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The Clinical and Electrocardiographic Phenotype of Patients with Genotype Negative Long QT Syndrome

Heart rhythm 2025年

作者： Vanessa Karlinski Vizentin Raquel Neves Sahej Bains Iuri Ferreira Felix David J Tester J Martijn Bos John R Giudicessi Michael J Ackerman Department of Molecular Pharmacology & Experimental Therapeutics (Windland Smith Rice Sudden Death Genomics Laboratory) Mayo Clinic Rochester MN. Department of Molecular Pharmacology & Experimental Therapeutics (Windland Smith Rice Sudden Death Genomics Laboratory) Mayo Clinic Rochester MN Medical Scientist Training Program Mayo Clinic Rochester MN. Deparment of Internal Medicine Mayo Clinic Rochester MN. Department of Cardiovascular Medicine (Divisions of Heart Rhythm Services and Circulatory Failure Windland Smith Rice Genetic Heart Rhythm Clinic) Mayo Clinic Rochester MN. Department of Cardiovascular Medicine (Divisions of Heart Rhythm Services and Circulatory Failure Windland Smith Rice Genetic Heart Rhythm Clinic) Mayo Clinic Rochester MN Department of Pediatric and Adolescent Medicine (Division of Pediatric Cardiology) Mayo Clinic Rochester MN. Electronic address: ackerman.michael@mayo.edu.

BACKGROUND:Long QT syndrome (LQTS) is a genetic heart disease that increases the risk for ventricular arrhythmias and sudden cardia arrest. Despite advances in genetic testing, a small subset of LQTS patients remain genetically elusive. OBJECTIVE:To determine the prevalence and clinical characteristics of patients with a phenotype of LQTS but genotype negative. METHODS:This study aimed to identify phenotype-positive, genotype-negative LQTS patients seen at Mayo Clinic (2000 - 2024). Retrospective data included demographics, clinical evaluations, ECGs, and genetic results. Diagnosis adhered to established criteria, and genotype-negative LQTS was defined by the absence of pathogenic variants despite clinical presentation. RESULTS:The study included 1,829 patients with LQTS. From these, 1,706 (93%) had pathogenic or likely pathogenic variants and 95 patients (5%) had upgraded clinically variants of uncertain significance, leaving 32 (1.7%) with negative genetic tests. Among the genotype-negative patients, 17 underwent next-generation sequencing, identifying a genetic cause in 6 cases (0.3% of the total). The mean age at diagnosis for the remaining 26 patients was 25 ± 15 years, 76% being female and an average initial QTc of 498 ± 41 ms. Fourteen patients (53%) experienced cardiac events prior to diagnosis, and 11 (44%) received an implantable cardioverter-defibrillator (ICD). The mean follow-up period was 8 ± 7 years. CONCLUSION:Genotype-negative LQTS accounted for <2% of our cohort, highlighting diagnostic and management challenges. Comprehensive clinical evaluation and advanced genetic testing remain essential for accurate diagnosis and care.

关键词： Genetic Heart Disease Genotype Negative Long QT syndrome Next Generation Sequencing Sudden Cardiac Death

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Publisher Correction: Structural basis of LRPPRC-SLIRP-dependent translation by the mitoribosome

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Nature structural & molecular biology 2024年第11期31卷 1809页

作者： Vivek Singh J Conor Moran Yuzuru Itoh Iliana C Soto Flavia Fontanesi Mary Couvillion Martijn A Huynen L Stirling Churchman Antoni Barrientos Alexey Amunts Science for Life Laboratory Department of Biochemistry and Biophysics Stockholm University Solna Sweden. Medical Scientist Training Program Department of Biochemistry and Molecular Biology University of Miami Miller School of Medicine Miami FL USA. Science for Life Laboratory Department of Biochemistry and Biophysics Stockholm University Solna Sweden. yuzuru.itoh@bs.s.u-tokyo.ac.jp. Department of Biological Sciences Graduate School of Science University of Tokyo Tokyo Japan. yuzuru.itoh@bs.s.u-tokyo.ac.jp. Blavatnik Institute Department of Genetics Harvard Medical School Boston MA USA. Department of Medical BioSciences Radboud University Medical Center Nijmegen The Netherlands. Blavatnik Institute Department of Genetics Harvard Medical School Boston MA USA. churchman@genetics.med.harvard.edu. Department of Neurology University of Miami Miller School of Medicine Miami FL USA. abarrientos@med.miami.edu. Science for Life Laboratory Department of Biochemistry and Biophysics Stockholm University Solna Sweden. alexey.amunts@***. Westlake University Hangzhou China. alexey.amunts@***.

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Clinical and histopathological spectrum of toxic erythema of chemotherapy in patients who have undergone allogeneic hematopoietic cell transplantation

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Hematology/ Oncology and Stem Cell Therapy 2019年第1期12卷 19-25页

作者： Hunjan, Manrup K. Nowsheen, Somaira Ramos-Rodriguez, Alvaro J. Hashmi, Shahrukh K. Bridges, Alina G. Lehman, Julia S. El-Azhary, Rokea St Johns Institute of Dermatology Guys and St Thomas’ Hospitals NHS Trust United Kingdom Mayo Clinic Medical Scientist Training Program Mayo Clinic School of Medicine Rochester MN United States Mayo Clinic Graduate School of Biomedical Sciences Mayo Clinic Rochester MN United States Department of Internal Medicine Icahn School of Medicine at Mount Sinai West New York NY United States Department of Hematology and Oncology Mayo Clinic Rochester MN United States Department of Dermatology Mayo Clinic Rochester MN United States Department of Laboratory Medicine and Pathology Mayo Clinic Rochester MN United States

Objective/Background: Toxic erythema of chemotherapy (TEC) is a well-recognized adverse cutaneous reaction to chemotherapy. Similar to many skin diseases, the clinical presentations may vary. Our objective is to expand on the typical and atypical clinical and histopathological presentations of TEC. Methods: Forty patients with a diagnosis of TEC were included from 500 patients who had undergone an allogeneic hematopoietic stem cell transplant. Relevant information and demonstrative photos and pathology were selected. Results: Classic clinical presentations included hand and foot erythema and dysesthesias;atypical presentations included facial involvement, hyperpigmentation, dermatomyositis-like, and erythroderma associated with capillary leak syndrome. Conclusion: The diagnosis of TEC should be considered after a correlation of clinical and histological findings in conjunction with a timeline of chemotherapy administration. Suggested criteria for the diagnosis of TEC may be helpful to dermatologists and clinicians when caring for these patients. © 2018 King Faisal Specialist Hospital & Research Centre

关键词： Cancer Capillary leak syndrome (CLS) Chemotherapy Stem cell transplant Toxic epidermal necrolysis Toxic erythema of chemotherapy

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Mitigation of Chromosome Loss in Clinical CRISPR-Cas9-Engineered T Cells

SSRN

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SSRN 2023年

作者： Tsuchida, Connor A. Brandes, Nadav Bueno, Raymund Trinidad, Marena Mazumder, Thomas Yu, Bingfei Hwang, Byungjin Chang, Christopher Liu, Jamin Sun, Yang Hopkins, Caitlin R. Parker, Kevin R. Qi, Yanyan Satpathy, Ansuman T. Stadtmauer, Edward A. Cate, Jamie H.D. Eyquem, Justin Fraietta, Joseph A. June, Carl H. Chang, Howard Y. Ye, Chun Jimmie Doudna, Jennifer A. University of California Berkeley - University of California San Francisco Graduate Program in Bioengineering University of California Berkeley BerkeleyCA United States Innovative Genomics Institute University of California Berkeley BerkeleyCA United States Division of Rheumatology Department of Medicine University of California San Francisco San FranciscoCA United States Center for Personal Dynamic Regulomes Stanford University StanfordCA United States Parker Institute for Cancer Immunotherapy Stanford University School of Medicine StanfordCA United States Biomedical Sciences Graduate Program University of California San Francisco San FranciscoCA United States Medical Scientist Training Program University of California San Francisco San FranciscoCA United States Department of Medicine University of California San Francisco San FranciscoCA United States Parker Institute for Cancer Immunotherapy San FranciscoCA United States Gladstone-UCSF Institute of Genomic Immunology San FranciscoCA United States Department of Biochemistry and Biophysics University of California San Francisco San FranciscoCA United States Abramson Cancer Center Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States Parker Institute for Cancer Immunotherapy Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States Center for Cellular Immunotherapies Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States Department of Pathology and Laboratory Medicine Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States Department of Microbiology Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States Department of Pathology Stanford University School of Medicine StanfordCA United States Division of Hematology-Oncology Department of Medicine Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States Department o

CRISPR-Cas9 genome editing has enabled advanced T cell therapies, but occasional loss of the targeted chromosome could be a safety concern. To investigate whether Cas9-induced chromosome loss is a universal phenomenon and evaluate its clinical significance, we conducted a systematic analysis in primary human T cells. Arrayed and pooled CRISPR screens revealed that partial or entire chromosome loss after Cas9-induced DNA cutting is a rare but generalized phenomenon, occurring also in pre-clinical chimeric antigen receptor T cells. T cells with chromosome loss persist for weeks in culture, implying potential interference with clinical use. A modified cell manufacturing process, employed in our first-in-human clinical trial of Cas9-engineered T cells, dramatically reduced chromosome loss while largely preserving genome editing efficacy. Expression of p53 correlated with the protection from chromosome loss observed with this protocol, suggesting both a mechanism and a strategy for T cell engineering that mitigates genotoxicity in the clinic. © 2023, The Authors. All rights reserved.

关键词： T-cells

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TRAF3 regulates the oncogenic proteins Pim2 and c-Myc to restrain survival in normal and malignant B cells (vol 9, 12884, 2019)

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SCIENTIFIC REPORTS 2019年第1期9卷 12884-12884页

作者： Whillock, Amy L. Mambetsariev, Nurbek Lin, Wai W. Stunz, Laura L. Bishop, Gail A. Department of Microbiology & Immunology University of Iowa Iowa City IA USA. Immunology Graduate Program University of Iowa Iowa City IA USA. Medical Scientist Training Program University of Iowa Iowa City IA USA. Holden Comprehensive Cancer Center University of Iowa Iowa City IA USA. Northwestern Memorial Hospital Chicago IL USA. Sanford-Burnham-Prebys Medical Discovery Institute La Jolla CA USA. Department of Microbiology & Immunology University of Iowa Iowa City IA USA. gail-bishop@uiowa.edu. Internal Medicine University of Iowa Iowa City IA USA. gail-bishop@uiowa.edu. Immunology Graduate Program University of Iowa Iowa City IA USA. gail-bishop@uiowa.edu. Medical Scientist Training Program University of Iowa Iowa City IA USA. gail-bishop@uiowa.edu. Holden Comprehensive Cancer Center University of Iowa Iowa City IA USA. gail-bishop@uiowa.edu. VA Medical Center Iowa City IA USA. gail-bishop@uiowa.edu.

TRAF3 is a versatile intracellular adapter protein with multiple context-specific roles. Uniquely in B cells, TRAF3 deficiency enhances survival and increases the risk of transformation, as loss of TRAF3 is observed in several types of B cell cancers. Here, we report a new mechanism for TRAF3 in the restraint of B cell survival. We found that TRAF3 deficiency was associated with induction of the pro-survival kinase Pim2 in mouse primary B cells and human malignant B cell lines. The increase in Pim2 was independent of NF-κB2 activation but was ameliorated with inhibition of STAT3 expression or function. TRAF3 deficiency also led to a Pim2-dependent increase in c-Myc protein levels and was associated with reduced c-Myc ubiquitination. TRAF3-deficient primary B cells were less sensitive to cell death induced by the Pim inhibitors SGI-1776 and TP-3654. Interestingly, human malignant B cell lines with low expression of TRAF3 were more sensitive to Pim inhibition-induced cell death. Combination treatment of TRAF3-deficient B cells and B cell tumor lines with c-Myc inhibitors enhanced their sensitivity to Pim inhibition, suggesting a possible therapeutic strategy. TRAF3 thus suppresses a Pim2-mediated B cell survival axis, which can be a potential target for treatment of B cell malignancies.

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75202 The New Normal: A Virtual Summer Foundations in Research

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Journal of Clinical and Translational Science 2021年第S1期5卷 62-62页

作者： Adriana Morales Gomez Kit Knier Joanna Yang Yowler Chris Pierret Linda M. Scholl Mayo Clinic Graduate School of Biomedical Sciences Mayo Clinic Rochester MN USA Mayo Clinic Medical Scientist Training Program Mayo Clinic Rochester MN USA Department of Research Mayo Clinic Jacksonville FL USA Department of Biochemistry and Molecular Biology Mayo Clinic Rochester MN USA Office of Applied Scholarship and Education Science Mayo Clinic College of Medicine Mayo Clinic Rochester MN USA

ABSTRACT IMPACT: The Summer Foundation on Research gave undergraduate students the opportunity to do research despite the new normal - COVID-19 pandemic. OBJECTIVES/GOALS: The COVID-19 pandemic prevented domestic and international undergraduate students from attending in-person Mayo Clinic Summer Undergraduate Research programs. Mayo decided to redesign this program as a virtual, 4-week Summer Foundations in Research (SFIR) program. The goal of this program was to give students a scientific research experience. METHODS/STUDY POPULATION: The SFIR included an Introduction to Experimental Design, Dialogue methodology for communicating science, scientific mentoring, asynchronous online modules and a Resiliency component. Evaluations of the program were undertaken to gather feedback for program improvement and to assess the educational and mental health impact on participants. These evaluations asked student to rate each section of the program. Additionally, students were encouraged to provide their own comments and feedback. Statistical analysis of quantitative data was performed using excel. The qualitative data was studied using the identification, analysis and interpretation of patterns method per the student’s comments on each of the questions addressed in the survey. RESULTS/ANTICIPATED RESULTS: These evaluations revealed positive outcomes across program components: 66% of the participants found the Resiliency component extremely worthwhile, 80% of participants liked the experimental design and 70% liked the educational courses. Qualitative data showed that mentor/mentee interactions were highly valued, and both participants and faculty suggested increasing the amount of time devoted to these interactions. Small group discussions gave students the opportunity to get to know other peers and encouraged further discussions about science and the community. Participants suggested minor improvements to the program, such as re-creating the online modules specific for unde

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

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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

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Bayesian multinomial logistic normal models through marginally latent matrix-T processes

arXiv

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arXiv 2019年

作者： Silverman, Justin D. Roche, Kimberly Holmes, Zachary C. David, Lawrence A. Mukherjee, Sayan Program in Computational Biology and Bioinformatics Duke University DurhamNC27708 United States Medical Scientist Training Program Duke University DurhamNC27708 United States Departments of Statistical Science Mathematics Computer Science Biostatistics & Bioinformatics Duke University DurhamNC27708 United States Center for Genomic and Computational Biology Duke University DurhamNC27708 United States Department of Molecular Genetics and Microbiology Duke University DurhamNC27708 United States

Bayesian multinomial logistic-normal (MLN) models are popular for the analysis of sequence count data (e.g., microbiome or gene expression data) due to their ability to model multivariate count data with complex covariance structure. However, existing implementations of MLN models are limited to handling small data sets due to the non-conjugacy of the multinomial and logistic-normal distributions. We introduce MLN models which can be written as marginally latent matrix-t process (LTP) models. Marginally LTP models describe a flexible class of generalized linear regression, non-linear regression, and time series models. We develop inference schemes for Marginally LTP models and, through application to MLN models, demonstrate that our inference schemes are both highly accurate and often 4-5 orders of magnitude faster than MCMC. Copyright © 2019, The Authors. All rights reserved.

关键词： Multivariant analysis

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Molecular and cellular evolution of the primate dorsolateral prefrontal cortex

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SCIENCE 2022年第6614期377卷 1511-+页

作者： Ma, Shaojie Skarica, Mario Li, Qian Xu, Chuan Risgaard, Ryan D. Tebbenkamp, Andrew T. N. Mato-Blanco, Xoel Kovner, Rothem Krsnik, Zeljka de Martin, Xabier Luria, Victor Marti-Perez, Xavier Liang, Dan Karger, Amir Schmidt, Danielle K. Gomez-Sanchez, Zachary Qi, Cai Gobeske, Kevin T. Pochareddy, Sirisha Debnath, Ashwin Hottman, Cade J. Spurrier, Joshua Teo, Leon Boghdadi, Anthony G. Homman-Ludiye, Jihane Ely, John J. Daadi, Etienne W. Mi, Da Daadi, Marcel Marin, Oscar Hof, Patrick R. Rasin, Mladen-Roko Bourne, James Sherwood, Chet C. Santpere, Gabriel Girgenti, Matthew J. Strittmatter, Stephen M. Sousa, Andre M. M. Sestan, Nenad Yale Sch Med Dept Neurosci New Haven CT 06510 USA Univ Wisconsin Madison Sch Med & Publ Hlth Waisman Ctr Madison WI 53705 USA Univ Wisconsin Madison Sch Med & Publ Hlth Med Scientist Training Program Madison WI 53705 USA Univ Pompeu Fabra Hosp Mar Med Res Inst IMIM Neurogen Grp Res Programme Biomed Informat GRIB Barcelona 08003 Spain Univ Zagreb Croatian Inst Brain Res Sch Med Zagreb 10000 Croatia Harvard Med Sch IT Res Comp Boston MA USA Yale Sch Med Div Neurocrit Care & Emergency Neurol Dept Neurol New Haven CT 06510 USA Yale Sch Med Dept Neurol Program Cellular Neurosci Neurodegenerat & Repair New Haven CT 06536 USA Monash Univ Australian Regenerat Med Inst 15 Innovat Walk Clayton Vic 3800 Australia MAEBIOS Alamogordo NM 88310 USA George Washington Univ Dept Anthropol Washington DC USA George Washington Univ Ctr Adv Study Human Paleobiol Washington DC USA Texas Biomed Res Inst Southwest Natl Primate Res Ctr San Antonio TX USA Tsinghua Univ IDG McGovern Inst Brain Res Sch Life Sci Tsinghua Peking Ctr Life Sci Beijing 100084 Peoples R China UT Hlth Long Sch Med Dept Cell Syst & Anat Radiol San Antonio TX USA NeoNeuron LLC Palo Alto CA 94306 USA Kings Coll London Inst Psychiat Psychol & Neurosci Ctr Dev Neurobiol London SE1 1UL England Kings Coll London MRC Ctr Neurodev Disorders London SE1 England Icahn Sch Med Mt Sinai Nash Family Dept Neuroscience New York NY 10029 USA Icahn Sch Med Mt Sinai Friedman Brain Inst New York NY 10029 USA Rutgers State Univ Robert Wood Johnson Med Sch Dept Neurosci & Cell Biol Piscataway NJ 08854 USA Yale Sch Med Dept Psychiat New Haven CT 06510 USA US Dept Vet Affairs Natl Ctr PTSD White River Jct VT USA Yale Sch Med Kavli Inst Neurosci New Haven CT 06510 USA Univ Wisconsin Madison Sch Med & Publ Hlth Dept Neurosci Madison WI 53705 USA Yale Sch Med Program Cellular Neurosci Neurodegenerat & Repair Dept Genet New Haven CT 06510 USA Yale Sch Med Program Cellular Neurosci Neurodegenerat & Repa

The granular dorsolateral prefrontal cortex (dlPFC) is an evolutionary specialization of primates that is centrally involved in cognition. We assessed more than 600,000 single-nucleus transcriptomes from adult human, chimpanzee, macaque, and marmoset dlPFC. Although most cell subtypes defined transcriptomically are conserved, we detected several that exist only in a subset of species as well as substantial species-specific molecular differences across homologous neuronal, glial, and non-neural subtypes. The latter are exemplified by human-specific switching between expression of the neuropeptide somatostatin and tyrosine hydroxylase, the rate-limiting enzyme in dopamine production in certain interneurons. The above molecular differences are also illustrated by expression of the neuropsychiatric risk gene FOXP2, which is human-specific in microglia and primate-specific in layer 4 granular neurons. We generated a comprehensive survey of the dlPFC cellular repertoire and its shared and divergent features in anthropoid primates.

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Direct stimulation of somatosensory cortex results in slower reaction times compared to peripheral touch in humans (vol 9, 3292, 2019)

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SCIENTIFIC REPORTS 2019年第1期9卷 1-11页

作者： Caldwell, David J. Cronin, Jeneva A. Wu, Jing Weaver, Kurt E. Ko, Andrew L. Rao, Rajesh P. N. Ojemann, Jeffrey G. Department of Bioengineering University of Washington Seattle USA. djcald@uw.edu. Medical Scientist Training Program University of Washington Seattle USA. djcald@uw.edu. National Science Foundation Center for Neurotechnology Seattle USA. djcald@uw.edu. Department of Bioengineering University of Washington Seattle USA. jcronin@uw.edu. National Science Foundation Center for Neurotechnology Seattle USA. jcronin@uw.edu. Department of Bioengineering University of Washington Seattle USA. National Science Foundation Center for Neurotechnology Seattle USA. Department of Radiology University of Washington Seattle USA. Department of Neurological Surgery University of Washington Seattle USA. Department of Computer Science and Engineering University of Washington Seattle USA.

Direct cortical stimulation (DCS) of primary somatosensory cortex (S1) could help restore sensation and provide task-relevant feedback in a neuroprosthesis. However, the psychophysics of S1 DCS is poorly studied, including any comparison to cutaneous haptic stimulation. We compare the response times to DCS of human hand somatosensory cortex through electrocorticographic grids with response times to haptic stimuli delivered to the hand in four subjects. We found that subjects respond significantly slower to S1 DCS than to natural, haptic stimuli for a range of DCS train durations. Median response times for haptic stimulation varied from 198 ms to 313 ms, while median responses to reliably perceived DCS ranged from 254 ms for one subject, all the way to 528 ms for another. We discern no significant impact of learning or habituation through the analysis of blocked trials, and find no significant impact of cortical stimulation train duration on response times. Our results provide a realistic set of expectations for latencies with somatosensory DCS feedback for future neuroprosthetic applications and motivate the study of neural mechanisms underlying human perception of somatosensation via DCS.

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