectivity. Subsequently, CG-CDs are explored to visualize nerve cell membrane impairment in depression models of living cells and zebrafish, unveiling the extensive heterogeneity of the lipid peroxidation process and indicating a positive correlation between MDA levels and depression.
RESUMEN
Light irradiation of stilbene supramolecular polymers produces [2+2] cycloadducts in the kinetically trapped state, which convert to the thermodynamically favorable state upon thermal annealing due to the shift of hydrogen bonds from intra- to inter-complexation modes.
RESUMEN
BACKGROUND: Liquid biopsies, for example, exosomal circular RNA (circRNA) can be used to assess potential predictive markers for hepatocellular carcinoma (HCC) in patients after curative resection. This study aimed to search for effective prognostic biomarkers for HCC in patients after surgical resection based on exosomal circRNA expression profiles. We developed two nomograms incorporating circRNAs to predict the postoperative recurrence-free survival (RFS) and overall survival (OS) of HCC patients. METHOD: Plasma exosomes isolated from HCC patients and healthy individuals were used for circRNA microarray analysis to explore differentially expressed circRNAs. Pearson correlation analysis was used to evaluate the correlation between circRNAs and clinicopathological features. Cox regression analysis was used to explore the correlation between circRNA and postoperative survival time as well as recurrence time. A nomogram based on circRNA and clinicopathological characteristics was established and further evaluated to predict prognosis and recurrence. RESULT: Among 60 significantly upregulated circRNAs and 25 downregulated circRNAs, hsa_circ_0029325 was selected to verify its power for predicting HCC outcomes. The high expression level of exosomal hsa_circ_0029325 was significantly correlated with OS (P = 0.001, HR = 2.04, 95% CI 1.41-3.32) and RFS (P = 0.009, HR = 1.62, 95% CI 1.14-2.30). Among 273 HCC patients, multivariate regression analysis showed that hsa_circ_0029325 (HR = 1.96, 95% CI 1.21-3.18), tumor size (HR = 2.11, 95% CI 1.33-3.32), clinical staging (HR = 2.31, 95% CI 1.54-3.48), and tumor thrombus (HR = 1.74, 95% CI 1.12-2.7) were independent risk factors for poor prognosis in HCC patients after radical resection. These independent predictors of prognosis were incorporated into the two nomograms. The AUCs under the 1-year, 3-year, and 5-year survival and recurrence curves of the OS and RFS nomograms were 0.755, 0.749, and 0.742 and 0.702, 0.685, and 0.642, respectively. The C-index, calibration curves, and clinical decision curves showed that the two prediction models had good predictive performance. These results were verified in the validation cohort with 90 HCC patients. CONCLUSION: Our study established two reliable nomograms for predicting recurrence and prognosis in HCC patients. We also show that it is feasible to screen potential predictive markers for HCC after curative resection through exosomal circRNA expression profile analysis.
RESUMEN
Acute rejection is an important factor affecting the survival of recipients after liver transplantation. Salidroside has various properties, including anti-inflammatory, antioxidant, and hepatoprotective properties. This study aims to investigate whether salidroside can prevent acute rejection after liver transplantation and to examine the underlying mechanisms involved. An in vivo acute rejection model is established in rats that are pretreated with tacrolimus (1â mg/kg/d) or salidroside (10 or 20â mg/kg/d) for seven days after liver transplantation. In addition, an in vitro experiment is performed using neutrophils incubated with salidroside (1, 10, 50 or 100â µM). Hematoxylin-eosin staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling staining, immunosorbent assays, immunofluorescence analysis, Evans blue staining, and western blot analysis are performed to examine the impact of salidroside on NET formation and acute rejection in vitro and in vivo. We find that Salidroside treatment reduces pathological liver damage, serum aminotransferase level, and serum levels of IL-1ß, IL-6, and TNF-α in vivo. The expressions of proteins associated with the HMGB1/TLR-4/MAPK signaling pathway (HMGB1, TLR-4, p-ERK1/2, p-JNK, p-P38, cleaved caspase-3, cleaved caspase-9, Bcl-2, Bax, IL-1ß, TNF-α, and IL-6) are also decreased after salidroside treatment. In vitro experiments show that the release of HMGB1/TLR-4/MAPK signaling pathway-associated proteins from neutrophils treated with lipopolysaccharide is decreased by salidroside. Moreover, salidroside inhibits NETosis and protects against acute rejection by regulating the HMGB1/TLR-4/MAPK signaling pathway. Furthermore, salidroside combined with tacrolimus has a better effect than either of the other treatments alone. In summary, salidroside can prevent acute liver rejection after liver transplantation by reducing neutrophil extracellular trap development through the HMGB1/TLR-4/MAPK signaling pathway.
Asunto(s)
Trampas Extracelulares , Glucósidos , Rechazo de Injerto , Proteína HMGB1 , Trasplante de Hígado , Neutrófilos , Fenoles , Receptor Toll-Like 4 , Animales , Fenoles/farmacología , Glucósidos/farmacología , Trampas Extracelulares/efectos de los fármacos , Trampas Extracelulares/metabolismo , Rechazo de Injerto/prevención & control , Rechazo de Injerto/patología , Rechazo de Injerto/tratamiento farmacológico , Rechazo de Injerto/metabolismo , Proteína HMGB1/metabolismo , Receptor Toll-Like 4/metabolismo , Masculino , Neutrófilos/efectos de los fármacos , Neutrófilos/metabolismo , Ratas , Ratas Sprague-Dawley , Hígado/efectos de los fármacos , Hígado/patología , Hígado/metabolismo , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Apoptosis/efectos de los fármacosRESUMEN
BACKGROUND: Sorafenib is a standard first-line treatment for advanced hepatocellular carcinoma (HCC), yet its effectiveness is often constrained. Emerging studies reveal that sorafenib triggers ferroptosis, an iron-dependent regulated cell death (RCD) mechanism characterized by lipid peroxidation. Our findings isolate the principal target responsible for ferroptosis in HCC cells and outline an approach to potentially augment sorafenib's therapeutic impact on HCC. METHODS: We investigated the gene expression alterations following sgRNA-mediated knockdown induced by erastin and sorafenib in HCC cells using CRISPR screening-based bioinformatics analysis. Gene set enrichment analysis (GSEA) and the "GDCRNATools" package facilitated the correlation studies. We employed tissue microarrays and cDNA microarrays for validation. Ubiquitination assay, Chromatin immunoprecipitation (ChIP) assay, RNA immunoprecipitation (RIP) assay, and dual-luciferase reporter assay were utilized to delineate the specific mechanisms underlying ferroptosis in HCC cells. RESULTS: Our study has revealed that pleiomorphic adenoma gene 1 (PLAG1), a gene implicated in pleomorphic adenoma, confers resistance to ferroptosis in HCC cells treated with sorafenib. Sorafenib leads to the opposite trend of protein and mRNA levels of PLAG1, which is not caused by affecting the stability or ubiquitination of PLAG1 protein, but by the regulation of PLAG1 at the transcriptional level by its upstream competitive endogenous long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1). Data from 139 HCC patients showed a significant positive correlation between PLAG1 and GPX4 levels in tumor samples, and PLAG1 is instrumental in redox homeostasis by driving the expression of glutathione peroxidase 4 (GPX4), the enzyme that reduces lipid peroxides (LPOs), which further leads to ferroptosis inhibition. CONCLUSIONS: Ferroptosis is a promising target for cancer therapy, especially for patients resistant to standard chemotherapy or immunotherapy. Our findings indicate that PLAG1 holds therapeutic promise and may enhance the efficacy of sorafenib in treating HCC.
Asunto(s)
Carcinoma Hepatocelular , Proteínas de Unión al ADN , Ferroptosis , Neoplasias Hepáticas , Fosfolípido Hidroperóxido Glutatión Peroxidasa , Sorafenib , Animales , Humanos , Ratones , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/metabolismo , Carcinoma Hepatocelular/patología , Carcinoma Hepatocelular/genética , Línea Celular Tumoral , Proteínas de Unión al ADN/metabolismo , Proteínas de Unión al ADN/genética , Ferroptosis/efectos de los fármacos , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/patología , Neoplasias Hepáticas/genética , MicroARNs/genética , MicroARNs/metabolismo , Fosfolípido Hidroperóxido Glutatión Peroxidasa/metabolismo , Fosfolípido Hidroperóxido Glutatión Peroxidasa/genética , Sorafenib/farmacología , Sorafenib/uso terapéutico , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismoRESUMEN
The emergence of a bilayer B48 cluster, which has been both theoretically predicted and experimentally observed, as well as the recent experimental synthesis of bilayer borophene sheets on Ag and Cu surfaces, has generated tremendous curiosity in the bilayer structures of boron clusters. However, the connection between bilayer boron cluster and bilayer borophene remains unknown. By combining a genetic algorithm and density functional theory calculations, a global search for the low-energy structures of the B63 cluster was conducted, revealing that the Cs bilayer structure with three interlayer B-B bonds is the most stable bilayer structure. This structure was further examined in terms of its structural stability, chemical bonding, and aromaticity. Interestingly, the interlayer bonds induce strong electronegativity and robust aromaticity. Furthermore, the dual aromaticity stems from diatropic currents originating from virtual translational transitions for both σ and π electrons. This unprecedent bilayer boron cluster is anticipated to enrich the concept of dual aromaticity and serve as a potential precursor for bilayer borophene.
RESUMEN
Thrombocytopenia, a prevalent hematologic challenge, correlates directly with the mortality of numerous ailments. Current therapeutic avenues for thrombocytopenia are not without limitations. Here, we identify genistin, an estrogen analogue, as a promising candidate for thrombocytopenia intervention, discovered through AI-driven compound library screening. While estrogen's involvement in diverse biological processes is recognized, its role in thrombopoiesis remains underexplored. Our findings elucidate genistin's ability to enhance megakaryocyte differentiation, thereby augmenting platelet formation and production. In vivo assessments further underscore genistin's remedial potential against radiation-induced thrombocytopenia. Mechanistically, genistin's efficacy is attributed to its direct interaction with estrogen receptor ß (ERß), with subsequent activation of both ERK1/2 and the Akt signaling pathways membrane ERß. Collectively, our study positions genistin as a prospective therapeutic strategy for thrombocytopenia, shedding light on novel interplays between platelet production and ERß.
Asunto(s)
Isoflavonas , Trombocitopenia , Humanos , Receptor beta de Estrógeno/genética , Trombocitopenia/tratamiento farmacológico , Bibliotecas de Moléculas PequeñasRESUMEN
Objective: To develop and validate nomograms for predicting the OS and CSS of patients with Solitary Hepatocellular Carcinoma (HCC). Methods: Using the TRIPOD guidelines, this study identified 5206 patients in the Surveillance, Epidemiology, and End Results (SEER) 17 registry database. All patients were randomly divided in a ratio of 7:3 into a training cohort (n = 3646) and a validation cohort (n = 1560), and the Chinese independent cohort (n = 307) constituted the external validation group. The prognosis-related risk factors were selected using univariate Cox regression analysis, and the independent prognostic factors of OS and CSS were identified using the Lasso-Cox regression model. The nomograms for predicting the OS and CSS of the patients were constructed based on the identified prognostic factors. Their prediction ability was evaluated using the concordance index (C-index), receiver operating characteristic (ROC) curve, and calibration curve in both the training and validation cohorts. Results: We identified factors that predict OS and CSS and constructed two nomograms based on the data. The ROC analysis, C-index analysis, and calibration analysis indicated that the two nomograms performed well over the 1, 3, and 5-year OS and CSS periods in both the training and validation cohorts. Additionally, these results were confirmed in the external validation group. Decision curve analysis (DCA) demonstrated that the two nomograms were clinically valuable and superior to the TNM stage system. Conclusion: We established and validated nomograms to predict 1,3, and 5-year OS and CSS in solitary HCC patients, and our results may also be helpful for clinical decision-making.
RESUMEN
Thrombocytopenia caused by long-term radiotherapy and chemotherapy exists in cancer treatment. Previous research demonstrates that 5-Hydroxtrayptamine (5-HT) and its receptors induce the formation of megakaryocytes (MKs) and platelets. However, the relationships between 5-HT1A receptor (5-HTR1A) and MKs is unclear so far. We screened and investigated the mechanism of vilazodone as a 5-HTR1A partial agonist in promoting MK differentiation and evaluated its therapeutic effect in thrombocytopenia. We employed a drug screening model based on machine learning (ML) to screen the megakaryocytopoiesis activity of Vilazodone (VLZ). The effects of VLZ on megakaryocytopoiesis were verified in HEL and Meg-01 cells. Tg (itga2b: eGFP) zebrafish was performed to analyze the alterations in thrombopoiesis. Moreover, we established a thrombocytopenia mice model to investigate how VLZ administration accelerates platelet recovery and function. We carried out network pharmacology, Western blot, and immunofluorescence to demonstrate the potential targets and pathway of VLZ. VLZ has been predicted to have a potential biological action. Meanwhile, VLZ administration promotes MK differentiation and thrombopoiesis in cells and zebrafish models. Progressive experiments showed that VLZ has a potential therapeutic effect on radiation-induced thrombocytopenia in vivo. The network pharmacology and associated mechanism study indicated that SRC and MAPK signaling are both involved in the processes of megakaryopoiesis facilitated by VLZ. Furthermore, the expression of 5-HTR1A during megakaryocyte differentiation is closely related to the activation of SRC and MAPK. Our findings demonstrated that the expression of 5-HTR1A on MK, VLZ could bind to the 5-HTR1A receptor and further regulate the SRC/MAPK signaling pathway to facilitate megakaryocyte differentiation and platelet production, which provides new insights into the alternative therapeutic options for thrombocytopenia.
Asunto(s)
Trombocitopenia , Clorhidrato de Vilazodona , Ratones , Animales , Clorhidrato de Vilazodona/efectos adversos , Clorhidrato de Vilazodona/metabolismo , Pez Cebra , Receptor de Serotonina 5-HT1A/metabolismo , Plaquetas/metabolismo , Trombocitopenia/tratamiento farmacológico , Trombocitopenia/metabolismo , Megacariocitos/metabolismo , TrombopoyesisRESUMEN
The roles of γδ T cells in liver cancer, especially in the potential function of immunotherapy due to their direct cytotoxic effects on tumor cells and secretion of important cytokines and chemokines, have aroused research interest. This review briefly describes the basic characteristics of γδ T cells, focusing on their diverse effects on liver cancer. In particular, different subtypes of γδ T cells have diverse or even opposite effects on liver cancer. We provide a detailed description of the immune regulatory network of γδ T cells in liver cancer from two aspects: immune components and nonimmune components. The interactions between various components in this immune regulatory network are dynamic and pluralistic, ultimately determining the biological effects of γδ T cells in liver cancer. We also integrate the current knowledge of γδ T-cell immunotherapy for liver cancer treatment, emphasizing the potential of these cells in liver cancer immunotherapy.
RESUMEN
BACKGROUND: Hybridization capture-based targeted next generation sequencing (NGS) is gaining importance in routine cancer clinical practice. DNA library preparation is a fundamental step to produce high-quality sequencing data. Numerous unexpected, low variant allele frequency calls were observed in libraries using sonication fragmentation and enzymatic fragmentation. In this study, we investigated the characteristics of the artifact reads induced by sonication and enzymatic fragmentation. We also developed a bioinformatic algorithm to filter these sequencing errors. RESULTS: We used pairwise comparisons of somatic single nucleotide variants (SNVs) and insertions and deletions (indels) of the same tumor DNA samples prepared using both ultrasonic and enzymatic fragmentation protocols. Our analysis revealed that the number of artifact variants was significantly greater in the samples generated using enzymatic fragmentation than using sonication. Most of the artifacts derived from the sonication-treated libraries were chimeric artifact reads containing both cis- and trans-inverted repeat sequences of the genomic DNA. In contrast, chimeric artifact reads of endonuclease-treated libraries contained palindromic sequences with mismatched bases. Based on these distinctive features, we proposed a mechanistic hypothesis model, PDSM (pairing of partial single strands derived from a similar molecule), by which these sequencing errors derive from ultrasonication and enzymatic fragmentation library preparation. We developed a bioinformatic algorithm to generate a custom mutation "blacklist" in the BED region to reduce errors in downstream analyses. CONCLUSIONS: We first proposed a mechanistic hypothesis model (PDSM) of sequencing errors caused by specific structures of inverted repeat sequences and palindromic sequences in the natural genome. This new hypothesis predicts the existence of chimeric reads that could not be explained by previous models, and provides a new direction for further improving NGS analysis accuracy. A bioinformatic algorithm, ArtifactsFinder, was developed and used to reduce the sequencing errors in libraries produced using sonication and enzymatic fragmentation.
Asunto(s)
Artefactos , Genoma Humano , Humanos , Biblioteca de Genes , Análisis de Secuencia de ADN/métodos , ADN de Neoplasias , Secuenciación de Nucleótidos de Alto Rendimiento/métodosRESUMEN
Background: Kounis syndrome is an acute coronary syndrome (ACS) caused by allergic reactions, including coronary artery spasm (type I) caused by allergies without coronary predisposing factors, pre-existing coronary atherosclerosis, and coronary artery disease. Anaphylaxis leads to plaque rupture or erosion leading to acute myocardial infarction (type II) and acute coronary stent thrombosis (type III). Here we share a case of Kounis syndrome type I caused by an allergy caused by a Cryptopteran bite. Case presentation: A 47-year-old woman was admitted to the hospital due to an insect bite for 2 days and chest distress for more than 3â h. Outside the hospital, electrocardiogram(ECG) showed sinus rhythm, ST-segment elevation in leads V1-V3, high-sensitivity troponin 2.54â ng/ml(0-0.5â ng/ml). One hour later, the ECG of the patient showed that the ST segment elevation of lead V1-V4 was 0.10-0.20â mV. Emergency coronary angiography showed coronary spasm and moderate lumen stenosis in the middle segment of left anterior descending artery (LAD). After treatment, the patient's symptoms were relieved, and the ST segment of lead V1-V4 of electrocardiogram returned to normal. Conclusion: Kunis syndrome is a life-threatening condition that can also cause myocardial ischemic injury in patients with or without coronary artery disease. Timely identification and anti-allergic treatment can achieve a good prognosis.
RESUMEN
Background: Therapeutic interventions such as synthetic drugs and microRNA (miR) modulators have created opportunities for mitigating hepatic ischemia/reperfusion injury (HIRI) by alleviating mitochondrial dysfunction. However, delivering multi-therapeutic ingredients with low toxicity to hepatocytes still lags behind its development. Methods: In this study, we endowed exosomes with delivery function to concentrate on hepatocytes for multidimensionally halting mitochondria dysfunction during HIRI. Concretely, exosomes were reprogrammed with a transmembrane protein CD47, which acted as a "camouflage cloak" to mimic the "don't eat me" mechanism to escape from immune surveillance. Besides, HuR was engineered bridging to the membrane by fusing with CD47 and located in the cytoplasm for miR loading. Results: This strategy successfully delivered dual payloads to hepatocytes and efficiently protected mitochondria by inhibiting the opening of mitochondrial permeability transition pore (mPTP) and upregulating mitochondrial transcription factor A (TFAM), respectively. Conclusions: The reprogramming of exosomes with CD47 and HuR for targeted delivery of CsA and miR inhibitors represents a promising therapeutic strategy for addressing HIRI. This approach shows potential for safe and effective clinical applications in the treatment of HIRI.
Asunto(s)
Exosomas , MicroARNs , Daño por Reperfusión , Humanos , Antígeno CD47/metabolismo , Proteínas de Transporte de Membrana Mitocondrial/metabolismo , Exosomas/metabolismo , Daño por Reperfusión/metabolismo , Mitocondrias/metabolismo , MicroARNs/metabolismoRESUMEN
Interleukins, a diverse family of cytokines produced by various cells, play crucial roles in immune responses, immunoregulation, and a wide range of physiological and pathological processes. In the context of megakaryopoiesis, thrombopoiesis, and platelet function, interleukins have emerged as key regulators, exerting significant influence on the development, maturation, and activity of megakaryocytes (MKs) and platelets. While the therapeutic potential of interleukins in platelet-related diseases has been recognized for decades, their clinical application has been hindered by limitations in basic research and challenges in drug development. Recent advancements in understanding the molecular mechanisms of interleukins and their interactions with MKs and platelets, coupled with breakthroughs in cytokine engineering, have revitalized the field of interleukin-based therapeutics. These breakthroughs have paved the way for the development of more effective and specific interleukin-based therapies for the treatment of platelet disorders. This review provides a comprehensive overview of the effects of interleukins on megakaryopoiesis, thrombopoiesis, and platelet function. It highlights the potential clinical applications of interleukins in regulating megakaryopoiesis and platelet function and discusses the latest bioengineering technologies that could improve the pharmacokinetic properties of interleukins. By synthesizing the current knowledge in this field, this review aims to provide valuable insights for future research into the clinical application of interleukins in platelet-related diseases.
RESUMEN
In current approaches for circularly polarized phosphorescent materials, the crystallization of chiral phosphors suffers from poor processability, while integrating them into an amorphous polymer matrix results in unsatisfactory chiroptical signals due to the absence of chirality communication. Here, we have developed an innovative strategy through chiral supramolecular polymerization of benzil phosphors facilitated by intermolecular hydrogen bonds. The inherent film-forming capabilities of non-covalent supramolecular polymers obviate the need for an external polymer matrix. The pronounced helical asymmetry of benzil phosphors resulting from chiral supramolecular polymerization leads to enhanced circularly polarized phosphorescence compared to their non-hydrogen-bonded counterparts. The circularly polarized phosphorescent signals can be further modulated by varying the location of stereogenic centers or introducing halogen bonding to benzils. Incorporation of platinum(II) phosphor into the benzil supramolecular polymers induces both chirality and triplet-to-triplet energy transfer, leading to a change in circularly polarized phosphorescent color from yellow to red. In summary, chiral supramolecular polymerization of phosphors represents a novel and effective approach to circularly polarized phosphorescent materials.
RESUMEN
The elimination of formaldehyde at room temperature holds immense potential for various applications, and the incorporation of a catalyst rich in surface hydroxyl groups and oxygen significantly enhances its catalytic activity towards formaldehyde oxidation. By employing a coprecipitation method, we successfully achieved a palladium domain confined within the manganese carbonate lattice and doped with iron. This synergistic effect between highly dispersed palladium and iron greatly amplifies the concentration of surface hydroxyl groups and oxygen on the catalyst, thereby enabling complete oxidation of formaldehyde at ambient conditions. The proposed method facilitates the formation of domain-limited palladium within the MnCO3 lattice, thereby enhancing the dispersion of palladium and facilitating its partial incorporation into the MnCO3 lattice. Consequently, this approach promotes increased exposure of active sites and enhances the catalyst's capacity for oxygen activation. The co-doping of iron effectively splits the doping sites of palladium to further enhance its dispersion, while simultaneously modifying the electronic modification of the catalyst to alter formaldehyde's adsorption strength on it. Manganese carbonate exhibits superior adsorption capability for activated surface hydroxyl groups due to the presence of carbonate. In situ infrared testing revealed that dioxymethylene and formate are primary products resulting from catalytic oxidation of formaldehyde, with catalyst surface oxygen and hydroxyl groups playing a crucial role in intermediate product decomposition and oxidation. This study provides novel insights for designing palladium-based catalysts.
RESUMEN
The southwest alpine canyon area is a typical ecologically fragile area. Understanding the characteristics of vegetation change here and its influencing factors can provide a theoretical basis for formulating countermeasures for ecological environment construction in the southwest alpine canyon area and has practical significance for realizing the harmonious and unified development of the regional economy, environment, and ecology. Based on the data set of NDVI, socio-economic factors, and natural factors from 2000 to 2019, the spatial and temporal variation and stability characteristics of NDVI in the southwest alpine canyon area were analyzed by using the methods of unary linear regression, Hurst index, geographic detector model, and coefficient of variation, and the influencing factors of the spatial differentiation of NDVI were also discussed. The results showed that:â in terms of spatial distribution, the vegetation was high in the southeast and low in the northwest. The area covered by medium and high vegetation accounted for 71.71%, and the vegetation cover was at a relatively high level. From the perspective of time, the area of vegetation showing an improvement trend accounted for 85.90%, and the recovery effect was obvious, and the future vegetation change trend will continue to be improved. â¡ Elevation, vegetation type, and soil type were the main factors affecting the spatial differentiation of NDVI, and the q value was no less than 0.40. Temperature and rainfall were secondary factors, with q values of 0.274 and 0.225, respectively. The dual-factor interaction enhanced the single factor influence, which was manifested as the dual-factor enhancement and nonlinear enhancement relationship. The highest q value was 0.714 for the combination of altitude â© vegetation, followed by 0.688 for the combination of altitude â© soil. ⢠The overall stability of NDVI during the study period was good, and the proportion of the regional area with low fluctuating changes and slightly low fluctuating changes was 89.95%. The area with moderate fluctuation accounted for 10.05%, concentrated in the relatively fragile ecological environment with factors such as high altitude, low temperature, little rainfall, barren soil, and sparse vegetation. Vegetation change is the result of a combination of multiple factors, so it is necessary to adapt to local conditions and adopt different strategies to restore the ecological environment of the southwest alpine canyon area.