Leonard Guarente,1,2, * David A. Sinclair,2,3 and Guido Kroemer2,4,5,6, *
1 Department of Biology, Massachusetts Institute for Technology, Cambridge, MA 02139
2 Academy for Healthspan and Lifespan Research (AHLR), New York, NY, USA
3 Blavatnik Institute, Genetics Department, Harvard Medical School, Boston, MA 02115, USA
4 Centre de Recherche des Cordeliers, Equipe labellise´ e par la Ligue contre le cancer, Universite´ Paris Cite´ , Sorbonne Universite´ , Inserm U1138, Institut Universitaire de France, Paris, France
5 Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France
6 Institut du Cancer Paris CARPEM, Department of Biology, Hoˆ pital Europe´ en Georges Pompidou, AP-HP, Paris, France
*Correspondence: 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (L.G.), 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (G.K.)
https://doi.org/10.1016/j.cmet.2023.12.007
SUMMARY
Here, we summarize the current knowledge on eight promising drugs and natural compounds that have been tested in the clinic: metformin, NAD+ precursors, glucagon-like peptide-1 receptor agonists, TORC1 inhibitors, spermidine, senolytics, probiotics, and anti-inflammatories. Multiple clinical trials have commenced to evaluate the efficacy of such agents against age-associated diseases including diabetes, cardiovascular disease, cancer, and neurodegenerative diseases. There are reasonable expectations that drugs able to decelerate or reverse aging processes will also exert broad disease-preventing or -attenuating effects. Hence, the outcome of past, ongoing, and future disease-specific trials may pave the way to the development of new anti-aging medicines. Drugs approved for specific disease indications may subsequently be repurposed for the treatment of organism-wide aging consequences.
Javier Ganz,1,2,3,8,9 Lovelace J. Luquette,4,8 Sara Bizzotto,1,2,3,5,8 Michael B. Miller,1,3,6 Zinan Zhou,1,2,3 Craig L. Bohrson,4
Hu Jin,4 Antuan V. Tran,4 Vinayak V. Viswanadham,4 Gannon McDonough,6 Katherine Brown,6 Yasmine Chahine,1
Brian Chhouk,1 Alon Galor,4 Peter J. Park,4,7,* and Christopher A. Walsh1,2,3,10,*
1 Division of Genetics and Genomics, Manton Center for Orphan Disease Research, Department of Pediatrics, and Howard Hughes Medical Institute, Boston Childrens Hospital, Boston, MA 02115, USA
2 Departments of Pediatrics and Neurology, Harvard Medical School, Boston, MA 02115, USA
3 Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA
4 Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA
5 Sorbonne Universite´ , Institut du Cerveau (Paris Brain Institute) ICM, Inserm, CNRS, Hoˆ pital de la Pitie´ Salpeˆ trie`re, 75013 Paris, France
6 Department of Pathology, Brigham and Womens Hospital, Harvard Medical School, Boston, MA 02115, USA
7 Division of Genetics, Brigham and Womens Hospital, Boston, MA 02115, USA
8 These authors contributed equally
9 Present address: Merck Research Laboratories, Cambridge, MA 02142, USA
10 Lead contact
*Correspondence: 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (P.J.P.), 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (C.A.W.)
https://doi.org/10.1016/j.cell.2024.02.025
Characterizing somatic mutations in the brain is important for disentangling the complex mechanisms of aging, yet little is known about mutational patterns in different brain cell types. Here, we performed wholegenome sequencing (WGS) of 86 single oligodendrocytes, 20 mixed glia, and 56 single neurons from neurotypical individuals spanning 0.4–104 years of age and identified >92,000 somatic single-nucleotide variants (sSNVs) and small insertions/deletions (indels). Although both cell types accumulate somatic mutations linearly with age, oligodendrocytes accumulated sSNVs 81% faster than neurons and indels 28% slower than neurons. Correlation of mutations with single-nucleus RNA profiles and chromatin accessibility from the same brains revealed that oligodendrocyte mutations are enriched in inactive genomic regions and are distributed across the genome similarly to mutations in brain cancers. In contrast, neuronal mutations are enriched in open, transcriptionally active chromatin. These stark differences suggest an assortment of active mutagenic processes in oligodendrocytes and neurons.
原创：伤口治疗及造口护理中心
糖尿病足骨髓炎（Diabetic foot osteomyelitis，DFO）与更高的踝上截肢率相关。尽管DFO有着很高的发生率和糟糕的预后，然而针对其治疗却缺乏高质量的证据。由于缺乏基于证据的指南，导致其治疗方法多种多样。作者咨询了14个外科专家，采用Delphi方法获得了关于DFO诊断、治疗和管理的专家共识。同时作者希望有更多有力的研究和更清晰的指南，以便能改善外科治疗的结果。
原创： 蔡秋妮 赫曼关爱健康
肉芽组织在伤口修复、愈合过程中起关键作用。伤口床中存在肉芽组织是伤口愈合的迹象,健康的肉芽组织表现为鲜红色或粉红色表面呈细颗粒状，柔软湿润，分泌物极少,无水肿,无痛觉，不易出血。
原创： 李梅 赫曼关爱健康
原创： 胡海涛 负压引流与创面修复
伤口世界平台生态圈，以“关爱人间所有伤口患者”为愿景，连接、整合和拓展线上和线下的管理慢性伤口的资源，倡导远程、就近和居家管理慢性伤口，解决伤口专家的碎片化时间的价值创造、诊疗经验的裂变复制、和患者的就近、居家和低成本管理慢性伤口的问题。
2019广东省医疗行业协会伤口管理分会年会
扫一扫了解详情:
任何关于疾病的建议都不能替代执业医师的面对面诊断。所有门诊时间仅供参考，最终以医院当日公布为准。
网友、医生言论仅代表其个人观点，不代表本站同意其说法，请谨慎参阅，本站不承担由此引起的法律责任。
