{"title":"Research Progress and Applications of Hydrophilic/Hydrophobic Composites for Antibacterial Hemostatic Dressings","authors":"Jingjing Zhao, Wenjing Liu, Zhaoxia Hou, Liying Wu, Zheng Zhao, XueYing Yang, Chaogang Zhou, Jiayue Chen, Wenli Zhang, Siwaluk Srikrajang, Suyanee Thongchot, Guorong Liu, Chuanbo Hu, Won-Chun Oh","doi":"10.1002/adbi.70132","DOIUrl":"10.1002/adbi.70132","url":null,"abstract":"<div>\u0000 \u0000 <p>To address the growing need for multifunctional wound dressings, this paper introduces the development of dressings with hydrophobic properties. It describes the preparation methods for hydrophilic/hydrophobic composite wound dressings, analyzes the healing mechanism of asymmetric hydrophobic dressings, emphasizing hemostasis on hydrophobic surfaces, improved wound adhesion, reduced bacterial adherence, and exudate removal, and finally discusses recent advances and future research directions in the preparation and application of hydrophilic/hydrophobic surfaces for antibacterial hemostatic dressings.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 7","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148454241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Advanced biologyPub Date : 2026-07-09DOI: 10.1002/adbi.202500680
Ping Wang, Yehai An, Xiaoyang Su, Qiyue Lin, Weiyi He, Wenhui Li, Ying Lv, Piao Luo, Wen Zhang, Zhiyu Ma
{"title":"Pirfenidone Ameliorates Paraquat-Induced Epithelial-Mesenchymal Transition via miR-9-8974-5p/RGS2 Axis","authors":"Ping Wang, Yehai An, Xiaoyang Su, Qiyue Lin, Weiyi He, Wenhui Li, Ying Lv, Piao Luo, Wen Zhang, Zhiyu Ma","doi":"10.1002/adbi.202500680","DOIUrl":"10.1002/adbi.202500680","url":null,"abstract":"<div>\u0000 \u0000 <p>Irreversible and extensive pulmonary fibrosis caused by paraquat (PQ) poisoning is the main cause of death induced by PQ poisoning in developing countries. Studies have confirmed that epithelial-mesenchymal transition (EMT) contributes to the process of pulmonary interstitial fibrosis caused by PQ poisoning. Many studies have proved that a variety of miRNAs are involved in the occurrence and development of EMT. Through animal and cell experiments, we established the model of EMT on mouse lung and MLE-12 cell. We found that the expression of Regulator of G-protein signaling 2 (RGS2) was decreased in mice lung tissue and MLE-12 induced by PQ, and over-expressed/inhibited miR-9-8974-5p can decrease/increase the level of RGS2. We found that pirfenidone (PFD) can relieve PQ-induced EMT in mice lung tissue and MLE-12 cells. Meanwhile, we found that it had high expression of RGS2 in PFD group. Mimic/inhibited miR-9-8974-5p can aggravate or relieve the EMT with decreasing /increasing the level of RGS2. In conclusion, miR-9-8974-5p can mediate the pulmonary EMT induced by PQ by regulating RGS2. PFD exerts a potential therapeutic effect on PQ-induced pulmonary EMT by regulating miR-9-8974-5p/RGS2 expression.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 7","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"RETRACTION: Devitalized Stem Cell Microsheets for Sustainable Release of Osteogenic and Vasculogenic Growth Factors and Regulation of Anti-Inflammatory Immune Response","authors":"ADBI ADBI","doi":"10.1002/adbi.70135","DOIUrl":"10.1002/adbi.70135","url":null,"abstract":"<p>S. Moeinzadeh, S. R. Pajoum Shariati, S. Kader, J. M. Melero-Martin and E. Jabbari, “Devitalized Stem Cell Microsheets for Sustainable Release of Osteogenic and Vasculogenic Growth Factors and Regulation of Anti-Inflammatory Immune Response,” <i>Advanced Biology</i> <i>1</i>, no. 3 (2017): 1600011, https://doi.org/10.1002/adbi.201600011.</p><p>The above article, published online on 07 March 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Kerstin Brachhold; and Wiley-VCH GmbH. The retraction has been agreed upon following concerns raised by a third party. A subsequent investigation identified abnormalities in the western blot presented in Figure 6e, such that the background in each panel is unusually similar and deviates from typical experimental results. Further concerns were noted regarding the flow cytometry data shown in Figure 8, where similar clusters were observed across the plots. The authors cooperated with the investigation but were unable to provide any acceptable raw data; they supplied some numerical data and TIFF images depicting the flow cytometry plots. They also acknowledged that the western blot images were constructed by cutting and pasting the bands onto the same background. The data and explanations provided were not sufficient to restore confidence in the results; therefore, the editors consider the results and conclusions to be unreliable. The authors disagree with the retraction.</p>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 7","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/adbi.70135","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410087","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":"MRC2 Links Collagen Turnover to Integrin/PI3K/AKT-Driven Fibrogenesis","authors":"Nuchanart Suntornnont, Jiranuwat Sapudom, Chaiyaboot Ariyachet","doi":"10.1002/adbi.70133","DOIUrl":"10.1002/adbi.70133","url":null,"abstract":"<div>\u0000 \u0000 <p>Liver fibrosis is characterized by excessive collagen accumulation, the principal component of the extracellular matrix (ECM), produced by activated hepatic stellate cells (HSCs). While the catabolic role of mannose receptor C-type 2 (MRC2) in binding and degradation of collagen is established, its role in regulating pro-fibrotic signaling remains undefined. We investigated the novel, non-canonical signaling function of the collagen receptor MRC2 as a regulator of HSC activation. Using doxycycline-inducible knockdown and overexpression systems in human HSCs, we show that MRC2 deficiency enhances activation phenotypes, including proliferation, migration, contraction, and collagen overproduction. Conversely, MRC2 overexpression suppressed these effects. Transcriptomic analysis of MRC2 knockdown cells revealed a pro-fibrotic transcriptional shift, with enrichment of pathways related to ECM organization, collagen biosynthesis, and the PI3K/AKT signaling axis. Mechanistically, MRC2 depletion induced transcriptional upregulation of ECM genes and components of the integrin/PI3K/AKT axis, accompanied by increased AKT phosphorylation. Pharmacological inhibition of either PI3K or integrins reversed ECM gene expression and collagen phenotypes induced by MRC2 depletion, establishing these pathways as required mediators. Our findings identify a novel, non-canonical signaling function of MRC2 as a negative regulator of HSC activation.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148196949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ying Lu, Lanlan Huang, Li Shen, Rajeev K. Singla, Xiaoming Zhu
{"title":"Integrative Database-Driven In Silico and In Vitro Study of Anemarrhena asphodeloides Bunge Highlighting Hippeastrine as a Regulator of the HSP90/PI3K/Akt/mTOR Axis in Oral Squamous Cell Carcinoma","authors":"Ying Lu, Lanlan Huang, Li Shen, Rajeev K. Singla, Xiaoming Zhu","doi":"10.1002/adbi.70129","DOIUrl":"10.1002/adbi.70129","url":null,"abstract":"<div>\u0000 \u0000 <p>Oral squamous cell carcinoma (OSCC) has a poor prognosis and limited effective therapies. <i>Anemarrhena asphodeloides</i> exhibits anticancer activity, but its efficacy in OSCC treatment remains underexplored. Network and protein-protein interaction analysis identified 275 overlapping targets and 12 hub genes, with HSP90AA1, HSP90AB1, and CASP3 upregulated in OSCC, linked to poorer survival. QSAR modeling, molecular docking, and molecular dynamics simulations demonstrated stable binding of key bioactive compounds with HSP90 and AKT1, highlighting hippeastrine as a promising candidate. ADMET analysis indicated their favorable pharmacokinetic profiles. To validate the therapeutic potential of hippeastrine, in vitro experiments were conducted using the CAL27 and SCC-9 cell lines. CCK-8 assay demonstrated that hippeastrine exerted significant and dose-dependent cytotoxicity against OSCC cells. Furthermore, hippeastrine treatment significantly suppressed colony formation and attenuated cell migration and invasion capabilities. Gene set enrichment analysis of TCGA-HNSC data revealed a positive correlation between HSP90AA1/AB1 expression and PI3K/Akt/mTOR signaling. Western blot analysis confirmed inhibition of the HSP90-PI3K-Akt-mTOR axis by hippeastrine. Moreover, functional rescue experiments with the PI3K activator 740 Y-P successfully reversed the hippeastrine-induced suppression of cell viability and PI3K/Akt phosphorylation. These findings indicate that hippeastrine exerts anti-OSCC effects by targeting the HSP90/PI3K/Akt/mTOR pathway, highlighting it as a novel therapeutic agent against OSCC.</p>\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}