Electronic Journal of Biotechnology最新文献

{"title":"ABL1-STAT3-NLRP3 axis attenuates pyroptosis and alleviates diabetic retinopathy","authors":"Lili Hu,&nbsp;Gong Chen,&nbsp;Haoning Pan,&nbsp;Shaoxin Pan","doi":"10.1016/j.ejbt.2026.100717","DOIUrl":"10.1016/j.ejbt.2026.100717","url":null,"abstract":"<div><h3>Background</h3><div>Diabetic retinopathy is a major microvascular complication of diabetes and a leading cause of vision loss. Persistent low-grade inflammation drives disease progression. Pyroptosis, characterized by its pro-inflammatory nature, is involved in several inflammatory diseases, yet the molecular mechanisms specific to diabetic retinopathy remain largely undefined. This study aimed to identify the key molecular drivers and regulatory pathways of pyroptosis in diabetic retinopathy.</div></div><div><h3>Results</h3><div>Five key pyroptosis-related genes were identified: ubiquitin-specific peptidase 24, signal transducer and activator of transcription 3, and ABL proto-oncogene 1 were upregulated, while tripartite motif containing 24 and tubulin beta 6 class VI were downregulated in diabetic retinopathy. High glucose exposure induced pyroptotic morphology and increased lactate dehydrogenase, interleukin-1 beta, and interleukin-18 levels. Functional assays demonstrated that ABL proto-oncogene 1 acts upstream of signal transducer and activator of transcription 3 to activate the NOD-like receptor family pyrin domain-containing 3 inflammasome, ultimately leading to pyroptosis. Signal transducer and activator of transcription 3 showed strong diagnostic value with an area under the curve exceeding 0.9.</div></div><div><h3>Conclusions</h3><div>This study identifies a novel ABL proto-oncogene 1–signal transducer and activator of transcription 3–NOD-like receptor family pyrin domain containing 3 signaling axis as a central regulator of pyroptosis in diabetic retinopathy. These findings provide insights into inflammation-induced retinal pathology and suggest candidate molecular targets for therapeutic intervention.</div><div><strong>How to cite:</strong> Hu L, Chen G, Pan H, et al. ABL1-STAT3-NLRP3 axis attenuates pyroptosis and alleviates diabetic retinopathy. Electron J Biotechnol 2026;82. <span><span>https://doi.org/10.1016/j.ejbt.2026.100717</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"82 ","pages":"Article 100717"},"PeriodicalIF":3.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148540241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of MORC2 via bioinformatics and machine learning reveals its transcriptional activation by PAX2 in NSCLC malignancy","authors":"Junyan Cao,&nbsp;Fang Cai,&nbsp;Jun Jia,&nbsp;Jiangtao Guo,&nbsp;Xiu Yang","doi":"10.1016/j.ejbt.2026.100718","DOIUrl":"10.1016/j.ejbt.2026.100718","url":null,"abstract":"<div><h3>Background</h3><div>Non-small cell lung cancer (NSCLC) represents the top contributor to cancer-associated deaths globally, and its suboptimal clinical outcomes are linked to late-stage detection and acquired resistance to existing therapies. Microrchidia family CW-type zinc finger 2 (MORC2) has been found to exhibit oncogenic potential in NSCLC, but its transcriptional regulatory mechanisms and role in glycolytic reprogramming remain unclear.</div></div><div><h3>Results</h3><div>As a key gene, MORC2 was found to be overexpressed in NSCLC and linked to poor prognosis. MORC2 silencing impaired cell proliferation, stemness, and invasion, diminished glycolysis, and enhanced apoptosis. PAX2 was confirmed to directly transcriptionally activate MORC2; overexpression of MORC2 reversed the defects in malignant phenotypes induced by PAX2 knockdown. <em>In vivo</em>, depletion of PAX2 suppressed tumor growth, which was partially rescued by MORC2 overexpression.</div></div><div><h3>Conclusions</h3><div>The PAX2/MORC2 axis was demonstrated to drive NSCLC malignancy, supporting MORC2 as a potential prognostic marker and therapeutic target for NSCLC.</div><div><strong>How to cite:</strong> Cao J, Cai F, Jia J, et al. Identification of MORC2 via bioinformatics and machine learning reveals its transcriptional activation by PAX2 in NSCLC malignancy. Electron J Biotechnol 2026;82. <span><span>https://doi.org/10.1016/j.ejbt.2026.100718</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"82 ","pages":"Article 100718"},"PeriodicalIF":3.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148539813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontal ligament stem cell-derived exosomes promote alveolar bone defect repair in periodontitis by mediating M2 macrophage polarization via regulation of the SEMA4D/PLXNB1 axis","authors":"YanZong Yang ,&nbsp;ChunBo Zhang","doi":"10.1016/j.ejbt.2026.100712","DOIUrl":"10.1016/j.ejbt.2026.100712","url":null,"abstract":"<div><h3>Background</h3><div>Periodontitis is a chronic inflammatory disease characterized by progressive alveolar bone loss. This study explored the role of exosomes derived from periodontal ligament stem cells (PDLSCs-Exo) in repairing alveolar bone defects in periodontitis.</div></div><div><h3>Results</h3><div>PDLSCs-Exo significantly promoted new bone formation and collagen deposition in the defect area while reducing pro-inflammatory factors and enhancing M2 macrophage polarization. The knockdown of semaphorin 4D (SEMA4D) or plexin B1 (PLXNB1) further enhanced exosome-mediated repair, whereas their overexpression attenuated it. Additionally, the upregulation of PLXNB1 reversed the reparative effects of SEMA4D downregulation on alveolar bone defects in periodontitis.</div></div><div><h3>Conclusions</h3><div>PDLSCs-Exo promotes M2 macrophage polarization by inhibiting the SEMA4D/PLXNB1 axis, alleviating local inflammation and accelerating alveolar bone defect repair in periodontitis. This finding provides a novel theoretical basis for the clinical treatment of periodontitis-related alveolar bone defects and identifies potential therapeutic targets for improving the efficacy of bone defect repair.</div><div><strong>How to cite:</strong> Yang Y, Zhang C. Periodontal ligament stem cell-derived exosomes promote alveolar bone defect repair in periodontitis by mediating M2 macrophage polarization via regulation of the SEMA4D/PLXNB1 axis. Electron J Biotechnol 2026;81. <span><span>https://doi.org/10.1016/j.ejbt.2026.100712</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"81 ","pages":"Article 100712"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147799172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutathione peroxidase 3 as a predictor of immune modulation in gastric adenocarcinoma","authors":"Ying Shao ,&nbsp;Shanpeng Cui ,&nbsp;Chunfeng Zhang ,&nbsp;Li Li ,&nbsp;Lijuan Ma","doi":"10.1016/j.ejbt.2026.100713","DOIUrl":"10.1016/j.ejbt.2026.100713","url":null,"abstract":"<div><h3>Background</h3><div>Gastric cancer is a highly prevalent and lethal malignancy worldwide, with its immune microenvironment playing a crucial role in tumor initiation and progression. Among selenoproteins, glutathione peroxidase 3 (GPX3) is an important antioxidant enzyme that has recently attracted attention for its roles in various cancers. However, the function of GPX3 and its impact on the immune microenvironment in stomach adenocarcinoma (STAD) remain insufficiently explored.</div></div><div><h3>Results</h3><div>Deep STAD tissues were more enriched in immune cells compared to superficial tumor tissues, particularly myeloid cells and fibroblasts. GPX3 was predominantly expressed in fibroblasts and myeloid cells, while its expression in T cells was relatively low, with no significant differences across different tumor layers. Moreover, GPX3 exhibited weak correlations with PD-1 and CTLA-4, suggesting that GPX3 may not directly mediate immune evasion via immune checkpoint pathways. These findings characterize the cellular distribution of GPX3 within the STAD immune microenvironment and provide initial insights into its potential regulatory function.</div></div><div><h3>Conclusions</h3><div>Although GPX3 may not directly influence immune checkpoint pathways, its high expression in myeloid cells and fibroblasts suggests that it might indirectly modulate immune responses by regulating the tumor microenvironment. These results lay a theoretical foundation for future research on GPX3 in gastric cancer and its potential as a therapeutic target.</div><div><strong>How to cite:</strong> Shao Y, Cui S, Zhang C, et al. Glutathione peroxidase 3 as a predictor of immune modulation in gastric adenocarcinoma. Electron J Biotechnol 2026;81. <span><span>https://doi.org/10.1016/j.ejbt.2026.100713</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"81 ","pages":"Article 100713"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147803547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AKT/p65-dependent upregulation of CD64 by LPS drives pathogenesis and diagnostic potential in sepsis","authors":"Lin Li ,&nbsp;Xiaoqing Fu ,&nbsp;Nayun Chen ,&nbsp;Daihua Fang","doi":"10.1016/j.ejbt.2026.100707","DOIUrl":"10.1016/j.ejbt.2026.100707","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis is a life-threatening condition characterized by organ dysfunction caused by a dysregulated host response to infection. Despite improvements in clinical management, both incidence and mortality remain high. Identifying biomarkers with high sensitivity and specificity is critical for early diagnosis. CD64, an Fcγ receptor upregulated on neutrophils during infection, has emerged as a promising diagnostic indicator. This study aimed to evaluate the diagnostic and mechanistic role of CD64 in pediatric sepsis.</div></div><div><h3>Results</h3><div>A total of 200 children with sepsis and 166 healthy controls were enrolled. At a cutoff value of 0.165, the CD64 index achieved a diagnostic sensitivity of 87.0% and specificity of 92.8%, outperforming conventional markers such as procalcitonin (PCT), C-reactive protein (CRP), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Mechanistic assays demonstrated that lipopolysaccharide (LPS) stimulation induced CD64 expression through the Protein Kinase B (AKT) signaling pathway. Both LPS exposure and AKT overexpression promoted p65 nuclear translocation, and chromatin immunoprecipitation confirmed p65 binding to the CD64 promoter, thereby enhancing CD64 transcription.</div></div><div><h3>Conclusions</h3><div>CD64 exhibits superior diagnostic and prognostic performance compared to traditional inflammatory markers and serves as a reliable biomarker for pediatric sepsis. Mechanistically, CD64 upregulation is mediated by the AKT/p65 signaling axis. These findings provide a foundation for integrating CD64 into early diagnostic workflows and developing targeted therapeutic strategies in sepsis management.</div><div><strong>How to cite:</strong> Li L, Fu X, Chen N, et al. AKT/p65-dependent upregulation of CD64 by LPS drives pathogenesis and diagnostic potential in sepsis. Electron J Biotechnol 2026;80. <span><span>https://doi.org/10.1016/j.ejbt.2026.100707</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"80 ","pages":"Article 100707"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147418600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systems-level analysis prioritizes the importance of IFNG, SULF1, and OAS3 genes in head and neck cancer","authors":"Juweria Khawar ,&nbsp;Jinlei Guo ,&nbsp;Saeed Akhtar ,&nbsp;Baogang Bai ,&nbsp;Syed Aun Muhammad","doi":"10.1016/j.ejbt.2026.100705","DOIUrl":"10.1016/j.ejbt.2026.100705","url":null,"abstract":"<div><h3>Background</h3><div>Head and neck cancer (HNC) is one of the most prevalent and challenging diseases affecting a large population worldwide. Functional genomics can help understand the disease, but expressed gene therapy is uncertain. The study sought to identify specific genetic mutations and protein expression profiles in HNC.</div></div><div><h3>Results</h3><div>We ranked IFNG, SULF1, and OAS3 as three HNC-related genes (<em>p</em> &lt; 0.05) based on the data mining. N-acetyleglucosamine-6-sulfatase activity, arylsulfatase, 2,5-oligoadenylate synthetase activity, interferon-gamma receptor binding, and other essential biological processes were all significantly correlated with the gene ontology (GO) terms. Nucleotide excision repair pathways, RNA polymerase-I transcription start and termination, RNA polymerase-II promoter escape, pyrimidine biosynthesis, and interferon-gamma signaling were all linked in the pathway enrichment. OAS1, IFIT1, CD4, STAT3, NFKBIA, RIPK1, SLCO5A1, and others are functionally connected to the co-expressed genes, while COL3A1 and SCEL are indirectly linked. Compared to controls, the quantitative PCR (qPCR) of these genes showed a significant two-fold change (FC) expression (2^−DDC_T) pattern of SULF1 (FC ≤ 1.2), OAS3 (FC ≤ 0.13), and IFNG (FC ≤ 0.12) compared to reference gene GAPDH (FC = 1). Pathophysiological cancer development is associated with up- and downregulated expression of these genes. The study found that personalized medicine can improve HNC treatment by adapting medication to each patient’s tumor’s molecular traits.</div></div><div><h3>Conclusions</h3><div>A substantial correlation between the pathophysiology of HNC and the <em>IFNG, SULF1</em>, and <em>OAS3</em> genes is found. This research could expedite the progress of drug discovery and aid in modifying HNC’s treatment approaches.</div><div><strong>How to cite:</strong> Khawar J, Guo J, Akhtar S, et al. Systems-level analysis prioritizes the importance of IFNG, SULF1, and OAS3 genes in head and neck cancer. Electron J Biotechnol 2026;80. <span><span>https://doi.org/10.1016/j.ejbt.2026.100705</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"80 ","pages":"Article 100705"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147418538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the molecular mechanism of resveratrol for the treatment of lung adenocarcinoma based on molecular docking","authors":"Nan Chen ,&nbsp;Yang Yang ,&nbsp;Zhuoyu Chen ,&nbsp;Huanzhen Fan ,&nbsp;Qing Lin ,&nbsp;Yanqiu Chen","doi":"10.1016/j.ejbt.2026.100706","DOIUrl":"10.1016/j.ejbt.2026.100706","url":null,"abstract":"<div><h3>Background</h3><div>Resveratrol (RES) has been found to inhibit the progression of lung cancer. Our study aims to explore the molecular mechanisms by which RES regulates lung adenocarcinoma (LUAD) progression.</div></div><div><h3>Results</h3><div>Our study unveils two key novel findings: First, our study demonstrates that EPHB2 is a direct functional target of RES in LUAD. Molecular docking and CETSA confirmed the binding, and crucially, EPHB2 overexpression reversed the anti-tumor effects of RES. Second, our study reveals a previously unrecognized role for EPHB2 in promoting glycolysis in LUAD, which is effectively suppressed by RES. Specifically, RES potently inhibited LUAD tumor growth <em>in vivo</em> and suppressed cell proliferation, migration, invasion, and glycolysis <em>in vitro</em>. These inhibitory effects were consistently abolished upon EPHB2 overexpression.</div></div><div><h3>Conclusions</h3><div>Collectively, our findings suggest that RES inhibits LUAD cell proliferation, migration, invasion, and glycolysis, with EPHB2 downregulation appearing to contribute to these effects. Further studies are needed to determine whether RES directly targets EPHB2 and to evaluate the translational potential of these findings.</div><div><strong>How to cite:</strong> Chen N, Yang Y, Chen Z, et al. Exploring the molecular mechanism of resveratrol for the treatment of lung adenocarcinoma based on molecular docking. Electron J Biotechnol 2026;80. <span><span>https://doi.org/10.1016/j.ejbt.2026.100706</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"80 ","pages":"Article 100706"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147417935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ANKRD1 knockdown attenuates doxorubicin-induced dilated cardiomyopathy by regulating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway","authors":"Jia Yuan ,&nbsp;Yu Zhou ,&nbsp;GuoHua Wei ,&nbsp;Tao Qi ,&nbsp;HaoLiang Sun ,&nbsp;Jian Shen","doi":"10.1016/j.ejbt.2025.08.002","DOIUrl":"10.1016/j.ejbt.2025.08.002","url":null,"abstract":"<div><h3>Background</h3><div>Doxorubicin (DOX), a widely used chemotherapeutic agent, causes severe cardiotoxicity that frequently progresses to dilated cardiomyopathy (DCM). While ankyrin repeat domain 1 protein (ANKRD1) plays critical roles in cardiovascular pathophysiology, its specific involvement in doxorubicin-induced DCM remains unknown. This study investigates the functional significance of ANKRD1 in DOX-induced DCM pathogenesis.</div></div><div><h3>Results</h3><div>DOX treatment significantly upregulated ANKRD1 expression in both rat models and H9c2 rat cardiomyocytes. <em>In vivo</em>, ANKRD1 knockdown ameliorated DOX-induced cardiac dysfunction, as demonstrated by improved left ventricular ejection fraction and fractional shortening, along with reduced serum levels of lactate dehydrogenase and creatine kinase-myocardial band. Conversely, ANKRD1 overexpression exacerbated cardiac impairment. Pathological examination revealed that ANKRD1 knockdown attenuated DOX-induced myocardial tissue damage and collagen deposition, while ANKRD1 overexpression intensified these pathological changes. Furthermore, ANKRD1 knockdown mitigated mitochondrial dysfunction and oxidative stress in DCM models both <em>in vivo</em> and <em>in vitro</em>. Mechanistically, ANKRD1 knockdown activated the AMP-activated protein kinase (AMPK)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling cascade, thereby attenuating DOX-induced cardiomyocyte toxicity, mitochondrial dysfunction, and oxidative stress. Rescue experiments using the AMPK inhibitor dorsomorphin confirmed this pathway’s involvement, as dorsomorphin treatment abolished the protective effects of ANKRD1 knockdown against DOX-induced cardiomyocyte damage.</div></div><div><h3>Conclusions</h3><div>ANKRD1 knockdown prevents DOX-induced DCM by ameliorating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway. These findings establish ANKRD1 as a promising therapeutic target for preventing DOX-induced cardiotoxicity and DCM.</div><div><strong>How to cite:</strong> Yuan J, Zhou Y, Wei G, et al. ANKRD1 knockdown attenuates doxorubicin-induced dilated cardiomyopathy by regulating mitochondrial dysfunction and oxidative stress through activation of the AMPK/AKT/mTOR pathway. Electron J Biotechnol 2026, 79. <span><span>https://doi.org/10.1016/j.ejbt.2025.08.002</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"79 ","pages":"Article 100696"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145749970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low-cost hybrid copper–carbon nanotube coating with antimicrobial properties in ambient conditions","authors":"Christian Pablo Romero ,&nbsp;Claudio Ramirez-Mora ,&nbsp;Rodolfo Salazar ,&nbsp;Cristobal Fernandez ,&nbsp;Cristian Acevedo ,&nbsp;Christian Orellana ,&nbsp;Maria Abellan ,&nbsp;David Aliaga","doi":"10.1016/j.ejbt.2025.100700","DOIUrl":"10.1016/j.ejbt.2025.100700","url":null,"abstract":"<div><h3>Background</h3><div>The development of bactericidal surfaces using nanotechnology has gained traction in high-tech sectors due to their effectiveness against pathogens. However, widespread adoption in low-income regions remains limited by the high cost of materials such as copper nanoparticles and the need for specialized application personnel. This study aims to develop a cost-effective bactericidal coating that minimizes nano-copper usage while maintaining strong antimicrobial performance and practical applicability in resource-limited environments.</div></div><div><h3>Results</h3><div>A polymer-based coating incorporating ≤3 wt% nano-copper and carbon nanotubes was formulated to enhance conductivity and mechanical stability. The fabrication process was optimized for on-site application under ambient conditions. Scanning Electron Microscopy (SEM) revealed a uniform surface distribution of nano-copper particles. Bactericidal activity tests confirmed efficacy against <em>Escherichia coli</em>, <em>Listeria monocytogenes</em>, and <em>Salmonella</em> spp. Techno-economic analysis indicated that the coating could be integrated into existing surface finishing systems at an incremental cost of 2.6–3.5 USD per gallon.</div></div><div><h3>Conclusions</h3><div>This work demonstrates the feasibility of producing and applying affordable nano-based bactericidal coatings under real-world conditions. The approach provides a practical pathway for implementing antimicrobial surface technologies in low-resource settings. Although the present study focused on wood substrates, future research should assess performance on diverse materials to broaden applicability. The combination of cost-effectiveness, efficacy, and scalability underscores the potential for both commercial adoption and significant public health benefits.</div><div><strong>How to cite:</strong> Romero CP, Ramirez-Mora C, Salazar R, et al. Low-cost hybrid copper–carbon nanotube coating with antimicrobial properties in ambient conditions. Electron J Biotechnol 2026;79. <span><span>https://doi.org/10.1016/j.ejbt.2025.100700</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"79 ","pages":"Article 100700"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145749971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HRMS-based profiling of metabolites, metal ions content and in-vitro cholinesterase inhibitory activities of Sonchus wightianus DC plant parts","authors":"Abhimat Subedi ,&nbsp;Bishnu Prasad Pandey ,&nbsp;Suman Prakash Pradhan ,&nbsp;G.C. Ashok ,&nbsp;Sumit Bhattarai ,&nbsp;Ankita Dahal ,&nbsp;Era Tuladhar ,&nbsp;Anupama Chapagain ,&nbsp;Mukti Ram Aryal ,&nbsp;Gopal Prasad Ghimire","doi":"10.1016/j.ejbt.2025.100702","DOIUrl":"10.1016/j.ejbt.2025.100702","url":null,"abstract":"<div><h3>Background</h3><div><em>Sonchus wightianus</em> DC is native to South Asia and has traditionally been known for its wide range of applications for the treatment of several human ailments. However, its application for the treatment of neurodegenerative diseases like Alzheimer’s disease (AD) has not been studied yet. In this present study, comprehensive metabolite profiling of plant parts and <em>in-vitro</em> cholinesterase inhibitory potential was examined to see the efficacy of plant extract against AD.</div></div><div><h3>Results</h3><div>The potent antioxidant activity was demonstrated by the flower extract in both DPPH and ABTS assays, with IC₅₀ values of 104.06 ± 2.05 µg/mL and 67.69 ± 1.58 µg/mL, respectively. The crude methanol extract of the leaf displayed the highest butyrylcholinesterase (BChE) inhibition potential with IC₅₀ values of 281.09 ± 14.64 µg/mL. In contrast, the flower extract exhibited the strongest acetylcholinesterase (AChE) inhibition with IC₅₀ values of 247.51 ± 11.15 µg/mL. Furthermore, the evaluated plant parts were a rich source of essential macro and micronutrients. Principal component analysis revealed the major contribution of total phenolic content (TPC), and total flavonoid content (TFC) in the plant extracts, which might be the prime reason for strong antioxidant and cholinesterase inhibition. Further, the HRMS profiling analysis revealed the presence of Linoleic acid, gingerol, kaempferol, genistein, daidzein, chlorogenic acid, fisetin and 12-oxo-phytodienoic acid.</div></div><div><h3>Conclusions</h3><div>The findings of this study suggest that <em>Sonchus wightianus</em> DC is a promising source of bioactive compounds and essential micronutrients, with notable potential as an anticholinesterase agent.</div><div><strong>How to cite:</strong> Subedi A, Pandey BP, Pradhan SP, et al. HRMS-based profiling of metabolites, metal ions content and <em>in-vitro</em> cholinesterase inhibitory activities of <em>Sonchus wightianus</em> DC plant parts. Electron J Biotechnol 2026;79. <span><span>https://doi.org/10.1016/j.ejbt.2025.100702</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"79 ","pages":"Article 100702"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145799179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}