Symposium on Aging May 20, 2019
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Beth Stevens: Casting Immune Cells As Brain Sculptors
Spectrum | Autism Research News https://www.spectrumnews.org PROFILES Beth Stevens: Casting immune cells as brain sculptors BY NICHOLETTE ZELIADT 24 SEPTEMBER 2015 Shortly after Beth Stevens launched her lab at Boston Children’s Hospital in 2008, she invited students from the Newton Montessori School, in a nearby suburb, to come for a visit. The children peered at mouse and rat brains bobbing in fluid-filled jars. They also learned how to position delicate slices of brain tissue on glass slides and inspect them with a microscope. This visit sparked a running relationship with the school, with a steady stream of students visiting the growing lab each year. Soon it became too complicated to bring so many children to the lab, so Stevens decided to take her neuroscience lessons on the road, visiting a number of local elementary schools each year. Last year, she dropped in on the classrooms of her 5- and 8-year- old daughters, Zoe and Riley. “The kids got really excited,” Stevens says. “It’s become such a thing that the principal wants me to come back for the whole school.” Stevens’ enthusiasm for science has left a lasting impression on researchers, too. Her pioneering work points to a surprise role in brain development for microglia, a type of cell once considered to simply be the brain’s immune defense system, cleaning up cellular debris, damaged tissue and pathogens. But thanks to Stevens, researchers now appreciate that these non-neuronal cells also play a critical role in shaping brain circuits. In a 2012 discovery that created a buzz among autism researchers, Stevens and her colleagues discovered that microglia prune neuronal connections, called synapses, in the developing mouse brain. -
PREDICTD: Parallel Epigenomics Data Imputation with Cloud-Based Tensor Decomposition
bioRxiv preprint doi: https://doi.org/10.1101/123927; this version posted April 4, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. PREDICTD: PaRallel Epigenomics Data Imputation with Cloud-based Tensor Decomposition Timothy J. Durham Maxwell W. Libbrecht Department of Genome Sciences Department of Genome Sciences University of Washington University of Washington J. Jeffry Howbert Jeff Bilmes Department of Genome Sciences Department of Electrical Engineering University of Washington University of Washington William Stafford Noble Department of Genome Sciences Department of Computer Science and Engineering University of Washington April 4, 2017 Abstract The Encyclopedia of DNA Elements (ENCODE) and the Roadmap Epigenomics Project have produced thousands of data sets mapping the epigenome in hundreds of cell types. How- ever, the number of cell types remains too great to comprehensively map given current time and financial constraints. We present a method, PaRallel Epigenomics Data Imputation with Cloud-based Tensor Decomposition (PREDICTD), to address this issue by computationally im- puting missing experiments in collections of epigenomics experiments. PREDICTD leverages an intuitive and natural model called \tensor decomposition" to impute many experiments si- multaneously. Compared with the current state-of-the-art method, ChromImpute, PREDICTD produces lower overall mean squared error, and combining methods yields further improvement. We show that PREDICTD data can be used to investigate enhancer biology at non-coding human accelerated regions. PREDICTD provides reference imputed data sets and open-source software for investigating new cell types, and demonstrates the utility of tensor decomposition and cloud computing, two technologies increasingly applicable in bioinformatics. -
October 2004
Myelin Repair Foundation Research Progress Summary October 2004 This summary outlines progress made by the Myelin Repair Foundation research team since June 2004 and includes findings from on-going research funded by other sources that members of the team found relevant to MRF research plan. Since the success of MRF is dependent on collaboration, rather than reporting on the progress of individual projects, this report describes progress towards MRF’s overall research goals and the contributions of various team members towards completing our understanding of critical aspects of myelination and how it is affected by the multiple sclerosis (MS) disease process. 1. Fundamental control of myelination: There are several MRF investigations focused on understanding the processes that control both myelination in development and remyelination after myelin loss due to inflammation and cell death: • Dr. Ben Barres’ lab has screened thousands of genes and identified 46 genes, specific to the myelination process, that show significantly higher or lower activity levels during developmental myelination than before or after the myelination process. In addition, Dr. Barres’ lab has demonstrated the timing of these changes during the developmental myelination process. The next step is to analyze the function of each of these 46 genes by artificially controlling its level of activity (expression) and observing the effect it has on myelin formation. Finding ways to artificially manipulate the expression of each gene is a formidable task. Although the functional analysis of each gene in this group is a significant project that may take several years to complete because of the large number of genes to be analyzed, the initial identification of these active genes is providing clues to other MRF researchers that will help prioritize which genes to evaluate first and which to ignore. -
NEUROBIOLOGY and Historical Perspective
sensation and central pattern generators. Relevant genetic techniques NEUROBIOLOGY and historical perspective. Student presentation. 4 units, Aut (Clandinin, Goodman) alternate years, not given 2004-05 Chair: Eric I. Knudsen Professors: Ben Barres, Eric I. Knudsen, Uel J. McMahan, William T. NBIO 218. Neural Basis of Behavior—Advanced seminar. The princi- Newsome, Eric M. Shooter, Howard Schulman, Lubert Stryer ples of information processing in the vertebrate central nervous system, Assistant Professor: Thomas Clandinin, Tirin Moore, Jennifer Raymond and the relationship of functional properties of neural systems with perception and behavior. Emphasis is on the visual and auditory systems. Department Offices: Fairchild Building, Second Floor Original papers, directed discussions, and student presentations. Mail Code: 94305-5125 Prerequisite: 200 or consent of instructor. Courses given in Neurobiology have the subject code NBIO. For a 4 units (Knudsen, Raymond) alternate years, given 2004-05 complete list of subject codes, see Appendix B. NBIO 220. Central Mechanisms in Visual Perception—Contempo- GRADUATE PROGRAM rary visual neuroscience, emphasizing the neural mechanisms underly- ing primate vision and visually guided behavior. Seven foundational Graduate students in the Department of Neurobiology obtain the Ph.D. topics in visual neuroscience; current papers concerning each topic. degree through the interdepartmental Neurosciences Ph.D. program. Student presentations. Computer-based demonstration exercises. Accepted students receive funding for tuition and a living stipend. Ap- 2-4 units, Spr (Newsome) alternate years, not given 2004-05 plicants should familiarize themselves with the research interests of the faculty and, if possible, indicate their preference on the application form NBIO 221. Frontiers in Translational Medicine—Pathways for com- which is submitted directly to the Neurosciences Program. -
Manolis Kellis Piotr Indyk
6.095 / 6.895 Computational Biology: Genomes, Networks, Evolution Manolis Kellis Rapid database search Courtsey of CCRNP, The National Cancer Institute. Piotr Indyk Protein interaction network Courtesy of GTL Center for Molecular and Cellular Systems. Genome duplication Courtesy of Talking Glossary of Genetics. Administrivia • Course information – Lecturers: Manolis Kellis and Piotr Indyk • Grading: Part. Problem sets 50% Final Project 25% Midterm 20% 5% • 5 problem sets: – Each problem set: covers 4 lectures, contains 4 problems. – Algorithmic problems and programming assignments – Graduate version includes 5th problem on current research •Exams – In-class midterm, no final exam • Collaboration policy – Collaboration allowed, but you must: • Work independently on each problem before discussing it • Write solutions on your own • Acknowledge sources and collaborators. No outsourcing. Goals for the term • Introduction to computational biology – Fundamental problems in computational biology – Algorithmic/machine learning techniques for data analysis – Research directions for active participation in the field • Ability to tackle research – Problem set questions: algorithmic rigorous thinking – Programming assignments: hands-on experience w/ real datasets • Final project: – Research initiative to propose an innovative project – Ability to carry out project’s goals, produce deliverables – Write-up goals, approach, and findings in conference format – Present your project to your peers in conference setting Course outline • Organization – Duality: -
Prof. Manolis Kellis April 15, 2008
Chromosomes inside the cell Introduction to Algorithms 6.046J/18.401J • Eukaryote cell LECTURE 18 • Prokaryote Computational Biology cell • Bio intro: Regulatory Motifs • Combinatorial motif discovery - Median string finding • Probabilistic motif discovery - Expectation maximization • Comparative genomics Prof. Manolis Kellis April 15, 2008 DNA packaging DNA: The double helix • Why packaging • The most noble molecule of our time – DNA is very long – Cell is very small • Compression – Chromosome is 50,000 times shorter than extended DNA • Using the DNA – Before a piece of DNA is used for anything, this compact structure must open locally ATATTGAATTTTCAAAAATTCTTACTTTTTTTTTGGATGGACGCAAAGAAGTTTAATAATCATATTACATGGCATTACCACCATATA ATATTGAATTTTCAAAAATTCTTACTTTTTTTTTGGATGGACGCAAAGAAGTTTAATAATCATATTACATGGCATTACCACCATATA ATCCATATCTAATCTTACTTATATGTTGTGGAAATGTAAAGAGCCCCATTATCTTAGCCTAAAAAAACCTTCTCTTTGGAACTTTC ATCCATATCTAATCTTACTTATATGTTGTGGAAATGTAAAGAGCCCCATTATCTTAGCCTAAAAAAACCTTCTCTTTGGAACTTTC AATACGCTTAACTGCTCATTGCTATATTGAAGTACGGATTAGAAGCCGCCGAGCGGGCGACAGCCCTCCGACGGAAGACTCTCCTC AATACGCTTAACTGCTCATTGCTATATTGAAGTACGGATTAGAAGCCGCCGAGCGGGCGACAGCCCTCCGACGGAAGACTCTCCTC GCGTCCTCGTCTTCACCGGTCGCGTTCCTGAAACGCAGATGTGCCTCGCGCCGCACTGCTCCGAACAATAAAGATTCTACAATACT GCGTCCTCGTCTTCACCGGTCGCGTTCCTGAAACGCAGATGTGCCTCGCGCCGCACTGCTCCGAACAATAAAGATTCTACAATACT TTTTATGGTTATGAAGAGGAAAAATTGGCAGTAACCTGGCCCCACAAACCTTCAAATTAACGAATCAAATTAACAACCATAGGATG TTTTATGGTTATGAAGAGGAAAAATTGGCAGTAACCTGGCCCCACAAACCTTCAAATTAACGAATCAAATTAACAACCATAGGATG AATGCGATTAGTTTTTTAGCCTTATTTCTGGGGTAATTAATCAGCGAAGCGATGATTTTTGATCTATTAACAGATATATAAATGGAA -
ENCODE Consortium Meeting
ENCODE Consortium Meeting June 17-19, 2008 Hilton Washington DC/Rockville Executive Meeting Center Rockville, Maryland PARTICIPANTS Bradley Bernstein Piero Carninci, Ph.D. Molecular Pathology Unit Leader Massachusetts General Hospital Functional Genomics Technology Team and 149 13th Street Omics Resource Development Unit Charlestown, MA 02129 Deputy Project Director (617) 726-6906 LSA Technology Development Group (617) 726-5684 Fax Omics Science Center [email protected] RIKEN Yokohama Institute 1-7-22 Suehiro-cho, Tsurumi-ku Ewan Birney Yokohama 230-0045 Joint Team Leader Japan Panda Group Nucleotides +81-(0)901-709-2277 Panda Coordination and Outreach [email protected] Panda Metabolism European Molecular Biology Laboratory Philip Cayting European Bioinformatics Institute Gerstein Laboratory Hinxton Outstation Department of Molecular Biophysics and Wellcome Trust Genome Campus Biochemistry Hinxton, Cambridge CB10 1SD Yale University United Kingdom P.O. Box 208114 +44-(0)1223-494 444, ext. 4420 New Haven, CT 06520-8114 +44-(0)1223-494 494 Fax (203) 432-6337 [email protected] [email protected] Michael Brent, Ph.D. Howard Y. Chang, M.D., Ph.D. Professor Assistant Professor Center for Genome Sciences Stanford University Washington University Center for Clinical Sciences Research, Campus Box 8510 Room 2155C 4444 Forest Park 269 Campus Drive Saint Louis, MO 63108 Stanford, CA 94305 (314) 286-0210 (650) 736-0306 [email protected] [email protected] James Bentley Brown Mike Cherry, Ph.D. Graduate Student Researcher Associate Professor Graduate Program in Applied Science and Department of Genetics Technology Stanford University Bickel Group 300 Pasteur Drive University of California, Berkeley Stanford, CA 94305-5120 Room 2 (650) 723-7541 1246 Hearst Avenue [email protected] Berkeley, CA 94702 (510) 703-4706 [email protected] Francis S. -
Unweaving)The)Circuitry)) Of)Complex)Disease!
Unweaving)the)circuitry)) of)complex)disease! Manolis Kellis Broad Institute of MIT and Harvard MIT Computer Science & Artificial Intelligence Laboratory Personal!genomics!today:!23!and!Me! Recombina:on)breakpoints) Me)vs.)) my)brother) Family)Inheritance) Dad’s)mom) My)dad) Mom’s)dad) Human)ancestry) Disease)risk) Genomics:)Regions))mechanisms)) Systems:)genes))combina:ons)) drugs) pathways) 1000s)of)diseaseHassociated)loci)from)GWAS) • Hundreds)of)studies,)each)with)1000s)of)individuals) – Power!of!gene7cs:!find!loci,!whatever!the!mechanism!may!be! – Challenge:!mechanism,!cell!type,!drug!target,!unexplained!heritability! GenomeHwide)associa:on)studies)(GWAS)) • Iden7fy!regions!that!coBvary!with!the!disease! • Risk!allele!G!more!frequent!in!pa7ents,!A!in!controls! • But:!large!regions!coBinherited!!!find!causal!variant! • Gene7cs!does!not!specify!cell!type!or!process! E environment causes syndrome G epigenomeX D S genome disease symptoms biomarkers effects Epidemiology The study of the patterns, causes, and effects of health and disease conditions in defined populations Gene:c) Tissue/) Molecular)Phenotypes) Organismal) Variant) cell)type) Epigene:c) Gene) phenotypes) Changes) Expression) Changes) Methyl.) ) Heart) Gene) Endo) DNA) expr.) phenotypes) Muscle) access.) ) Lipids) Cortex) Tension) CATGACTG! Enhancer) CATGCCTG! Lung) ) Gene) Heartrate) Disease) H3K27ac) expr.) Metabol.) Blood) ) Drug)resp) Skin) Promoter) Disease! ) Gene) cohorts! Nerve) Insulator) expr.) GTEx!/! ENCODE/! GTEx! Environment) Roadmap! Epigenomics/! Epigenomics! -
Lesson Plan Ben Barres: Neurobiology Pioneer and Champion for Equity in STEM
Lesson Plan Ben Barres: Neurobiology Pioneer and Champion for Equity in STEM By: Hannah Pell, Research Assistant November 2019 Neurobiologist Ben Barres, before his death in 2017. Photo credit to Timothy Archibald, from the journal Nature. Grade Level(s): 11-12, General College Subject(s): History, Social Activism, Equity in STEM In-Class Time: 50 min – 1 hour Prep Time: 15 min – 20 min Materials • Lesson Plan • Copies of: (See Supplemental Materials) o “Ben Barres (1954 – 2017)” o “Ben Barres - gender champion” o “Does gender matter?” and Discussion Worksheet • Classroom internet access Objective This two-part lesson is about introducing students to Ben Barres (1954 – 2017), a successful neurobiologist and gender equity activist. Students will learn about his life and experiences as a female- to-male transgender scientist through excerpts and a review of his posthumously published book, The Autobiography of a Transgender Scientist (2017). Additionally, students will read his famous Prepared by the Center for the History of Physics at AIP 1 commentary in Nature, titled “Does gender matter?,” and discuss Barres’ arguments for why women are not advancing in science as quickly as men. Students can also explore the Queer in Stem online research project to collect information about LGBTQ+ scientists’ career experiences. The teacher should be prepared to discuss the importance of diverse representation in academic leadership and role models in science, issues such as subtle discrimination1, as well as how students can be allies in cultivating an equitable learning community. The guide is divided into two parts, which can be used together or as independent lessons: (1) an introduction to Ben Barres’ life as a scientist and activist, and (2) resources for understanding LGBTQ+ experiences in STEM and increasing their visibility in the scientific community. -
Precision Medicine in Type 2 Diabetes and Cardiovascular Disease 31 August–1 September 2016 in Båstad · Sweden
Berzelius symposium 91 Precision Medicine in Type 2 Diabetes and Cardiovascular Disease 31 August–1 September 2016 in Båstad · Sweden Programme · General information · Lectures abstracts · Poster abstracts Generously supported by: PRECISION MEDICINE IN TYPE 2 DIABETES AND CARDIOVASCULAR DISEASE · 31 AUGUST–1 SEPTEMBER 2016 1 Berzelius symposium 91 Precision Medicine in Type 2 Diabetes and Cardiovascular Disease Purpose statement: Cardiovascular disease (CVD) and type 2 diabetes are devastating and costly diseases whose prevalence is increasing rapidly around the world, projected to exceed billions of people worldwide within the next deca- des. Although drug and lifestyle interventions are used widely to prevent and treat CVD and diabetes, neither is highly effective; for example, in high risk adults, intensive lifestyle intervention delays the onset of disease by roughly 3-years and with metformin by 18-months compared to placebo control interven- tion (Knowler et al, Lancet, 2009), with diabetes “prevention” being the excep- tion, rather than the rule. Moreover, whilst some patients respond very well to therapies, others benefit little or not at all, progressing rapidly through the pre-diabetic phase of beta-cell decline and later developing life-threatening complications such as retinopathy, nephropathy, peripheral neuropathy, and CVD. As such, there is an urgent need to develop innovative and effective prevention and treatment strategies. Human biology is complex and people differ in their genetic and molecular characteris- tics, which underlies the variable response to interventions and rates of disease progression. Thus, a huge, as yet unrealised opportunity exists to optimize the prevention and treatment of CVD and type 2 diabetes by tailoring therapies to the patient’s unique biology. -
Symposium 2017
UCSF WEILL INSTITUTE FOR NEUROSCIENCES SYMPOSIUM 2017 MAY.25.2017 UCSF MISSION BAY Sanford I. "Sandy" and Joan Weill Welcome to the inaugural symposium! It is with great pleasure that we invite you to the inaugural UCSF Weill Institute for Neurosciences Symposium. Bringing together leaders in science and medicine, this event will showcase innovative research, inspiring ideas, and new paths towards discovery. Each symposium will highlight a different theme, offering a fresh perspective on key issues and disease areas across the neurosciences. Featuring a truly exciting panel of speakers, this inaugural event will focus on neurodegenerative diseases including Alzheimer's, Parkinson's and ALS. Schedule of Events 8:00AM Registration (coffee/tea available) 9:00AM Welcome & Opening Remarks Stephen Hauser; Sandy and Joan Weill 9:15AM Don W. Cleveland, Ph.D. Gene Silencing Therapy for Human Neurodegenerative Disease 10:00AM M. Elizabeth Ross, M.D., Ph.D. Fetal Development Genes Repurposed in Brain Plasticity and Aging 10:45AM Break 11:00AM Thomas C. Südhof, M.D. Synaptic and Non-Synaptic Signaling by ApoE: Implications for Alzheimer's Disease 11:45AM Beth Stevens, Ph.D. Immune Mechanisms of Synapse Loss in Health & Disease 12:30PM Lunch break (box lunch provided) 1:30PM Kristine Yaffe, M.D. Neurodegeneration: A Population Health Perspective 2:00PM Bruce L. Miller, M.D. The Landscape of Neurodegenerative Diseases 2:30PM Lennart Mucke, M.D. Addressing the Multifactoriality of Neurodegenerative Diseases in Research and Therapeutic Development 3:00PM Stanley B. Prusiner, M.D. Therapeutic Challenges and Opportunities 3:30PM Roundtable Discussion 4:15PM Reception Don W. Cleveland, Ph.D. -
UNIVERSITY of CALIFORNIA RIVERSIDE RNA-Seq
UNIVERSITY OF CALIFORNIA RIVERSIDE RNA-Seq Based Transcriptome Assembly: Sparsity, Bias Correction and Multiple Sample Comparison A Dissertation submitted in partial satisfaction of the requirements for the degree of Doctor of Philosophy in Computer Science by Wei Li September 2012 Dissertation Committee: Dr. Tao Jiang , Chairperson Dr. Stefano Lonardi Dr. Marek Chrobak Dr. Thomas Girke Copyright by Wei Li 2012 The Dissertation of Wei Li is approved: Committee Chairperson University of California, Riverside Acknowledgments The completion of this dissertation would have been impossible without help from many people. First and foremost, I would like to thank my advisor, Dr. Tao Jiang, for his guidance and supervision during the four years of my Ph.D. He offered invaluable advice and support on almost every aspect of my study and research in UCR. He gave me the freedom in choosing a research problem I’m interested in, helped me do research and write high quality papers, Not only a great academic advisor, he is also a sincere and true friend of mine. I am always feeling appreciated and fortunate to be one of his students. Many thanks to all committee members of my dissertation: Dr. Stefano Lonardi, Dr. Marek Chrobak, and Dr. Thomas Girke. I will be greatly appreciated by the advice they offered on the dissertation. I would also like to thank Jianxing Feng, Prof. James Borneman and Paul Ruegger for their collaboration in publishing several papers. Thanks to the support from Vivien Chan, Jianjun Yu and other bioinformatics group members during my internship in the Novartis Institutes for Biomedical Research.