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Aqueous zinc ion batteries have received widespread attention due to their merits of high safety, high theoretical specific capacity, low cost, and environmental benignity. Nevertheless, the irreversible issues of Zn anode deriving from side reactions and dendrite growth have hindered its commercialization in large-scale energy storage systems. Herein, a zinc phosphate tetrahydrate (Zn3(PO4)2·4H2O, ZnPO) coating layer is in situ formed on the bare Zn by spontaneous redox reactions at room temperature to tackle the above issues. Particularly, the dense and brick-like ZnPO layer can effectively separate the anode surface from the aqueous electrolyte, thus suppressing the serious side reactions. Moreover, the ZnPO layer with high ionic conductivity, high Zn2+ transference number, and low nucleation barrier permits rapid Zn2+ transport and enables uniform Zn deposition, ensuring dendrite-free Zn deposition. As a result, the ZnPO@Zn symmetric battery achieves a high Coulombic efficiency of 99.8% and displays ultrahigh cycle stability over 6000 h (> 8 months), far surpassing its counterparts. Furthermore, the ZnPO@Zn||MnO2 full battery exhibits excellent electrochemical performances. Therefore, this work provides a new reference for simple and large-scale preparation of highly reversible Zn metal anodes, and has great potential for practical applications.
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BACKGROUND: Aquaporin-8 (AQP8) is involved in impacting glioma proliferation and can effect tumour growth by regulating Intracellular reactive oxygen species (ROS) signalling levels. In addition to transporting H2O2, AQP8 has been shown to affect ROS signaling, but evidence is lacking in gliomas. In this study, we aimed to investigate how AQP8 affects ROS signaling in gliomas. MATERIALS AND METHODS: We constructed A172 and U251 cell lines with AQP8 knockdown and AQP8 rescue by CRISPR/Cas9 technology and overexpression of lentiviral vectors. We used CCK-8 and flow cytometry to test cell proliferation and cycle, immunofluorescence and Mito-Tracker CMXRos to observe the distribution of AQP8 expression in glioma cells, Amplex and DHE to study mitochondria release of H2O2, mitochondrial membrane potential (MMP) and NAD+/NADH ratio to assess mitochondrial function and protein blotting to detect p53 and p21 expression. RESULT: We found that AQP8 co-localised with mitochondria and that knockdown of AQP8 inhibited the release of H2O2 from mitochondria and led to increased levels of ROS in mitochondria, thereby impairing mitochondrial function. We also discovered that AQP8 knockdown resulted in suppression of cell proliferation and was blocked at the G0/G1 phase with increased expression of mitochondrial ROS signalling-related p53/p21. CONCLUSIONS: This finding provides further evidence for mechanistic studies of AQP8 as a prospective target for the treatment of gliomas.
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Aquaporinas , Proliferação de Células , Glioma , Peróxido de Hidrogênio , Mitocôndrias , Espécies Reativas de Oxigênio , Humanos , Mitocôndrias/metabolismo , Glioma/metabolismo , Glioma/patologia , Glioma/genética , Peróxido de Hidrogênio/farmacologia , Peróxido de Hidrogênio/metabolismo , Aquaporinas/metabolismo , Aquaporinas/genética , Linhagem Celular Tumoral , Espécies Reativas de Oxigênio/metabolismo , Potencial da Membrana Mitocondrial , Neoplasias Encefálicas/metabolismo , Neoplasias Encefálicas/patologia , Neoplasias Encefálicas/genética , Transdução de SinaisRESUMO
BACKGROUND: We have previously identified an unsuspected role for GJB3 showing that the deficiency of this connexin protein induces aneuploidy in human and murine cells and accelerates cell transformation as well as tumor formation in xenograft models. The molecular mechanisms by which loss of GJB3 leads to aneuploidy and cancer initiation and progression remain unsolved. METHODS: GJB3 expression levels were determined by RT-qPCR and Western blot. The consequences of GJB3 knockdown on genome instability were assessed by metaphase chromosome counting, multinucleation of cells, by micronuclei formation and by the determination of spindle orientation. Interactions of GJB3 with α-tubulin and F-actin was analyzed by immunoprecipitation and immunocytochemistry. Consequences of GJB3 deficiency on microtubule and actin dynamics were measured by live cell imaging and fluorescence recovery after photobleaching experiments, respectively. Immunohistochemistry was used to determine GJB3 levels on human and murine bladder cancer tissue sections. Bladder cancer in mice was chemically induced by BBN-treatment. RESULTS: We find that GJB3 is highly expressed in the ureter and bladder epithelium, but it is downregulated in invasive bladder cancer cell lines and during tumor progression in both human and mouse bladder cancer. Downregulation of GJB3 expression leads to aneuploidy and genomic instability in karyotypically stable urothelial cells and experimental modulation of GJB3 levels alters the migration and invasive capacity of bladder cancer cell lines. Importantly, GJB3 interacts both with α-tubulin and F-actin. The impairment of these interactions alters the dynamics of these cytoskeletal components and leads to defective spindle orientation. CONCLUSION: We conclude that deregulated microtubule and actin dynamics have an impact on proper chromosome separation and tumor cell invasion and migration. Consequently, these observations indicate a possible role for GJB3 in the onset and spreading of bladder cancer and demonstrate a molecular link between enhanced aneuploidy and invasive capacity cancer cells during tumor cell dissemination.
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Actinas , Aneuploidia , Invasividade Neoplásica , Tubulina (Proteína) , Neoplasias da Bexiga Urinária , Animais , Humanos , Camundongos , Actinas/metabolismo , Actinas/genética , Linhagem Celular Tumoral , Movimento Celular/genética , Instabilidade Genômica , Microtúbulos/metabolismo , Ligação Proteica , Tubulina (Proteína)/metabolismo , Tubulina (Proteína)/genética , Neoplasias da Bexiga Urinária/patologia , Neoplasias da Bexiga Urinária/genética , Neoplasias da Bexiga Urinária/metabolismo , Urotélio/patologia , Urotélio/metabolismo , Conexinas/metabolismoRESUMO
We have recently shown that loss of ORP3 leads to aneuploidy induction and promotes tumor formation. However, the specific mechanisms by which ORP3 contributes to ploidy-control and cancer initiation and progression is still unknown. Here, we report that ORP3 is highly expressed in ureter and bladder epithelium while its expression is downregulated in invasive bladder cancer cell lines and during tumor progression, both in human and in mouse bladder cancer. Moreover, we observed an increase in the incidence of N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN)-induced invasive bladder carcinoma in the tissue-specific Orp3 knockout mice. Experimental data demonstrate that ORP3 protein interacts with γ-tubulin at the centrosomes and with components of actin cytoskeleton. Altering the expression of ORP3 induces aneuploidy and genomic instability in telomerase-immortalized urothelial cells with a stable karyotype and influences the migration and invasive capacity of bladder cancer cell lines. These findings demonstrate a crucial role of ORP3 in ploidy-control and indicate that ORP3 is a bona fide tumor suppressor protein. Of note, the presented data indicate that ORP3 affects both cell invasion and migration as well as genome stability through interactions with cytoskeletal components, providing a molecular link between aneuploidy and cell invasion and migration, two crucial characteristics of metastatic cells.
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Actinas , Neoplasias da Bexiga Urinária , Animais , Humanos , Camundongos , Aneuploidia , Instabilidade Genômica , Microtúbulos , Invasividade Neoplásica , Bexiga Urinária , Neoplasias da Bexiga Urinária/genéticaRESUMO
Aryl-ketone derivatives have been acknowledged as promising organic photocatalysts for photosynthesis. However, they are limited by their photostability and have been less explored for photoinduced electron transfer (PET) applications. Herein we demonstrate a novel strategy to cover the shortage of aryl-ketone photocatalysts and control the photoreactivity by implanting symmetric aryl ketones into the conjugated covalent organic frameworks (COFs). To prove the concept, three comparative materials with the same topology and varied electronic structures were built, adopting truxenone knot and functionalized terephthalaldehyde linkers. Spectroscopic investigation and excited carrier dynamics analysis disclosed improvements in the photostability and electronic transfer efficiency as well as the structure-performance relationships toward N-aryl tetrahydroisoquinoline oxidation. This system provides a robust rule of thumb for designing new-generation aryl-ketone photocatalysts.
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Optical absorption and scattering result in quality degradation of underwater images, which hampers the performance of underwater vision tasks. In practice, a well-posed underwater image recovery requires a combination of scene specificity and adaptability. To this end, this paper breaks down the overall recovery process into in-situ enhancement and data-driven correction modules, and proposes a Multi-stage Underwater Image Enhancement (MUIE) method to cascade the modules. In the in-situ enhancement module, a channel compensation with scene-relevant supervision is designed to address different degrees of unbalanced attenuation, and then the duality-based computation inverts the result of running a enhancement on inverted intensities to recover the degraded textures. In response to different scenarios, a data-driven correction, encoding corrected color-constancy information under data supervision, is performed to correct the improper color appearance of in-situ enhanced results. Further, under the collaboration between scene and data information, the recovery of MUIE avoids ill-posed response and reduces the prior dependence of specific scenes, resulting in a robust performance in different underwater scenes. Recovery comparison results confirm that the recovery of MUIE shows the superiority of scene clarity, realistic color appearance and evaluation scores. With the recovery of MUIE, the Underwater Image Quality Measurement (UIQM) scores of recovery-challenging images in the UIEB dataset were improved from 1.59 to 3.92.
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A cascade spiroannulation of 2-mercaptoquinoline-3-carbaldehydes with α,α-dicyanoalkenes as well as a cascade spiroannulation of 2-mercaptoquinoline-3-carbaldehydes aldehydes with α-bromocarbonyl compounds was investigated based on a synergistic strategy, providing a series of diverse spiro-fused heterocyclic compounds containing more different functional groups. The features of this strategy directed towards molecular complexity and diversity include step economy, mild conditions, and high bond-forming efficiency, but important polycyclic heterocyclic products, which could be transformed into potential biologically interesting heterocyclic structures.
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BACKGROUND: The interleukin-1-receptor antagonist IL1RA (encoded by the IL1RN gene) is a potent competitive antagonist to interleukin-1 (IL1) and thereby is mainly involved in the regulation of inflammation. Previous data indicated a role of IL1RA in muscle-invasive urothelial carcinoma of the bladder (UCB) as well as an IL1-dependent decrease in tissue barrier function, potentially contributing to cancer cell invasion. OBJECTIVE: Based on these observations, here we investigated the potential roles of IL1RA, IL1A, and IL1B in bladder cancer cell invasion in vitro. METHODS: Cell culture, real-time impedance sensing, invasion assays (Boyden chamber, pig bladder model), qPCR, Western blot, ELISA, gene overexpression. RESULTS: We observed a loss of IL1RA expression in invasive, high-grade bladder cancer cell lines T24, UMUC-3, and HT1197 while IL1RA expression was readily detectable in the immortalized UROtsa cells, the non-invasive bladder cancer cell line RT4, and in benign patient urothelium. Thus, we modified the invasive human bladder cancer cell line T24 to ectopically express IL1RA, and measured changes in cell migration/invasion using the xCELLigence Real-Time-Cell-Analysis (RTCA) system and the Boyden chamber assay. The real-time observation data showed a significant decrease of cell migration and invasion in T24 cells overexpressing IL1RA (T24-IL1RA), compared to cells harboring an empty vector (T24-EV). Concurrently, tumor cytokines, e.g., IL1B, attenuated the vascular endothelial barrier, which resulted in a reduction of the Cell Index (CI), an impedance-based dimensionless unit. This reduction could be reverted by the simultaneous incubation with IL1RA. Moreover, we used an ex vivo porcine organ culture system to evaluate cell invasion capacity and showed that T24-IL1RA cells showed significantly less invasive capacity compared to parental T24 cells or T24-EV. CONCLUSIONS: Taken together, our results indicate an inverse correlation between IL1RA expression and tumor cell invasive capacity and migration, suggesting that IL1RA plays a role in bladder carcinogenesis, while the exact mechanisms by which IL1RA influences tumor cells migration/invasion remain to be clarified in future studies. Furthermore, we confirmed that real-time impedance sensing and the porcine ex vivo organ culture methods are powerful tools to discover differences in cancer cell migration and invasion.
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Movimento Celular/genética , Células Epiteliais/metabolismo , Proteína Antagonista do Receptor de Interleucina 1/genética , Interleucina-1alfa/genética , Interleucina-1beta/genética , Neoplasias da Bexiga Urinária/genética , Animais , Carcinogênese/genética , Carcinogênese/metabolismo , Carcinogênese/patologia , Linhagem Celular Tumoral , Proliferação de Células , Células Epiteliais/patologia , Regulação Neoplásica da Expressão Gênica , Humanos , Proteína Antagonista do Receptor de Interleucina 1/metabolismo , Interleucina-1alfa/metabolismo , Interleucina-1beta/metabolismo , Invasividade Neoplásica , Transdução de Sinais , Suínos , Bexiga Urinária/metabolismo , Bexiga Urinária/patologia , Neoplasias da Bexiga Urinária/metabolismo , Neoplasias da Bexiga Urinária/patologiaRESUMO
Invasive urothelial carcinomas of the bladder (UCB) characteristically show a loss of differentiation markers. The transcription factor Grainyhead-like 3 (GRHL3) plays an important role in the development and differentiation of normal urothelium. The contribution to UCB progression is still elusive. Differential expression of GRHL3 was assessed in normal human urothelium and in non-invasive and invasive bladder cancer cell lines. The contribution of GRHL3 to cell proliferation, viability and invasion in UCB cell lines was determined by gain- and loss-of-function assays in vitro and in an organ culture model using de-epithelialized porcine bladders. GRHL3 expression was detectable in normal human urothelial cells and showed significantly higher mRNA and protein levels in well-differentiated, non-invasive RT4 urothelial carcinoma cells compared to moderately differentiated RT112 cells. GRHL3 expression was absent in anaplastic and invasive T24 cells. Ectopic de novo expression of GRHL3 in T24 cells significantly impaired their migration and invasion properties in vitro and in organ culture. Its downregulation improved the invasive capacity of RT4 cells. The results indicate that GRHL3 may play a role in progression and metastasis in UCB. In addition, this work demonstrates that de-epithelialized porcine bladder organ culture can be a useful, standardized tool to assess the invasive capacity of cancer cells.
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Carcinoma/genética , Proteínas de Ligação a DNA/genética , Fatores de Transcrição/genética , Neoplasias da Bexiga Urinária/genética , Urotélio/metabolismo , Animais , Carcinoma/patologia , Carcinoma de Células de Transição , Diferenciação Celular/genética , Movimento Celular/genética , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Invasividade Neoplásica/genética , Invasividade Neoplásica/patologia , Metástase Neoplásica , Técnicas de Cultura de Órgãos , Suínos , Neoplasias da Bexiga Urinária/patologia , Urotélio/patologiaRESUMO
Sc2(MoO4)3 shows negative thermal expansion (NTE) properties between -93 and +750 °C. Recently, electrochemical activation has been demonstrated to dramatically alter the phase evolution of structurally analogous Sc2(WO4)3. Electrochemical activation involves placing the material of choice in an electrochemical cell with Li, Na or K counter electrodes and discharging (or reacting Li+, Na+ and K+) which is followed by extraction of the activated electrode and subsequent thermal treatment. Here such a process is applied to Sc2(MoO4)3 and the results compared with the evolution of Sc2(WO4)3. For 12.5% lithium discharged Sc2(MoO4)3(12.5% of fully discharge capacity) the coefficient of thermal expansion (CTE) below 425 °C is -13.83(1) × 10-6/°C which is larger than parent material, and a new LixMoO2 phase forms at about 425 °C. The 25% lithium discharged Sc2(MoO4)3 shows the formation of a new Li2MoO4 phase after discharging (electrochemical-based structural change) and on subsequent heat treatment the electrode mix transforms to Li3ScMo3O12. Interestingly, a range of new phases at various temperatures in the sodium and potassium discharged samples appear during heat treatment. For example, Na0.9Mo2O4 forms during thermal treatment of the 50% sodium discharged Sc2(MoO4)3 while KMo4O6 and K2MoO4 form with thermal treatment of 100% potassium discharged Sc2(MoO4)3. This work showcases the rich diversity in the phases that can be accessed during and post thermal treatment of Li, Na, and K discharged Sc2(MoO4)3 electrodes.
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BACKGROUND: Currently, the role of UPR signaling in prostate cancer (PCa) is unclear. To evaluate the relationship between UPR signaling pathway and the prognosis of PCa, we explored the expression of IRE1, PERK, and ATF6 in tissues. METHODS: A total of 160 PCa and 30 benign prostate hyperplasia (BPH) tissues were collected. The expression of UPR signaling factors was assessed by immunohistochemistry. The staining characteristics were identified and evaluated for associations with clinicopathologic parameters, PSA recurrence survival, and prostate cancer-specific morality. RESULTS: The expressions of ATF6α, PERK, and IRE1α were significantly associated with Gleason grade, PSA level, T stages and M stage, while this association was not significant in N stage. Additionally, UPR signaling factors expressed correlatively with each other. In further studies, high expression level of UPR signaling factors was usually detected in patients who suffered poor prognosis. Patients with positive UPR signaling factors meet shorter survival duration both on cancer-specific morality and PSA recurrence. Multivariate analysis showed that IRE1α (HR = 4.461 95%CI = 1.270-15.670 P = 0.020) could be a potential factor in predicting PSA recurrence independently. CONCLUSIONS: UPR signaling factors were co-activated and activation of UPR signaling was implicated to the malignant progression and worse prognosis of PCa. The mechanism and function of UPR signaling in PCa are still to be determined. Prostate 77:274-281, 2017. © 2016 Wiley Periodicals, Inc.
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Progressão da Doença , Hiperplasia Prostática/metabolismo , Neoplasias da Próstata/metabolismo , Transdução de Sinais/fisiologia , Resposta a Proteínas não Dobradas/fisiologia , Idoso , Idoso de 80 Anos ou mais , Estudos de Coortes , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Hiperplasia Prostática/patologia , Neoplasias da Próstata/patologia , Estudos RetrospectivosRESUMO
Ras and a-factor-converting enzyme 1 (Rce1) is located in the endoplasmic reticulum (ER) and is thought to be responsible for endoproteolytic processing of the vast majority of CAAX proteins. Endoplasmic reticulum stress (ERS) plays an important role in renal cell carcinoma (RCC); however, the expression and role of Rce1 in RCC have not been extensively studied. We aimed to investigate the expression of Rce1 in RCC tissues and its molecular mechanism in ERS-induced apoptosis in RCC 786-O cells. We first used western blotting, quantitative reverse transcriptase-polymerase chain reaction, and immunohistochemistry to detect the Rce1 expression in renal carcinoma tissues and paracancerous tissues. It was found that Rce1 expression was upregulated in RCC tissues, and its positive expression level was strongly associated with clinicopathologic features. Next, we detected the expression of Rce1 in human embryonic kidney cell line HEK293 and human renal carcinoma cell lines 786-O, ACHN, and A498. Higher expression of Rce1 was found in human renal carcinoma cell lines, especially in 786-O cells. Knockdown of Rce1 in 786-O cells increased apoptosis and inhibited proliferation (P < 0.05). Moreover, downregulation of Rce1 upregulated the expression of the pro-apoptotic protein Bax, but downregulated the expression of the anti-apoptotic protein Bcl-2. Further studies showed that downregulation of Rce1 also affected the expression of ERS factors. In conclusion, our results indicated that Rce1 plays a key role in RCC. Low expression of Rce1 might indirectly increase apoptosis and inhibit proliferation of renal carcinoma cells through ERS.
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Apoptose , Carcinoma de Células Renais/patologia , Endopeptidases/metabolismo , Estresse do Retículo Endoplasmático , Regulação Neoplásica da Expressão Gênica , Neoplasias Renais/patologia , Fator 4 Ativador da Transcrição/genética , Fator 4 Ativador da Transcrição/metabolismo , Carcinoma de Células Renais/genética , Carcinoma de Células Renais/metabolismo , Estudos de Casos e Controles , Proliferação de Células , Endopeptidases/genética , Retículo Endoplasmático/metabolismo , Retículo Endoplasmático/patologia , Fator de Iniciação 2 em Eucariotos/genética , Fator de Iniciação 2 em Eucariotos/metabolismo , Feminino , Humanos , Neoplasias Renais/genética , Neoplasias Renais/metabolismo , Masculino , Pessoa de Meia-Idade , Prognóstico , Proteínas Proto-Oncogênicas c-bcl-2/genética , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , eIF-2 Quinase/genética , eIF-2 Quinase/metabolismoRESUMO
To effectively manage water constraints (WCs) within a basin, it is crucial to first scientifically delineate their spatial distribution and thoroughly understand the interactions between WCs. Investigating the complex driving mechanisms at multiple scales is also essential. In this study, a basin WC evaluation framework is constructed using a conflict risk assessment model. The spatiotemporal variations of four types of WCs across three spatial scales in the Taihu Lake Basin (TLB) are thoroughly investigated. Furthermore, the study quantifies the trade-offs, synergy effects, and bundle patterns of these water constraints. The study employs the Optimal Parameters-based Geographic Detector (OPGD) and multivariate linear regression to identify the key socio-ecological drivers of WCs. Our findings indicate that between 2010 and 2020, water resource constraint (WREC), water environment constraint (WENC), water safety constraint (WSAC), water ecology constraint (WECC), and the comprehensive WC (CWC) displayed varying degrees of heterogeneity. Particularly, the mean values of WSAC, WECC, and CWC witnessed an increase over the decade. Additionally, all WCs exhibited a strong positive spatial autocorrelation. Synergistic interactions among WCs were predominantly observed in pairs such as WREC-WSAC, WREC-WECC, and WSAC-WECC, while a weaker trade-off effect was noted in the WENC-WECC pair. At multiple scales, we identified eight types of WC bundles capable of undergoing mutual transformations, especially at the basin scale. The primary drivers of WCs varied across different stages and scales, with most factors collectively exerting a more significant impact than individually. Notably, factors like secondary and tertiary industry GDP (X2), population density (X3), precipitation (X6), and elevation (X7) were identified as core drivers influencing the evolution of WCs in the TLB. Integrating these spatiotemporal characteristics and driving mechanisms of WC interactions into basin planning and management can significantly support the alleviation of multidimensional water constraints in territorial spaces.
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Heat shock protein 20 (HSP20) serves as a chaperone and plays roles in numerous biological processes, but the codon usage bias (CUB) of its genes has remained unexplored. This study identified 140 HSP20 genes from four cruciferous species, Arabidopsis thaliana, Brassica napus, Brassica rapa, and Camelina sativa, that were identified from the Ensembl plants database, and we subsequently investigated their CUB. As a result, the base composition analysis revealed that the overall GC content of HSP20 genes was below 50%. The overall GC content significantly correlated with the constituents at three codon positions, implying that both mutation pressure and natural selection might contribute to the CUB. The relatively high ENc values suggested that the CUB of the HSP20 genes in four cruciferous species was relatively weak. Subsequently, ENc exhibited a negative correlation with gene expression levels. Analyses, including ENc-plot analysis, neutral analysis, and PR2 bias, revealed that natural selection mainly shaped the CUB patterns of HSP20 genes in these species. In addition, a total of 12 optimal codons (ΔRSCU > 0.08 and RSCU > 1) were identified across the four species. A neighbor-joining phylogenetic analysis based on coding sequences (CDS) showed that the 140 HSP20 genes were strictly and distinctly clustered into 12 subfamilies. Principal component analysis and cluster analysis based on relative synonymous codon usage (RSCU) values supported the fact that the CUB pattern was consistent with the genetic relationship at the gene level and (or) species levels. These results will not only enrich the HSP20 gene resource but also advance our understanding of the CUB of HSP20 genes, which may underlie the theoretical basis for exploration of their genetic and evolutionary pattern.
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Structuring a stable artificial coating to mitigate dendrite growth and side reactions is an effective strategy for protecting the Zn metal anode. Herein, a Cu-Ag double-layer metal coating is constructed on the Zn anode (Zn@Cu-Ag) by simple and in-situ displacement reactions. The Cu layer enhances the bond between the Ag layer and Zn substrate by acting as an intermediary, preventing the Ag coating from detachment. Concurrently, the Ag layer serves to improve the corrosion resistance of Cu metal. During plating, the initial Cu sheets and Ag particles on the surface of Zn@Cu-Ag electrode gradually transform into a flat and smooth layer, resulting in the formation of AgZn, AgZn3, and (Ag, Cu)Zn4 alloys. Alloys play a multifunctional role in inhibiting dendrite growth and side reactions due to decreased resistance, low nucleation barrier, enhanced zincophilicity, and strong corrosion resistance. Consequently, the Zn@Cu-Ag symmetric cell exhibits continuous stable performance for 3750 h at 1 mA cm-2. Furthermore, the Zn@Cu-Ag||Zn3V3O8 full cell achieves an initial capacity of 293.4 mAh g-1 and realizes long cycling stability over 1200 cycles. This work provides new insight into the engineering of an efficient artificial interface for highly stable and reversible Zn metal anodes.
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In interactions between pathogens and plants, pathogens secrete many molecules that facilitate plant infection, and some of these compounds are recognized by plant pattern recognition receptors (PRRs), which induce immune responses. Molecules in both pathogens and plants that trigger immune responses in plants are termed elicitors. On the basis of their chemical content, elicitors can be classified into carbohydrates, lipopeptides, proteinaceous compounds and other types. Although many studies have focused on the involvement of elicitors in plants, especially on pathophysiological changes induced by elicitors in plants and the mechanisms mediating these changes, there is a lack of up-to-date reviews on the characteristics and functions of proteinaceous elicitors. In this mini-review, we provide an overview of the up-to-date knowledge on several important families of pathogenic proteinaceous elicitors (i.e., harpins, necrosis- and ethylene-inducing peptide 1 (nep1)-like proteins (NLPs) and elicitins), focusing mainly on their structures, characteristics and effects on plants, specifically on their roles in plant immune responses. A solid understanding of elicitors may be helpful to decrease the use of agrochemicals in agriculture and gardening, generate more resistant germplasms and increase crop yields.
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Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory illness. It arises from emphysema and chronic bronchitis and is characterized by progressive and irreversible airflow limitation and chronic inflammation of the lungs, which eventually progresses to pulmonary hypertension, chronic pulmonary heart disease and respiratory failure. Autophagy is a highly conserved cellular homeostasis maintenance mechanism that involves the transport of damaged organelles and proteins to lysosomes for destruction. Dysregulation of autophagy is one of the pathogenic mechanisms of many diseases and is strongly associated with the development of COPD, although the precise mechanisms are unknown. In this paper, we focus on macroautophagy, a type of autophagy that has been thoroughly studied, and describe the characteristics, processes, regulatory pathways, and functions of autophagy, and discuss its relationship with COPD from the perspectives of inflammation, emphysema, mucus hypersecretion, cilia structure and function, airway remodeling, vascular remodeling, and bacterial infections, with a view to searching for the therapeutic targets of COPD from the perspective of autophagy, which is hoped to be helpful for the clinical treatment.
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Enfisema , Hipertensão Pulmonar , Doença Pulmonar Obstrutiva Crônica , Enfisema Pulmonar , Humanos , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Enfisema Pulmonar/etiologia , Doença Crônica , Autofagia/fisiologia , Inflamação/patologia , Hipertensão Pulmonar/complicaçõesRESUMO
BACKGROUND: Shaoyao Gancao decoction (SGD), a classic traditional Chinese herbal formula, has been widely used to treat febrile diseases in the clinic for centuries. In recent years, a growing number of studies have found that SGD has a favorable anti-liver injury effect. PURPOSE: In this study, we want to know the potential active components of SGD treatment in liver injury. STUDY DESIGN: A novel method combining computer simulation and in vivo experiment was established for the first time and used to investigate this problem. METHODS: A network pharmacology was used to explore the active components of SGD treatment in liver injury, and preliminarily verified the results of network pharmacology through molecular docking. To further understand the active compounds of SGD in the treatment of liver injury, we compared the prototypes and metabolites of SGD in healthy rats and rats with liver injury after oral administration. In addition, a UPLC-MS/MS method was developed and successfully applied to investigate the pharmacokinetics of 9 compounds of SGD in healthy and liver injury rats. RESULTS: It showed that SGD exerted protective effects against liver injury by the active components of liquiritin and albiflorin, etc. The values of the AUC0-t, AUC0-∞, t1/2, Tmax were significantly different after oral administration of SGD in healthy and liver injury rats. This indicates that the pharmacokinetic study in the pathological state of liver injury can provide more valuable information for guiding clinical medication. CONCLUSION: In this study, the integration of network pharmacology and experiments in vivo provides a novel strategy to explore active components of TCMs to treat diseases.
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Farmacologia em Rede , Espectrometria de Massas em Tandem , Ratos , Animais , Simulação por Computador , Simulação de Acoplamento Molecular , Cromatografia Líquida , Espectrometria de Massas em Tandem/métodosRESUMO
Non-small cell lung cancer (NSCLC) is one of the most serious diseases affecting human health today, and current research is focusing on gut flora. There is a correlation between intestinal flora imbalance and lung cancer, but the specific mechanism is not clear. Based on the "lung and large intestine being interior-exteriorly related" and the "lung-intestinal axis" theory. Here, based on the theoretical comparisons of Chinese and western medicine, we summarized the regulation of intestinal flora in NSCLC by active ingredients of traditional Chinese medicine and Chinese herbal compounds and their intervention effects, which is conducive to providing new strategies and ideas for clinical prevention and treatment of NSCLC.
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Carcinoma Pulmonar de Células não Pequenas , Medicamentos de Ervas Chinesas , Microbioma Gastrointestinal , Neoplasias Pulmonares , Humanos , Medicina Tradicional Chinesa , Carcinoma Pulmonar de Células não Pequenas/tratamento farmacológico , Medicamentos de Ervas Chinesas/uso terapêuticoRESUMO
PURPOSE: The purpose of this work is to examine the impact of AQP8 on the proliferation and development of human glioma cell lines A172 and U251 and to determine if aquaporin 8 (AQP8) is associated with GSK-3ß phosphorylation and nuclear transport of ß-catenin in the Wnt signaling pathway. METHODS: AQP8 knockdown cell lines were constructed using a CRISPR/Cas9 double vector lentivirus infection. SAM/dCas9 was used to construct AQP8 overexpression cell lines and the CV084 lentivirus vector was used to construct AQP8 rescue cell lines. AQP8 and its mRNA, and phosphorylated GSK-3ß, ß-catenin, and other related proteins, were detected using western blot and qRT-PCR. Glioma cell apoptosis was detected using Hoechst 33342 dye. The migration of glioma cells was discovered using a wound healing assay. ß-catenin localization in cells was detected using immunofluorescence staining. RESULTS: The proliferative and migratory capacities of A172 and U251 cells were significantly enhanced after AQP8 overexpression. The Wnt signaling pathways appeared to have higher levels of phosphorylated GSK-3ß and ß-catenin, and a rise in the fluorescence intensity ratio of ß-catenin in the nucleus and cytoplasm, which suggests that ß-catenin translocated into the nucleus, while AQP8 knockdown produced the opposite effect. Further, overexpression of AQP8 in AQP8 knockdown cell lines rescued the reduction of related protein levels caused by AQP8 knockdown. CONCLUSION: High AQP8 expression promotes proliferation and growth of glioma cells, a process associated with phosphorylation of GSK-3ß and nuclear translocation of ß-catenin.