Oxidative Medicine and Cellular Longevity最新文献

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Correction to "Potential Roles of Endoplasmic Reticulum Stress and Cellular Proteins Implicated in Diabesity". 更正“内质网应激和细胞蛋白在糖尿病中的潜在作用”。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-29 eCollection Date: 2026-01-01 DOI: 10.1155/omcl/9817849
{"title":"Correction to \"Potential Roles of Endoplasmic Reticulum Stress and Cellular Proteins Implicated in Diabesity\".","authors":"","doi":"10.1155/omcl/9817849","DOIUrl":"10.1155/omcl/9817849","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/2021/8830880.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 ","pages":"9817849"},"PeriodicalIF":0.0,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12854160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146106437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Excessive Vitamin E Supplementation: Implications for Ovarian Physiology and Reproductive Health. 过量补充维生素E:对卵巢生理和生殖健康的影响。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-22 eCollection Date: 2026-01-01 DOI: 10.1155/omcl/1330508
Farzaneh Rabiee, Masoud Fattahi, Mohammad Iranzad, Mohsen Rahimi Andani, Farnoosh Jafarpour, Mohammad Hossein Sanei, Joel R Drevet, Mohammad Hossein Nasr-Esfahani
{"title":"Excessive Vitamin E Supplementation: Implications for Ovarian Physiology and Reproductive Health.","authors":"Farzaneh Rabiee, Masoud Fattahi, Mohammad Iranzad, Mohsen Rahimi Andani, Farnoosh Jafarpour, Mohammad Hossein Sanei, Joel R Drevet, Mohammad Hossein Nasr-Esfahani","doi":"10.1155/omcl/1330508","DOIUrl":"10.1155/omcl/1330508","url":null,"abstract":"<p><p>Infertility, a major global health problem affecting ~17.5% of couples, is influenced by various intrinsic (e.g., individual genetics) and extrinsic (e.g., related to environmental stimuli) factors. Oxidative stress and reactive oxygen species (ROS) are at the crossroads of these different stimulus-response pathways for both male and female gametes. While ROS are essential for ovarian processes such as folliculogenesis and oocyte maturation, changes in the ovarian ROS generation/recycling equilibrium can lead to impaired reproductive outcomes. Against this backdrop, noninvasive therapeutic approaches aimed at supplementing antioxidant (AO) molecules have emerged to correct prooxidant imbalances encountered in various stress situations. Numerous molecules have been tested, alone or in combination, for their beneficial effects on reproductive success in both men and women. The aim of this study was to investigate the effects of vitamin E supplementation at different levels on female reproductive performance and the molecular pathways involved. Groups of mice were treated with three different doses of vitamin E (optimal, overdose and severe overdose) and compared with control groups (no supplementation, sham groups [water and olive oil]). The results showed that both overdose and severe overdose of vitamin E showed significant reductions in pregnancy rates, litter size, and oocyte development capacity compared to the other groups. Blastocyst formation rates and quality were also significantly lower in these vitamin E overdosed groups, reflecting compromised embryonic quality. Severe vitamin E overdosage resulted in impaired folliculogenesis, with fewer antral follicles and corpora lutea and an increased number of atretic follicles. Notably, uterine thickness was significantly reduced in the severe vitamin E overdose group. Molecular analyses revealed increased GSH/GSSG ratios and higher ROS levels in granulosa cells. Intriguingly, in a context of increased ROS, we did not record any stimulation of the Nrf2 pathway and associated genes. A decrease in apoptosis in the ovarian environment marked by a lower Bax/Bcl2 ratio accompanied situations of vitamin E overdose. These findings shed new light on the consequences of excessive vitamin E intake and its implications for reproductive health. While optimal supplementation promotes fertility, excessive intake disrupts the redox balance, adversely affecting ovarian function and reproductive outcomes. This study highlights the importance of precise AO management to mitigate stress-induced infertility and provides a framework for further research into the molecular mechanisms underlying vitamin E's effects on ovarian physiology.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 ","pages":"1330508"},"PeriodicalIF":0.0,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12824594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146053237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Oxidative and Inflammatory Mechanisms Induced by Intermittent Hypoxia Leading to Vascular Alterations in Rodents: A Systematic Review and Meta-Analysis. 间歇性缺氧导致啮齿动物血管改变的氧化和炎症机制:系统综述和荟萃分析。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-14 eCollection Date: 2026-01-01 DOI: 10.1155/omcl/9967028
Marc Adrien Reveyaz, Célian Peyronnel, Quentin Boëte, Joey Fournier, Claire Arnaud, Elise Belaïdi, Olfa Harki, Jean-Louis Pépin, Charles Khouri, Gilles Faury, Anne Briançon-Marjollet
{"title":"Oxidative and Inflammatory Mechanisms Induced by Intermittent Hypoxia Leading to Vascular Alterations in Rodents: A Systematic Review and Meta-Analysis.","authors":"Marc Adrien Reveyaz, Célian Peyronnel, Quentin Boëte, Joey Fournier, Claire Arnaud, Elise Belaïdi, Olfa Harki, Jean-Louis Pépin, Charles Khouri, Gilles Faury, Anne Briançon-Marjollet","doi":"10.1155/omcl/9967028","DOIUrl":"10.1155/omcl/9967028","url":null,"abstract":"<p><strong>Objectives: </strong>Obstructive sleep apnea (OSA) and the related intermittent hypoxia (IH) are recognized as major cardiovascular risk factors. In a previous meta-analysis, we confirmed the impact of IH on structural and functional remodeling of vessels in rodent models of IH. Here, we conducted a systematic review and meta-analysis to investigate the molecular mechanisms related to vascular remodeling induced by IH and to analyze the impacts of patterns of exposure on the effect of IH.</p><p><strong>Methods: </strong>We searched PubMed, Web of Science, and EMBASE and included 52 articles, among them 44 concerning wild type (WT) rodents and eight concerning apolipoprotein E knockout (ApoE<sup>-/-</sup>) mice. We used standardized mean difference (SMD) to compare results between studies. A hypoxic score was designed and calculated, and metaregressions were performed to explore the impact of IH exposure parameters on the selected outcomes.</p><p><strong>Results: </strong>IH induced an increase in oxidative stress, inflammation markers, leucocyte infiltration, and apoptosis, and a decrease in endothelial nitric oxide synthase (eNOS) expression and activity in arteries of WT mice. In metaregressions, inflammation and oxidative stress markers were associated with total duration of IH exposure, and eNOS was associated with hypoxic score. In ApoE<sup>-/-</sup> mice, inflammation markers were significantly increased in atherosclerotic plaques, but leukocyte infiltration and oxidative stress were not modified by IH. Rodent characteristics had only few impacts on the outcomes.</p><p><strong>Conclusions: </strong>Our meta-analysis confirms that IH, independently of measured confounders, has a major impact on oxido-inflammatory mechanisms in vessels, and that the duration of IH can modulate these effects. Our findings strengthen our understanding of molecular mechanisms associated with vascular alterations in IH/OSA.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 ","pages":"9967028"},"PeriodicalIF":0.0,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12802560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Correction to "Dexmedetomidine Attenuates Oxidative Stress Induced Lung Alveolar Epithelial Cell Apoptosis In Vitro". 更正“右美托咪定在体外减轻氧化应激诱导的肺泡上皮细胞凋亡”。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-07 eCollection Date: 2026-01-01 DOI: 10.1155/omcl/9890530
{"title":"Correction to \"Dexmedetomidine Attenuates Oxidative Stress Induced Lung Alveolar Epithelial Cell Apoptosis <i>In Vitro</i>\".","authors":"","doi":"10.1155/omcl/9890530","DOIUrl":"10.1155/omcl/9890530","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/2015/358396.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 ","pages":"9890530"},"PeriodicalIF":0.0,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12778939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145934675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Correction to "Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension Through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress". 更正“控制性出血通过独立于内质网应激的脑肾素-血管紧张素系统的激活使血管紧张素ii引起的高血压增敏”。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-07 eCollection Date: 2026-01-01 DOI: 10.1155/omcl/9829207
{"title":"Correction to \"Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension Through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress\".","authors":"","doi":"10.1155/omcl/9829207","DOIUrl":"10.1155/omcl/9829207","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1155/2022/6371048.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 ","pages":"9829207"},"PeriodicalIF":0.0,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12778936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145934755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Kidney Dysfunction, Biochemical Changes, DNA Alteration, and MAPKs Regulation Following Chronic Exposure to Regular and Occasional Hookah Smoke in Mice. 长期暴露于定期和不定期水烟烟雾的小鼠肾功能障碍、生化变化、DNA改变和MAPKs调控。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-07 eCollection Date: 2026-01-01 DOI: 10.1155/omcl/6069542
Naserddine Hamadi, Anas Nemmar, Sumaya Beegam, Nur Elena Zaaba, Ozaz Elzaki, Abderrahim Nemmar
{"title":"Kidney Dysfunction, Biochemical Changes, DNA Alteration, and MAPKs Regulation Following Chronic Exposure to Regular and Occasional Hookah Smoke in Mice.","authors":"Naserddine Hamadi, Anas Nemmar, Sumaya Beegam, Nur Elena Zaaba, Ozaz Elzaki, Abderrahim Nemmar","doi":"10.1155/omcl/6069542","DOIUrl":"10.1155/omcl/6069542","url":null,"abstract":"<p><p>Regular hookah smoking (Reg-HS) has become a major global public health issue, linked to significant health risks, including kidney damage. A less frequent pattern of use, known as occasional hookah smoking (Occ-HS), is also common; however, there has been little progress in understanding the direct impact of Occ-HS on kidneys. To investigate how varying frequencies of HS inhalation affect the kidney, we exposed mice to nose-only HS under two regimens, occasional (30 min once weekly) and regular (30 min five times per week) for a duration of 6 months. This study explored the impact on renal damage, inflammatory responses, oxidative stress levels, genotoxicity, and mitochondrial activity as well as the possible modulation of MAPK signaling pathway. Both Occ-HS and Reg-HS led to a marked elevations in plasma levels of urea and creatinine (<i>p</i> < 0.05-<i>p</i> < 0.0001). Additionally, concentrations of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) were significantly increased in both groups (<i>p</i> < 0.01-<i>p</i> < 0.0001). Notably, only the Reg-HS regimen induced a substantial rise in plasma levels of indoxyl sulfate, cystatin C, and adiponectin (<i>p</i> < 0.01-<i>p</i> < 0.0001). Similarly, relative to the control group, mice subjected to Reg-HS exposure exhibited significantly elevated levels of proinflammatory cytokines, tumor necrosis factor-<i>α</i>, and interleukin-6 (<i>p</i> < 0.0001). Exposure to either Occ-HS or Reg-HS caused significant increase in interleukin-1<i>β</i> (<i>p</i> < 0.05, <i>p</i> < 0.0001), thiobarbituric acid reactive substances (TBARS; <i>p</i> < 0.05, <i>p</i> < 0.0001) compared with air-exposed mice. Our findings revealed that Occ-HS inhalation triggered only a decrease in superoxide dismutase (SOD) activity (<i>p</i> < 0.001). On the other hand, nitric oxide (NO; <i>p</i> < 0.001), SOD (<i>p</i> < 0.0001), and Glutathione (GSH; <i>p</i> < 0.0001) levels were significantly decreased in Reg-HS group. Furthermore, DNA damage marker, 8-Hydroxy-2<sup>'</sup>-deoxyguanosine was significantly augmented in both regimens (<i>p</i> < 0.0001). Exposure to both regimens resulted in significant elevation in mitochondrial complexes I, II and III, and IV (<i>p</i> < 0.0001). Increased expression of activation of mitogen-activated protein kinases (MAPKs) was observed exclusively in the Reg-HS group, as evidenced by increased levels of p-JNK, p-p38, and p-ERK (<i>p</i> < 0.001-<i>p</i> < 0.0001). In conclusion, our study is the first to demonstrate that despite the significant differences in the amount of smoke inhaled, both Occ-HS or Reg-HS inhalation deteriorate kidney function and induce oxidative damage, inflammatory response, DNA injury, and mitochondrial impairment with modulation of the MAPK signaling. These findings highlight the importance of further research into the public health risks associated with occasional hookah smoking.</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 ","pages":"6069542"},"PeriodicalIF":0.0,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12779612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145952214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: Sesamin Enhances Nrf2-Mediated Protective Defense against Oxidative Stress and Inflammation in Colitis via AKT and ERK Activation. 撤回:芝麻素通过AKT和ERK激活增强nrf2介导的对结肠炎氧化应激和炎症的保护性防御。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-05 eCollection Date: 2025-01-01 DOI: 10.1155/omcl/9830464
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Sesamin Enhances Nrf2-Mediated Protective Defense against Oxidative Stress and Inflammation in Colitis via AKT and ERK Activation.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9830464","DOIUrl":"10.1155/omcl/9830464","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.1155/2019/2432416.].</p>","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2025 ","pages":"9830464"},"PeriodicalIF":0.0,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12771608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145918231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation. 结论:普罗布考对大鼠心肺复苏后氧化应激引起的心功能障碍有保护作用。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9812128
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Probucol Protects Rats from Cardiac Dysfunction Induced by Oxidative Stress following Cardiopulmonary Resuscitation.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9812128","DOIUrl":"10.1155/omcl/9812128","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9812128"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13059081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147634028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Correction to "Metformin Reduces the Senescence of Renal Tubular Epithelial Cells in Diabetic Nephropathy via the MBNL1/miR-130a-3p/STAT3 Pathway". 更正“二甲双胍通过MBNL1/miR-130a-3p/STAT3通路减缓糖尿病肾病肾小管上皮细胞的衰老”。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9781279
{"title":"Correction to \"Metformin Reduces the Senescence of Renal Tubular Epithelial Cells in Diabetic Nephropathy via the MBNL1/miR-130a-3p/STAT3 Pathway\".","authors":"","doi":"10.1155/omcl/9781279","DOIUrl":"10.1155/omcl/9781279","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9781279"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13042344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: Exosomes Released from CaSR-Stimulated PMNs Reduce Ischaemia/Reperfusion Injury. 收缩:从casr刺激的PMNs释放的外泌体减少缺血/再灌注损伤。
2区 生物学
Oxidative Medicine and Cellular Longevity Pub Date : 2026-01-01 DOI: 10.1155/omcl/9769386
Oxidative Medicine And Cellular Longevity
{"title":"RETRACTION: Exosomes Released from CaSR-Stimulated PMNs Reduce Ischaemia/Reperfusion Injury.","authors":"Oxidative Medicine And Cellular Longevity","doi":"10.1155/omcl/9769386","DOIUrl":"https://doi.org/10.1155/omcl/9769386","url":null,"abstract":"","PeriodicalId":19657,"journal":{"name":"Oxidative Medicine and Cellular Longevity","volume":"2026 1","pages":"e9769386"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13100975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147777906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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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