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Since the initial introduction of whole-cell bioreporters (WCBs) nearly 30 years ago, their high sensitivity, selectivity, and suitability for on-site detection have rendered them highly promising for environmental monitoring, medical diagnosis, food safety, biomanufacturing, and other fields. Especially in the environmental field, the technology provides a fast and efficient way to assess the bioavailability of pollutants in the environment. Despite these advantages, the technology has not been commercialized. This lack of commercialization is confusing, given the broad application prospects of WCBs. Over the years, numerous research papers have focused primarily on enhancing the sensitivity and selectivity of WCBs, with little attention paid to their wider commercial applications. So far, there is no a critical review has been published yet on this topic. Therefore, in this article we critically reviewed the research progress of WCBs over the past three decades, assessing the performance and limitations of current systems to understand the barriers to commercial deployment. By identifying these obstacles, this article provided researchers and industry stakeholders with deeper insights into the challenges hindering market entry and inspire further research toward overcoming these barriers, thereby facilitating the commercialization of WCBs as a promising technology for environmental monitoring.
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Per- and polyfluoroalkyl substances (PFASs), comprising over 9,000 persistent synthetic organic contaminants, are extensively found in the environment and pose significant risks to both human and ecological health. Among the strategies for addressing PFAS contamination, adsorption processes have proven to be cost-effective. Traditional sorbents such as ion-exchange resins and activated carbon have been found to exhibit low adsorption capacities and slow equilibration times. Recent innovations in porous materials, including metal-organic frameworks (MOFs), covalent organic frameworks (COFs), and porous organic polymers (POPs), however, offer significant improvements in the efficiency of PFAS adsorption. This review thoroughly examines the latest advancements in these materials, analyzing their mechanisms of adsorption, and concludes by suggesting directions for future research that could further enhance their effectiveness in PFAS management.
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Cadmium (Cd) and sulfamethoxazole (SMX) frequently coexist in farmlands, yet their synergistic toxicological impacts on terrestrial invertebrates remain unexplored. In this study, earthworms were exposed to artificial soils percolated with Cd (5 mg/kg), SMX (5 mg/kg) or combination of them for 7 days, followed by a 12-day elimination phase in uncontaminated soil. The uptake of Cd and SMX by the earthworms, along with their subcellular distribution, was meticulously analyzed. Additionally, a suite of biomarkers-including superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and weight loss-were evaluated to assess the health status of the earthworms and the toxicological effects of the Cd and SMX mixture. Notably, the cotreatment with Cd and SMX resulted in a significantly higher weight loss in Eisenia fetida (41.25 %) compared to exposure to Cd alone (26.84 %). Moreover, the cotreatment group exhibited substantially higher concentrations of Cd in the total internal body, fraction C (cytosol), and fraction E (tissue fragments and cell membranes) in Eisenia fetida compared to Cd alone counterparts. The combined exposure also significantly elevated the SMX levels in the total body and fraction C compared with the SMX-only treated earthworms. Additionally, Eisenia fetida subjected to the combined treatment showed markedly increased activities of SOD, CAT, and MDA compared to those treated with Cd alone. The effect addition indices (EAIs), ranging from 1.00 to 2.23, unequivocally demonstrated a synergistic effect of the combined treatments. Interestingly, relocating the earthworms to clean soil did not mitigate the observed adverse effects. These findings underscore the increased risk posed by the Cd-SMX complex to terrestrial invertebrates in agricultural areas.
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Biomarcadores , Cadmio , Oligoquetos , Contaminantes del Suelo , Sulfametoxazol , Oligoquetos/efectos de los fármacos , Oligoquetos/fisiología , Animales , Sulfametoxazol/toxicidad , Cadmio/toxicidad , Contaminantes del Suelo/toxicidad , Biomarcadores/metabolismo , Malondialdehído/metabolismo , Superóxido Dismutasa/metabolismo , Catalasa/metabolismoRESUMEN
BACKGROUND: Although the fusion of the transmembrane serine protease 2 gene (TMPRSS2) with the erythroblast transformation-specific-related gene (ERG), or TMPRSS2-ERG, occurs frequently in prostate cancer, its impact on clinical outcomes remains controversial. Roughly half of TMPRSS2-ERG fusions occur through intrachromosomal deletion of interstitial genes and the remainder via insertional chromosomal rearrangements. Because prostate cancers with deletion-derived TMPRSS2-ERG fusions are more aggressive than those with insertional fusions, we investigated the impact of interstitial gene loss on prostate cancer progression. METHODS: We conducted an unbiased analysis of transcriptome data from large collections of prostate cancer samples and employed diverse in vitro and in vivo models combined with genetic approaches to characterize the interstitial gene loss that imposes the most important impact on clinical outcome. RESULTS: This analysis identified FAM3B as the top-ranked interstitial gene whose loss is associated with a poor prognosis. The association between FAM3B loss and poor clinical outcome extended to fusion-negative prostate cancers where FAM3B downregulation occurred through epigenetic imprinting. Importantly, FAM3B loss drives disease progression in prostate cancer. FAM3B acts as an intermediator of a self-governing androgen receptor feedback loop. Specifically, androgen receptor upregulates FAM3B expression by binding to an intronic enhancer to induce an enhancer RNA and facilitate enhancer-promoter looping. FAM3B, in turn, attenuates androgen receptor signaling. CONCLUSION: Loss of FAM3B in prostate cancer, whether through the TMPRSS2-ERG translocation or epigenetic imprinting, causes an exit from this autoregulatory loop to unleash androgen receptor activity and prostate cancer progression. These findings establish FAM3B loss as a new driver of prostate cancer progression and support the utility of FAM3B loss as a biomarker to better define aggressive prostate cancer.
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Neoplasias de la Próstata , Receptores Androgénicos , Masculino , Humanos , Receptores Androgénicos/genética , Retroalimentación , Neoplasias de la Próstata/genética , Neoplasias de la Próstata/metabolismo , Transcriptoma , Proteínas de Fusión Oncogénica/genética , Regulador Transcripcional ERG/genética , Regulador Transcripcional ERG/metabolismo , Proteínas de Neoplasias/genética , Citocinas/genéticaRESUMEN
BACKGROUND AND OBJECTIVE: The herb Rheum tanguticum (RT), a member of the Polygonaceae family, is listed in the Chinese Pharmacopoeia and has been widely used to treat cardiovascular and gastrointestinal disease. The research aimed to identify the different substances from two kinds of RT extraction methods and the in vivo biotransformation of RT components. METHODS: In this study, by using ultrahigh-performance liquid chromatography coupled with quadrupole-time-of-flight tandem mass spectrometry (UHPLC-Q-TOF-MS/MS), we have investigated the metabolomic variation and the in vivo metabolism of RT. A post-acquisition data processing software, PeakView, was applied to an accurate qualitative analysis of the chemical components in RT. RESULTS: Through plant metabolomics analysis, 24 related, differentially expressed metabolites of RT water extract and alcohol extract were obtained. Combined with novel identification strategies and systematic in vivo metabolism analysis, a total of 101 compounds were discovered or tentatively identified in rat serum (including 15 prototype compounds and 86 metabolites). CONCLUSION: In this study, a combination of extraction methods, liquid chromatography-mass spectrometry (LC-MS) technology, and in vivo animal metabolism studies have been established for the screening, identification, and research of chemical active components of natural medicines. LC-MS analysis combined with plant metabolomics was used to study the differential metabolites between different extraction methods of RT. Based on UHPLC-Q-TOF-MS/MS technology, the composition and metabolism of rat plasma before and after RT administration were analysed in vivo, and 15 prototype components and 86 metabolites were detected.
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Etanol , Rheum , Animales , Ratas , Espectrometría de Masas en Tándem , Cromatografía Líquida de Alta Presión , MetabolómicaRESUMEN
Tumor cells have significant heterogeneity in metabolism and are closely related to prognosis, gene mutation, and subtype. However, this association has not been demonstrated in reports of gastrointestinal tumors. In this study, we constructed four metabolic subtypes and identified four gene signatures using the expression data and clinical information of 252 metabolism-related genes from TCGA and NCBI databases for gastric adenocarcinoma (STAD) and colorectal cancer (COAD and READ). MC1 had the worst prognosis compared to other classifications. GSig1 was mainly related to drug metabolism and was the highest in MC1 with the worst prognosis, while the other subtypes were mainly related to glucose metabolism pathways. This difference also existed in other different malignant tumors. In addition, metabolic typing was associated with chemotherapeutic drug response and tumor heterogeneity, which indicated that monitoring metabolic typing could contribute to drug efficacy and gene-targeted therapy. In conclusion, we identified differences among subtypes in clinical characteristics such as prognosis and revealed the potential function of metabolic subtype in response to chemotherapeutic agents and oncogene mutations. This work highlighted the potential clinical meaning of metabolic subtype and characteristics in drug therapy and prognosis assessment of malignant tumors.
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Adenocarcinoma , Neoplasias Gastrointestinales , Neoplasias Gástricas , Humanos , Neoplasias Gastrointestinales/tratamiento farmacológico , Neoplasias Gastrointestinales/genética , Bases de Datos Factuales , Terapia GenéticaRESUMEN
Studies in recent years have highlighted an elaborate crosstalk between T cells and bone cells, suggesting that T cells may be alternative therapeutic targets for the maintenance of bone homeostasis. Here, it is reported that systemic administration of low-dose staphylococcal enterotoxin C2 (SEC2) 2M-118, a form of mutant superantigen, dramatically alleviates ovariectomy (OVX)-induced bone loss via modulating T cells. Specially, SEC2 2M-118 treatment increases trabecular bone mass significantly via promoting bone formation in OVX mice. These beneficial effects are largely diminished in T-cell-deficient nude mice and can be rescued by T-cell reconstruction. Neutralizing assays determine interferon gamma (IFN-γ) as the key factor that mediates the beneficial effects of SEC2 2M-118 on bone. Mechanistic studies demonstrate that IFN-γ stimulates Janus kinase/signal transducer and activator of transcription (JAK-STAT) signaling, leading to enhanced production of nitric oxide, which further activates p38 mitogen-activated protein kinase (MAPK) and Runt-related transcription factor 2 (Runx2) signaling and promotes osteogenic differentiation. IFN-γ also directly inhibits osteoclast differentiation, but this effect is counteracted by proabsorptive factors tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1ß) secreted from IFN-γ-stimulated macrophages. Taken together, this work provides clues for developing innovative approaches which target T cells for the prevention and treatment of osteoporosis.
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Ductal carcinoma in situ (DCIS) is a common precursor of invasive breast cancer. Our understanding of its genomic progression to recurrent disease remains poor, partly due to challenges associated with the genomic profiling of formalin-fixed paraffin-embedded (FFPE) materials. Here, we developed Arc-well, a high-throughput single-cell DNA-sequencing method that is compatible with FFPE materials. We validated our method by profiling 40,330 single cells from cell lines, a frozen tissue, and 27 FFPE samples from breast, lung, and prostate tumors stored for 3-31 years. Analysis of 10 patients with matched DCIS and cancers that recurred 2-16 years later show that many primary DCIS had already undergone whole-genome doubling and clonal diversification and that they shared genomic lineages with persistent subclones in the recurrences. Evolutionary analysis suggests that most DCIS cases in our cohort underwent an evolutionary bottleneck, and further identified chromosome aberrations in the persistent subclones that were associated with recurrence.
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Neoplasias de la Mama , Carcinoma Ductal de Mama , Carcinoma Intraductal no Infiltrante , Femenino , Humanos , Neoplasias de la Mama/patología , Carcinoma Ductal de Mama/genética , Carcinoma Intraductal no Infiltrante/genética , Carcinoma Intraductal no Infiltrante/patología , Progresión de la Enfermedad , Genómica/métodos , Análisis de Expresión Génica de una Sola Célula , Línea Celular TumoralRESUMEN
Consensus on the stage of liver hepatocellular carcinoma (LIHC) in patients is difficult, which restricts the diagnosis and treatment of liver cancer. Molecular typing based on genes related to the lipid metabolism pathways can reflect deeper characteristics of liver cancer and complement the deficiency of the clinical staging system. In this study, we constructed and verified two cell subtypes: C1 and C2 in LIHC, based on six lipid metabolic pathway-associated genes identified in two independent external validation cohorts comprising single-cell RNA-sequencing technology (scRNA-Seq) data and bulk RNA-seq data downloaded from Gene Expression Omnibus (GEO) database and The Cancer Genome Atlas (TCGA) database. The C2 subtype showed poorer prognosis, higher immune scores, and greater correlation with pathways associated with tumor progression as compared to the C1 subtype. Moreover, the sensitivity of many tested targeted drugs in C1 was relative to C2. Furthermore, Gene Set Enrichment Analysis (GSEA) revealed several significantly enriched oncological signatures and metabolic processes, which might help elucidate the underlying molecular mechanisms. At the same time, we identified there were significantly different metabolites in C1 and C2 subtypes using 11 LIHC tissue samples. In conclusion, we constructed two molecular subtypes based on the lipid metabolism-associated genes, which may provide valuable information to further study the pathogenesis and devise clinical management strategies for LIHC.
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Lacking self-repair abilities, injuries to articular cartilage can lead to cartilage degeneration and ultimately result in osteoarthritis. Tissue engineering based on functional bioactive scaffolds are emerging as promising approaches for articular cartilage regeneration and repair. Although the use of cell-laden scaffolds prior to implantation can regenerate and repair cartilage lesions to some extent, these approaches are still restricted by limited cell sources, excessive costs, risks of disease transmission and complex manufacturing practices. Acellular approaches through the recruitment of endogenous cells offer great promise for in situ articular cartilage regeneration. In this study, we propose an endogenous stem cell recruitment strategy for cartilage repair. Based on an injectable, adhesive and self-healable o-alg-THAM/gel hydrogel system as scaffolds and a biophysio-enhanced bioactive microspheres engineered based on hBMSCs secretion during chondrogenic differentiation as bioactive supplement, the as proposed functional material effectively and specifically recruit endogenous stem cells for cartilage repair, providing new insights into in situ articular cartilage regeneration.
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The adult human breast is comprised of an intricate network of epithelial ducts and lobules that are embedded in connective and adipose tissue1-3. Although most previous studies have focused on the breast epithelial system4-6, many of the non-epithelial cell types remain understudied. Here we constructed the comprehensive Human Breast Cell Atlas (HBCA) at single-cell and spatial resolution. Our single-cell transcriptomics study profiled 714,331 cells from 126 women, and 117,346 nuclei from 20 women, identifying 12 major cell types and 58 biological cell states. These data reveal abundant perivascular, endothelial and immune cell populations, and highly diverse luminal epithelial cell states. Spatial mapping using four different technologies revealed an unexpectedly rich ecosystem of tissue-resident immune cells, as well as distinct molecular differences between ductal and lobular regions. Collectively, these data provide a reference of the adult normal breast tissue for studying mammary biology and diseases such as breast cancer.
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Mama , Perfilación de la Expresión Génica , Análisis de la Célula Individual , Adulto , Femenino , Humanos , Mama/citología , Mama/inmunología , Mama/metabolismo , Neoplasias de la Mama/metabolismo , Neoplasias de la Mama/patología , Células Endoteliales/clasificación , Células Endoteliales/metabolismo , Células Epiteliales/clasificación , Células Epiteliales/metabolismo , Genómica , InmunidadRESUMEN
The adult human breast comprises an intricate network of epithelial ducts and lobules that are embedded in connective and adipose tissue. While previous studies have mainly focused on the breast epithelial system, many of the non-epithelial cell types remain understudied. Here, we constructed a comprehensive Human Breast Cell Atlas (HBCA) at single-cell and spatial resolution. Our single-cell transcriptomics data profiled 535,941 cells from 62 women, and 120,024 nuclei from 20 women, identifying 11 major cell types and 53 cell states. These data revealed abundant pericyte, endothelial and immune cell populations, and highly diverse luminal epithelial cell states. Our spatial mapping using three technologies revealed an unexpectedly rich ecosystem of tissue-resident immune cells in the ducts and lobules, as well as distinct molecular differences between ductal and lobular regions. Collectively, these data provide an unprecedented reference of adult normal breast tissue for studying mammary biology and disease states such as breast cancer.
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The knowledge of osteoarthritis (OA) has nowadays been extended from a focalized cartilage disorder to a multifactorial disease. Although recent investigations have reported that infrapatellar fat pad (IPFP) can trigger inflammation in the knee joint, the mechanisms behind the role of IPFP on knee OA progression remain to be defined. Here, dysregulated osteopontin (OPN) and integrin ß3 signaling are found in the OA specimens of both human and mice. It is further demonstrated that IPFP-derived OPN participates in OA progression, including activated matrix metallopeptidase 9 in chondrocyte hypertrophy and integrin ß3 in IPFP fibrosis. Motivated by these findings, an injectable nanogel is fabricated to provide sustained release of siRNA Cd61 (RGD- Nanogel/siRNA Cd61) that targets integrins. The RGD- Nanogel possesses excellent biocompatibility and desired targeting abilities both in vitro and in vivo. Local injection of RGD- Nanogel/siRNA Cd61 robustly alleviates the cartilage degeneration, suppresses the advancement of tidemark, and reduces the subchondral trabecular bone mass in OA mice. Taken together, this study provides an avenue for developing RGD- Nanogel/siRNA Cd61 therapy to mitigate OA progression via blocking OPN-integrin ß3 signaling in IPFP.
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Cartílago Articular , Osteoartritis de la Rodilla , Humanos , Ratones , Animales , Integrina beta3 , Nanogeles , Osteopontina , Articulación de la Rodilla , Tejido Adiposo , ARN Interferente Pequeño/genética , OligopéptidosRESUMEN
The deadliest anaplastic thyroid cancer (ATC) often transforms from indolent differentiated thyroid cancer (DTC); however, the complex intratumor transformation process is poorly understood. We investigated an anaplastic transformation model by dissecting both cell lineage and cell fate transitions using single-cell transcriptomic and genetic alteration data from patients with different subtypes of thyroid cancer. The resulting spectrum of ATC transformation included stress-responsive DTC cells, inflammatory ATC cells (iATCs), and mitotic-defective ATC cells and extended all the way to mesenchymal ATC cells (mATCs). Furthermore, our analysis identified 2 important milestones: (a) a diploid stage, in which iATC cells were diploids with inflammatory phenotypes and (b) an aneuploid stage, in which mATCs gained aneuploid genomes and mesenchymal phenotypes, producing excessive amounts of collagen and collagen-interacting receptors. In parallel, cancer-associated fibroblasts showed strong interactions among mesenchymal cell types, macrophages shifted from M1 to M2 states, and T cells reprogrammed from cytotoxic to exhausted states, highlighting new therapeutic opportunities for the treatment of ATC.
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Carcinoma Anaplásico de Tiroides , Neoplasias de la Tiroides , Humanos , Transcriptoma , Neoplasias de la Tiroides/genética , Neoplasias de la Tiroides/metabolismo , Carcinoma Anaplásico de Tiroides/genética , Perfilación de la Expresión Génica , Aneuploidia , Línea Celular TumoralRESUMEN
Background: The molecular classification of HCC premised on metabolic genes might give assistance for diagnosis, therapy, prognosis prediction, immune infiltration, and oxidative stress in addition to supplementing the limitations of the clinical staging system. This would help to better represent the deeper features of HCC. Methods: TCGA datasets combined with GSE14520 and HCCDB18 datasets were used to determine the metabolic subtype (MC) using ConsensusClusterPlus. ssGSEA method was used to calculate the IFNγ score, the oxidative stress pathway scores, and the score distribution of 22 distinct immune cells, and their differential expressions were assessed with the use of CIBERSORT. To generate a subtype classification feature index, LDA was utilized. Screening of the metabolic gene coexpression modules was done with the help of WGCNA. Results: Three MCs (MC1, MC2, and MC3) were identified and showed different prognoses (MC2-poor and MC1-better). Although MC2 had a high immune microenvironment infiltration, T cell exhaustion markers were expressed at a high level in MC2 in contrast with MC1. Most oxidative stress-related pathways are inhibited in the MC2 subtype and activated in the MC1 subtype. The immunophenotyping of pan-cancer showed that the C1 and C2 subtypes with poor prognosis accounted for significantly higher proportions of MC2 and MC3 subtypes than MC1, while the better prognostic C3 subtype accounted for significantly lower proportions of MC2 than MC1. As per the findings of the TIDE analysis, MC1 had a greater likelihood of benefiting from immunotherapeutic regimens. MC2 was found to have a greater sensitivity to traditional chemotherapy drugs. Finally, 7 potential gene markers indicate HCC prognosis. Conclusion: The difference (variation) in tumor microenvironment and oxidative stress among metabolic subtypes of HCC was compared from multiple angles and levels. A complete and thorough clarification of the molecular pathological properties of HCC, the exploration of reliable markers for diagnosis, the improvement of the cancer staging system, and the guiding of individualized treatment of HCC all gain benefit greatly from molecular classification associated with metabolism.
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Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/diagnóstico , Carcinoma Hepatocelular/genética , Pronóstico , Neoplasias Hepáticas/genética , Estrés Oxidativo/genética , Complejo CD3 , Microambiente Tumoral/genéticaRESUMEN
Osteoporosis, a common systematic bone homeostasis disorder related disease, still urgently needs innovative treatment methods. Several natural small molecules were found to be effective therapeutics in osteoporosis. In the present study, quercetin was screened out from a library of natural small molecular compounds by a dual luciferase reporter system. Quercetin was found to upregulate Wnt/ß-catenin while inhibiting NF-κB signaling activities, and thereby rescuing osteoporosis-induced tumor necrosis factor alpha (TNFα) impaired BMSCs osteogenesis. Furthermore, a putative functional lncRNA, Malat1, was shown to be a key mediator in quercetin regulated signaling activities and TNFα-impaired BMSCs osteogenesis, as mentioned above. In an ovariectomy (OVX)-induced osteoporosis mouse model, quercetin administration could significantly rescue OVX-induced bone loss and structure deterioration. Serum levels of Malat1 were also obviously rescued in the OVX model after quercetin treatment. In conclusion, our study demonstrated that quercetin could rescue TNFα-impaired BMSCs osteogenesis in vitro and osteoporosis-induced bone loss in vivo, in a Malat1-dependent manner, suggesting that quercetin may serve as a therapeutic candidate for osteoporosis treatment.
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Enfermedades Óseas Metabólicas , Osteoporosis , ARN Largo no Codificante , Ratones , Animales , Femenino , Humanos , Osteogénesis/genética , ARN Largo no Codificante/genética , ARN Largo no Codificante/uso terapéutico , Factor de Necrosis Tumoral alfa/farmacología , Quercetina/farmacología , Quercetina/uso terapéutico , Médula Ósea/patología , Osteoporosis/etiología , Osteoporosis/genética , Ovariectomía/efectos adversos , Células Madre/patología , Diferenciación Celular , Vía de Señalización WntRESUMEN
The high mortality rate of patients with diabetic foot ulcers is urging the appearance of an effective biomedical drug. Senescence is one of the major reasons of aging-induced decline in the diabetic wound. Our previous studies have demonstrated the anti-senescence effect of secretomes derived from human fetal mesenchymal stem cells (hfMSC). The present study tends to explore the potential role of hfMSC secretome (HFS) in wound healing through anti-aging. Meanwhile, we try to overcome several obstacles in the clinical application of stem cell secretome. A verticle bioreactor and microcarriers are employed to expand hfMSC and produce the HFS on a large scale. The HFS was then subjected to lyophilization (L-HFS). The PLGA (poly lactic-co-glycolic acid) particles were used to encapsulate and protect L-HFS from degradation in the streptozotocin (STZ)-induced diabetic rat model. Results showed that HFS-PLGA significantly enhanced wound healing by promoting vascularization and inhibiting inflammation in the skin wound bed. We further analyzed the contents of HFS. Isobaric tag for relative and absolute quantitation (ITRAQ) and label-free methods were used to identify peptides in the secretome. Bioinformatics analysis indicated that exosome production-related singling pathways and heat-shock protein family could be used as bio-functional markers and quality control for stem cell secretome production.
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The existing QuEChERS-combined analytical pretreatment methods are limited by large reagent consumption, high environmental burden, and mediocre effects. To provide an efficient and green pretreatment method, this study developed pH-responsive switchable deep eutectic solvents (SDESs) to extract triazole fungicides (TFs) from fruit peel wastes, which could enhance the preconcentration effect of target compounds in food waste samples with complex matrices. The mechanisms of pH-induced phase transition and hydrophobicity-hydrophilicity conversion of pH-responsive SDESs were investigated by pH phase diagrams and chemical characterization techniques, respectively. We validated the established method by high-performance liquid chromatography-diode array detector (HPLC-DAD), and lower LOD (0.089-0.351 ng mL-1), LOQ (0.297-1.172 ng mL-1), RSD (≤8.8 %) and satisfactory recoveries (90.6 %-110.9 %) and preconcentration factors (389-512) were obtained in rotting grape peel, watermelon peel, and orange peel samples. Our findings highlight the potential of pH-responsive SDESs in the extraction and analysis of various natural food products.
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Fungicidas Industriales , Microextracción en Fase Líquida , Eliminación de Residuos , Disolventes Eutécticos Profundos , Triazoles , Alimentos , Solventes/química , Concentración de Iones de Hidrógeno , Microextracción en Fase Líquida/métodosRESUMEN
We develop a poly (lactic-co-glycolic acid)/ß-calcium phosphate (PLGA/TCP)-based scaffold through a three-dimensional (3D) printing technique incorporating icaritin (ICT), a unique phytomolecule, and secretome derived from human fetal mesenchymal stem cells (HFS), to provide mechanical support and biological cues for stimulating bone defect healing. With the sustained release of ICT and HFS from the composite scaffold, the cell-free scaffold efficiently facilitates the migration of MSCs and promotes bone regeneration at the femoral defect site in the ovariectomy (OVX)-induced osteoporotic rat model. Furthermore, mechanism study results indicate that the combination of ICT and HFS additively activates the Integrin-FAK (focal adhesion kinase)-ERK1/2 (extracellular signal-regulated kinase 1/2)-Runx2 (Runt-related transcription factor 2) axis, which could be linked to the beneficial recruitment of MSCs to the implant and subsequent osteogenesis enhancement. Collectively, the PLGA/TCP/ICT/HFS (P/T/I/S) bioactive scaffold is a promising biomaterial for repairing osteoporotic bone defects, which may have immense implications for their translation to clinical practice.
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Fe-N co-doped biochar is recently an emerging carbocatalyst for persulfate activation in situ chemical oxidation (ISCO). However, the involved catalytic mechanisms remain controversial and distinct effects of coexisting water components are still not very clear. Herein, we reported a novel N-doped biochar-coupled crystallized Fe phases composite (Fe@N-BC800) as efficient and low-cost peroxydisulfate (PDS) activators to degrade bisphenol A (BPA), and the underlying influencing mechanism of coexisting inorganic anions (IA) and humic constituent. Due to the formation of graphitized nanosheets with high defects (AI index>0.5, ID/IG = 1.02), Fe@N-BC800 exhibited 2.039, 5.536, 8.646, and 23.154-fold higher PDS catalytic activity than that of Fe@N-BC600, Fe@N-BC400, N-BC, BC. Unlike radical pathway driven by carbonyl group and pyrrolic N of low/mid-temperature Fe@N-BCs. The defective graphitized nanosheets and Fe-Nx acted separately as electron transfer and radical pathway active sites of Fe@N-BC800, where π-π sorption assisted with pyrrolic N and pore-filling facilitated BPA degradation. The strong inhibitory effects of PO43- and NO2- were ascribed to competitive adsorption of phosphate (61.11 mg g-1) and nitrate (23.99 mg g-1) on Fe@N-BC800 via electrostatic attraction and hydrogen bonding. In contrast, HA competed for the pyrrolic-N site and hindered electron delivery. Moreover, BPA oxidation pathways initiated by secondary free radicals were proposed. The study facilitates a thorough understanding of the intrinsic properties of designed biochar and contributes new insights into the fate of degradation byproducts formed from ISCO treatment of micropollutants.