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Strengthening the bond with the scientific community: FEBS Open Bio in 2025 加强与科学界的联系:2025年的FEBS开放生物
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2025-01-06 DOI: 10.1002/2211-5463.13956
Sara Fuentes, Miguel A. De la Rosa
{"title":"Strengthening the bond with the scientific community: FEBS Open Bio in 2025","authors":"Sara Fuentes,&nbsp;Miguel A. De la Rosa","doi":"10.1002/2211-5463.13956","DOIUrl":"https://doi.org/10.1002/2211-5463.13956","url":null,"abstract":"<p><i>FEBS Open Bio</i> remains dedicated to serving the scientific community by ensuring rapid publication of rigorous science and pioneering initiatives to support researchers. In this editorial, we reflect on a year of achievements, and look forward to the new developments planned for 2025.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 1","pages":"4-10"},"PeriodicalIF":2.8,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13956","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143110194","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}
引用次数: 0
CD44v, S1PR1, HER3, MET and cancer-associated amino acid transporters are promising targets for the pancreatic cancers characterized using mAb CD44v, S1PR1, HER3, MET和癌症相关的氨基酸转运蛋白是用单抗表征胰腺癌的有希望的靶点。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2025-01-05 DOI: 10.1002/2211-5463.13963
Takashi Nakano, Kouki Okita, Shogo Okazaki, Soshi Yoshimoto, Sachiko Masuko, Hideki Yagi, Kazunori Kato, Yoshihisa Tomioka, Kenichi Imai, Yoichi Hamada, Kazue Masuko, Kayoko Shimada-Takaura, Noriaki Nagai, Hideyuki Saya, Tomio Arai, Toshiyuki Ishiwata, Takashi Masuko
{"title":"CD44v, S1PR1, HER3, MET and cancer-associated amino acid transporters are promising targets for the pancreatic cancers characterized using mAb","authors":"Takashi Nakano,&nbsp;Kouki Okita,&nbsp;Shogo Okazaki,&nbsp;Soshi Yoshimoto,&nbsp;Sachiko Masuko,&nbsp;Hideki Yagi,&nbsp;Kazunori Kato,&nbsp;Yoshihisa Tomioka,&nbsp;Kenichi Imai,&nbsp;Yoichi Hamada,&nbsp;Kazue Masuko,&nbsp;Kayoko Shimada-Takaura,&nbsp;Noriaki Nagai,&nbsp;Hideyuki Saya,&nbsp;Tomio Arai,&nbsp;Toshiyuki Ishiwata,&nbsp;Takashi Masuko","doi":"10.1002/2211-5463.13963","DOIUrl":"10.1002/2211-5463.13963","url":null,"abstract":"<p>Effective therapies have yet to be established for pancreatic ductal adenocarcinomas (PDAC) even though it is the most aggressive cancer. In the present study, PDAC was analyzed using novel rat mAbs against membrane proteins in conjunction with flow cytometry and immunohistochemistry. Human epidermal growth receptor (HER)1–4, mesenchymal to epithelial transition factor (MET), sphingosine-1-phospahate receptor 1 (S1PR1), <span>l</span>-type amino acid transporter 1 (LAT1), system x<sup>−</sup><sub>c</sub> transporter (xCT), alanine-serine-cysteine transporter (ASCT2), cationic amino acid transporter 1 (CAT1) and variant CD44 (CD44v) were expressed at high frequencies in both <i>in vitro</i> and <i>in vivo</i> PDAC. Internalization of membrane proteins by mAbs and growth inhibition by toxin-linked mAbs were demonstrated in many PDAC cell lines, and mAbs against S1PR1, ASCT2, HER3 and CD44v inhibited the growth of xenografted MIA PaCa-2 PDAC cells. Furthermore, CD44v-high PDAC showed high mRNA expression of HER1–3, MET and CD44v, and was correlated with poor prognosis. Taken together, our results suggest that CD44v, S1PR1, HER3, MET and the above-mentioned cancer-associated amino acid transporters might be promising targets for the diagnosis and treatment of PDAC.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 5","pages":"867-884"},"PeriodicalIF":2.8,"publicationDate":"2025-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13963","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930863","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}
引用次数: 0
CDK5 interacts with MST2 and modulates the Hippo signalling pathway CDK5与MST2相互作用并调节Hippo信号通路。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-30 DOI: 10.1002/2211-5463.13962
Mehak Passi, Jan B. Stöckl, Thomas Fröhlich, Simone Moser, Angelika M. Vollmar, Stefan Zahler
{"title":"CDK5 interacts with MST2 and modulates the Hippo signalling pathway","authors":"Mehak Passi,&nbsp;Jan B. Stöckl,&nbsp;Thomas Fröhlich,&nbsp;Simone Moser,&nbsp;Angelika M. Vollmar,&nbsp;Stefan Zahler","doi":"10.1002/2211-5463.13962","DOIUrl":"10.1002/2211-5463.13962","url":null,"abstract":"<p>MST2 (STK3) is a major upstream kinase in the Hippo signalling pathway, an evolutionary conserved pathway in regulation of organ size, self-renewal and tissue homeostasis. Its downstream effectors are the transcriptional regulators YAP and TAZ. This pathway is regulated by a variety of factors, such as substrate stiffness or cell–cell contacts. Using a yeast two-hybrid screen, we detected a novel interaction between the kinases MST2 and CDK5, which we further confirmed by co-immunoprecipitation experiments. Cyclin-dependent kinase 5 (CDK5) is an unusual member of the family of cyclin-dependent kinases, involved in tumour growth and angiogenesis. Although a link between CDK5 and Hippo has been previously postulated, the mode of action is still elusive. Here, we show that knockdown of CDK5 causes reduced transcriptional activity of YAP and that CDK5 influences the phosphorylation levels of the Hippo upstream kinase LATS1. Moreover, a phosphoproteomics approach revealed that CDK5 interferes with the phosphorylation of DLG5, another upstream kinase, which regulates the Hippo pathway. Hence, CDK5 seems to act as a signalling hub for integrating the Hippo pathway and other signalling cascades. These interactions might have important implications for the use of CDK5 inhibitors, which are already in clinical use for tumour diseases.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 4","pages":"647-660"},"PeriodicalIF":2.8,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13962","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909455","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}
引用次数: 0
Enhancing human ACE2 expression in mouse models to improve COVID-19 research 增强人ACE2在小鼠模型中的表达以改善COVID-19研究。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-29 DOI: 10.1002/2211-5463.13934
Sun Jiaoyang, Cheng Shaofei, Hong Guangliang, Quan Xiongzhi, Lin Haofeng, Mao Rui, Johannes Grillari, Shi Zheng-Li, Chen Jiekai, Liu Meiqin, Wu Haoyu, Wu Guangming
{"title":"Enhancing human ACE2 expression in mouse models to improve COVID-19 research","authors":"Sun Jiaoyang,&nbsp;Cheng Shaofei,&nbsp;Hong Guangliang,&nbsp;Quan Xiongzhi,&nbsp;Lin Haofeng,&nbsp;Mao Rui,&nbsp;Johannes Grillari,&nbsp;Shi Zheng-Li,&nbsp;Chen Jiekai,&nbsp;Liu Meiqin,&nbsp;Wu Haoyu,&nbsp;Wu Guangming","doi":"10.1002/2211-5463.13934","DOIUrl":"10.1002/2211-5463.13934","url":null,"abstract":"<p>Mice are one of the most common biological models for laboratory use. However, wild-type mice are not susceptible to COVID-19 infection due to the low affinity of mouse ACE2, the entry protein for SARS-CoV-2. Although mice with human ACE2 (hACE2) driven by <i>Ace2</i> promoter reflect its tissue specificity, these animals exhibit low ACE2 expression, potentially limiting their fidelity in mimicking COVID-19 manifestations and their utility in viral studies. Here, we created and compared hACE2 mouse models generated with different strategies. Our findings show that distinct β-globin insertion within hACE2 cassette significantly influences its expression, with downstream placement enhancing transcription. Moreover, optimizing hACE2 codons (opt-hACE2) improves translation efficiency in multiple tissues. Notably, opt-hACE2 mice displayed more active immune responses and severe COVID-19 phenotypes following SARS-CoV-2 challenge compared to other models. Our study demonstrates the dual regulatory role of β-globin element in transgene transcription and suggests that opt-hACE2 mice might serve as valuable tools for SARS-CoV-2 research.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 2","pages":"324-334"},"PeriodicalIF":2.8,"publicationDate":"2024-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13934","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142906842","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}
引用次数: 0
RETRACTION: Effect of a Neural Relay on Liver Regeneration in Mice: Activation of Serotonin Release from the Gastrointestinal Tract 神经接力对小鼠肝脏再生的影响:胃肠道血清素释放的激活。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-25 DOI: 10.1002/2211-5463.13961
{"title":"RETRACTION: Effect of a Neural Relay on Liver Regeneration in Mice: Activation of Serotonin Release from the Gastrointestinal Tract","authors":"","doi":"10.1002/2211-5463.13961","DOIUrl":"10.1002/2211-5463.13961","url":null,"abstract":"<p><b>RETRACTION:</b> R. Inoue, K. Kamimura, T. Nagoya, N. Sakai, T. Yokoo, R. Goto, K. Ogawa, Y. Shinagawa-Kobayashi, Y. Watanabe-Mori, A. Sakamaki, S. Abe, H. Kamimura, N. Miyamura, H. Nishina, and S. Terai, “Effect of a Neural Relay on Liver Regeneration in Mice: Activation of Serotonin Release from the Gastrointestinal Tract,” <i>FEBS Open Bio</i> 8, no. 3 (2018): 449-460, https://doi.org/10.1002/2211-5463.12382.</p><p>The above article, published online on 16 January 2018, in Wiley Online Library (http://onlinelibrary.wiley.com/),has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The journal received a report from a third party which indicated that the Day 2 and Day 4 panels in Figure 3A had been duplicated and rotated. Additional investigation by the journal discovered multiple inappropriate image duplications and overlaps in Figure 6A. The authors responded to an inquiry by the journal, confirmed that images had been duplicated in both figures, and provided what was labelled as the correct data. Following receipt of the authors' explanation and new data, the journal requested an investigation by the authors' institution.</p><p>The institutional investigation reported that there was insufficient evidence of intentional image manipulation and concluded that the image duplications were due to errors in image preparation by the authors. However, given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised. As a result, the Editor-in-Chief, FEBS Press, and John Wiley and Sons Ltd. have determined that a retraction is necessary. The authors disagree with the retraction.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 5","pages":"889"},"PeriodicalIF":2.8,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13961","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893306","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}
引用次数: 0
Cost-effective and simple flow cytometry quantification of receptor-mediated autophagy using fluorescent tagging 成本效益和简单的流式细胞术定量受体介导的自噬使用荧光标记。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-23 DOI: 10.1002/2211-5463.13958
Mija Marinković, Ana Rožić, Denis Polančec, Ivana Novak
{"title":"Cost-effective and simple flow cytometry quantification of receptor-mediated autophagy using fluorescent tagging","authors":"Mija Marinković,&nbsp;Ana Rožić,&nbsp;Denis Polančec,&nbsp;Ivana Novak","doi":"10.1002/2211-5463.13958","DOIUrl":"10.1002/2211-5463.13958","url":null,"abstract":"<p>Mitophagy, a selective clearance of damaged or superfluous mitochondria via autophagy machinery and lysosomal degradation, is an evolutionarily conserved process essential for various physiological functions, including cellular differentiation and immune responses. Defects in mitophagy are implicated in numerous human diseases, such as neurodegenerative disorders, cancer, and metabolic conditions. Despite significant advancements in mitophagy research over recent decades, novel and robust methodologies are necessary to elucidate its molecular mechanisms comprehensively. In this study, we present a detailed protocol for quantitatively assessing mitophagy through flow cytometry using a mitochondria-targeted fluorescent mitophagy receptor, GFP-BNIP3L/NIX. This method offers a rapid alternative to conventional microscopy or immunoblotting techniques for analyzing mitophagy activity. Additionally, this approach can theoretically be adapted to utilize any fluorescent-tagged selective autophagy receptor, enabling the direct and rapid analysis of various types of receptor-mediated selective autophagy.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 4","pages":"587-598"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13958","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881643","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}
引用次数: 0
NPC1 promotes the progression of hepatocellular carcinoma by mediating the accumulation of neutrophils into the tumor microenvironment NPC1通过介导中性粒细胞在肿瘤微环境中的积累促进肝细胞癌的进展。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-20 DOI: 10.1002/2211-5463.13951
Songhai Yang, Jiangming Chen, Kun Xie, Fubao Liu
{"title":"NPC1 promotes the progression of hepatocellular carcinoma by mediating the accumulation of neutrophils into the tumor microenvironment","authors":"Songhai Yang,&nbsp;Jiangming Chen,&nbsp;Kun Xie,&nbsp;Fubao Liu","doi":"10.1002/2211-5463.13951","DOIUrl":"10.1002/2211-5463.13951","url":null,"abstract":"<p>Hepatocellular carcinoma remains a significant threat to human health. Recent studies have found that the intake of cellular cholesterol contributes to the development and progression of hepatocellular carcinoma, although the exact mechanisms remain unclear. Our analysis of transcriptomic and proteomic databases has identified increased mRNA and protein expression levels of NPC1, a cholesterol intracellular transporter protein, in hepatocellular carcinoma tissues. This increase is significantly associated with a worse prognosis for patients. To corroborate these findings, we performed immunohistochemical staining of NPC1 on liver tissue samples from patients, revealing significantly higher expression levels of NPC1 in hepatocellular carcinoma tissues compared to normal tissues. Subsequent investigations have revealed that NPC1 expression does not significantly influence the proliferation of hepatocellular carcinoma cells <i>in vitro</i>. However, it has a substantial inhibitory effect on the progression of hepatocellular carcinoma tumors when observed <i>in vivo</i>. Utilizing flow cytometry to monitor cellular changes within the tumor microenvironment has led us to discover that NPC1 plays a crucial role in the regulation of neutrophil recruitment within the tumor. Using further neutrophil depletion experiments, we determined that the role of NPC1 in advancing hepatocellular carcinoma progression truly relies on neutrophils. These observations are further reinforced by a comprehensive analysis of clinical databases alongside immunohistochemistry findings. In conclusion, our research suggests that NPC1's overexpression could contribute to hepatocellular carcinoma progression by promoting neutrophil recruitment, positioning NPC1 as a promising new biomarker and therapeutic target for hepatocellular carcinoma.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 4","pages":"661-673"},"PeriodicalIF":2.8,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13951","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871936","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}
引用次数: 0
Dexmedetomidine suppresses glucose-stimulated insulin secretion in pancreatic β-cells 右美托咪定抑制胰β细胞中葡萄糖刺激的胰岛素分泌。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-20 DOI: 10.1002/2211-5463.13960
Munenori Kusunoki, Kiichi Hirota, Tomohiro Shoji, Takeo Uba, Yoshiyuki Matsuo, Mikio Hayashi
{"title":"Dexmedetomidine suppresses glucose-stimulated insulin secretion in pancreatic β-cells","authors":"Munenori Kusunoki,&nbsp;Kiichi Hirota,&nbsp;Tomohiro Shoji,&nbsp;Takeo Uba,&nbsp;Yoshiyuki Matsuo,&nbsp;Mikio Hayashi","doi":"10.1002/2211-5463.13960","DOIUrl":"10.1002/2211-5463.13960","url":null,"abstract":"<p>Proper glycemic control is crucial for patient management in critical care, including perioperative care, and can influence patient prognosis. Blood glucose concentration determines insulin secretion and sensitivity and affects the intricate balance between the glucose metabolism. Human and other animal studies have demonstrated that perioperative drugs, including volatile anesthetics and intravenous anesthetics, affect glucose-stimulated insulin secretion (GSIS). Dexmedetomidine (DEX) decreases insulin release and affects glucose metabolism; however, the specific mechanism underlying this phenomenon remains largely unknown. Thus, we investigated the effect and mechanism of DEX on insulin secretion using mouse and rat pancreatic β-cell-derived MIN6 and INS-1 cell lines and primary pancreatic β-cells/islets extracted from mice. The amount of insulin secreted into the culture medium was determined using an enzyme-linked immunosorbent assay. Cell viability, cytotoxicity, and electrophysiological effects were investigated. Clinically relevant doses of DEX suppressed GSIS in MIN6 cells, INS-1 cells, and pancreatic β-cells/islets. Furthermore, DEX suppressed insulin secretion facilitated by insulinotropic factors. There was no significant difference in oxygen consumption rate, intracellular ATP levels, or caspase-3/7 activity. Electrophysiological evaluation using the patch-clamp method showed that DEX did not affect ATP-sensitive potassium (K<sub>ATP</sub>) channels, voltage-dependent potassium channels, or voltage-gated calcium channels. We demonstrated that clinically relevant doses of DEX significantly suppressed GSIS. These findings suggest that DEX inhibits a signaling pathway via α2-adrenoceptor or insulin vesicle exocytosis, resulting in GSIS suppression. Our results support the hypothesis that DEX suppresses insulin secretion and reveal some underlying mechanisms.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 4","pages":"634-646"},"PeriodicalIF":2.8,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13960","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863892","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}
引用次数: 0
Evaluating frailty scores across experimental groups in rodent models: bridging physical and cognitive domains 评估脆弱评分跨实验组在啮齿动物模型:桥接物理和认知领域。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-19 DOI: 10.1002/2211-5463.13955
Aleksandra Mladenovic, Smilja Pracer
{"title":"Evaluating frailty scores across experimental groups in rodent models: bridging physical and cognitive domains","authors":"Aleksandra Mladenovic,&nbsp;Smilja Pracer","doi":"10.1002/2211-5463.13955","DOIUrl":"10.1002/2211-5463.13955","url":null,"abstract":"<p>Frailty, a reversible clinical geriatric syndrome, impairs the ability to maintain homeostasis, leading to severe consequences such as hospitalization and death. Cognitive frailty, characterized by the co-occurrence of physical frailty and cognitive impairment, has garnered increasing attention in recent years. Preclinical models, especially rodent studies, are essential for understanding frailty and developing interventions to mitigate associated conditions. Traditionally, animal studies have focused solely on physical frailty. We have pioneered the inclusion of cognitive parameters by developing a novel physical-cognitive frailty score (FS) in animal research, in order to assess the effectiveness of anti-aging interventions. Here, we provide a detailed example of the FS calculation at the group level, which can serve as a guide for other studies. This dual-focus approach also helps in understanding how physical frailty and cognitive impairment interact to exacerbate adverse health outcomes and provides an opportunity to evaluate potential interventions that target both physical and cognitive dimensions of frailty more reliably.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 4","pages":"599-607"},"PeriodicalIF":2.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13955","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863893","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}
引用次数: 0
Synergistic antibacterial activity of baicalin in combination with oxacillin sodium against methicillin-resistant Staphylococcus aureus 黄芩苷联合奥西林钠对耐甲氧西林金黄色葡萄球菌的协同抑菌作用。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-15 DOI: 10.1002/2211-5463.13952
Xin Meng, Mengna Kang, Zhiyun Yu, Changyou Li, Yang Chen, Taicheng Jin, Kai Wang, Haiyong Guo
{"title":"Synergistic antibacterial activity of baicalin in combination with oxacillin sodium against methicillin-resistant Staphylococcus aureus","authors":"Xin Meng,&nbsp;Mengna Kang,&nbsp;Zhiyun Yu,&nbsp;Changyou Li,&nbsp;Yang Chen,&nbsp;Taicheng Jin,&nbsp;Kai Wang,&nbsp;Haiyong Guo","doi":"10.1002/2211-5463.13952","DOIUrl":"10.1002/2211-5463.13952","url":null,"abstract":"<p>Methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) poses a challenge for clinical treatment and combining antibiotics with other agents might be a promising strategy to overcome this challenge. This study explored the synergistic antibacterial activity of baicalin (traditional Chinese medicine extract) and the narrow-spectrum beta-lactam antibiotic oxacillin sodium, both of which are poorly active against MRSA <i>in vitro</i>. The combination of baicalin and oxacillin sodium showed a synergistic effect with a fractional inhibitory concentration index of 0.5. Mechanistically, the supplementation of baicalin increased the permeability of bacterial cell walls and cell membranes, enhancing oxacillin sodium entry and bactericidal action. The combination of baicalin and oxacillin sodium also significantly inhibited MRSA USA300 biofilm formation by further reducing polysaccharide intercellular adhesion production. Therefore, the combination of baicalin and oxacillin sodium offers a new therapeutic option for addressing clinical MRSA resistance. Further studies, including clinical trials, will be required to validate the observed <i>in vitro</i> results.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 4","pages":"608-621"},"PeriodicalIF":2.8,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/2211-5463.13952","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827951","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}
引用次数: 0
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