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Present Post: Previous Positions Held: Honors/Awards Membership In
CURRICULUM VITAE Name: Vassilis Pachnis, M.D., Ph.D., FMedSci Date of Birth: 24 January 1953 Place of Birth: Athens, Greece Contact details: National Institute for Medical Research Institute of Molecular Biology and Biotechnology The Ridgeway, Mill Hill, Foundation for Research and Technology‐Hellas London NW7 1AA, UK. N. Plastira 100, GR‐70013, Heraklion, Greece tel. (+44) 02088162113 Tel. (+30) 2810391100 email: [email protected] Email: [email protected] Education: July 1980 University of Athens Medical School (Athens, Greece) M.D. magna cum laude June 1986 University of Pennsylvania, Philadelphia, PA (USA) Degree: Ph.D., Genetics Supervisor: Prof. Shirley Tilghman Nov 1986 – Mar 1988 Howard Hughes Medical Institute Center for Neurobiology and Behavior Columbia University, New York, NY (USA) Postdoctoral Fellow in Prof. Richard Axel's laboratory Apr 1988 – May 1991 Department of Genetics and Development Columbia University, New York, NY (USA) Postdoctoral fellow in Dr. Frank Costantini's laboratory Present Post: ‐ Head of Division of Molecular Neurobiology, National Institute for Medical Research, Medical Research Council (London, UK) ‐ Director of the Institute of Molecular Biology and Biotechnology of the Foundation for Research and Technology‐Hellas (Heraklion, Greece) Previous positions held: May 1991 – Feb 1997 Senior Scientific Staff, Group Leader, MRC National Institute for Medical Research, London (5/91‐2/97) Feb 1997 – Aug 2000 Tenured Senior Scientist, MRC National Institute for Medical Research, London Honors/Awards ‐ Scholarship from the National Scholarship Foundation of Greece for Academic excellence in Medical School ‐ Special Fellowship Award from the Leukemia Society of America (Jul 1989‐May 1991) ‐ Janssen Award for Life Time Achievement in Gastroenterology (2002) Membership in Academies ‐ Elected Fellow of the Academy of Medical Sciences, UK (2000). -
Medical Research Council
OFFICIAL MEDICAL RESEARCH COUNCIL 03 Should not be viewed by CEO due to Author: Sam Bartholomew Conflict of interest Should not be viewed by deputy CEO due to Conflict of interest Trade Union Side access: In part Minutes of the Council meeting held at the Chelsea Harbour Hotel on 7 March 2018 Present: Council Head Office staff Mr Donald Brydon (Chair) Ms Sam Bartholomew Sir John Savill (CEO) Professor David Lomas Professor Jonathan Bisson Dr Rob Buckle Dr John Brown Mr Hugh Dunlop Professor Doreen Cantrell Dr Declan Mulkeen Professor Chris Day Dr Tony Peatfield Professor Dame Janet Finch Mrs Helen Page Professor John Iredale Dr Rachel Quinn Mr Richard Murley Dr Frances Rawle Baroness Onora O’Neill Ms Pauline Mullin (item 9a&b only) Dr Mene Pangalos Professor Irene Tracey Guests – item 8 Dr Pauline Williams Nick Lemoine, Chair MRF Trust Angela Hind, CEO MRF Observers Ms Jenny Dibden (BEIS) Professor Fiona Watt, MRC Executive Chair Designate 1. Announcements Mr Brydon welcomed members to the last meeting of the MRC Council as currently constituted, prior to the transition to UK Research and Innovation. He introduced Professor Fiona Watt, MRC Executive Chair Designate, and Professor Jonathan Bisson who was attending his first meeting since being appointed as a Council member in the summer. He offered congratulations to those MRC-associated people whose achievements had been recognised in the New Year’s Honours: • Sir Keith Peters Sir Keith, lately Regius Professor of Physic at the University of Cambridge, was appointed Knight Grand Cross of the Order of the British Empire (GBE) for services to 1 OFFICIAL the advancement of medical science. -
Biology Powerhouse Raises Railway Alarm
NEWS IN FOCUS to enrol all participants by 2018. Certain factors make researchers optimis- tic that the British study will succeed where the US one failed. One is the National Health Service, which provides care for almost all pregnant women and their children in the United Kingdom, and so offers a centralized means of recruiting, tracing and collecting medical information on study participants. In the United States, by contrast, medical care is provided by a patchwork of differ- ent providers. “I think that most researchers in the US recognize that our way of doing population-based research here is simply different from the way things can be done in the UK and in Europe, and it will almost always be more expensive here,” says Mark Klebanoff, a paediatric epidemiologist at Nationwide Children’s Hospital in Colum- bus, Ohio, who was involved in early dis- cussions about the US study. The Francis Crick Institute sits at the nexus of three central London railway hubs. At one stage, US researchers had planned to knock on doors of random houses looking URBAN SCIENCE for women to enrol before they were even pregnant. “It became obvious that that wasn’t going to be a winning formula,” says Philip Pizzo, a paediatrician at Stanford University Biology powerhouse in Palo Alto, California, who co-chaired the working group that concluded that the National Children’s Study was not feasible. raises railway alarm “The very notion that someone was going to show up on your doorstep as a representa- tive from a government-funded study and Central London’s Francis Crick Institute fears that proposed say ‘Are you thinking of getting pregnant?’ train line will disrupt delicate science experiments. -
New Editor on Journal of Cell Science Michael Way (Editor-In-Chief)
© 2019. Published by The Company of Biologists Ltd | Journal of Cell Science (2019) 132, jcs229740. doi:10.1242/jcs.229740 EDITORIAL New Editor on Journal of Cell Science Michael Way (Editor-in-Chief) As someone who has worked on things related to the actin cytoskeleton my whole research career, the nucleus was not something I paid much attention to. Yes, there were scattered historical reports of actin in the nucleus long before I started my PhD, but no one believed actin was really there of course – it was all an artefact of fixation, you know. Nuclear actin was taboo and no one talked about it at the meetings I went to as a student and postdoc. How wrong we were – today nuclear actin is alive and kicking, although there are definitely more questions than answers concerning what it is actually doing there. We now appreciate that the nucleus contains a wide assortment of proteins associated with the cytoplasmic actin cytoskeleton including myosin motors and actin nucleators such as the Arp2/3 complex. In addition, it should not be forgotten that many chromatin-associated complexes including SWI/SNF and INO80/ SWR also contain multiple actin-related proteins, as well as actin itself. It strikes me that maybe we should all be paying more attention to the nucleus and not just because it contains my favourite proteins! Maybe that’s why, in recent years, we’ve been seeing more submissions to JCS that are focused on different aspects of the nucleus and that traditionally appeared in journals with ‘molecular’ in their titles. -
Bloomsbury Scientists Ii Iii
i Bloomsbury Scientists ii iii Bloomsbury Scientists Science and Art in the Wake of Darwin Michael Boulter iv First published in 2017 by UCL Press University College London Gower Street London WC1E 6BT Available to download free: www.ucl.ac.uk/ ucl- press Text © Michael Boulter, 2017 Images courtesy of Michael Boulter, 2017 A CIP catalogue record for this book is available from the British Library. This book is published under a Creative Commons Attribution Non-commercial Non-derivative 4.0 International license (CC BY-NC-ND 4.0). This license allows you to share, copy, distribute and transmit the work for personal and non-commercial use providing author and publisher attribution is clearly stated. Attribution should include the following information: Michael Boulter, Bloomsbury Scientists. London, UCL Press, 2017. https://doi.org/10.14324/111.9781787350045 Further details about Creative Commons licenses are available at http://creativecommons.org/licenses/ ISBN: 978- 1- 78735- 006- 9 (hbk) ISBN: 978- 1- 78735- 005- 2 (pbk) ISBN: 978- 1- 78735- 004- 5 (PDF) ISBN: 978- 1- 78735- 007- 6 (epub) ISBN: 978- 1- 78735- 008- 3 (mobi) ISBN: 978- 1- 78735- 009- 0 (html) DOI: https:// doi.org/ 10.14324/ 111.9781787350045 v In memory of W. G. Chaloner FRS, 1928– 2016, lecturer in palaeobotany at UCL, 1956– 72 vi vii Acknowledgements My old writing style was strongly controlled by the measured precision of my scientific discipline, evolutionary biology. It was a habit that I tried to break while working on this project, with its speculations and opinions, let alone dubious data. But my old practices of scientific rigour intentionally stopped personalities and feeling showing through. -
Functional Effects Detailed Research Plan
GeCIP Detailed Research Plan Form Background The Genomics England Clinical Interpretation Partnership (GeCIP) brings together researchers, clinicians and trainees from both academia and the NHS to analyse, refine and make new discoveries from the data from the 100,000 Genomes Project. The aims of the partnerships are: 1. To optimise: • clinical data and sample collection • clinical reporting • data validation and interpretation. 2. To improve understanding of the implications of genomic findings and improve the accuracy and reliability of information fed back to patients. To add to knowledge of the genetic basis of disease. 3. To provide a sustainable thriving training environment. The initial wave of GeCIP domains was announced in June 2015 following a first round of applications in January 2015. On the 18th June 2015 we invited the inaugurated GeCIP domains to develop more detailed research plans working closely with Genomics England. These will be used to ensure that the plans are complimentary and add real value across the GeCIP portfolio and address the aims and objectives of the 100,000 Genomes Project. They will be shared with the MRC, Wellcome Trust, NIHR and Cancer Research UK as existing members of the GeCIP Board to give advance warning and manage funding requests to maximise the funds available to each domain. However, formal applications will then be required to be submitted to individual funders. They will allow Genomics England to plan shared core analyses and the required research and computing infrastructure to support the proposed research. They will also form the basis of assessment by the Project’s Access Review Committee, to permit access to data. -
Transcriptional Regulation by Extracellular Signals 209
Cell, Vol. 80, 199-211, January 27, 1995, Copyright © 1995 by Cell Press Transcriptional Regulation Review by Extracellular Signals: Mechanisms and Specificity Caroline S. Hill and Richard Treisman Nuclear Translocation Transcription Laboratory In principle, regulated nuclear localization of transcription Imperial Cancer Research Fund factors can involve regulated activity of either nuclear lo- Lincoln's Inn Fields calization signals (NLSs) or cytoplasmic retention signals, London WC2A 3PX although no well-characterized case of the latter has yet England been reported. N LS activity, which is generally dependent on short regions of basic amino acids, can be regulated either by masking mechanisms or by phosphorylations Changes in cell behavior induced by extracellular signal- within the NLS itself (Hunter and Karin, 1992). For exam- ing molecules such as growth factors and cytokines re- ple, association with an inhibitory subunit masks the NLS quire execution of a complex program of transcriptional of NF-KB and its relatives (Figure 1; for review see Beg events. While the route followed by the intracellular signal and Baldwin, 1993), while an intramolecular mechanism from the cell membrane to its transcription factor targets may mask NLS activity in the heat shock regulatory factor can be traced in an increasing number of cases, how the HSF2 (Sheldon and Kingston, 1993). When transcription specificity of the transcriptional response of the cell to factor localization is dependent on regulated NLS activity, different stimuli is determined is much less clear. How- linkage to a constitutively acting NLS may be sufficient to ever, it is possible to understand at least in principle how render nuclear localization independent of signaling (Beg different stimuli can activate the same signal pathway yet et al., 1992). -
Female Fellows of the Royal Society
Female Fellows of the Royal Society Professor Jan Anderson FRS [1996] Professor Ruth Lynden-Bell FRS [2006] Professor Judith Armitage FRS [2013] Dr Mary Lyon FRS [1973] Professor Frances Ashcroft FMedSci FRS [1999] Professor Georgina Mace CBE FRS [2002] Professor Gillian Bates FMedSci FRS [2007] Professor Trudy Mackay FRS [2006] Professor Jean Beggs CBE FRS [1998] Professor Enid MacRobbie FRS [1991] Dame Jocelyn Bell Burnell DBE FRS [2003] Dr Philippa Marrack FMedSci FRS [1997] Dame Valerie Beral DBE FMedSci FRS [2006] Professor Dusa McDuff FRS [1994] Dr Mariann Bienz FMedSci FRS [2003] Professor Angela McLean FRS [2009] Professor Elizabeth Blackburn AC FRS [1992] Professor Anne Mills FMedSci FRS [2013] Professor Andrea Brand FMedSci FRS [2010] Professor Brenda Milner CC FRS [1979] Professor Eleanor Burbidge FRS [1964] Dr Anne O'Garra FMedSci FRS [2008] Professor Eleanor Campbell FRS [2010] Dame Bridget Ogilvie AC DBE FMedSci FRS [2003] Professor Doreen Cantrell FMedSci FRS [2011] Baroness Onora O'Neill * CBE FBA FMedSci FRS [2007] Professor Lorna Casselton CBE FRS [1999] Dame Linda Partridge DBE FMedSci FRS [1996] Professor Deborah Charlesworth FRS [2005] Dr Barbara Pearse FRS [1988] Professor Jennifer Clack FRS [2009] Professor Fiona Powrie FRS [2011] Professor Nicola Clayton FRS [2010] Professor Susan Rees FRS [2002] Professor Suzanne Cory AC FRS [1992] Professor Daniela Rhodes FRS [2007] Dame Kay Davies DBE FMedSci FRS [2003] Professor Elizabeth Robertson FRS [2003] Professor Caroline Dean OBE FRS [2004] Dame Carol Robinson DBE FMedSci -
Diversity Data Report 2019 Diversity Data Report 2019 Issued: November 2020 DES6507
Diversity data report 2019 Diversity data report 2019 Issued: November 2020 DES6507 The text of this work is licensed under the terms of the Creative Commons Attribution License which permits unrestricted use, provided the original author and source are credited. The license is available at: creativecommons.org/licenses/by/4.0 Images are not covered by this license. This report can be viewed online at: royalsociety.org/diversity Contents Introduction .....................................................4 The Fellowship ..................................................11 Committees, panels and working groups ..........................19 Research Fellowship Grants ......................................26 Scientific programmes ...........................................38 Public engagement .............................................50 Publishing ......................................................62 Schools engagement ............................................67 Royal Society staff ..............................................72 Gender pay gap .................................................75 Definitions .....................................................77 DIVERSITY DATA REPORT 2019 3 Introduction The Royal Society is a Fellowship of many of the world’s most eminent scientists and is the oldest scientific academy in continuous existence. The Society is committed to increasing sections of this report such as organisers, diversity in science, technology, engineering chairs and speakers at scientific meetings, and mathematics (‘STEM’) -
The Ubiquitin Proteasome System and Its Involvement in Cell Death Pathways
Cell Death and Differentiation (2010) 17, 1–3 & 2010 Macmillan Publishers Limited All rights reserved 1350-9047/10 $32.00 www.nature.com/cdd Editorial The ubiquitin proteasome system and its involvement in cell death pathways F Bernassola1, A Ciechanover2 and G Melino1,3 Cell Death and Differentiation (2010) 17, 1–3; doi:10.1038/cdd.2009.189 Following the awarding of the 2004 Nobel Prize in Chemistry Inactivation of the proteasome following caspase-mediated to Aaron Ciechanover, Avram Hershko, and Irwin A Rose cleavage may disable the proteasome, interfering with its for the discovery of ubiquitin (Ub)-mediated degradation, role in the regulation of key cellular processes and thereby Cell Death and Differentiation has drawn the attention of facilitating induction of apoptosis. The noted recent develop- its readers to the Ub Proteasome System (UPS) and its ments show how understanding of these functions is just involvement in regulating cell death pathways.1–4 The current starting to emerge. For example, why does dIAP1 associate set of reviews is an update on this theme.5–16 with multiple E2s via its RING finger? Does dIAP1 also interact From previous review articles published in Cell Death and with the E3 – the F-box protein Morgue, which is a part of an Differentiation, it was apparent that the UPS has a major SCF E3 complex? Why does dIAP1, which is an E3, have to mechanistic role in regulating cell death via modification and interact with other ligases such as the N-end rule UBR1 and degradation of key regulatory proteins involved in -
Linking Neurons to Immunity: Lessons from Hydra COMMENTARY Yuuki Obataa and Vassilis Pachnisa,1
COMMENTARY Linking neurons to immunity: Lessons from Hydra COMMENTARY Yuuki Obataa and Vassilis Pachnisa,1 According to the Greek mythology (1), Heracles’ sec- Hydra offers unique advantages to neuroscience re- ond labor was the destruction of the Lernaean Hydra, search as well. Its nervous system is an anatomically a fearsome fire-breathing monster with a dog-like simple network of sensory and ganglion neurons body and nine snake heads. Many had tried to slay that control a range of behaviors, including sponta- the Lernaean Hydra but in vain: Any head that was neous body contractions (5, 6). Remarkably, the an- cut off regrew and multiplied. It is remarkable how atomical organization and functional output of consistent the narrative of this myth is with our recent Hydra’s nervous system are reminiscent of the intrin- understanding of tissue and organ regeneration. Her- sic neural networks of the gastrointestinal tract in acles was successful not only because of his divine vertebrates, known as the enteric nervous system origin (he was the son of Zeus after all) and the help (ENS). The ENS is an assembly of nerve cells within of Athena, but particularly because of the assistance the gut wall, which are organized into the ganglia he received from his nephew Iolaus, who was assigned of the myenteric and submucosal plexus (7) and regu- the job of cauterizing the exposed stumps of the Hy- late most intestinal functions, including coordination of dra’s severed heads. Of course, we now understand smooth muscle contractions, the basis of intestinal why Iolaus’ contribution was so critical: His flame con- peristalsis (8). -
Gilaie-Dotan, Sharon; Rees, Geraint; Butterworth, Brian and Cappelletti, Marinella
Gilaie-Dotan, Sharon; Rees, Geraint; Butterworth, Brian and Cappelletti, Marinella. 2014. Im- paired Numerical Ability Affects Supra-Second Time Estimation. Timing & Time Perception, 2(2), pp. 169-187. ISSN 2213-445X [Article] http://research.gold.ac.uk/23637/ The version presented here may differ from the published, performed or presented work. Please go to the persistent GRO record above for more information. If you believe that any material held in the repository infringes copyright law, please contact the Repository Team at Goldsmiths, University of London via the following email address: [email protected]. The item will be removed from the repository while any claim is being investigated. For more information, please contact the GRO team: [email protected] Timing & Time Perception 2 (2014) 169–187 brill.com/time Impaired Numerical Ability Affects Supra-Second Time Estimation Sharon Gilaie-Dotan 1,∗, Geraint Rees 1,2, Brian Butterworth 1 and Marinella Cappelletti 1,3,∗ 1 UCL Institute of Cognitive Neuroscience, 17 Queen Square, London, WC1N 3AR, UK 2 Wellcome Trust Centre for Neuroimaging, University College London, 12 Queen Square, London WC1N 3BG, UK 3 Psychology Department, Goldsmiths College, University of London, UK Received 24 September 2013; accepted 11 March 2014 Abstract It has been suggested that the human ability to process number and time both rely on common magni- tude mechanisms, yet for time this commonality has mainly been investigated in the sub-second rather than longer time ranges. Here we examined whether number processing is associated with timing in time ranges greater than a second. Specifically, we tested long duration estimation abilities in adults with a devel- opmental impairment in numerical processing (dyscalculia), reasoning that any such timing impairment co-occurring with dyscalculia may be consistent with joint mechanisms for time estimation and num- ber processing.