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Systemic factors as mediators of brain homeostasis, ageing and neurodegeneration (vol 21, pg 93, 2020)

NATURE REVIEWS NEUROSCIENCE 2020年第5期21卷 298-298页

作者： Pluvinage, John V. Wyss-Coray, Tony Medical Scientist Training Program Stanford University School of Medicine Stanford CA USA Stem Cell Biology and Regenerative Medicine Graduate Program Stanford University School of Medicine Stanford CA USA Department of Neurology and Neurological Sciences Stanford University School of Medicine Stanford CA USA Veterans Administration Palo Alto Healthcare System Palo Alto CA USA Paul F. Glenn Center for the Biology of Aging Stanford University School of Medicine Stanford CA USA Wu Tsai Neurosciences Institute Stanford University Stanford CA USA

A rapidly ageing population and a limited therapeutic toolbox urgently necessitate new approaches to treat neurodegenerative diseases. Brain ageing, the key risk factor for neurodegeneration, involves complex cellular and molecular processes that eventually result in cognitive decline. Although cell-intrinsic defects in neurons and glia may partially explain this decline, cell-extrinsic changes in the systemic environment, mediated by blood, have recently been shown to contribute to brain dysfunction with age. Here, we review the current understanding of how systemic factors mediate brain ageing, how these factors are regulated and how we can translate these findings into therapies for neurodegenerative diseases.

关键词： Alzheimer's disease Neural ageing Neuroimmunology Parkinson's disease

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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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Combining multiplexed functional data to improve variant classification

arXiv

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arXiv 2025年

作者： Calhoun, Jeffrey D. Dawood, Moez Rowlands, Charlie F. Fayer, Shawn Radford, Elizabeth J. McEwen, Abbye E. Turnbull, Clare Spurdle, Amanda B. Starita, Lea M. Jagannathan, Sujatha Ken and Ruth Davee Department of Neurology Northwestern Feinberg School of Medicine ChicagoIL United States Human Genome Sequencing Center Baylor College of Medicine HoustonTX United States Department of Molecular and Human Genetics Baylor College of Medicine HoustonTX United States Medical Scientist Training Program Baylor College of Medicine HoustonTX United States Division of Genetics and Epidemiology The Institute of Cancer Research London United Kingdom Brotman Baty Institute for Precision Medicine SeattleWA United States Department of Genome Sciences University of Washington SeattleWA United States Wellcome Sanger Institute HinxtonCB10 1SA United Kingdom Department of Pediatrics University of Cambridge Cambridge Biomedical Campus Level 8 CambridgeCB2 0QQ United Kingdom Department of Laboratory Medicine and Pathology University of Washington Seattle United States Population Health Program QIMR Berghofer Medical Research Institute HerstonQLD4006 Australia Faculty of Medicine The University of Queensland BrisbaneQLD4006 Australia Department of Biochemistry and Molecular Genetics University of Colorado Anschutz Medical Campus AuroraCO United States RNA Bioscience Initiative University of Colorado Anschutz Medical Campus AuroraCO United States

With the surge in the number of variants of uncertain significance (VUS) reported in ClinVar in recent years, there is an imperative to resolve VUS at scale. Multiplexed assays of variant effect (MAVEs), which allow the functional consequence of 100s to 1000s of genetic variants to be measured in a single experiment, are emerging as a source of evidence which can be used for clinical gene variant classification. Increasingly, there are multiple published MAVEs for the same gene, sometimes measuring different aspects of variant impact. Where multiple functional consequences may need to be considered to get a more complete understanding of variant effects for a given gene, combining data from multiple MAVEs may lead to the assignment of increased evidence strength which could impact variant classifications. Here, we provide guidance for combining such multiplexed functional data, incorporating a stepwise process from data curation and collection to model generation and validation. We illustrate the potential of this approach by showing the integration of multiplexed functional data from four MAVEs for the gene TP53. By following these steps, researchers can maximize the value of MAVEs, strengthen the functional evidence for clinical variant classification, reclassify more VUS, and potentially uncover novel mechanisms of pathogenicity for clinically relevant genes. © 2025, CC BY.

关键词： Genome

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The emerging role of microbiota derived SCFAs in neurodegenerative disorders

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Brain, Behavior, and Immunity - Health 2025年 46卷 101012-101012页

作者： Wachamo, Samuel Gaultier, Alban Department of Neuroscience University of Virginia Charlottesville VA United States Neuroscience Graduate Program University of Virginia Charlottesville VA United States Center for Brain Immunology and Glia University of Virginia Charlottesville VA United States Medical Scientist Training Program School of Medicine University of Virginia Charlottesville VA United States

The microbiota-gut-brain axis (MGBA), the bidirectional communication network between the gastrointestinal tract and the central nervous system, plays a significant role in the pathophysiology of neurodegenerative disorders. Emerging research highlights how gut microbiota dysbiosis, or an imbalance in the microbial community, is linked to the etiology and pathology of these conditions. Microbiota dysbiosis leads to changes in the production of microbial metabolites, such as short-chain fatty acids (SCFAs), which can cross the intestinal barrier and influence the brain either directly or indirectly. Understanding the mechanisms by which dysfunction in the MGBA contributes to neurodegeneration opens potential avenues for novel therapeutic strategies, including microbiota-targeted interventions. This review introduces the MGBA, discusses the role of SCFAs within the MGBA in the context of neurodegenerative disorders, and suggests future research directions. © 2025 The Authors

关键词： Dysbiosis Microbiota Microbiota-gut-brain axis (MGBA) Neurodegenerative disorders Short-chain fatty acids (SCFAs)

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STAT1-mediated interferon signatures are associated with preclinical JAK inhibitor sensitivity in T-ALL

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Blood 2025年第23期145卷 2793-2798页

作者： Xu, Jason Sussman, Jonathan H. Yang, Austin Yoshimura, Satoshi Hu, Jianzhong Chen, Changya Vincent, Tiffaney Bandyopadhyay, Shovik Li, Elizabeth Y. Lim, Tristan Elghawy, Omar Barsouk, Adam Karanfilovski, Damjan Wald, Shira L. Chen, Gregory M. Wu, David Newman, Haley Li, Alexander Sun, Yusha Chen, Chia-Hui Bernt, Kathrin Wood, Brent L. Winter, Stuart S. Dunsmore, Kimberly P. Raetz, Elizabeth Devidas, Meenakshi Pounds, Stanley Loh, Mignon Hunger, Stephen P. Chiang, Mark Y. Diorio, Caroline Di Giacomo, Danika Pölönen, Petri Mullighan, Charles G. Yang, Jun J. Tan, Kai Teachey, David T. Graduate Group in Genomics and Computational Biology Perelman School of Medicine University of Pennsylvania Philadelphia PA United States Medical Scientist Training Program Perelman School of Medicine University of Pennsylvania Philadelphia PA United States Division of Oncology and Center for Childhood Cancer Research Children's Hospital of Philadelphia Philadelphia PA United States Department of Pharmacy and Pharmaceutical Sciences St. Jude Children's Research Hospital Memphis TN United States Graduate Group in Cell and Molecular Biology University of Pennsylvania Philadelphia PA United States Department of Pediatrics Yale School of Medicine New Haven CT United States Department of Internal Medicine Perelman School of Medicine University of Pennsylvania Philadelphia PA United States Department of Pathology Perelman School of Medicine University of Pennsylvania Philadelphia PA United States Department of Pediatrics Perelman School of Medicine University of Pennsylvania Philadelphia PA United States Department of Pathology and Laboratory Medicine Children's Hospital Los Angeles Los Angeles CA United States Division of Hematology Oncology Children's Minnesota Eagan MN United States Division of Oncology University of Virginia Health Sciences Center Charlottesville VA United States Department of Pediatrics New York University Langone Health New York NY United States Department of Biostatistics St. Jude Children's Research Hospital Memphis TN United States 1Ben Towne Center for Childhood Cancer Research Seattle Children's Hospital Fred Hutch Cancer Center University of Washington Seattle WA United States Division of Hematology and Oncology University of Michigan Ann Arbor MI United States Department of Pathology St. Jude Children's Research Hospital Memphis TN United States Department of Chemistry Biology and Biotechnology University of Perugia Via del Giochetto Perugia Italy Center for Single-Cell Biology Children's Hospital of Philadelp

We used single-cell genomics to characterize a patient with T-cell acute lymphoblastic leukemia treated on the Children's Oncology Group AALL0434 with poor clinical outcome despite favorable genomic features, identifying a STAT1-mediated interferon-related transcriptional signature and inflammatory microenvironment associated with sensitivity to small-molecule JAK inhibition. © 2025 American Society of Hematology

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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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Food DNA Sequencing Reveals Associations between Dietary Perturbations and Patient Outcomes in Hematopoietic Stem Cell Transplant

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Transplantation and Cellular Therapy 2024年第2期30卷 S132-S132页

作者： Zeng, Jun Bergens, Matthew Jiang, Sharon Petrone, Brianna Bush, Amy Johnson, Ernaya Hill, Lauren David, Lawrence, PhD Sung, Anthony D, MD Department of Molecular Genetics & Microbiology Duke University School of Medicine Durham NC Division of Hematologic Malignancies and Cellular Therapy Duke University School of Medicine Durham NC Medical Scientist Training Program Duke University School of Medicine Durham NC Duke Cancer Institue Durham NC

Malnutrition affects 80% of cancer patients and is a well-documented prognostic factor for survival. However, assessing dietary patterns has been challenging as dietary recall surveys are limited by memory and literacy. To overcome these limitations, we leveraged a novel food DNA sequencing pipeline,FoodSeq, which amplifies and sequences plant and animal DNA markers derived from residual food materials found in stool samples. This permits retroactive examination of patients’ diets at various timepoints pre- and post-transplant. We applied FoodSeq to stool samples collected from 162 patients with hematologic malignancies who underwent hematopoietic stem cell transplantation (HCT) from 2015 to 2021. FoodSeq illuminated multiple unique clinical findings from the stool samples of our cohort. Principal component analysis (PCA) on abundances of food taxa showed significant changes in patients' diet across HCT timeline (PERMANOVA p = 0.001) (Figure 1). The first principal component (PC1) captures overall consumption of common foods, whereas the second (PC2) moderately reflect food preferences. This highlights that patients experienced a dietary perturbation during transplant. We next evaluate how patients' dietary quality changed during HCT. We evaluated patients’ diet using plant and animal metabarcoding diversity (referred to as pMR and aMR respectively) across HCT timeline and observed a significant reduction of plant dietary diversity (pMR) within the first 4 weeks post-transplant (Figure 2). Also, we found a significant reduction of animal dietary diversity (aMR) within the first 3 weeks post-transplant, but not on week 4 (p=0.067). To evaluate how diet correlates to engraftment outcomes, we compared by transplant type and conditioning regimen intensity using the same PC1 and pMR data sets in stool samples collected in the first two-weeks post-transplant. Taxonomic abundance (PC1) was negatively correlated with faster platelet recovery (the first of three consecutive

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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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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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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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