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Compared to lithium (Li) anode, the alloy/Li-alloy anodes show more compatible with sulfide solid electrolytes (SSEs), and are promising candidates for practical SSE-based all-solid-state Li batteries (ASSLBs). In this work, a porous Li-Al alloy (LiAl-p) anode is crafted using a straightforward mechanical pressing method. Various characterizations confirm the porous nature of such anode, as well as rich oxygen species on its surface. To the best knowledge, such LiAl-p anode demonstrates the best room temperature cell performance in comparison with reported Li and alloy/Li-alloy anodes in SSE-based ASSLBs. For example, the LiAl-p symmetric cells deliver a record critical current density of 6.0 mA cm-2 and an ultralong cycling of 5000 h; the LiAl-p|LiNi0.8Co0.1Mn0.1O2 full cells achieve a high areal capacity of 11.9 mAh cm-2 and excellent durability of 1800 cycles. Further in situ and ex situ experiments reveal that the porous structure can accommodate volume changes of LiAl-p and ensure its integrity during cycling; and moreover, a robust Li inorganics-rich solid electrolyte interphase can be formed originated from the reaction between SSE and surface oxygen species of LiAl-p. This study offers inspiration for designing high-performance alloy anodes by focusing on designing special architecture to alleviate volume change and constructing stable interphase.
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BACKGROUND: Bronchopulmonary dysplasia (BPD) is a chronic lung disorder predominantly affecting preterm infants. Oxygen therapy, a common treatment for BPD, often leads to hyperoxia-induced pulmonary damage, particularly targeting alveolar epithelial cells (AECs). Crucially, disrupted lung epithelium-fibroblast interactions significantly contribute to BPD's pathogenesis. Previous studies on interleukin-11 (IL-11) in lung diseases have yielded conflicting results. Recent research, however, highlights IL-11 as a key regulator of fibrosis, stromal inflammation, and epithelial dysfunction. Despite this, the specific role of IL-11 in BPD remains underexplored. Our transcriptome analysis of normal and hyperoxia-exposed murine lung tissues revealed an increased expression of IL-11 RNA. This study aimed to investigate IL-11's role in modulating the disrupted interactions between AECs and fibroblasts in BPD. METHODS: BPD was modeled in vivo by exposing C57BL/6J neonatal mice to hyperoxia. Histopathological changes in lung tissue were evaluated with hematoxylin-eosin staining, while lung fibrosis was assessed using Masson staining and immunohistochemistry (IHC). To investigate IL-11's role in pulmonary injury contributing to BPD, IL-11 levels were reduced through intraperitoneal administration of IL-11RαFc in hyperoxia-exposed mice. Additionally, MLE-12 cells subjected to 95% oxygen were collected and co-cultured with mouse pulmonary fibroblasts (MPFs) to measure α-SMA and Collagen I expression levels. IL-11 levels in the supernatants were quantified using an enzyme-linked immunosorbent assay (ELISA). RESULTS: Both IHC and Masson staining revealed that inhibiting IL-11 expression alleviated pulmonary fibrosis in neonatal mice induced by hyperoxia, along with reducing the expression of fibrosis markers α-SMA and collagen I in lung tissue. In vitro analysis showed a significant increase in IL-11 levels in the supernatant of MLE-12 cells treated with hyperoxia. Silencing IL-11 expression in MLE-12 cells reduced α-SMA and collagen I concentrations in MPFs co-cultured with the supernatant of hyperoxia-treated MLE-12 cells. Additionally, ERK inhibitors decreased α-SMA and collagen I levels in MPFs co-cultured with the supernatant of hyperoxia-treated MLE-12 cells. Clinical studies found increased IL-11 levels in tracheal aspirates (TA) of infants with BPD. CONCLUSION: This research reveals that hyperoxia induces IL-11 secretion in lung epithelium. Additionally, IL-11 derived from lung epithelium emerged as a crucial mediator in myofibroblast differentiation via the ERK signaling pathway, highlighting its potential therapeutic value in BPD treatment.
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Cervical cancer seriously affects the health of women worldwide. Persistent infection of high-risk HPV (Human Papilloma Virus) can lead to cervical cancer. There is a great need for timely and efficient screening methods for cervical cancer. The current screening methods for cervical cancer are mainly based on cervical cytology and HPV testing. Cervical cytology is made of Pap smear and liquid-based cytology, while HPV testing is based on immunological and nucleic acid level detection methods. This review introduces cervical cancer screening methods based on cytology and human papillomavirus testing in detail. The advantages and limitations of the screening methods are also summarized and compared.
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Detección Precoz del Cáncer , Neoplasias del Cuello Uterino , Humanos , Neoplasias del Cuello Uterino/diagnóstico , Femenino , Papillomaviridae/aislamiento & purificación , Infecciones por Papillomavirus/diagnósticoRESUMEN
Peanut (Arachis hypogaea L.) is an important crop that provides essential proteins and oils for human and animal consumption. 9-cis-epoxycarotenoid dioxygenase (NCED) have been found can play a vital role in abscisic acid (ABA) biosynthesis and may be a response to drought stress. Until now, in Arachis hypogaea, no information about the NCED gene family has been reported and the importance of NCED-related drought tolerance is unclear. In this study, eight NCED genes in Arachis hypogaea, referred to as AhNCEDs, are distributed across eight chromosomes, with duplication events in AhNCED1 and AhNCED2, AhNCED3 and AhNCED4, and AhNCED6 and AhNCED7. Comparative analysis revealed that NCED genes are highly conserved among plant species, including Pisum sativum, Phaseolus vulgaris, Glycine max, Arabidopsis thaliana, Gossypium hirsutum, and Oryza sativa. Further promoter analysis showed AhNCEDs have ABA-related and drought-inducible elements. The phenotyping of Arachis hypogaea cultivars NH5 and FH18 demonstrated that NH5 is drought-tolerant and FH18 is drought-sensitive. Transcriptome expression analysis revealed the differential regulation of AhNCEDs expression in both NH5 and FH18 cultivars under drought stress. Furthermore, compared to the Arachis hypogaea cultivar FH18, the NH5 exhibited a significant upregulation of AhNCED1/2 expression under drought. To sum up, this study provides an insight into the drought-related AhNCED genes, screened out the potential candidates to regulate drought tolerance and ABA biosynthesis in Arachis hypogaea.
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Arachis , Dioxigenasas , Sequías , Regulación de la Expresión Génica de las Plantas , Proteínas de Plantas , Estrés Fisiológico , Arachis/genética , Arachis/metabolismo , Estrés Fisiológico/genética , Dioxigenasas/genética , Dioxigenasas/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Ácido Abscísico/metabolismo , Filogenia , Perfilación de la Expresión Génica , Regiones Promotoras Genéticas/genéticaRESUMEN
Infectious diseases pose a significant threat to global health, yet traditional microbiological identification methods suffer from drawbacks, such as high costs and long processing times. Raman spectroscopy, a label-free and noninvasive technique, provides rich chemical information and has tremendous potential in fast microbial diagnoses. Here, we propose a novel Combined Mutual Learning Net that precisely identifies microbial subspecies. It demonstrated an average identification accuracy of 87.96% in an open-access data set with thirty microbial strains, representing a 5.76% improvement. 50% of the microbial subspecies accuracies were elevated by 1% to 46%, especially for E. coli 2 improved from 31% to 77%. Furthermore, it achieved a remarkable subspecies accuracy of 92.4% in the custom-built fiber-optical tweezers Raman spectroscopy system, which collects Raman spectra at a single-cell level. This advancement demonstrates the effectiveness of this method in microbial subspecies identification, offering a promising solution for microbiology diagnosis.
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Escherichia coli , Pinzas Ópticas , Espectrometría Raman/métodosRESUMEN
Mitochondria are the centers of energy and material metabolism, and they also serve as the storage and dispatch hubs of metal ions. Damage to mitochondrial structure and function can cause abnormal levels and distribution of metal ions, leading to cell dysfunction and even death. For a long time, mitochondrial quality control pathways such as mitochondrial dynamics and mitophagy have been considered to inhibit metal-induced cell death. However, with the discovery of new metal-dependent cell death including ferroptosis and cuproptosis, increasing evidence shows that there is a complex relationship between mitochondrial quality control and metal-dependent cell death. This article reviews the latest research results and mechanisms of crosstalk between mitochondrial quality control and metal-dependent cell death in recent years, as well as their involvement in neurodegenerative diseases, tumors and other diseases, in order to provide new ideas for the research and treatment of related diseases.
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Muerte Celular , Metales , Mitocondrias , Humanos , Mitocondrias/metabolismo , Metales/metabolismo , Animales , Mitofagia , Ferroptosis , Dinámicas Mitocondriales , Enfermedades Neurodegenerativas/metabolismo , Enfermedades Neurodegenerativas/patologíaRESUMEN
The increased rate of antibiotic resistance strongly limits the resolution of Salmonella enterica serovar Typhimurium (S. Typhimurium) infection. Therefore, new strategies to control bacterial infections are urgently needed. Bacillus subtilis (B. subtilis) and its metabolites are desirable antibacterial agents. Here, we aimed to evaluate the antibacterial activity of the novel B. subtilis strain GXYX (No: PRJNA940956) crude lipopeptide against S. Typhimurium. In vitro, GXYX crude lipopeptides affected S. Typhimurium biofilm formation and swimming and attenuated the adhesion and invasion abilities of S. Typhimurium toward BHK-21 cells; in addition, it inhibited the mRNA expression of the filA, filC, csgA, and csgB genes, which are related to the adhesion and invasion ability of S. Typhimurium. In vivo, pretreatment with GXYX crude lipopeptide via intragastric administration improved the survival rate by 30%, which was related to reductions in organ bacterial loads and clinical signs in mice. Intragastric administration of GXYX crude lipopeptide significantly downregulated the mRNA levels of TNF-α, IL-1ß, IL-12 and IL-6 in response to S. Typhimurium-induced inflammation compared with intraperitoneal injection. Moreover, it significantly improved the intestinal barrier-related gene (ZO-1, claudin-1, occludin-1) mRNA levels in intestinal tissue damaged by S. Typhimurium infection. In conclusion, GXYX crude lipopeptides were effective at reducing S. Typhimurium colonization, laying a foundation for the further development of novel antibacterial agents.
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Nuclear receptor coactive 4 (NCOA4), which functions as a selective cargo receptor, is a critical regulator of the particularly autophagic degradation of ferritin, a process known as ferritinophagy. Mechanistically, NCOA4-mediated ferritinophagy performs an increasingly vital role in the maintenance of intracellular iron homeostasis by promoting ferritin transport and iron release as needed. Ferritinophagy is not only involved in iron-dependent responses but also in the pathogenesis and progression of various human diseases, including metabolism-related, neurodegenerative, cardiovascular and infectious diseases. Therefore, ferritinophagy is of great importance in maintaining cell viability and function and represents a potential therapeutic target. Recent studies indicated that ferritinophagy regulates the signalling pathway associated with ferroptosis, a newly discovered type of cell death characterised by iron-dependent lipid peroxidation. Although accumulating evidence clearly demonstrates the importance of the interplay between dysfunction in iron metabolism and ferroptosis, a deeper understanding of the double-edged sword effect of ferritinophagy in ferroptosis has remained elusive. Details of the mechanisms underlying the ferritinophagy-ferroptosis axis in regulating relevant human diseases remain to be elucidated. In this review, we discuss the latest research findings regarding the mechanisms that regulate the biological function of NCOA4-mediated ferritinophagy and its contribution to the pathophysiology of ferroptosis. The important role of the ferritinophagy-ferroptosis axis in human diseases will be discussed in detail, highlighting the great potential of targeting ferritinophagy in the treatment of diseases.
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Autofagia , Ferritinas , Ferroptosis , Hierro , Coactivadores de Receptor Nuclear , Humanos , Ferroptosis/fisiología , Ferritinas/metabolismo , Coactivadores de Receptor Nuclear/metabolismo , Coactivadores de Receptor Nuclear/genética , Autofagia/fisiología , Hierro/metabolismo , Animales , Transducción de Señal , Enfermedades Neurodegenerativas/metabolismo , Enfermedades Neurodegenerativas/patologíaRESUMEN
N6-methyladenosine (m6A) regulates gene expression and governs many important biological processes. However, the function of m6A in the development of bronchopulmonary dysplasia (BPD) remains poorly characterized. Thus, the purpose of this investigation was to evaluate the effects of m6A RNA methylation regulators on the development of BPD. BPD-related transcriptome data were downloaded from the GEO database. Differentially expressed m6A methylation regulators between BPD and control group were identified. Consensus clustering was conducted for the classification of BPD and association between clusters and BPD phenotypes were explored. Analysis of differentially expressed genes (DEGs) and immune-related DEGs was performed. The GSEA, GO and KEGG analyses were used to interpret the functional enrichments. The composition of immune cell subtypes in BPD subsets was predicted by CIBERSORT analysis. Compared with the control group, expression of most m6A regulators showed significant alteration, especially for IGF2BP1/2/3. BPD was classified into 2 subsets, and cluster 1 was correlated with severe BPD. Furthermore, the results of functional enrichment analyses showed a disturbed immune-related signaling pathway. Based on CIBERSORT analysis, we found that the proportion of immune cell subsets changed between cluster 1 and cluster 2. Our study revealed the implication of m6A methylation regulators in the development of BPD, which might provide a novel insight for the diagnosis and treatment of BPD.
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OBJECTIVE: Pathologic cardiac hypertrophy (PCH) is a precursor to heart failure. Amydrium sinense (Engl.) H. Li (AS), a traditional Chinese medicinal plant, has been extensively utilized to treat chronic inflammatory diseases. However, the therapeutic effect of ASWE on PCH and its underlying mechanisms are still not fully understood. METHODS: A cardiac hypertrophy model was established by treating C57BL/6 J mice and neonatal rat cardiomyocytes (NRCMs) in vitro with isoprenaline (ISO) in this study. The antihypertrophic effects of AS water extract (ASWE) on cardiac function, histopathologic manifestations, cell surface area and expression levels of hypertrophic biomarkers were examined. Subsequently, the impact of ASWE on inflammatory factors, p65 nuclear translocation and NF-κB activation was investigated to elucidate the underlying mechanisms. RESULTS: In the present study, we observed that oral administration of ASWE effectively improved ISO-induced cardiac hypertrophy in mice, as evidenced by histopathological manifestations and the expression levels of hypertrophic markers. Furthermore, the in vitro experiments demonstrated that ASWE treatment inhibited cardiac hypertrophy and suppressed inflammation response in ISO-treated NRCMs. Mechanically, our findings provided evidence that ASWE suppressed inflammation response by repressing p65 nuclear translocation and NF-κB activation. ASWE was found to possess the capability of inhibiting inflammation response and cardiac hypertrophy induced by ISO. CONCLUSION: To sum up, ASWE treatment was shown to attenuate ISO-induced cardiac hypertrophy by inhibiting cardiac inflammation via preventing the activation of the NF-kB signaling pathway. These findings provided scientific evidence for the development of ASWE as a novel therapeutic drug for PCH treatment.
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Araceae , FN-kappa B , Animales , Ratones , Ratas , Ratones Endogámicos C57BL , Isoproterenol/toxicidad , Transducción de Señal , Iones , Litio , Artesunato , Cardiomegalia/inducido químicamente , Cardiomegalia/tratamiento farmacológico , Inflamación/inducido químicamente , Inflamación/tratamiento farmacológicoRESUMEN
Zinc oxide nanoparticles (ZnO NPs) are widely used in many fields due to their unique physicochemical properties. However, the renal toxicity of ZnO NPs and the underlying mechanisms have not been well studied. We found that ZnO NPs induced injury in human renal proximal tubular epithelial cells (HK-2) in a dose- and size-dependent manner, as revealed by CCK-8, LDH and Annexin V-FITC assays. Mechanistically, ZnO NPs promoted oxidative stress and mitochondrial damage by generating ROS and induced apoptosis in HK-2 cells, as evidenced by the upregulation of Bax and Caspase 3 and downregulation of Beclin 1. In vivo, ZnO NPs induced tubular epithelial cell apoptosis and increased serum creatinine, serum urea nitrogen, and urinary protein in mice, suggesting damage to renal structure and function. These findings clarified our understanding of the biological mechanisms underlying ZnO NP-induced renal tubular epithelial cell injury and contributed to estimating the risk of ZnO NPs to the kidney.
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Nanopartículas , Óxido de Zinc , Humanos , Ratones , Animales , Óxido de Zinc/toxicidad , Óxido de Zinc/química , Especies Reactivas de Oxígeno/metabolismo , Apoptosis , Estrés Oxidativo , Nanopartículas/toxicidad , Nanopartículas/química , Riñón/metabolismo , Células Epiteliales/metabolismoRESUMEN
Nanoattapulgite (nano-ATP), a magnesium-aluminum silicate clay, can absorb substances and is a suitable material for bone repair and regeneration. In this study, using three-dimensional printing technology, a nano-ATP/polycaprolactone (PCL) scaffold was fabricated and modified using NaOH to form a rough surface. Biomimetic hydroxyapatite (HA) on nano-ATP/PCL scaffolds was fabricated using a biomineralized approach. The scaffold provided structural support through PCL and was modified with ATP and HA to improve hydrophilicity and promote the delivery of nutrients. The biocompatibility and osteogenic induction of scaffolds were assessed in vitro using mouse bone marrow mesenchymal stem cells. According to the in vitro study results, the nano-ATP/PCL/HA composite scaffold significantly boosted the expression levels of genes related to osteogenesis (p < 0.05), attributed to its superior alkaline phosphatase activity and calcium deposition capabilities. The outcomes of in vivo experimentation demonstrated an augmentation in bone growth at the rat cranial defect site when treated with the ATP/PCL/HA composite scaffold. It can be inferred from the results that the implementation of ATP and HA for the bone tissue engineering repair material displays encouraging prospects.
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Durapatita , Andamios del Tejido , Ratas , Ratones , Animales , Durapatita/farmacología , Durapatita/química , Andamios del Tejido/química , Ingeniería de Tejidos/métodos , Biomimética , Regeneración Ósea , Impresión Tridimensional , Adenosina Trifosfato/farmacología , CráneoRESUMEN
Objective: To establish a juvenile mouse asthma model by postnatal hyperoxia exposure combined with early ovalbumin (OVA) sensitization. Methods: Female C57BL/6J newborn mice were exposed to hyperoxia (95 % O2) from postnatal day-1 (PND1) to PND7; intraperitoneally injected with OVA suspension on PND21, PND28; and stimulated by nebulized inhalation of 1 % OVA from PND36 to PND42. Within 48 h of the last challenge, we observed their activity performance and evaluated airway responsiveness (AHR). All mice were executed at PND44. Female (n = 32) were divided into four groups as follows: room airï¼RAï¼+phosphate-buffered saline (PBS) group; O2 (hyperoxia, 95 % O2) + PBS group; RA + OVA group; O2+OVA group. We obtained the serum, bronchoalveolar lavage fluid (BALF), and lung tissues. The Wright-Giemsa staining was performed for leukocyte classification in BALF and HE staining for pathological examination. The levels of IL-2, IL-5, IL-13, IL-17A and IL-10 in BALF and tIgE and sIgE in serum were detected by ELISA. Results: Compared with OVA sensitization or hyperoxia exposure alone, the mice in the model group (O2+OVA) showed asthma-like symptoms and increased airway hyperreactivity,The levels of IL-5,IL-13 IL-17A were increased in BLAF,and total leukocyte and eosinophil counts were also significant increasesed. The levels of tIgE and sIgE in serum were increased. Conclusion: Postnatal hyperoxia exposure combined with early OVA sensitization might establish a juvenile mouse asthma model.
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Due to their appealing physiochemical properties, metal-organic frameworks (MOFs) have been widely employed in biomedical fields. In this study, we utilize ferric ions and fluorine-containing organic ligands as both structural and functional units to develop a stimulus-responsive nanoagent, 19FIMOF-TA nanoparticles, for activatable 19F magnetic resonance imaging (MRI) and synergistic therapy of tumors. This nanoagent could respond to excess GSH in a tumor microenvironment, discharging fluorinated organic ligands and reduced ferrous ions. The release of these fluorine-containing small molecules results in boosting of the 19F MRI signals, which could be further enhanced by the photothermal effect of this nanoagent to achieve a responsive cascaded amplification of 19F MRI signals for tumor visualization. Meanwhile, ferroptosis promoted by the ferrous ions leads to significant tumor cell death, which is synergistically aggravated by the photothermal effect. The encouraging results illustrate the promising potential of our nanoagent for effective tumor imaging and combinative cancer therapy.
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Estructuras Metalorgánicas , Nanopartículas , Neoplasias , Humanos , Estructuras Metalorgánicas/uso terapéutico , Estructuras Metalorgánicas/química , Flúor/química , Hierro , Imagen por Resonancia Magnética/métodos , Neoplasias/diagnóstico por imagen , Neoplasias/terapia , Neoplasias/patología , Nanopartículas/química , Iones , Línea Celular Tumoral , Microambiente TumoralRESUMEN
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that specifically affects preterm infants. Oxygen therapy administered to treat BPD can lead to hyperoxia-induced lung injury, characterized by apoptosis of lung alveolar epithelial cells. Our epitranscriptomic microarray analysis of normal mice lungs and hyperoxia-stimulated mice lungs revealed elevated RNA expression levels of IL-33, as well as increased m6A RNA methylation levels of IL-33 and PVT1 in the hyperoxia-stimulated lungs. This study aimed to investigate the role of the PVT1/IL-33 axis in BPD. A mouse model of BPD was established through hyperoxia induction, and lung histological changes were assessed by hematoxylin-eosin staining. Parameters such as radial alveolar count and mean chord length were measured to assess lung function. Mouse and human lung alveolar epithelial cells (MLE12 and A549, respectively) were stimulated with hyperoxia to create an in vitro BPD model. Cell apoptosis was detected using Western blotting and flow cytometry analysis. Our results demonstrated that silencing PVT1 suppressed apoptosis in MLE12 and A549 cells and improved lung function in hyperoxia-stimulated lungs. Additionally, IL-33 reversed the effects of PVT1 both in vivo and in vitro. Through online bioinformatics analysis and RNA-binding protein immunoprecipitation assays, YTHDC1 was identified as a RNA-binding protein (RBP) for both PVT1 and IL-33. We found that PVT1 positively regulated IL-33 expression by recruiting YTHDC1 to mediate m6A modification of IL-33. In conclusion, silencing PVT1 demonstrated beneficial effects in alleviating BPD by facilitating YTHDC1-mediated m6A modification of IL-33. Inhibition of the PVT1/IL-33 axis to suppress apoptosis in lung alveolar epithelial cells may hold promise as a therapeutic approach for managing hyperoxia-induced lung injury in BPD.
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Conventional electrospinning produces nanofibers with smooth surfaces that limit biomineralization ability. To overcome this disadvantage, we fabricated a tetramethylpyrazine (TMP)-loaded matrix-mimicking biomineralization in PCL/Gelatin composite electrospun membranes with bubble-shaped nanofibrous structures. PCL/Gelatin membranes (PG), PCL/Gelatin membranes containing biomineralized hydroxyapatite (HA) (PGH), and PCL/Gelatin membranes containing biomineralized HA and loaded TMP (PGHT) were tested. In vitro results indicated that the bubble-shaped nanofibrous surface increased the surface roughness of the nanofibers and promoted mineralization. Furthermore, sustained-release TMP had an excellent drug release efficiency. Initially released vigorously, it reached stabilization at day 7, and the slow-release rate stabilized at 61.0 ± 1.8% at 28 days. All membranes revealed an intact cytoskeleton, cell viability, and superior adhesion and proliferation when stained with Ghost Pen Cyclic Peptide, CCK-8, cell adhesion, and EdU. In PGHT membranes, the osteogenic and vascularized gene expression of BMSCs and human vascular endothelial cells was significantly upregulated compared with that in other groups, indicating the PGHT membranes exhibited an effective vascularization role. Subsequently, the membranes were implanted in a rat cranium defect model for 4 and 8 weeks. Micro-CT and histological analysis results showed that the PGHT membranes had better bone regenerative patterns. Additionally, the levels of CD31 and VEGF significantly increased in the PGHT membrane compared with those in other membranes. Thus, PGHT membranes could accelerate the repair of cranium defects in vivo via HA and TMP synergistic effects.
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Nanofibras , Ratas , Humanos , Animales , Nanofibras/química , Gelatina/química , Células Endoteliales , Regeneración Ósea , Durapatita/química , Cráneo , Poliésteres/química , Andamios del Tejido , Proliferación Celular , Ingeniería de Tejidos/métodosRESUMEN
Bronchial asthma is not considered a singular disease, but rather a collection of syndromes with multiple phenotypes and mechanisms that involve various signaling pathways. It typically emerges during the preschool years, and its etiology is intricate and diverse. In recent years, the advancement of high-throughput sequencing technology has revealed that early alterations in lung microbiota may be associated with asthma incidence and progression. Moreover, significant variations in lung microbiota have been observed among different airway inflammation profiles, known as asthma endotypes. Hence, a comprehensive understanding of the characteristics of lung microbiota in children with asthma can aid in managing disease progression and improving long-term prognosis. Additionally, such insights may spark novel approaches to diagnosing and treating childhood asthma.
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Asma , Microbiota , Niño , Preescolar , Humanos , Asma/etiología , Asma/diagnóstico , Pulmón , Inflamación , FenotipoRESUMEN
Polystyrene nanoplastics (PS-NPs) have recently been found to be present in human blood and kidney. However, the renal toxicity of PS-NPs and the underlying mechanisms have not been fully elucidated. Here, we found that exposure of PS-NPs induced apoptosis of human renal proximal tubular epithelial cells (HK-2) in a size- and dose-dependent manner as revealed by AnnexinV-FITC assay. In addition, PS-NPs promoted ROS production and caused structure changes of mitochondrial and endoplasmic reticulum. Mechanistically, transcriptional sequencing indicated the involvement of MAPK pathway in apoptosis, which was further confirmed by the upregulation of p-p38, p-ERK, CHOP, BAX, cytochrome C, and caspase 3 expression. This study clarified the molecular mechanism underlying PS-NP-induced apoptosis in HK-2 cells and contributed to our risk estimation of PS-NPs in human kidney.
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Nanopartículas , Poliestirenos , Humanos , Poliestirenos/metabolismo , Microplásticos , Túbulos Renales Proximales/metabolismo , Línea Celular , Estrés Oxidativo , Sistema de Señalización de MAP Quinasas , Células Epiteliales , ApoptosisRESUMEN
Histopathological image analysis plays an important role in the diagnosis and treatment of cholangiocarcinoma. This time-consuming and complex process is currently performed manually by pathologists. To reduce the burden on pathologists, this paper proposes a histopathological image classification method for cholangiocarcinoma based on spatial-channel feature fusion convolutional neural networks. Specifically, the proposed model consists of a spatial branch and a channel branch. In the spatial branch, residual structural blocks are used to extract deep spatial features. In the channel branch, a multi-scale feature extraction module and some multi-level feature extraction modules are designed to extract channel features in order to increase the representational ability of the model. The experimental results of the Multidimensional Choledoch Database show that the proposed method performs better than other classical CNN classification methods.
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Ambient carbonyls are important precursors of radicals and ground-level ozone (O3). In this study, sources, precursors, and impacts on radicals and O3 of carbonyls were investigated based on online observations of volatile organic compounds (VOCs) at an urban site in Beijing during June 2021. Carbonyls accounted for 36% and 42% of mixing ratios and OH reactivity for total measured VOCs, respectively. Formaldehyde was the most abundant carbonyl, with the mean level of 4.13 ± 2.28 ppb. Source apportionment results based on the multi linear regression (MLR) method suggested that secondary production contributed 41%, 25%, 36%, and 30% of formaldehyde, acetaldehyde, propanal, and acetone, respectively. Key precursors of carbonyls were then identified based on the calculation of their production rates. It was found that alkenes contributed 59%-80% of aldehydes production. Impacts of carbonyls on HOx radicals (OH and HO2) and O3 production were explored using a box model based on observations (OBM). Photolysis of HONO, formaldehyde, and O3 were the dominant primary sources of HOx radicals during daytime of O3 pollution days, with average relative contributions of 52%, 28%, and 19% to the total primary production rate of HOx, respectively. Aldehydes accounted for 32% (20% from formaldehyde) of average HOx removal rates. The relative incremental reactivity (RIR) values of NOx determined by the OBM were negative, suggesting that the O3-VOCs-NOx sensitivity was in the VOCs-limited regime. Using the observed concentrations of carbonyls as constraints of OBM, the absolute values of RIR for NOx tended to increase but those for anthropogenic VOCs tended to decrease. Formaldehyde showed the largest RIR value for anthropogenic VOCs during O3 pollution days. These findings indicated the important impacts of carbonyls on O3 production and O3-VOCs-NOx sensitivity.