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Systems genetic dissection of Alzheimer's disease brain gene expression networks

Alzheimer's & dementia : the journal of the Alzheimer's Association 2021年第Sup2期17卷 e058716页

作者： Zhao, Pinghan Mangleburg, Carl Grant Al-Ramahi, Ismael Botas, Juan Shulman, Joshua M. Baylor College of Medicine TX Houston United States Jan and Dan Duncan Neurological Research Institute Texas Children's Hospital TX Houston United States Baylor College of Medicine Neuroscience Program TX Houston United States Baylor College of Medicine Medical Scientist Training Program TX Houston United States

BACKGROUND: Alzheimer's disease (AD) is the most prevalent cause of dementia. Large RNA-Sequencing data sets have provided detailed molecular profiles of AD, but they cannot differentiate causal vs. non-causal gene expression changes. METHOD: We combined bioinformatic prioritization of human data with genetic screens in Drosophila melanogaster to identify human brain transcriptional changes that exacerbate or ameliorate neurodegeneration induced by Tau or amyloid-β (Aβ), the proteins which form the hallmark pathologic aggregates that define AD. First, we used large, AD-associated coexpression networks derived from Accelerating Medicines Partnership (AMP)-AD human brain RNA-Seq data to nominate candidate AD drivers based on multiple bioinformatic criteria. We then tested nominated drivers for modification of Tau- or Aβ-induced neurodegeneration in vivo using a locomotor assay in Drosophila. For one module of our interest, PHGbrown, we analyzed its overlap with published differentially expressed gene (DEG) sets from mouse models to explore its potential functional roles in AD. Finally, we used the L1000 Connectivity Map database of perturbation-associated gene expression changes to select small molecules which either reverse or promote the implicated AD-associated gene expression signatures that are causally linked with disease progression. RESULT: Through our screen, we identified a module, PHGbrown, with 14 of its 27 prioritized genes (51.9%) significantly modifying Tau/Aβ neurotoxicity in our screen. We integrated our screen data with PHGbrown's module structure to identify a subnetwork containing genes involved in synaptic function including GRIN2A, GRIN2B, KCNJ6, GABRB2, and GABRB3. This synaptic subnetwork is downregulated in human AD and contains multiple loss-of-function suppressors of Tau/Aβ neurotoxicity. Interestingly, PHGbrown shows overlap and concordant down-regulation with published mouse models of excitotoxicity. Our results suggest that PHGbrown down-

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CCL5 Protects Cortical Neuron Function by Regulating M2 Microglia Activation After Mild Traumatic Brain Injury

SSRN

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SSRN 2022年

作者： Tsai, Yih-Jeng Ho, Man-Hau Yen, Chia-Hung Wang, Jia-Yi Burnouf, Thierry Chen, Chia-Yen Wang, Yun Chiang, Yung-Hsiao Hoffer, Barry J. Chou, Szu-Yi Department of Otolaryngology Head and Neck Surgery Shin Kong Wu HoSu Memorial Hospital Taipei Taiwan School of Medicine Fu Jen Catholic University New Taipei City Taiwan Ph.D. Program in Medical Neuroscience College of Medical Science and Technology Taipei Medical University National Health Research Institute Taiwan Graduate Institute of Neural Regenerative Medicine College of Medical Science and Technology Taipei Medical University Taipei Taiwan Department of Biological Science and Technology National Pingtung University of Science and Technology Neipu Pingtung91201 Taiwan Graduate Institute of Medical Sciences College of Medicine Taipei Medical University Taipei11031 Taiwan Department of Neurosurgery Taipei Medical University Hospital Taipei11031 Taiwan Neuroscience Research Center Taipei Medical University Taipei11031 Taiwan International PhD Program in Biomedical Engineering College of Biomedical Engineering Taipei Medical University Taipei Taiwan Graduate Institute of Biomedical Materials and Tissue Engineering College of Biomedical Engineering Taipei Medical University Taipei Taiwan NeuroTMULille International Laboratory Taipei Medical University Taipei Taiwan International PhD Program in Cell Therapy and Regeneration Medicine College of Medicine Taipei Medical University Taipei Taiwan Brain and Consciousness Research Centre TMU Shuang Ho Hospital New Taipei City Taiwan Center for Neuropsychiatric Research National Health Research Institutes Zhunan Miaoli County Taiwan Department of Surgery School of Medicine College of Medicine Taipei Medical University 11031 Taiwan Department of Neurosurgery Case Western Reserve University School of Medicine ClevelandOH United States Scientist Emeritus National Institutes of Health United States International Master Program in Medical Neuroscience College of Medical Science and Technology Taipei Medical University Taipei Taiwan

Cytokines and chemokines play important roles in inflammation and repair following brain injury. M1 microglia are pro-inflammatory which produce cytokines and lead to neural injury;in contrast, M2 microglia are anti-inflammatory, release neurotrophic factors, and promote neural repair processes. Chemokine CCL5, increased after TBI, shows a neuroprotective function by reducing oxidative stress. CCL5 may contribute to the balance between oxidative stress and immune responses after brain injury. Herein, we investigated the role of CCL5 in microglial polarization after mild traumatic brain injury, focusing on the cerebral cortex.C57BL/6 and CCL5 knockout (CCL5-KO) mice were given a mild traumatic brain injury (TBI) using weight-drop. Neurological parameters such as motor and sensory functions were analyzed by mNSS score, accelerating rotarod, beam walking, and adhesive removal tests. Oxidative stress and neuron damage were measured by NADPH oxidase activity, hypoxyloprobe staining and FJC. Performance of motor and sensory functions in both WT and CCL5-KO mice were impaired after brain injury which recovered after 7 days-post-injury (dpi) in the WT group but only after 14 days in the CCL5-KO mouse group. RT-qPCR analysis revealed that pro-inflammation cytokines - IL-1β, TNF-α, and IL-6 were higher in CCL5-KO mice compared to WT mice at 4 and 14 dpi. In contrast, M2-like microglia markers - IL-10 and Agr-1 were increased in WT mouse cortical tissue at 4 dpi. Oxidative stress increased both M1 and M2- related cytokine expression in BV2 cells treated with H 2 O 2;CCL5 treatment increased M2- but suppressed M1- related cytokine gene activation. Intranasal delivery of CCL5 reduced neuronal oxidative stress, increased IL-10 expression and improved motor and sensory functions in CCL5-KO mice after brain *** summary, CCL5, which alters immune responses and protects neurons from TBI damage, has an important function in regulating M2-like microglial polarization during post-

关键词： Polarization

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The acoustic properties, syllable structure, and syllable sequences of ultrasonic vocalizations (USVs) during neonatal opioid withdrawal in FVB/N mouse substrains

Addiction Neuroscience

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Addiction neuroscience 2025年

作者： Kelly K. Wingfield Teodora Misic Sophia A. Miracle Carly S. McDermott Kaahini Jain Nalia M. Abney Kayla T. Richardson Mia B. Rubman Jacob A. Beierle Elisha M. Wachman Camron D. Bryant Laboratory of Addiction Genetics Center for Drug Discovery Department of Pharmaceutical Sciences Northeastern University Boston MA USA T32 Biomolecular Pharmacology Training Program Boston University Chobanian & Avedisian School of Medicine Boston MA USA Graduate Program for Neuroscience Boston University Boston MA USA Post-Baccalaureate Research Education Program Boston University Chobanian & Avedisian School of Medicine NIH/NIDA Summer Undergraduate Fellowship Program Transformative Training Program in Addiction Science Boston University Chobanian & Avedisian School of Medicine Department of Pediatrics Boston University Chobanian & Avedisian School of Medicine Boston Medical Center Boston MA USA

Concomitant with the opioid epidemic, there has been a rise in pregnant women diagnosed with opioid use disorder and infants born with neonatal opioid withdrawal syndrome (NOWS). NOWS refers to withdrawal signs following cessation of prenatal opioid exposure that comprise neurological, gastrointestinal, and autonomic system dysfunction. A critical indicator of NOWS severity is excessive, high-pitched crying. However, NOWS evaluation is mostly subjective, and additional cry features may not be easily recognized during clinical assessment. Thus, there is a need for more objective measures of NOWS severity. We used a third trimester-approximate opioid exposure paradigm to model NOWS traits in genetically similar inbred substrains of FVB/N mice (NJ, NCrl, NHsd, and NTac). Pups were injected twice daily from postnatal day 1 (P1) to P14 with morphine (10 mg/kg, s.c.) or saline (20 microliters/g, s.c.). Because there were very few minor substrain differences in spontaneous withdrawalinduced ultrasonic vocalization (USV) profiles, we collapsed across substrains to evaluate the effects of morphine withdrawal on additional USV properties. We identified syllable sequences unique to morphine-withdrawn and saline-control FVB/N pups on P7 and P14. We also observed an effect of spontaneous morphine withdrawal on the acoustic properties of USVs on P7 and P14. Some withdrawal traits correlated with acoustic properties of USVs in morphine-withdrawn FVB/N pups on P7 and P14. This in-depth investigation of mouse USV features during spontaneous neonatal opioid withdrawal has implications for predicting neonatal opioid withdrawal severity in mice and applying objective approaches to understanding cries in human infants suffering from NOWS.

关键词： neonatal abstinence syndrome reduced complexity cross opiate opioid use disorder fentanyl

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Single-cell panleukemia signatures of HSPC-like blasts predict drug response and clinical outcome

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Blood 2025年第23期145卷 2685-2700页

作者： Chen, Changya Xu, Jason Sussman, Jonathan H. Vincent, Tiffaney Tumulty, Joseph S. Yoshimura, Satoshi Alikarami, Fatemeh Yu, Wenbao Ding, Yang-yang Chen, Chia-hui Li, Elizabeth Y. Yang, Austin Qin, Xiaohuan Bandyopadhyay, Shovik Peng, Jacqueline Pölönen, Petri Newman, Haley Wood, Brent L. Hu, Jianzhong Shraim, Rawan Hughes, Andrew D. Diorio, Caroline Uppuluri, Lahari Shi, Gongping Ryan, Theresa Fuller, Tori Loh, Mignon L. Raetz, Elizabeth A. Hunger, Stephen P. Pounds, Stanley B. Mullighan, Charles G. Frank, David Yang, Jun J. Bernt, Kathrin M. Teachey, David T. Tan, Kai State Key Laboratory of Experimental Hematology National Clinical Research Center for Blood Diseases Haihe Laboratory of Cell Ecosystem Institute of Hematology and Blood Diseases Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Tianjin China Tianjin Institutes of Health Science Tianjin China Division of Oncology and Center for Childhood Cancer Research Children's Hospital of Philadelphia Philadelphia PA Graduate Group in Genomics and Computational Biology Perelman School of Medicine University of Pennsylvania Philadelphia PA Medical Scientist Training Program Perelman School of Medicine University of Pennsylvania Philadelphia PA Department of Pharmacy and Pharmaceutical Sciences St. Jude Children's Research Hospital Memphis TN United States Department of Pediatrics Perelman School of Medicine University of Pennsylvania Philadelphia PA Departments of Oncology and Pediatrics Johns Hopkins University School of Medicine and Sidney Kimmel Comprehensive Cancer Center Baltimore MD School of Medicine Yale University New Haven CT Graduate Group in Cell and Molecular Biology University of Pennsylvania Philadelphia PA Department of Pathology St. Jude Children's Research Hospital Memphis TN United States Department of Pathology and Laboratory Medicine Children's Hospital Los Angeles Los Angeles CA Induced Proximity Platform Amgen Thousand Oaks CA United States Ben Towne Center for Childhood Cancer and Blood Disorders Research Seattle Children's Hospital Seattle WA United States Division of Pediatric Hematology Oncology Bone Marrow Transplant and Cellular Therapy Seattle Children's Hospital Seattle WA United States Department of Pediatrics and Perlmutter Cancer Center New York University Langone Health New York NY Department of Biostatistics St. Jude Children's Research Hospital Memphis TN United States Hematological Malignancies Program St. Jude Children's Research Hospital Memphis TN United States Division of Cardiology Childre

The critical role of leukemia-initiating cells as a therapy-resistant population in myeloid leukemia is well established. However, the molecular signatures of such cells in acute lymphoblastic leukemia remain underexplored. Moreover, their role in therapy response and patient prognosis is yet to be systematically investigated across various types of acute leukemia. We used single-cell multiomics to analyze diagnostic specimens from 96 pediatric patients with acute lymphoblastic, myeloid, and lineage-ambiguous leukemias. Through the integration of single-cell multiomics with extensive bulk RNA sequencing and clinical data sets, we uncovered a prevalent, chemotherapy-resistant subpopulation that resembles hematopoietic stem and progenitor cells (HSPC-like) and is associated with poor clinical outcomes across all subtypes investigated. We identified a core transcriptional regulatory network (TRN) in HSPC-like blasts that is combinatorially controlled by HOXA/AP1/CEBPA. This TRN signature can predict chemotherapy response and long-term clinical outcomes. We identified shared potential therapeutic targets against HSPC-like blasts, including FLT3, BCL2, and the PI3K pathway. Our study provides a framework for linking intratumoral heterogeneity with therapy response, patient outcomes, and the discovery of new therapeutic targets for pediatric acute leukemias. © 2025 American Society of Hematology

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Electron spin dynamics guide cell motility

arXiv

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arXiv 2025年

作者： Wang, Kai Gilmer, Gabrielle Araña, Matheus Cândia Iijima, Hirotaka Bergmann, Juliana Woollard, Antonio Mesits, Boris McGraw, Meghan Zoltowski, Brian Cappellaro, Paola Ungar, Alex Pekker, David Waldeck, David H. Saxena, Sunil Lloyd, Seth Ambrosio, Fabrisia Discovery Center for Musculoskeletal Recovery Schoen Adams Research Institute at Spaulding BostonMA United States Department of Physical Medicine & Rehabilitation Spaulding Rehabilitation Hospital BostonMA United States Department of Physical Medicine & Rehabilitation Harvard Medical School BostonMA United States Cellular and Molecular Pathology Graduate Program University of Pittsburgh PittsburghPA United States Medical Scientist Training Program School of Medicine University of Pittsburgh PittsburghPA United States École Polytechnique Institut Polytechnique de Paris Palaiseau France Department of Physics & Astronomy University of Pittsburgh PittsburghPA United States Department of Chemistry Southern Methodist University DallasTX United States Department of Nuclear Science and Engineering Massachusetts Institute of Technology CambridgeMA02139 United States Department of Physics Massachusetts Institute of Technology CambridgeMA02139 United States Department of Chemistry University of Pittsburgh PittsburghPA United States Department of Mechanical Engineering Massachusetts Institute of Technology BostonMA United States

Diverse organisms exploit the geomagnetic field (GMF) for migration. Migrating birds employ an intrinsically quantum mechanical mechanism for detecting the geomagnetic field: absorption of a blue photon generates a radical pair whose two electrons precess at different rates in the magnetic field, thereby sensitizing cells to the direction of the GMF. In this work, using an in vitro injury model, we discovered a quantum-based mechanism of cellular migration. Specifically, we show that migrating cells detect the GMF via an optically activated, electron spin-based mechanism. Cell injury provokes acute emission of blue photons, and these photons sensitize muscle progenitor cells to the magnetic field. We show that the magnetosensitivity of muscle progenitor cells is (a) activated by blue light, but not by green or red light, and (b) disrupted by the application of an oscillatory field at the frequency corresponding to the energy of the electron-spin/magnetic field interaction. A comprehensive analysis of protein expression reveals that the ability of blue photons to promote cell motility is mediated by activation of calmodulin calcium sensors. Collectively, these data suggest that cells possess a light-dependent magnetic compass driven by electron spin dynamics. © 2025, CC BY.

关键词： Spin dynamics

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STIMULUS-INDEPENDENT ACTIVITY IN THE DEVELOPING BRAIN: A PERSPECTIVE FROM THE FLY

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IBRO neuroscience Reports 2023年 15卷 S45-S45页

作者： Sassan Suarez Jun Reichl Harpreet Randhawa Orkun Akin University California Los Angeles Neuroscience Interdepartmental Program Los Angeles United States of America David Geffen School of Medicine University California Los Angele Medical Scientist Training Program Los Angeles United States of America David Geffen School of Medicine University California Los Angeles Department Of Neurobiology Los Angeles United States of America

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Single-Cell and Bulk RNA Sequencing Analysis of Adult Patients with Acute Myeloid Leukemia to Identify Potential for Transferability of Pediatric Trivalent CAR-T Approaches

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Transplantation and Cellular Therapy 2025年第2期31卷 S203-S203页

作者： Seir, Gabriel E, BS Bubb, Quenton Rashawn, MPhil, PhD Salzman, Gabriel, MD, PhD Czechowicz, Agnieszka, MD, PhD Zhang, Tian Y, MD, PhD Kennedy, Vanessa E, MD Department of Bioengineering Stanford University Stanford CA Stem Cell Biology and Regenerative Medicine Graduate Program Medical Scientist Training Program Stanford University Stanford CA Hematology and Medical Oncology Fellowship Program Stanford Health Care Stanford California Stanford University Stanford CA Department of Pediatrics； Division of Hematology Oncology Stem Cell Transplantation and Regenerative Medicine Stanford University School of Medicine Stanford CA Department of Medicine Division of Hematology Stanford University Stanford CA Division of Blood and Marrow Transplantation & Cellular Therapy Stanford University Stanford CA

IntroductionChimeric antigen receptor (CAR) T-cells have shown success in B-cell malignancies but have yet to extend to acute myeloid leukemia (AML) due to disease heterogeneity hindering targeting with mono or even bivalent CARs. Our group previously engineered a trivalent CAR targeting the KIT, MPL, and FLT3 hematopoietic receptors based on bulk and single-cell (SC) RNA-seq analysis from pediatric AML samples showing specificity of these targets to stem-like compartments and potent activity in xenograft murine models. We investigated if this approach could extend to adult AML. MethodsWe used data from The Cancer Genome Atlas (TCGA) (n = 173) and BEAT AML (n = 395) to analyze bulk expression of KIT, MPL and FLT3 across AML genetic subtypes. We used a published dataset of newly diagnosed AML (van Galen et al, 2019; n = 16) to analyze SC expression by cell type and differentiation state (assessed via CytoTRACE). Data analysis was conducted via Seurat. ResultsAt the bulk-RNA level, at least one of KIT, MPL, or FLT3 was expressed in >85% of patients in both cohorts. A high proportion of tumors with ELN adverse-risk disease had expression ≥1 of the putative targets, at 84.4% (n=45) and 90.0% (n=148) for TCGA and BEAT AML, respectively. Notably, 100% (n=5) and 88.0% (n=25) of TP53-mutant tumors and 91.9% (n=37) and 91.1% (n=202) of poor cytogenetic tumors had ≥1 gene expressed. Triple-negative tumors were rare, at 13.8% and 14.6%. Of these triple-negative tumors, no single genetic subtype was over-represented, and most were intermediate-risk disease. Expression of any combination of KIT, MPL, and FLT3, was not associated with overall survival in either dataset. SC RNA-seq analysis showed KIT was highly expressed, largely confined to immature blasts with high differentiation potential (CytoTRACE score close to 1). Further, differential expression of FLT3 was observed among most leukemic cells, some expression in non-malignant myeloid cells, and minimal expression in lymph

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Regulation of sister chromatid cohesion by nuclear PD-L1

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细胞研究（英文版） 2020年第7期30卷 590-601页

作者： Jia Yu Bo Qin Ann M.Moyer Somaira Nowsheen Xinyi Tu Haidong Dong Judy C.Boughey Matthew P.Goetz Richard Weinshilboum Zhenkun Lou Liewei Wang Department of Molecular Pharmacology and Experimental Therapeutics Mayo Clinic Rochester MN 55905 USA Department of Oncology Mayo Clinic Rochester MN 55905USA Department of Laboratory Medicine and Pathology Mayo Clinic Rochester MN 55905 USA Mayo Clinic Graduate School of Biomedical Sciences Mayo Clinic School of Medicine and the Mayo Clinic Medical Scientist Training Program Mayo Clinic Rochester MN 55905 USA Departments of Urology and Immunology Mayo Clinic Rochester MN 55905 USA Department of Surgery Mayo Clinic Rochester MN 55905 USA

programmed death ligand-1 (PD-L1 or B7-H1) is well known for its role in immune checkpoint regulation,but its function inside the tumor cells has rarely been *** we report that nuclear PD-L1 is important for cancer cell sister chromatid *** found that depletion of PD-L1 suppresses cancer cell proliferation,colony formation in vitro,and tumor growth in vivo in immunedeficient NSG mice independent of its role in immune ***,PD-L1 functions as a subunit of the cohesin complex,and its deficiency leads to formation of multinucleated cells and causes a defect in sister chromatid ***,PD-L1 compensates for the loss of Sororin,whose expression is suppressed in cancer cells overexpressing ***-L1 competes with Wing Apart-Like (WAPL) for binding to PDS5B,and secures proper sister chromatid cohesion and *** findings suggest an important role for nuclear PD-L1 in cancer cells independent of its function in immune checkpoint.

关键词： Cell division Oncogenes

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Engineered Invariant Natural Killer T Cells (iNKT cells) Targeting CD 117 As a Novel Treatment for Acute Myeloid Leukemia.

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Transplantation and Cellular Therapy 2025年第2期31卷 S201-S202页

作者： Boonchalermvichian, Chaiyaporn, MD, PhD Yan, Hao, PhD Baker, Jeanette Bubb, Quenton Rashawn, MPhil, PhD Gupta, Biki, PhD Czechowicz, Agnieszka, MD, PhD Negrin, Robert S., MD Division of Blood and Marrow Transplantation & Cellular Therapy Stanford University School of Medicine Stanford CA Department of Medicine Division of Blood and Marrow Transplantation Stanford University School of Medicine Stanford CA Stem Cell Biology and Regenerative Medicine Graduate Program Medical Scientist Training Program Stanford University Stanford CA Department of Pediatrics； Division of Hematology Oncology Stem Cell Transplantation and Regenerative Medicine Stanford University School of Medicine Stanford CA

BackgroundOur research aims to develop a CAR based therapy for the treatment of acute myeloid leukemia (AML) using engineered invariant natural killer T (iNKT) cells targeting the CD117 molecule. iNKT cells are specialized subset of innate T cells with an invariant T-cell receptor that have demonstrated cytotoxicity against cancer cells, making them a promising candidate for adoptive cell therapy. Moreover, their ability to suppress or prevent graft-versus-host disease (GVHD) while maintaining potent antitumor activity makes iNKT cells a possible " off-the-shelf" product for treating various hematologic and solid tumor malignancies. MethodsPeripheral blood mononuclear cells were isolated by gradient centrifugation from buffy coats using Ficoll Pague Plus Media, followed by enrichment using anti-iNKT microbeads. Stimulation of iNKT cells with irradiated allogeneic PBMC, α-Galcer, and key cytokines (IL2, IL15, IL21) on days 0 and 10 facilitated expansion. After 14 days of expansion (67-80-fold expansion), the iNKT cells were transduced with an MSGV1 gamma-retroviral vector that was modified to include a CAR sequence. CAR constructs consist of single chain variable fragment (scFv) binding to CD117. The fibronectin enhanced retroviral transduction of human iNKT cells achieved transfection efficacies ranging from 72% – 91.2%, depending on donors. In vitro cytotoxicity assay was done by co-culturing either CD117- CAR-iNKT cells or CD117- CAR-T cells (effector cells) with luciferase-transduced CD117 leukemia cell lines (target cells) for 24 hours. To study the impact of CD117 CAR iNKT cells in vivo(Figure 1), NSG mice (6 mice per group) were irradiated (250 cGy/ mouse) on D0 and engrafted with luc-transduced CD117 leukemia cell lines (Kasumi-1) on D4. Mice were treated with either 1.5 × 10 7 CD117- CAR-iNKT cells or untransduced iNKT cells, 3 days after the engraftment of leukemia cell lines to compare efficacy and mortality. Animals also received IL2 intraperitoneally (1,

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55564 Interactive mindfulness and dialogue sessions are integral components of research training.

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Journal of Clinical and Translational Science 2021年第S1期5卷 64-65页

作者： Kit Knier Adriana Morales Gomez 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: This work demonstrates the integration of interactive mindfulness and dialogue sessions in curricula is both desired by students and effective in conferring resilience, a protective factor that may aid in maintaining wellbeing of trainees interested in pursuing graduate studies in biomedical research and science. OBJECTIVES/GOALS: To support student futures in the field of biomedicine, Mayo Clinic graduate School of Biological Sciences utilized digital platforms to deliver a summer research program in the summer of 2020. One goal of this program, in addition to scholastic outcomes and research experience, was to support and improve the wellbeing of college student participants. METHODS/STUDY POPULATION: Following the cancellation of in-person summer research programs, students were invited to attend a digital Summer Foundations in Research program. The 4-week program included 4 small group dialogue sessions led by trained facilitators and 4 large group mindfulness seminars followed with 3 Q/A style small group sessions. Surveys were delivered on days 1, 27, and 3 months following the program. Wellbeing measures included Brief Resilience, Perceived Stress, and Satisfaction with Life Scales. Students were prompted to indicate how worthwhile they found course components and comment on why they rated each component the way they did. Wellbeing results were assessed using paired t-tests with Bonferroni correction for multiple comparisons. Thematic analysis was used to interpret qualitative results. RESULTS/ANTICIPATED RESULTS: Students improved across all wellbeing measures at the program conclusion, including resilience (mean difference(SE) pre- to post-program +0.22(0.06) p=0.0007), perceived stress (-1.71(0.66) p=0.0116), and life satisfaction (+1.57(0.52) p=0.0037). Gains in resilience were maintained 3 months out (pre-program to 3 month survey +0.28(0.06) p<0.0001). To our surprise, mindfulness was the highest rated component of the research program

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