检索结果-内蒙古大学图书馆

Obesity alters pathology and treatment response in inflammatory disease

四川生理科学杂志 2022年第3期44卷 446-446页

作者： Sagar P Bapat NOMIS Center for Immunobiology and Microbial Pathogenesis The Salk Institute for Biological Studies La Jolla CA USA Gene Expression Laboratory The Salk Institute for Biological Studies La Jolla CA USA Medical Scientist Training Program University of California San Diego La Jolla CA USA Department of Laboratory Medicine University of California San Francisco San Francisco CA USA Department of Microbiology and Immunology University of California San Francisco San Francisco CA USA Diabetes Center University of California San Francisco San Francisco CA USA Medical Scientist Training Program University of California San Francisco CA USA Division of Pulmonary Critical Care Allergy and Sleep Department of Medicine University of California San Francisco San Francisco CA USA School of Pharmaceutical Sciences Xiamen University Xiamen China Department of Dermatology University of California San Diego La Jolla CA USA Department of Surgery University of California San Francisco San Francisco CA USA Department of Medicine University of California San Francisco San Francisco CA USA Sandler Asthma Basic Research Center University of California San Francisco San Francisco CA USA School of Medicine Wake Forest University Winston–Salem NC USA Department of Dermatology Icahn School of Medicine at Mount Sinai New York NY USA Lung Biology Center Department of Medicine University of California San Francisco San Francisco CA USA Department of Biomedical Science Graduate School Kyungpook National University Kyungpook National University Hospital Daegu South Korea Department of Dermatology University of California San Francisco San Francisco CA USA Department of Pathology University of California San Francisco San Francisco CA USA Department of Internal Medicine Division of Pulmonary Critical Care and Sleep Medicine University of Kentucky Lexington KY USA Pulmonary Critical Care Section Department of Medicine Veterans Affairs San Diego Hea

Decades of work have elucidated cytokine signalling and transcriptional pathways that control T cell differentiation and have led the way to targeted biologic therapies that are effective in a range of autoimmune,allergic and inflammatory *** evidence indicates that obesity and metabolic disease can also influence the immune system1-7,although the mechanisms and effects on immunotherapy outcomes remain largely ***,using two models of atopic dermatitis,we show that lean and obese mice mount markedly different immune *** converted the classical type 2 T helper(TH2)-predominant disease associated with atopic dermatitis to a more severe disease with prominent TH17 *** also observed divergent responses to biologic therapies targeting TH2 cytokines,which robustly protected lean mice but exacerbated disease in obese ***-cell RNA sequencing coupled with genome-wide binding analyses revealed decreased activity of nuclear receptor peroxisome proliferator-activated receptor-γ(PPARγ)in TH2 cells from obese mice relative to lean mice.

关键词： dermatitis inflammatory allergic

来源：评论

学校读者我要写书评

暂无评论

LC-MS/MS proteomics identifies plasma proteins related to cognition over 9-year follow-up

引用

Alzheimer's & dementia : the journal of the Alzheimer's Association 2025年第6期21卷 e70276页

作者： Hailey A Adegboye Khiry L Patterson Julia Libby Yunyi Sun Panpan Zhang Dandan Liu W Hudson Robb Amalia J Peterson Keith R Cole Albert B Arul Nekesa C Oliver Marsalas D Whitaker Kimberly R Pechman Logan Dumitrescu Corey J Bolton Kaj Blennow Henrik Zetterberg Timothy J Hohman Renã A S Robinson Angela L Jefferson Vanderbilt Memory and Alzheimer's Center Vanderbilt University School of Medicine Nashville Tennessee USA. Medical Scientist Training Program Vanderbilt University School of Medicine Nashville Tennessee USA. Department of Chemistry Vanderbilt University Nashville Tennessee USA. Department of Biostatistics Vanderbilt University Medical Center Nashville Tennessee USA. Department of Neurology Vanderbilt University Medical Center Nashville Tennessee USA. Department of Orthopaedic Surgery Vanderbilt University Medical Center Nashville Tennessee USA. Department of Medicine Vanderbilt University Medical Center Nashville Tennessee USA. Department of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden. Clinical Neurochemistry Laboratory Sahlgrenska University Hospital Mölndal Sweden. Paris Brain Institute ICM Hôpital Pitié Paris France. Neurodegenerative Disorder Research Center Division of Life Sciences and Medicine and Department of Neurology Institute on Aging and Brain Disorders University of Science and Technology of China and First Affiliated Hospital of USTC Hefei China. Department of Neurodegenerative Disease UCL Institute of Neurology Queen Square London UK. UK Dementia Research Institute at UCL London UK. Hong Kong Center for Neurodegenerative Diseases InnoHK Hong Kong China. Wisconsin Alzheimer's Disease Research Center University of Wisconsin School of Medicine and Public Health University of Wisconsin-Madison Madison Wisconsin USA.

INTRODUCTION:This project identified plasma proteins predictive of cognitive decline across a robust neuropsychological protocol over a 9-year period. METHODS:Vanderbilt Memory and Aging Project participants (n = 336, 73 ± 7 years, 59% male, 87% non-Hispanic White, 10% Black/African American) underwent blood draw for baseline plasma protein abundance using mass spectrometry analysis of tandem mass tag (TMT)-labeled peptides and serial neuropsychological assessment (follow-up = 6.1 ± 2.3 years). Linear mixed-effects regressions related protein levels to neuropsychological outcomes in fully adjusted models. False discovery rate correction was applied. RESULTS:Initial proteomics analyses yielded 3764 unique protein identifications across 23 16-plex TMT batches, and 686 proteins passed quality control. Proteins were identified predicting longitudinal decline in language (EGFR, RTN4RL2), information processing speed (EGFR, NOMO2, CLEC3B), executive function (A1BG), and visuospatial skills (RTN4RL2, GALNT1, SERPINA4, SERPINA5, C8A, ALDOB), but not episodic memory. DISCUSSION:Large-scale proteomics analyses identified 10 plasma proteins that predicted subsequent cognitive decline over a 9-year follow-up in multiple cognitive domains. HIGHLIGHTS:There were 3764 unique protein identifications across 23 16-plex TMT batches. Rigorous quality control yielded 686 proteins used as predictors in analyses. Identified proteins related to all domains assessed, except for episodic memory. Many proteins identified were differentially expressed in MCI.

关键词： Alzheimer's disease LC‐MS/MS cognition mild cognitive impairment plasma proteomics

来源：评论

学校读者我要写书评

暂无评论

Correction to: USP20 positively regulates tumorigenesis and chemoresistance through β-catenin stabilization

引用

Cell death and differentiation 2023年第3期30卷 857-858页

作者： Chenming Wu Kuntian Luo Fei Zhao Ping Yin Ying Song Min Deng Jinzhou Huang Yuping Chen Lei Li SeungBaek Lee JungJin Kim Qin Zhou Xinyi Tu Somaira Nowsheen Qifeng Luo Xiumei Gao Zhenkun Lou Zhongmin Liu Jian Yuan Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Department of Pathology East Hospital Shanghai 200120 China. Mayo Clinic Medical Scientist Training Program Mayo Clinic School of Medicine and Mayo Clinic Graduate School of Biomedical Sciences Mayo Clinic Rochester MN 55905 USA. Department of Molecular Pharmacology and Experimental Therapeutics Mayo Clinic Rochester MN 55905 USA. Department of Gastrointestinal Surgery Shanghai East Hospital School of Medicine Tongji University Shanghai 200120 Shanghai P. R. China. Tianjin State Key Laboratory of Modern Chinese Medicine Tianjin University of Traditional Chinese Medicine 300193 Tianjin China. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Lou.zhenkun@mayo.edu. Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Zhongmin_Liu@***. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Zhongmin_Liu@***. Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Yuanjian229@***. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Yuanjian229@***. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Yuanjian229@***. Department of Molecular Pharmacology and Experimental Therapeutics Mayo Clinic Rochester MN 55905 USA. Yuanjian229@***.

来源：评论

学校读者我要写书评

暂无评论

Using MARRVEL v1.2 for Bioinformatics Analysis of Human Genes and Variant Pathogenicity

引用

Current Protocols in Bioinformatics 2019年第1期67卷 Using MARRVEL vl.2 for/1-Using MARRVEL vl.2 for/24页

作者： Wang, Julia Mao, Dongxue Fazal, Fatima Kim, Seon-Young Yamamoto, Shinya Bellen, Hugo Liu, Zhandong Program in Developmental Biology Medical Scientist Training Program Baylor College of Medicine Houston TX United States Department of Pediatrics-Neurology Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital Baylor College of Medicine Houston TX United States Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital Baylor College of Medicine Houston TX United States Department of Molecular and Human Genetics Baylor College of Medicine Howard Hughes Medical Institute Houston TX United States Department of Molecular and Human Genetics Baylor College of Medicine Jan and Dan Duncan Neurological Research Institute Texas Children's Hospital Houston TX United States Department of Neuroscience Baylor College of Medicine Jan and Dan Duncan Neurological Research Institute Texas Children's Hospital Houston TX United States Program in Developmental Biology Baylor College of Medicine Jan and Dan Duncan Neurological Research Institute Texas Children's Hospital Houston TX United States Department of Pediatrics Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital Houston TX United States Computational and Integrative Biomedical Research Center Baylor College of Medicine Houston TX United States Department of Pediatrics-Neurology Baylor College of Medicine Houston TX United States

One of the greatest challenges in the bioinformatic analysis of human sequencing data is identifying which variants are pathogenic. Numerous databases and tools have been generated to address this difficulty. However, these many useful data and tools are broadly dispersed, requiring users to search for their variants of interest through human genetic databases, variant function prediction tools, and model organism databases. To solve this problem, we collected data and observed workflows of human geneticists, clinicians, and model organism researchers to carefully select and display valuable information that facilitates the evaluation of whether a variant is likely to be pathogenic. This program, Model organism Aggregated Resources for Rare Variant ExpLoration (MARRVEL) v1.2, allows users to collect relevant data from 27 public sources for further efficient bioinformatic analysis of the pathogenicity of human variants. © 2019 by John Wiley & Sons, Inc. © 2019 John Wiley & Sons, Inc.

关键词： genes of unknown significance genetics genomics databases model organisms variants of unknown significance

来源：评论

学校读者我要写书评

暂无评论

Author Correction: A framework for clinical cancer subtyping from nucleosome profiling of cell-free DNA

引用

Nature communications 2023年第1期14卷 403页

作者： Anna-Lisa Doebley Minjeong Ko Hanna Liao A Eden Cruikshank Katheryn Santos Caroline Kikawa Joseph B Hiatt Robert D Patton Navonil De Sarkar Katharine A Collier Anna C H Hoge Katharine Chen Anat Zimmer Zachary T Weber Mohamed Adil Jonathan B Reichel Paz Polak Viktor A Adalsteinsson Peter S Nelson David MacPherson Heather A Parsons Daniel G Stover Gavin Ha Division of Public Health Sciences and Human Biology Fred Hutchinson Cancer Center Seattle WA USA. Molecular and Cellular Biology Graduate Program University of Washington Seattle WA USA. Medical Scientist Training Program University of Washington Seattle WA USA. Department of Genome Sciences University of Washington Seattle WA USA. Dana-Farber Cancer Institute Boston MA USA. Division of Medical Oncology Department of Medicine University of Washington Seattle WA USA. Ohio State University Comprehensive Cancer Center Columbus OH USA. Laboratory Medicine and Pathology University of Washington Seattle WA USA. Brotman Baty Institute for Precision Medicine Seattle WA USA. Department of Oncological Sciences Icahn School of Medicine Mount Sinai New York NY USA. Broad Institute of MIT and Harvard Cambridge MA USA. Division of Public Health Sciences and Human Biology Fred Hutchinson Cancer Center Seattle WA USA. gha@***. Department of Genome Sciences University of Washington Seattle WA USA. gha@***. Brotman Baty Institute for Precision Medicine Seattle WA USA. gha@***.

来源：评论

学校读者我要写书评

暂无评论

HMGA2 and protein leucine methylation drive pancreatic cancer lineage plasticity

引用

Nature communications 2025年第1期16卷 4866页

作者： Stephanie Dobersch Naomi Yamamoto Aidan Schutter Sarah M Cavender Tess M Robertson Nithya Kartha Annie N Samraj Ben Doron Lisa A Poole Cynthia L Wladyka Amy Zhang Gun Ho Jang Aswanth H Mahalingam Guillermo Barreto Srivatsan Raghavan Goutham Narla Faiyaz Notta Robert N Eisenman Andrew C Hsieh Sita Kugel Human Biology Division Fred Hutchinson Cancer Center Seattle WA USA. Medical Scientist Training Program University of Washington Seattle WA USA. Molecular & Cellular Biology Graduate Program University of Washington Seattle WA USA. Division of Transfusion Medicine Department of Laboratory Medicine University of Washington School of Medicine Seattle WA USA. PanCuRx Translational Research Initiative Ontario Institute for Cancer Research Toronto Ontario Canada. Department of Medical Oncology Dana-Farber Cancer Institute Boston MA USA. Université de Lorraine CNRS Laboratoire IMoPA Nancy France. Lung Cancer Epigenetic Max-Planck-Institute for Heart and Lung Research Bad Nauheim Germany. Broad Institute of MIT and Harvard Cambridge MA USA. Harvard Medical School Boston MA USA. Department of Medicine Brigham and Women's Hospital Boston MA USA. Division of Genetic Medicine Department of Internal Medicine University of Michigan Ann Arbor MI USA. Rogel Cancer Center University of Michigan Ann Arbor MI USA. Princess Margaret Cancer Centre University Health Network Toronto ON Canada. Department of Medical Biophysics University of Toronto Toronto ON Canada. Basic Sciences Division Fred Hutchinson Cancer Center Seattle WA USA. Department of Medicine University of Washington Seattle WA USA. Department of Genome Sciences University of Washington Seattle WA USA. Human Biology Division Fred Hutchinson Cancer Center Seattle WA USA. skugel@***. Department of Genome Sciences University of Washington Seattle WA USA. skugel@***.

Basal pancreatic ductal adenocarcinoma (PDAC) has the worst overall survival and is the only subtype that serves as an independent poor prognostic factor. We identify elevated levels of LIN28B and its downstream target, HMGA2, in basal PDAC. Notably, LIN28B significantly accelerates KRAS-driven PDAC progression in a mouse model. Here, we show that HMGA2 promotes basal PDAC pathogenesis by enhancing mRNA translation downstream of LIN28B. Mechanistically, HMGA2 suppresses leucine carboxyl methyltransferase 1 (LCMT1) at the chromatin level, reducing PP2A methylation and activity. This leads to increased phosphorylation of S6K and eIF4B, boosting mRNA translation. Additionally, HMGA2 downregulates B56α (PPP2R5A), disrupting functional PP2A holoenzyme assembly and further sustaining phosphorylated S6K levels. Impaired PP2A function mimics HMGA2's effects, reinforcing increased mRNA translation and basal lineage features. This work uncovers a critical link between the LIN28B/HMGA2 axis, protein synthesis, and PDAC lineage specificity via LCMT1-mediated PP2A methylation and B56α-PP2A disruption.

关键词：

来源：评论

学校读者我要写书评

暂无评论

GWAS meta-analysis of over 29,000 people with epilepsy identifies 26 risk loci and subtype-specific genetic architecture

引用

Nature genetics 2023年第9期55卷 1471-1482页

作者： Remi Stevelink Dorothee Kasteleijn-Nolst Trenite Bobby P. C. Koeleman Dick Lindhout Anja C. M. Sonsma Ciarán Campbell Gianpiero L. Cavalleri Norman Delanty Hany El-Naggar Austin Lacey Peter Widdess-Walsh Colin P. Doherty Siwei Chen Claire Churchhouse Mark J. Daly Yen-Chen A. Feng Daniel P. Howrigan Mitja I. Kurki Benjamin M. Neale Aarno Palotie Wei Zhou Namrata Gupta Henrike O. Heyne Bassel Abou-Khalil Kevin F. Haas R. S. Taneja Oluyomi M. Adesoji Michael Nothnagel Peter Nürnberg Thomas Sander Zaid Afawi Ilan Blatt Amos D. Korczyn Elisabetta Amadori Ganna Balagura Antonella Riva Marcello Scala Paolo Scudieri Pasquale Striano Federico Zara Michele Iacomino Francesca Madia Alison Anderson Patrick Kwan Terence J. O’Brien Slavé Petrovski K. Meng Tan Marian Todaro Joseph Anderson Danielle M. Andrade Quratulain Zulfiqar Ali Grazia Annesi Pauls Auce Andreja Avbersek Simona Balestrini Vera Braatz Claudia B. Catarino Krishna Chinthapalli Jennifer Jamnadas-Khoda Dalia Kasperavičiūte Costin Leu Josemir W. Sander Sanjay M. Sisodiya Sara Zagaglia Melanie Bahlo Karen L. Oliver Mark D. Baker Beata Fonferko-Shadrach William O. Pickrell Carmen Barba Claudia Bianchini Viola Doccini Renzo Guerrini Davide Mei Martino Montomoli Elena Parrini Annalisa Vetro Karen Barboza Fabrice Bartolomei Thomas Bast Bernhard J. Steinhoff Larry Baum Stacey S. Cherny Pak Sham Tobias Baumgartner Christian E. Elger Kerstin Hallmann Wolfram S. Kunz Rainer Surges Randi von Wrede Gábor Zsurka Betül Baykan Nerses Bebek Yeşim Kesim Albert J. Becker Susanne Schoch Felicitas Becker Caitlin A. Bennett Samuel F. Berkovic Stephanie L. Leech Brigid M. Regan Ingrid E. Scheffer Bianca Berghuis Ahmad Beydoun Wassim Nasreddine Francesca Bisulli Lidia Di Vito Lorenzo Ferri Tania Giangregorio Laura Licchetta Raffaella Minardi Barbara Mostacci Carlotta Stipa Paolo Tinuper Lorenzo Muccioli Federica Pondrelli Dheeraj R. Bobbili Emadeldin Hassanin Roland Krause Zied Landoulsi Patrick May Ingo Borggraefe Christian Bosselmann Christian Hengsbach Josua Kegele Stephen Lauxmann Department of Genetics University Medical Center Utrecht Utrecht The Netherlands Stichting Epilepsie Instellingen Nederland (SEIN) Heemstede The Netherlands School of Pharmacy and Biomolecular Sciences The Royal College of Surgeons in Ireland Dublin Ireland The FutureNeuro Research Centre Dublin Ireland Department of Neurology Beaumont Hospital Dublin Ireland Department of Neurology St. James’s Hospital Dublin Ireland Analytic and Translational Genetics Unit Department of Medicine Massachusetts General Hospital and Harvard Medical School Boston MA USA Program in Medical and Population Genetics Broad Institute of MIT and Harvard Cambridge MA USA Stanley Center for Psychiatric Research Broad Institute of Harvard and M.I.T Cambridge MA USA Institute for Molecular Medicine Finland (FIMM) University of Helsinki Helsinki Finland Psychiatric & Neurodevelopmental Genetics Unit Department of Psychiatry Massachusetts General Hospital and Harvard Medical School Boston MA USA Division of Biostatistics Institute of Epidemiology and Preventive Medicine College of Public Health National Taiwan University Taipei Taiwan Hasso Plattner Institute Digital Health Center University of Potsdam Potsdam Germany Hasso Plattner Institute Mount Sinai School of Medicine New York City NY USA Department of Neurology Vanderbilt University Medical Center Nashville TN USA Cologne Center for Genomics (CCG) University of Cologne Faculty of Medicine and University Hospital Cologne Cologne Germany University Hospital Cologne Cologne Germany Department of Neurology Charité Universitaetsmedizin Berlin Campus Virchow-Clinic Berlin Germany Tel-Aviv University Sackler Faculty of Medicine Ramat Aviv Israel Department of Neurology Sheba Medical Center Ramat Gan Israel Department of Neurosciences Rehabilitation Ophthalmology Genetics Maternal and Child Health University of Genova Genova Italy IRCCS Istituto Giannina Gaslini Genova Italy Department of Medicine University of Melbour

Epilepsy is a highly heritable disorder affecting over 50 million people worldwide, of which about one-third are resistant to current treatments. Here we report a multi-ancestry genome-wide association study including 29,944 cases, stratified into three broad categories and seven subtypes of epilepsy, and 52,538 controls. We identify 26 genome-wide significant loci, 19 of which are specific to genetic generalized epilepsy (GGE). We implicate 29 likely causal genes underlying these 26 loci. SNP-based heritability analyses show that common variants explain between 39.6% and 90% of genetic risk for GGE and its subtypes. Subtype analysis revealed markedly different genetic architectures between focal and generalized epilepsies. Gene-set analyses of GGE signals implicate synaptic processes in both excitatory and inhibitory neurons in the brain. Prioritized candidate genes overlap with monogenic epilepsy genes and with targets of current antiseizure medications. Finally, we leverage our results to identify alternate drugs with predicted efficacy if repurposed for epilepsy treatment.

关键词：

来源：评论

学校读者我要写书评

暂无评论

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A (vol 603, pg 131, 2022)

引用

NATURE 2024年第8020期631卷 E7-E7页

作者： Brown, Anna-Leigh Wilkins, Oscar G. Keuss, Matthew J. Hill, Sarah E. Zanovello, Matteo Lee, Weaverly Colleen Bampton, Alexander Lee, Flora C. Y. Masino, Laura Qi, Yue A. Bryce-Smith, Sam Gatt, Ariana Hallegger, Martina Fagegaltier, Delphine Phatnani, Hemali Phatnani, Hemali Newcombe, Jia Gustavsson, Emil K. Seddighi, Sahba Reyes, Joel F. Coon, Steven L. Ramos, Daniel Schiavo, Giampietro Fisher, Elizabeth M. C. Raj, Towfique Secrier, Maria Lashley, Tammaryn Ule, Jernej Buratti, Emanuele Humphrey, Jack Ward, Michael E. Fratta, Pietro UCL Queen Square Motor Neuron Disease Centre Department of Neuromuscular Diseases UCL Queen Square Institute of Neurology UCL London UK The Francis Crick Institute London UK UK Dementia Research Institute University College London London UK Department of Molecular Biology and Nanobiotechnology National Institute of Chemistry Ljubljana Slovenia National Institute of Neurological Disorders and Stroke NIH Bethesda MD USA Medical Scientist Training Program Johns Hopkins University School of Medicine Baltimore MD USA Center for Alzheimer’s and Related Dementias National Institutes of Health Bethesda MD USA Queen Square Brain Bank UCL Queen Square Institute of Neurology University College London London UK Department of Neurodegenerative Disease UCL Queen Square Institute of Neurology University College London London UK Great Ormond Street Institute of Child Health Genetics and Genomic Medicine University College London London UK Center for Genomics of Neurodegenerative Disease New York Genome Center (NYGC) New York NY USA NeuroResource Department of Neuroinflammation UCL Queen Square Institute of Neurology London UK Molecular Genomics Core Eunice Kennedy Shriver National Institute of Child Health and Human Development NIH Bethesda MD USA Nash Family Department of Neuroscience and Friedman Brain Institute Icahn School of Medicine at Mount Sinai New York NY USA Ronald M. Loeb Center for Alzheimer’s Disease Icahn School of Medicine at Mount Sinai New York NY USA Department of Pathology Fishberg Department of Neuroscience Icahn School of Medicine at Mount Sinai New York NY USA Department of Genetics and Genomic Sciences and Icahn Institute for Data Science and Genomic Technology Icahn School of Medicine at Mount Sinai New York NY USA Estelle and Daniel Maggin Department of Neurology Icahn School of Medicine at Mount Sinai New York NY USA Department of Genetics Evolution and Environment UCL Genetics Institute University College London London UK Mole

来源：评论

学校读者我要写书评

暂无评论

Publisher Correction: Female aging: when translational models don't translate

Nature aging

引用

Nature aging 2024年第1期4卷 164页

作者： Gabrielle Gilmer Zachary R Hettinger Yetsa Tuakli-Wosornu Elizabeth Skidmore Julie K Silver Rebecca C Thurston Dawn A Lowe Fabrisia Ambrosio Discovery Center for Musculoskeletal Recovery Schoen Adams Research Institute at Spaulding Rehabilitation Boston MA USA. Department of Physical Medicine and Rehabilitation Spaulding Rehabilitation Hospital Charlestown MA USA. Medical Scientist Training Program School of Medicine University of Pittsburgh Pittsburgh PA USA. Cellular and Molecular Pathology Graduate Program University of Pittsburgh Pittsburgh PA USA. Department of Physical Medicine & Rehabilitation Harvard Medical School Boston MA USA. Department of Geriatric Medicine University of Pittsburgh Pittsburgh PA USA. Department of Social and Behavioral Sciences Yale School of Public Health Yale University New Haven CT USA. Department of Physical Medicine and Rehabilitation University of Pittsburgh School of Medicine Pittsburgh PA USA. Department of Occupational Therapy School of Health and Rehabilitation Sciences University of Pittsburgh Pittsburgh PA USA. Department of Physical Medicine and Rehabilitation Massachusetts General Hospital Boston MA USA. Department of Physical Medicine and Rehabilitation Brigham and Women's Hospital Boston MA USA. Department of Psychiatry University of Pittsburgh School of Medicine Pittsburgh PA USA. Divisions of Rehabilitation Science and Physical Therapy Department of Rehabilitation Medicine University of Minnesota Minneapolis MN USA. Discovery Center for Musculoskeletal Recovery Schoen Adams Research Institute at Spaulding Rehabilitation Boston MA USA. fambrosio@mgh.harvard.edu. Department of Physical Medicine and Rehabilitation Spaulding Rehabilitation Hospital Charlestown MA USA. fambrosio@mgh.harvard.edu. Department of Physical Medicine & Rehabilitation Harvard Medical School Boston MA USA. fambrosio@mgh.harvard.edu.

来源：评论

学校读者我要写书评

暂无评论

Exposure to Static Magnetic and Electric Fields Treats Type 2 Diabetes (vol 32, pg 561, 2020)

引用

CELL METABOLISM 2020年第6期32卷 1076-1076页

作者： Carter, Calvin S. Huang, Sunny C. Searby, Charles C. Cassaidy, Benjamin Miller, Michael J. Grzesik, Wojciech J. Piorczynski, Ted B. Pak, Thomas K. Walsh, Susan A. Acevedo, Michael Zhang, Qihong Mapuskar, Kranti A. Milne, Ginger L. Milne, Ginger L. Hinton, Antentor O., Jr. Guo, Deng-Fu Weiss, Robert Bradberry, Kyle Taylor, Eric B. Rauckhorst, Adam J. Dick, David W. Akurathi, Vamsidhar Falls-Hubert, Kelly C. Wagner, Brett A. Carter, Walter A. Wang, Kai Norris, Andrew W. Rahmouni, Kamal Buettner, Garry R. Hansen, Jason M. Spitz, Douglas R. Abel, E. Dale Sheffield, Val C. Department of Pediatrics and Division of Medical Genetics and Genomics University of Iowa Hospitals & Clinics Iowa City IA USA Medical Scientist Training Program Roy J. and Lucille A. Carver College of Medicine University of Iowa Iowa City IA USA Department of Physics and Astronomy University of Iowa Iowa City IA USA Fraternal Order of Eagles Diabetes Research Center Roy J. and Lucille A. Carver College of Medicine University of Iowa Iowa City IA USA Department of Physiology and Developmental Biology Brigham Young University Provo UT USA Department of Radiology Division of Nuclear Medicine University of Iowa Hospitals & Clinics Iowa City IA USA Free Radical and Radiation Biology Program Department of Radiation Oncology Holden Comprehensive Cancer Center University of Iowa Hospitals & Clinics Iowa City IA USA Department of Pharmacology Vanderbilt University Medical Center Nashville TN USA Department of Neuroscience and Pharmacology University of Iowa Hospitals & Clinics Iowa City IA USA Department of Internal Medicine Division of Cardiology University of Iowa Hospitals & Clinics Iowa City IA USA Department of Molecular Physiology and Biophysics University of Iowa Hospitals & Clinics Iowa City IA USA Department of Internal Medicine Division of Endocrinology and Metabolism University of Iowa Hospitals & Clinics Iowa City IA USA College of Public Health Department of Biostatistics University of Iowa Iowa City IA USA

Aberrant redox signaling underlies the pathophysiology of many chronic metabolic diseases, including type 2 diabetes (T2D). Methodologies aimed at rebalancing systemic redox homeostasis have had limited success. A noninvasive, sustained approach would enable the long-term control of redox signaling for the treatment of T2D. We report that static magnetic and electric fields (sBE) noninvasively modulate the systemic GSH-to-GSSG redox couple to promote a healthier systemic redox environment that is reducing. Strikingly, when applied to mouse models of T2D, sBE rapidly ameliorates insulin resistance and glucose intolerance in as few as 3 days with no observed adverse effects. Scavenging paramagnetic byproducts of oxygen metabolism with SOD2 in hepatic mitochondria fully abolishes these insulin sensitizing effects, demonstrating that mitochondrial superoxide mediates induction of these therapeutic changes. Our findings introduce a remarkable redox-modulating phenomenon that exploits endogenous electromagneto-receptive mechanisms for the noninvasive treatment of T2D, and potentially other redox-related diseases.

关键词： redox type 2 diabetes insulin resistance electromagnetic fields ROS superoxide glutathione radical pair mechanism mitochondria liver

来源：评论

学校读者我要写书评

暂无评论

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案：

请选择收藏分类：

通借通还

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：