EXCLI Journal最新文献

{"title":"Artificial intelligence in the cath lab: Bridging predictive models and real-time procedural decision support.","authors":"Inderbir Padda, Shirobhi Sharma, Yashendra Sethi, Sneha Annie Sebastian, Harshan Atwal, Inderjeet Bharaj, Khushal Choudhary, Charles Sineri","doi":"10.17179/excli2026-9524","DOIUrl":"10.17179/excli2026-9524","url":null,"abstract":"<p><p>The integration of Artificial Intelligence (AI) in medicine has been revolutionary, particularly in cardiology, where AI offers transformative tools for data integration, image analysis, and predictive modeling. In procedural settings such as percutaneous coronary intervention (PCI) planning, where timely decision-making is crucial, AI represents a promising avenue for real-time risk prediction. However, current clinical scores and risk models often fall short in dynamic environments like the catheterization (cath) lab due to their static nature and limited adaptability to intra-procedural complexities. Emerging AI models aim to leverage high-frequency physiological data, procedural metadata, and multimodal imaging to recognize evolving patterns and anticipate complications. Nevertheless, most existing applications remain retrospective, lack real-time integration, and are constrained by limited external validation. Looking ahead, the implementation of real-time AI systems in the cath lab holds significant potential to enhance procedural safety and outcomes by delivering anticipatory alerts and actionable insights that support clinical decision-making during PCI. However, it is important to note that most currently available AI models remain retrospective or observational in nature, and prospective evidence demonstrating improved clinical outcomes through real-time AI-guided interventions remains limited. See also the graphical abstract(Fig. 1).</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1303-1315"},"PeriodicalIF":6.2,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Injectable extracellular matrix microparticles for regenerative and biocompatible soft tissue augmentation.","authors":"Javad Khanali, Yasamin Ostadi, Fatemeh A Tehrani, Tahereh Tayebi, Roghayeh Tarasi, Younes Yassaghi, Yasaman Nazerian, Maryam Salimi, Feizollah Niazi, Soheyl Bahrami, Hassan Niknejad","doi":"10.17179/excli2026-9490","DOIUrl":"10.17179/excli2026-9490","url":null,"abstract":"<p><p>Decellularized extracellular matrices (DEMs) have been widely investigated as promising biomaterials for soft tissue augmentation. In contrast, the use of decellularized human amniotic membrane (dHAM) represents a novel approach within this field, offering unique potential for clinical application. The objective of this study is to develop an \"off-the-shelf\" bioactive soft tissue filler from crosslinked and non-crosslinked dHAM in the injectable microparticle formulation. We used physical and enzymatic processes for decellularization and milling for fabricating the injectable matrix. The decellularization, crosslinking and detoxification protocol removed immunogenic cellular components, preserved collagen and glycosaminoglycan content, and reduced residual crosslinker to sub-cytotoxic levels. Consequently, both crosslinked and non-crosslinked powder extractions promoted cell viability and proliferation and did not affect cell migration in culture. Moreover, the crosslinked powder showed higher stability upon <i>in vitro</i> enzymatic degradation and prolonged volume retention in the subcutaneous guinea pig model. Histopathologic evaluation of the implants showed that immune cell infiltration markedly resolved over the 12-week study period. Moreover, immunohistochemistry staining for CD68 and CD163 macrophage markers indicated the abundance of CD163-positive cells, commonly associated with an anti-inflammatory or M2-like phenotype. Staining for CD31 endothelial cell marker demonstrated the formation of blood vessels with intraluminal RBCs and endothelial cell lining within the implants, which is indicative of neovascularization. Therefore, dHAM demonstrated long-term volume retention, reduced immune cell infiltration, and was associated with a CD163-positive macrophage phenotype and evidence of vascularization in the animal model. This study suggests dHAM as a readily deliverable biomaterial and a promising candidate to address clinical translational needs for soft tissue reconstruction. See also the graphical abstract(Fig. 1).</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1279-1302"},"PeriodicalIF":6.2,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Andes hantavirus aboard an expedition cruise ship: A sentinel event for travel medicine and maritime biosurveillance.","authors":"Paulo Ricardo Martins-Filho, Thialla Andrade Carvalho, Adriano Antunes de Souza Araújo, Lucindo José Quintans-Júnior","doi":"10.17179/excli2026-9613","DOIUrl":"10.17179/excli2026-9613","url":null,"abstract":"","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1276-1278"},"PeriodicalIF":6.2,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generative AI and the changing meaning of survey responses in digital health research.","authors":"Pyae Linn Aung","doi":"10.17179/excli2026-9602","DOIUrl":"10.17179/excli2026-9602","url":null,"abstract":"","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1273-1275"},"PeriodicalIF":6.2,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of T cell activation: Integrating signaling pathways, experimental models, and therapeutic implications.","authors":"Mohammed Ageeli Hakami, Rabab Fatima, Yumna Khan, Ahad Amer Alsaiari, Jawaher Amer Alsaiari, Md Sadique Hussain","doi":"10.17179/excli2026-9572","DOIUrl":"10.17179/excli2026-9572","url":null,"abstract":"<p><p>T cell activation is a central mechanism in adaptive immunity, modulating immune surveillance, host defense, and immune-mediated pathology. It is a highly coordinated mechanism including antigen recognition, co-stimulatory and co-inhibitory signaling, and cytokine-mediated regulation. This work aims to synthesize existing knowledge on the molecular mechanisms modulating T cell activation, with emphasis on integrated signaling cascades, experimental models, and therapeutic implications. A narrative review of the literature was conducted, focusing on key signaling cascades, regulatory mechanisms, and experimental methods used to analyze T cell activation in both basic and translational immunology. T cell activation is orchestrated via the mediation of T cell receptor (TCR) signaling with co-stimulatory and co-inhibitory cascades, alongside cytokine-mediated cues that collectively determine T cell fate and function. Critical intracellular signaling cascades, offer pivotal function in transcriptional and metabolic reprogramming. Experimental models such as in vitro stimulation systems, flow cytometry-based analyses, and advanced imaging approaches have significantly improved mechanistic knowledge of T cell responses. These insights have informed therapeutic approaches targeting T cell activation in cancer immunotherapy, autoimmune diseases, and infectious conditions. Although, obstacles in clinical translation remain. A comprehensive understanding of T cell activation needs integration of molecular, experimental, and clinical perspectives. Importantly, this review emphasizes the comparative strengths and limitations of contemporary experimental models and discusses how multi-omics integration and computational modeling can improve reproducibility, physiological relevance, and translational predictability in T cell research. Advancements in this field continue to offer opportunities for the development of targeted immunotherapies and enhanced disease intervention approaches. See also the graphical abstract(Fig. 1).</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1219-1272"},"PeriodicalIF":6.2,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Retraction of the landmark glyphosate safety publication by Williams, Kroes and Munro (2000) should be reversed.","authors":"Christopher J Borgert, Mohammad Abdollahi, Jay M Ansell, Michael Aschner, Christopher A Bates, Sir Colin Berry, Brad Bolon, Peter J Boogaard, Robert A Budinksy, Lyle D Burgoon, Gary Burin, James S Bus, Harvey Clewell, Samuel M Cohen, Thomas Colnot, Paul S Darby, Wolfgang Dekant, John DeSesso, Daniel R Dietrich, Mirjana Djukic, Anca Oana Docea, Jose L Domingo, David L Eaton, Jeffery A Engelhardt, Anne Fairbrother, Allan Felsot, Penelope A Fenner-Crisp, Robinan Gentry, Jay I Goodman, Gio B Gori, Helmut Greim, J S Heslop-Harrison, Jan G Hengstler, Hartmut Jaeschke, Norbert E Kaminski, Sam Kacew, James Kim, Anthony L Kiorpes, Curtis Klaassen, James E Klaunig, Anne Loccisano, James S MacDonald, Angela Mally, Hans W J Marquardt, M Sue Marty, John C Matthews, Roger O McClellan, Robert G Meeks, Glenn C Millner, Michael W Pariza, Dennis Paustenbach, Olavi Pelkonen, David Sarvadi, Kai Savolainen, Ted W Simon, Carr J Smith, Keith R Solomon, Stanley M Tarka, Aristidis M Tsatsakis, Joyce Tsuji, Nico P E Vermeulen, Kendall B Wallace, Michael Wernke, Jonathan P Williams, Raphael J Witorsch, Hiroshi Yamazaki","doi":"10.17179/excli2026-9686","DOIUrl":"https://doi.org/10.17179/excli2026-9686","url":null,"abstract":"<p><p>[This corrects the article on p. 1107 in vol. 25, PMID: 42517087.].</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1215-1218"},"PeriodicalIF":6.2,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WEE1 kinase in cancer: Molecular mechanisms and inhibitor insights.","authors":"Ankush Kumar, Keshav Raj Paudel, Rajwinder Kaur, Rohit Bhatia","doi":"10.17179/excli2026-9568","DOIUrl":"10.17179/excli2026-9568","url":null,"abstract":"<p><p>WEE1 kinase is a main regulator of the G2/M cell cycle checkpoint. It plays an important role in maintaining genomic stability by inhibiting CDK1 through a phosphorylation process at Tyr15. WEE1 is found to be overexpressed in several cancers and also act as a protective mechanism that allows cancer cells to repair DNA damage and survive under replicative stress. So, pharmacological inhibition of WEE1 has emerged as a promising therapeutic strategy. Many conventional chemotherapeutic agents act by inducing DNA damage, so it enables the activation of WEE1 in cancer cells to arrest the cell cycle and repair this damage by preventing cell death. Inhibition of WEE1 disrupts this protective checkpoint, which ultimately leads to mitotic catastrophe. Therefore, targeting WEE1 represents a promising and rational therapeutic approach, mainly in tumors with TP53 mutations. We have comprehensively discussed the structural features of WEE1, its regulation in DNA damage response, epigenetic control, and its role in cancer progression. We have also summarized the clinical development of major WEE1 inhibitors such as adavosertib, azenosertib (ZN-c3), and Debio 0123. Moreover, recently synthesized small-molecule inhibitors are also discussed with special focus on structure-activity relationship (SAR) insights, dual-target inhibitors, and PROTACs and molecular glue-based degraders. Two compounds, 8 and 11, were found to be the most potent WEE1 inhibitors with excellent enzymatic inhibition. This explains the importance of rational scaffold optimization and electron-withdrawing group insertion for enhanced activity. Overall, this review serves as a valuable reference for medicinal chemists in the development of next-generation WEE1 inhibitors. See also the graphical abstract(Fig. 1).</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1186-1214"},"PeriodicalIF":6.2,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overview of recent advances in zearalenone (ZEN) research.","authors":"Gabriela Pilarska, Magdalena Twaruzek","doi":"10.17179/excli2026-9422","DOIUrl":"10.17179/excli2026-9422","url":null,"abstract":"<p><p>Zearalenone (ZEN) is a <i>Fusarium</i> derived mycotoxin widely detected in cereals and cereal-based products and recognized for its pronounced estrogenic activity. Although the fundamental aspects of ZEN chemistry, metabolism, and toxicological effects have been well described, recent research has revealed a more complex picture of its biological significance and exposure pathways. Increasing attention has been devoted to biomonitoring approaches that allow the assessment of internal exposure rather than relying solely on contamination levels in food or feed matrices. At the same time, studies on modified and masked forms of ZEN suggest that these derivatives may represent an additional and often underestimated source of exposure. Recent findings also indicate that the toxicological impact of ZEN extends beyond endocrine disruption and may involve effects on intestinal barrier integrity, metabolic regulation, and inflammatory processes. Furthermore, advances in analytical techniques and research on enzymatic degradation and inhibition of <i>Fusarium</i> biosynthesis are expanding possibilities for more effective monitoring and mitigation strategies. This review summarizes recent developments in the understanding of ZEN occurrence, metabolism, toxicity, and detection, highlighting emerging research directions relevant to food safety, animal health, and modern exposure assessment. See also the graphical abstract(Fig. 1).</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1171-1185"},"PeriodicalIF":6.2,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of distinct and similar pathological features between diabetes and Alzheimer's disease.","authors":"Joshua Reed, Stephen C Bain, Venkateswarlu Kanamarlapudi","doi":"10.17179/excli2026-9429","DOIUrl":"10.17179/excli2026-9429","url":null,"abstract":"<p><p>Type 1 diabetes (T1D), type 2 diabetes (T2D) and Alzheimer's disease (AD), which are heterogeneous multifactorial diseases, have become major global healthcare burdens and significant concerns for the future. Historically, the pathogeneses of these diseases were regarded as being largely distinct, but recent research suggests that this view is now outdated, with a lack of insulin and/or insulin resistance playing an important role in both forms of diabetes and AD. The current state of knowledge on the epidemiology, aetiology, and pathogenesis of T1D, T2D, and AD is summarised in this review. The evidence demonstrating overlapping pathological features between these diseases is also discussed here. Studies have demonstrated that islet autoimmunity, dysfunctional glucagon secretion, insulin resistance and islet amyloidosis manifest in both T1D and T2D. AD has been suggested to be type 3 diabetes (T3D), due to the associated abnormal brain insulin resistance, which is speculated to drive the progressive pathogenesis. Additionally, T1D and T2D are risk factors for AD and vice versa, and most AD patients also have diabetes or glucose intolerance, indicating bidirectional relationships. Thus, the association between AD and diabetes is already well established. Further understanding the connection between these diseases using recent scientific evidence may allow for the development of more efficient therapeutic strategies, which is highly desirable, given the prevalence of post-diagnosis complications. Evidence suggests that GLP-1R agonists can alleviate the phenotypes of all of these diseases, and these agonists could be used in the future to simultaneously treat them in subjects or prevent/delay their manifestation in at-risk individuals. See also the graphical abstract(Fig. 1).</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1124-1170"},"PeriodicalIF":6.2,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13550658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148911288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction of the landmark glyphosate safety publication by Williams, Kroes and Munro (2000) should be reversed.","authors":"Christopher J Borgert, Mohammad Abdollahi, Jay M Ansell, Michael Aschner, Christopher A Bates, Sir Colin Berry, Brad Bolon, Peter J Boogaard, Robert A Budinksy, Lyle D Burgoon, Gary Burin, James S Bus, Harvey Clewell, Samuel M Cohen, Thomas Colnot, Paul S Darby, Wolfgang Dekant, John DeSesso, Daniel R Dietrich, Mirjana Djukic, Anca Oana Docea, Jose L Domingo, David L Eaton, Jeffery A Engelhardt, Anne Fairbrother, Allan Felsot, Penelope A Fenner-Crisp, Robinan Gentry, Jay I Goodman, Gio B Gori, Helmut Greim, J S Heslop-Harrison, Jan G Hengstler, Hartmut Jaeschke, Norbert E Kaminski, Sam Kacew, James Kim, Anthony L Kiorpes, Curtis Klaassen, James E Klaunig, Anne Loccisano, James S MacDonald, Angela Mally, Hans W J Marquardt, M Sue Marty, John C Matthews, Roger O McClellan, Robert G Meeks, Glenn C Millner, Michael W Pariza, Dennis Paustenbach, Olavi Pelkonen, David Sarvadi, Kai Savolainen, Ted W Simon, Carr J Smith, Keith R Solomon, Stanley M Tarka, Aristidis M Tsatsakis, Joyce Tsuji, Nico P E Vermeulen, Kendall B Wallace, Michael Wernke, Jonathan P Williams, Raphael J Witorsch, Hiroshi Yamazaki","doi":"10.17179/excli2026-9644","DOIUrl":"10.17179/excli2026-9644","url":null,"abstract":"<p><p>The decision by the co-Editor-in-Chief of Regulatory Toxicology and Pharmacology, Prof. Martin van den Berg, to retract the 2000 review article by Williams, Kroes, and Munro has elicited widespread criticism within the scientific community. Issued in late 2025, the retraction decision cites procedural concerns including potential ghostwriting, undisclosed conflicts of interest, and omission of certain unpublished studies, invoking Committee on Publication Ethics guidelines despite lacking evidence of fraud or scientific flaws. This editorial argues that the retraction decision involves editorial overreach and misapplication of the guidelines. The alleged omissions stemmed from proprietary data access limitations that were disclosed in the original paper. Subsequent reviews by several independent expert panels and regulatory authorities with access to all glyphosate data, including the studies cited by the retracting editor, reached similar conclusions. Claims of ghostwriting were previously investigated and found lacking, including a declaration by EFSA as to the clarity of the conflict disclosures. The retraction's timing, reliance on litigation documents, and apparent biases that were not disclosed in the retraction notice raise questions of ideological interference. Absent substantive rebuttals based on scientific merit rather than speculative claims of inappropriate authorship and data access, this retraction decision sets a dangerous precedent for retroactive censorship, potentially chilling beneficial industry-academic collaborations and eroding trust in the integrity of scientific publishing. With the strongest conviction, we assert that retracting a paper without scientific flaws isn't protection-it is censorship. We therefore call for the immediate reversal of this flawed and unjustified retraction to preserve trust in peer-reviewed literature.</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"25 ","pages":"1107-1116"},"PeriodicalIF":6.2,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13402740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}