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HomeAutoHarley-Davidson celebrates 120 years with limited-edition models
Harley-Davidson celebrates 120 years with limited-edition models
By: Aradhya
Harley-Davidson is a motorbike brand that is well-known among motorcycle enthusiasts all over the world. This is the legacy of the American brand, which is celebrating its 120th year this year. To mark the occasion, Harley-Davidson has introduced limited-edition editions of seven of its motorcycles. Aside from that, Harley-Davidson presented new updated models such as the Breakout performance cruiser, the Road Glide 3 trike, the Nightster Special middleweight sport motorcycle, and the Freewheeler trike model, which will be covered in a separate piece.
"Since 1903, Harley-Davidson has pioneered American motorcycle design, technology, and performance, and today marks the start of a year-long celebration of Harley-120th Davidson's Anniversary," stated Jochen Zeitz, Chairman, President, and CEO of Harley-Davidson, when the motorcycles were unveiled.
"We're thrilled to present the first batch of 2023 Harley-Davidson motorcycles; additional releases will follow later in the year. We hope you can join us in 2023 as we celebrate the history, culture, and community of Harley-Davidson. It will be an amazing milestone for the company."
Intricate paint schemes are used for the 120th anniversary model of Harley-Davidson. Anniversary Black is applied as a base coat to the models, and then Heirloom Red is applied in panels. Each of the panels is bordered with a hand-applied scallop of gold paint and a vivid red pinstripe. The head and wings of a soaring eagle are depicted by subtle details incorporated within the panels, and the gold-plated tank medallion also features an Art Deco interpretation of the eagle, which is a defining feature of H-D design. Alcantara seat surfaces with red and gold stitching are also included for the versions. Only a few of the following units are available for each of the seven types.
ALSO READ: KTM to take electric scooters into Europe with Chetak launch
Harley-Davidson Nightster S
Reset your Windows 11 computer easily with this step-by-step guide
PM Modi: Listen to this plea from the man who inspired '3 Idiots'
Aradhyahttp://thevocalnews.com
Aaradhya is working as a Sub-Editor at The Vocal News. She enjoys writing about gadgets and automobiles because she is a tech and automotive fanatic. She has done her bachelors in Journalism and Mass communication from Makhanlal Chaturvedi Rashtriya Patrakarita Vishwavidyalaya. "I write to discover what I know."


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By Kenya Roberson Monroe Black Chamber
Support Black Owned Businesses
Photo Monroe Black Chamber Executive Director Kenya Roberson
We are continuing our support of Black owned businesses throughout the month. Thursday, November 17, 2022 - Support Black-owned publications like The Monroe Dispatch, operated by Mr. Frank DeTiege and The Free Press Newspaper, owned by Mr. Roosevelt Wright. Each of these businesses publish their newspapers on Thursdays. Please stop by a local convenience store to purchase. Friday, November 18, 2022 - Visit Coney Island Connection, located at 2635 North 7th Street, West Monroe, LA. The hours of operation are 10:00 AM - 7:00 PM. The owner is Mr. Chris Lewis. Saturday, November 19, 2022 -...
Mrs. Frances Reddix's Treasured Legacy

redpajama_set_name: RedPajamaCommonCrawl


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Jamie I var ett dreadnought-slagskepp i Spaniens flotta. Hon var det sist byggda av tre systerfartyg i España-klassen, som hon bildade tillsammans med España och Alfonso XIII. Jamie I och hennes systrar tillkom i samband med en upprustning av den spanska flottan, följande landets nederlag mot Förenta Staterna i Spansk-amerikanska kriget 1898. Slagskeppet förde en huvudbestyckning av åtta 30,5 cm kanoner i fyra dubbeltorn, och en sekundär bestyckning av 20 stycken 10,2 cm kanoner i kasematter.

Jamie I byggdes av ett spanskt-brittiskt konsortium. Fartyget kölsträcktes i Ferrol och sjösattes den 21 september 1914. Första världskrigets utbrott samma år sänkte dock byggnadstakten avsevärt, då mycket av materielen till henne importerades från Storbritannien, vilket betydde att hon inte kunde levereras förrän 1921. När Spanska inbördeskriget bröt ut sommaren 1936 förblev Jamie I i regeringssidans händer. När fartyget låg under reparation i Cartagena, efter att ha angripits av italienskt bombflyg, föll hon offer för en intern explosion och skadades så illa att hon fick huggas upp 1939. Fartyget fick sitt namn efter den aragoniske kungen Jacob I, som levde på 1200-talet.

Referenser

Externa länkar

Spanska örlogsfartyg
Spanska slagskepp
Fartyg sjösatta 1914
Fartyg byggda i Spanien
España-klass

redpajama_set_name: RedPajamaWikipedia


The transportation sector accounts for 50% of greenhouse gas emissions and 80 percent of smog-causing pollutants. Governor Brown has set a target of 5 million zero emission vehicles by 2030 to meet California's clean air standards and climate goals. This initiative includes a new eight-year rebate for zero-emission vehicles (ZEVs) and clean fuels charging and refueling stations. This $2.5 billion initiative will help bring 250,000 vehicle charging stations and 200 hydrogen fueling stations to California by 2025. Grant programs are available for developing an alternative and renewable fuel station network. If you need help with meeting your grant requirements or obtaining related permits and approvals, please contact Valerie Rosenkrantz.


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IDK CRM
IDK CMS
IDK DMS
IDK SMS
Short message service
UX & Design
Let's Make Something Great
VR Web browsing might ultimately be one of Samsung and Oculus best tricks
Of all the things to be excited about regarding virtual reality – gaming, 360-degree movies, and all sorts of cool new experiences – the last thing I expected to intrigue me is a virtual reality Web browser.
Yet after trying Samsung's new browser made for the Gear VR, I think it might ultimately end up being one of the platform's most useful tricks – even if it's extremely limited at the moment.
It's like Web browsing in 'Minority Report'. Tabs are presented as floating windows around you, and you simply shift your head slightly to look at another tab. In fact, it feels a lot like a multi-monitor set-up, except you probably can't afford or have the space for five 40-inch monitors.
Navigating around is relatively simple. You scroll using the Gear VR's touchpad (I didn't have a game controller with me), and URL and search input defaults to dictation.
Voice recognition works really well, but you can also type in an address by moving your head around and tapping on the touchpad. That sounds more cumbersome than it actually is, since Samsung's motion tracking is excellent (think typing with a mouse or stylus). Not ideal, but it works.
One practical benefit of having the browser is that you can use it to watch 360-degree videos on YouTube; the standard YouTube app -which now supports Google Cardboard – doesn't work in the Oculus OS layer, but the Web interface provides an essentially identical experience.
Everything runs surprisingly smoothly too, despite the extra rendering my S6 Edge+ has to do for the 3D interface.
The app itself is pretty barebones in terms of functionality at the moment though. You can't import bookmarks, but there's no way to adjust settings like cookies or default to using desktop sites. My bluetooth keyboard didn't work while browsing either, which is a shame, as it would have been nice as a distraction-free writing interface.
The pixel density on the Gear VR is also too low for what we've come to expect from our devices for sharp text- it's usable, but feels like working with 1024×768 panels.
But despite all those qualms, the possibilities are still enticing. Once the specs, features, and peripheral support have caught up, imagine being being able to make your computer screen any size you'd like and having as many of them as you need. Perhaps even better: you could easily turn off a distracting environment to zone into a task.
Right now, browsing on the GR VR is more of a nice-to-have feature than something that could change the way you work. But if it's any indication of what's to come, then the future looks pretty awesome.
07.12.2015. | TNW by Napier Lopez
Imagine what we can do, TOGETHER.
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French green clay helps draw out impurities within pores while tea tree helps reduce the appearance of blemishes and other imperfections. Non-drying formula features squalane to help boost the performance of tea tree as well as replenish hydration, help calm, and keep skin feeling ultra-soft.
Our formula is enriched with tea tree that originates from Australia and is grown with the highest quality eco-friendly farming practices that meet ISO standards.
For external use only. Use only as directed. Avoid eye area. We recommend a patch test prior to use if you are particularly sensitive. If irritation occurs, consult a dermatologist.
*Based on a single use clinical study of 35 women, age 18 – 40.
**Based on a 7-day consumer use study of 35 women, ages 18-40, twice weekly.
May be used as an all-over facial mask or only on areas of concern.


Current Medical Education is a series of interactive eLearning modules for GPs, based on breaking global medical news. Developed in partnership with expert GP reviewers, modules are in five languages and target a global audience. A range of topics are covered, including managing migraine in primary care, the role of vitamin D and calcium in fracture prevention, and addressing peanut allergy. The project is provided for univadis, a service from MSD.
The Hong Kong Diabetes Advisory Panel (HKDAP) met to discuss clinical treatment guidelines from the International Diabetes Federation (IDF). Local adaptations to the guidelines are summarized in a newsletter from the HKDAP.
Swine Flu pandemic is just one example. In partnership with univadis a service from MSD, International Medical Press has produced factsheets summarising the current situation and up-to-date management recommendations for healthcare professionals and their patients.
International Medical Press produce webcasts, videos and podcasts in partnership with therapeutic experts from around the world.
Hear the latest on adverse events in HIV from the faculty of the International Workshop on Adverse Drug Reactions and Co-morbidities in HIV.
Learn about incretin-based therapies in diabetes.
GP News Channel is a daily news service for general practitioners provided for univadis a service from MSD. International Medical Press provides newswire searches, editorial, copywriting and liaison with GP faculty. International Medical Press has produced Cantonese language videos on hepatitis B, in collaboration with leading regional gastroenterologists, for use in specialist out-patient departments in Hong Kong hospitals.
Please contact us for more information on these projects.


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The Korean League Cup was a professional football competition in South Korean football. It was held by the K League Federation from 1986 to 2012.

Sponsorship

Champions

List of finals

Titles by club
K League's principle of official statistics is that final club succeeds to predecessor club's history and records.

Titles by city/province
K League introduced home and away system in 1987.

Titles by region
K League introduced home and away system in 1987.

Awards

Best Player

Top goalscorer

Top assist provider

See also
 Adidas Cup
 Korean League Cup (Supplementary Cup)
 Samsung Hauzen Cup
 K League
 Korean FA Cup
 Korean Super Cup
 List of Korean FA Cup winners

References

External links
Official website
RSSSF

League Cup
National association football league cups
Recurring sporting events established in 1992
Recurring sporting events disestablished in 2012
1992 establishments in South Korea
2012 disestablishments in South Korea


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Specialist Project Engineer | WAIO | Jimblebar | FIFO
Location: Western Australia
About BHP
At BHP we support our people to grow, learn, develop their skills and reach their potential. With a global portfolio of operations, we offer a diverse and inclusive environment with extraordinary career opportunities. Our strategy is to focus on creating a safe work environment where our employees feel strongly connected to our values and objectives, and where the capability of our people is key to our success.
Come and be a part of this success.
This is a dynamic career role for an experienced Project management professional with excellent stakeholder engagement skills to join our Jimblebar Engineering team, fulfilling a broad scope of responsibilities across the project lifecycle from concept to handover; concept study, engineering design, technical, contractual and commercial requirements through to tender execution management and closeout.
Reporting to the Lead Project Engineer within the Engineering Modifications and Small Projects team on site you will manage and track approved modifications and small projects to the defined scope, budget and schedule, in accordance with relevant processes and standards.
Development of Project budgets, plans and schedules and supporting feasibility studies and cost- benefit analyses where required
Engaging and coordinating stakeholders during the execution of work including operations, maintenance, Project Supervisors, contractors and other functional groups
Engage and manage external consultants and contractors, ensuring their work is completed within the terms of the Contact and safely achieves the required outcomes
Providing technical input to the design of Engineering solutions
Monitoring and regularly reporting on project progress, ensuring action is taken to address deviations from the project program
Contributing to a safety orientated culture and ensuring the safety and quality of execution activities
You will have a genuine desire to develop your career yet contribute positively to team objectives, recognising the value of relationship building to influence and achieve business outcomes, communicating effectively at all levels.
You may also have the following:
A tertiary/degree qualification in Project Management and/or Engineering (preferred)
Experience across all aspects of the Project lifecycle
Previous leadership experience of contractors and small teams is desirable
Distinctive proficiency in executing Engineering Modifications & Small Projects, preferably in a mining or aligned environment
Exemplary interpersonal and communication skills
Experience managing the contractual and commercial components of project management
Demonstrated high-level negotiation and influencing skills to liaise and negotiate within internal and external departments and contractors
With this role you will be fly-in fly-out from Perth to Newman on a 5/2, 4/3 roster.
You will be working at Jimblebar mine site, which is located approximately 30kms from the Newman airport. The outstanding facilities at the FIFO villages include; a fully equipped gym, swimming pool, tennis and basketball court, beach volleyball court and recreation room including a pool table, darts, table tennis, TV and DVD player. All rooms at the village have their own en-suite bathroom, television, refrigerator and air-conditioning.
Remuneration and Benefits
Join us and be rewarded with interesting, challenging work in a supportive team culture. Develop skills for life whilst enjoying access to benefits including; incentive bonus, award winning share scheme, education assistance and generous superannuation scheme. As part of our commitment to inclusion and diversity, we offer a range of family friendly work practices, including flexible work arrangements, and a substantial parental leave policy, includes retirement savings / superannuation contributions during parental leave
Please apply online before 29 January 2023
You may be requested to complete a short video assessment as part of your application.
About Our Process
At BHP, we are committed to employing individuals who align with the BHP Charter Values and meet the requirements of the role. As part of the recruitment process, there are a number of checks which may be conducted to demonstrate applicants suitability for a role including police / criminal background checks, medical, drug and alcohol testing, due diligence checks, right to work checks, and/or reference checks.
To ensure the safety and wellbeing of our people, BHP requires employees in Australia to be fully vaccinated against Covid-19 in line with BHP's Covid Policy and any relevant State health directives. If you are applying for a role at BHP please consider this requirement when submitting your application. BHP will also adhere to any relevant health directives that may be made that affects our workforce.
Supporting a Diverse Workforce
The size and magnitude of our business not only provides significant opportunity for professional development, but also attractive salary packages with performance-based bonuses and a unique BHP employee share program.
At BHP, we recognise that we are strengthened by diversity. We are committed to providing a work environment in which everyone is included, treated fairly and with respect. We are an Equal Opportunity employer and we encourage applications from women and Indigenous people. We know there are many aspects of our employees' lives that are important, and work is only one of these, so we offer benefits to enable your work to fit with your life. These benefits include flexible working options, a generous paid parental leave policy, other extended leave entitlements and parent rooms.
IndustryMining, resources & energy
"It's similar to childcare in the sense that you're always moving around and it's very hands on. I'm clocking up about 15 kilometres of walking a day. Sometimes the shifts are long but then you get days off, so the flexibility is definitely there."
Karen Hogan
Process Technician


What do the different ship stats do?
For example what's the difference between hull and masts and sails? What do they affect?
Hull seems to be how much damage a ship can take in combat. When its hull reaches zero, it sinks.
Keel seems to be added in with hull somehow. When you take hull damage in combat, sometimes you need to do keel repairs when you get to port.
Masts and sails are also reduced in combat. I think when a ship loses all of its masts in combat, it surrenders. I think I've seen ships with no sails, but still having masts, continue to fight. I suspect sails has more effect on speed. I think that if you have more sails that your opponent, you have a better chance of controlling the range. So you can escape if you want to, or prevent your opponent from escaping. I'd also assume that the number of sails your ship has will affect it's speed when travelling as well, but I haven't tested this.
I've lost all my masts and died, told that a lucky shot brought the mast down.
In real life if you lose a mast -- in a single masted ship -- you stop dead in the water. But they still have to board you if they want to capture your ship. Of course if they managed to set the sails on fire, and the mast comes down, you have to put the fire out, as well, before the whole ship is a-blaze.
On sailing ships which only have cannon on the sides (generally all of them in the age of sail), once you've taken down your opponent's masts you can sail past his bow or stern where he can't return firs and blast away with impunity. This was known as "crossing his T". So once a ship's masts are down, it really has no choice but to surrender.
I second this question. I have been making comparissons to ST RPG but some of it obviously can't translate. Is this info up on another thread already?
Definitely check out the game Guide, available from the main menu in Age of Pirates.
That was the first place I looked Cory. I just checked again and the guide doesn't display any info on ship stats.
Thank you sir. You rock, as always. Now that I am finding some relaxation time to game again, it is a blast re-discovering all of the games you and fallen make. This one is definitely tertiary compared to all your other work, but I will always have a soft spot for carribean-esque pirate games.


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Brainflammation: The Role of the Innate Immune System in CNS Disorders
The New York Academy of Sciences
Presented by the Biochemical Pharmacology Discussion Group and the New York Chapter of the American Chemical Society
Neuroinflammation has been implicated in nearly every disorder of the CNS. As the resident innate immune cells of the CNS, microglia are the vanguard in host defense and in tissue repair. Their constant surveillance of the CNS enables them to rapidly respond to invading pathogens as well as mechanical or chemical injury. However, a growing body of evidence indicates that chronic or maladaptive activation of these very same cells plays a critical role in a variety of CNS disorders (including autism, psychiatric disorders, epilepsy, and neurodegenerative diseases such as AD, PD, ALS, and MS). Furthermore, recent work suggests that peripheral monocytes (another component of the innate immune system) may also become activated and then recruited to the CNS where they contribute to the regulation of neuroinflammation and the course of such disorders. These two cell populations, separated by the blood brain barrier and time, may therefore provide a key link between peripheral and central inflammatory processes. This symposium gathers experts on microglia/monocyte biology to discuss the role of the innate immune system in neurological disorders, what insights can be learned about their biology from their dysfunction in various disease contexts, and possible therapeutic interventions.
Networking reception to follow.
Member $25
Student / Postdoc / Fellow Member $10
Student / Postdoc / Fellow Nonmember $40
Nonmember Academic $60
Nonmember Not for Profit $60
Nonmember Corporate $80
* Presentation times are subject to change.
Registration & Continental Breakfast
Sean Pintchovski, PhD and Roland Staal, PhD, Lundbeck Research USA
The Impact of Systemic Inflammation on the Healthy and Diseased Brain
V. Hugh Perry, DPhil, University of Southampton, UK
Microglia and Monocytes: Kith or Kin?
Richard Ransohoff, MD, Lerner Research Institute
Microglia / Macrophage Responses during Chronological Aging
Dave Morgan, PhD, University of South Florida
CD45 and CD40 Modulation of Microglial Activation: Implications for Alzheimer's and HIV Associated Dementias
Jun Tan, MD, PhD, University of South Florida College of Medicine
Dysfunctional Microglia in the Pathogenic Mechanisms Underlying Autism
Carlos A. Pardo-Villamizar, PhD, Johns Hopkins University School of Medicine
An Imbalanced Neuro-immuno-endocrine Set Point as a Cause for Major Mental Disorders
Hemmo A. Drexhage, MD, PhD, Erasmus Medical Center
Seizing Opportunities in Microglial Biology for Epilepsy
Annamaria Vezzani, PhD, Mario Negri Institute for Pharmacological Research
Microglia, What a (Neuropathic) Pain!
Ru-Rong Ji, PhD, Harvard University and Brigham & Women's Hospital
Robert Martone
Covance Biomarker Center of Excellence
Robert Martone is Neuroscience Therapeutic Area Lead for the Covance Biomarker Center of Excellence. He has extensive experience in the pharmaceutical industry leading neuroscience drug discovery and technology teams through all phases of discovery from target identification through clinical trials with expertise in both small molecule and protein therapeutics. He also has several years of academic research experience in molecular neurobiology, with a focus on the molecular genetics of familial neuropathies, and CNS tumor biomarker development.
Sean Pintchovski, PhD
Lundbeck Research USA
Dr. Pintchovski earned a BS with Honors from the California Institute of Technology and a PhD in Neuroscience from the University of California, San Francisco while working at the Gladstone Institute of Neurological Disease and studying the regulation of neuronal gene expression underlying memory and cognition. After completing a postdoctoral fellowship at Elan Pharmaceuticals, where he worked to further elucidate key processes that contribute to cognitive decline in Alzheimer's disease, Dr. Pintchovski joined the Neuroinflammation Department at Lundbeck as a research scientist in early 2010. At Lundbeck his efforts have focused on applying a range of cutting edge techniques, including ex vivo FACS, to uncover how dysregulation of the immune system contributes to the pathogenesis of various neurodegenerative and psychiatric conditions. Dr. Pintchovski is driven by the desire to translate such fundamental discoveries into novel therapeutic approaches that will address the medical and social challenges posed by these devastating diseases.
Roland Staal, PhD
Roland Staal received his PhD in Pharmacology from the University of Medicine and Dentistry of NJ with a focus on in vivo models of dopaminergic neurodegeneration, including amphetamines and MPTP, an animal model of Parkinson's disease. He did his post-doctoral studies at Columbia University, where he studied the function of alpha-synuclein as well as its role in sensitizing mice to the Parkinsonian neurotoxin MPTP. He then joined Wyeth Research's department of neurodegeneration, studying protein mis-folding and potential therapeutic interventions including aggregation inhibitors and immunotherapies for both Parkinson's and Alzheimer's disease. He then joined Lundbeck Research, where he was instrumental in establishing the Neuroinflammation biology unit. The unit works with various technologies including flow cytometry, cell sorting, ELISAs and Cellomics to evaluate various markers and outcomes of Neuroinflammation in in vivo models as well as cell lines and primary neuronal and microglial cultures. His current focus is on targeting neuroinflammatory aspects of CNS diseases, in particular, neuronal–microglial communication.
Jennifer Henry, PhD
Hemmo A. Drexhage, MD, PhD
Erasmus Medical Center
Dr. Hemmo A. Drexhage is professor in Medical Immunology at the ErasmusMC (Rotterdam). He graduated from medical school in 1974 (Amsterdam), defended his immunology PhD thesis in 1977 (Amsterdam) and studied immunology/medical immunology with Brigid Balfour/John Humphrey (Mill Hill) and Ivan Roitt and Deborah Doniach (Middlesex Hospital) in London from 1976–1981 (on exchange grants of the Royal Dutch and English Societies of Science). His subject of studies has ever since been focussed on the clinical picture and immune diagnosis of autoimmune diseases of endocrine glands (thyroid, islets of Langerhans, adrenal, ovary, pituitary) and the initiating role of aberrant dendritic cells and macrophages in thepathogenesis of these diseases. The higher prevalence of endocrine autoimmunities in severe mood disorders sparkled in 1996 his interest into studies on the role of immune cells in bipolar disorder, major depressive disorder, post partum psychosis and schizophrenia. He has published over 350 articles/book chapters on these subjects and supervised more than 30 PhD students.
Ru-Rong Ji, PhD
Harvard University and Brigham & Women's Hospital
Ru-Rong Ji received his PhD degree in Neurobiology at Shanghai Institute of Physiology, Chinese Academy of Sciences. He had postdoctoral trainings in Peking University, Karolinska Institute, and Harvard Medical School. Currently he is an associate professor at Brigham and Women's Hospital, Harvard Medical School. He is also director of Sensory Plasticity Laboratory and associate director of the Pain Research Center. He has been working on spinal cord mechanisms of chronic pain for 20 years. His work has demonstrated important roles of glial cells (eg., microglia), MAP kinase signaling pathways, and cytokines/chemokines in the control of neuropathic pain. His recent work has also revealed important role of pro-resolution lipid mediators in the resolution of inflammation and pain. Dr. Ji has published more than one hundred papers on chronic pain mechanisms and treatments.
Dave Morgan, PhD
Dave Morgan is Chief Executive Officer/Director of the USF Health Byrd Alzheimer Institute, Distinguished Professor of Molecular Pharmacology and Physiology, and Director of Neuroscience Research for the College of Medicine and at the University of South Florida. Dr. Morgan's research interests are aging and brain function, focusing on drugs to treat Alzheimer's dementia. Morgan participated in the development of a transgenic mouse model of Alzheimer's disease (APP+PS1). His work focuses largely on the neuro-immune interactions associated with the Alzheimer phenotype, and the role of astrocytes and microglia in the disease process. He is presently testing anti-amyloid immunotherapy and gene therapy to treat the Alzheimer-like changes in transgenic mouse models of the disease. This work is supported by multiple grants from the NIH, private foundations and contracts from industrial partners. Morgan regularly sits on review panels for NIH and other agencies evaluating grants to develop new drugs to treat Alzheimer's and other neurodegenerative disorders.
Carlos A. Pardo-Villamizar, MD
Dr. Pardo is an Associate Professor of Neurology and clinician-scientist at Johns Hopkins University School of Medicine, Department of Neurology (Division of Neuroimmunology and Neuroinfectious Disorders) and Pathology (Neuropathology) in Baltimore, Maryland. He is the principal investigator of the Neuroimmunopathology Laboratory, member of the HIV Neurosciences Research Group and clinical neurologist at the Multiple Sclerosis and Transverse Myelitis Centers at Johns Hopkins Hospital. Dr. Pardo's research interest and laboratory work focuses on studies of the 1) Immunopathological and molecular mechanisms of associated with neuroimmune disorders such as multiple sclerosis, neuroAIDS as well as epilepsy and autism, 2) the role of cytokines and chemokines in neurobiological processes and pathogenic mechanisms in neurological disorders, 3) Studies of biomarkers of neuroimunological disease in cerebrospinal fluid and blood and 4) Animal models of neuroimmunological disorders. Dr. Pardo's interest on autism centers on the role of neuroimmune factors and neuroglia in the pathogenesis of this neurodevelopmental disorder. His laboratory has contributed to the study of the role of microglia activation in the cerebral cortex and the function of cytokines and chemokines as factors involved in neurobiological processes associated with disturbances of developmental and neurobehavioral trajectories that characterize autism. His laboratory is also working on the identification of CSF and blood biomarkers that may facilitate a better understanding of pathogenesis and phenotypic characterization of autism.
V. Hugh Perry, DPhil
University of Southampton, UK
Hugh Perry obtained his first degree at the University of Oxford where he completed his DPhil in neuroscience in 1977. He remained at the University of Oxford and was appointed to a Locke Fellow of the Royal Society and then a Wellcome Trust Senior Research Fellow. He was appointed Professor in Experimental Neuropathology (1996). In 1998 he moved to the University of Southampton to take up his current post. His research interests are in the field of interactions between the immune system and nervous system. He has published more than 275 peer-reviewed papers. He has sat on research advisory and funding panels for the Medical Research Council, and a number of biomedical charities including the Multiple Sclerosis Society, International Spinal Research Trust and Motor Neuron Disease Association: he chaired the Cellular and Molecular Neuroscience panel of the Wellcome Trust 2004–2007. He has acted as a consultant for biotechnology and pharmaceutical companies in the area of neuroinflammation and neurodegenerative disease. He was elected a Fellow of the Academy of Medical Sciences (2005), is Deputy Chair of the Nuffield Council on Bioethics. He has been appointed to Chair of the Medical Research Council Neuroscience and Mental Health Board from 1st April 2012.
Richard Ransohoff, MD
Lerner Research Institute
Richard M. Ransohoff serves at the Cleveland Clinic as Director of the Neuroinflammation Research Center in the Department of Neurosciences of the Lerner Research Institute; Professor of Molecular Medicine at the Cleveland Clinic Lerner College of Medicine; and Staff Neurologist in the Mellen Center for MS Treatment and Research.
Among his many awards are a Physician's Research Training Award from the American Cancer Society (1984–86); a Clinical Investigator Development Award from the National Institutes of Health (NIH; 1988–1993); the Cleveland Clinic Lerner Research Institute's Award for Excellence in Science in 2006; the Cleveland Clinic's Scientific Achievement Award in Basic Science 2009. He was invited to give the F. E. Bennett Memorial Lecture to the American Neurological Association in 2009. He has been cited from 1996 through the present in "Best Doctors in America" for his expertise in the clinical care of patients with multiple sclerosis (MS).
Dr. Ransohoff serves as regular member on study sections of the NIH and NMSS (as Chair) and is currently a regular member of the CMBG Study Section. He has served on the Editorial Boards of The Journal of Immunology, (2002–2005 as Section Editor) Trends in Immunology, the Journal of Neuroimmunology; Nature Reviews Immunology, and Neurology (Associate Editor).
Dr. Ransohoff's research focuses on the functions of chemokines and chemokine receptors in development, cell biology and pathology of the nervous system. With a longstanding interest in the mechanisms of action of interferon-beta. Dr. Ransohoff has received continuous research support from the NIH and the NMSS for more than 20 years. In Entrez/PubMed, he lists more than 275 articles of which more than 215 are peer-reviewed scientific reports. He has written numerous book chapters, and edited five books.
Dr. Ransohoff is a member of the American Academy of Neurology, the American Neurological Association, and the American Association of Physicians and is a Fellow of the American Association for the Advancement of Science.
Jun Tan, MD, PhD
In 1983, Dr. Jun Tan received his Bachelors of Medicine at the Third Medical University in Chongqing, China. He went on to earn his Masters of Science in human genetics at Fudan University, Shanghai in 1989. Three years later, he completed his Doctoral Degree at the Third Medical University/Fudan University. Following, he was promoted to both full Professor and Chief of the Department of Molecular Genetics from 1990 to 1994 at the Third Medical University in Chongqing, China. He completed postdoctoral studies in 1996 at the Department of Human Genetics/Immunology at the University of Michigan, Ann Arbor. Dr. Tan then completed his research fellowship in 1998 at H. Lee Moffitt Cancer & Research Institute in Tampa, Florida. Upon completion, he became Assistant Professor of Psychiatry and Microbiology & Immunology at the University of South Florida (USF) in 1998 and Associate Professor 2004. In 2007, Dr. Tan was named the Robert A. Silver Endowed Chair in Developmental Neurobiology and currently directs the Developmental Neurobiology Laboratory at the Silver Child Development Center, USF Department of Psychiatry. Dr. Tan has published over 100 scientific papers, several of them in journals such as Science, Nature Neuroscience, Nature Medicine, EMBO J, PNAS, Journal of Neuroscience, Journal of Immunology, JBC, PloS One, Neurobiology of Disease, and The European Journal of Immunology. Based on these works, Dr. Tan is the recipient of a number of federal grants as PI, including NIH/NINDS (R01/2004), NIH/NIA (P01/2006), NIH/NIA (R01/2009), NIH/NIMH (R21/2007/2010), NIH/NIA (R21/2010) and NIH/NIA (STTR/SBIR/2006/2008/2009). In addition, he also receives funding from the James A. Haley VA Medical Center (2009), the Alzheimer's Association (2004), as well as the Johnny Byrd Alzheimer Center & Institute (2005/2006), and The Institute for the Study of Aging (ISOA/2006).
Annamaria Vezzani, PhD
Mario Negri Institute for Pharmacological Research
Annamaria Vezzani, PhD degree in Neuropharmacology in Milano at the Mario Negri Inst for Pharmacol Res (IRFMN). She spent her post-doctoral period at the Univ of Maryland in Baltimore working in experimental models of epilepsy. Additional post-doctoral periods were done at the Univ of Stockholm and at the Karolinska Institute. She was on sabbatical at the Albert Einstein College of Medicine in 2002 in the laboratory of Developmental Epilepsy.
The present research is on the functional role of neuroactive peptides and inflammatory mediators in the modulation of seizures and in the mechanisms of pharmacoresistance. Since 1997 she is Head of the Laboratory of Experimental Neurology in the Department of Neuroscience at the IRFMN.
Dr. Vezzani is member of the Editorial Board of Epilepsy Currents, Epilepsy Research, Epilepsy and Treatments and Neuroscience and Associate Editor of Basic Science for Epilepsia. She has been appointed (2006–2009) of the Chair of the Commission on Neurobiology of International League Against Epilepsy promoting initiatives for improving translational research in epilepsy. She received the Research Recognition Award for translational research in 2009 by the American Epilepsy Society.
For sponsorship opportunities please contact Carmen McCaffery at cmccaffery@nyas.org or 212.298.8642.
This activity is supported by an educational donation provided by Amgen.
Academy Friends
Alzheimer Research Forum
Dana Foundation
V. Hugh Perry, DPhil, University of Southampton
The resident macrophages of the brain, the microglia, are observed to be morphologically activated and increase in number during the progression of many chronic neurodegenerative diseases. Observational studies in human postmortem material and studies in animal models seek to define the contribution that this innate immune response makes to the pathogenesis and rate of progression of these diseases. It is well recognized that age is a significant risk factor for diseases such as Alzheimer's disease and Parkinson's diseases and that elderly people commonly have systemic co-morbidities that give rise to systemic inflammation. There is a growing body of evidence to show that systemic infection and inflammation impacts on the progression of chronic neurodegeneration in animal models and that this involves the switching of the microglia phenotype to an aggressive tissue damaging phenotype by the systemic inflammation. Clinical studies in patients with Alzheimer's disease show that chronic systemic inflammation and acute infections are associated with accelerated cognitive decline and exacerbation of the symptoms of sickness. These findings offer new routes to therapeutic interventions to improve the quality of life of those suffering from chronic neurodegenerative disease.
Richard Ransohoff, MD, Lerner Research Institute, Cleveland Clinic
Microglia are the resident mononuclear phagocytes (MNP) of the central nervous system (CNS). In the healthy brain, parenchymal microglia exhibit are pressed phenotype, maintained by soluble and membrane-associated inhibitory factors of adjacent neurons and astrocytes, and contingent as well upon the blood-brain barrier's exclusion of plasma proteins. Microglial processes are constitutively motile, monitoring the local microenvironment and palpate synapses. In response to disturbance of CNS homeostasis, microglia undergo morphological and phenotypic changes collectively termed 'activation'. Effector functions of activated microglia are enormously diverse and can either enable or impede CNS recovery, dependent on context. Often, CNS disorders featuring microglial activation are also accompanied by accumulation of blood-derived monocytes in the parenchymal tissues. Both microglia and monocytes give rise to macrophages. Several lines of evidence indicate functional differences between monocyte-derived macrophages as compared with those differentiated from microglia. However, no immunohistochemical markers distinguish monocyte-derived macrophages from resident microglial macrophages. Novel murine genetic models discriminate between resident microglia and infiltrating monocytes, both in the healthy brain and during autoimmune inflammation. Understanding the differential and context-depending roles of hematogenous as compared with brain-derived macrophages will add a new dimension of refinement to therapeutic strategies that target neuroinflammation.
Microglial activation in the brain is thought to confer either beneficial or detrimental impacts on the nervous system depending upon the context and type of activation. Most studies of microglia activation in response to various stimuli use either young mice or cells in culture. We have found that the microglial response to activating stimuli in mouse brain differs as a function of mouse age. Moreover, the classical and alternative forms of activation seem to respond to age and antibody therapy in opposite directions. A still unanswered question is the degree to which circulating monocytes can infiltrate the immune system. We find that in brain that is perturbed by the presence of amyloid deposits that sufficient circulating monocytes enter the brain to supply it with a potentially therapeutic gene (neprilysin). Moreover, we find that age appears to increase the extent of monocyte infiltration in both normal as well as mice with amyloid deposits. These results caution that data obtained in young mice may not translate effectively to aged human brain.
Deposition of amyloid-β peptide (Aβ) as β-amyloid plaques in the setting of microgliosis is a defining pathological hallmark of Alzheimer's disease (AD). However, reactive microglia ultimately fail to clear Aβ in brains of AD patients and in mouse models of the disease. It has even been suggested that chronic microglial immune responses contribute to AD pathogenesis by promoting Aβ plaque formation, but the molecular mechanisms underlying this deleterious response have remained elusive. The main focus of our research has been on the role of the CD40–CD40 ligand (CD40L) interactions in regulation of microglia for the treatment of neurodegenerative disease. Over the past years, we discovered that the CD40–CD40L interaction plays a critical role in abnormal amyloid β (Aβ)-induced microglial activation. We have investigated the role of CD45, a membrane-bound protein–tyrosine phosphatase (PTP), in negative regulation of this pathway. The latter work has suggested that triggering CD45 is beneficial because it blocks a very early step in the development of AD. Most recently, we have shown that transgenic mice overproducing Aβ, but deficient in CD45 (PSAPP/CD45−/− mice), faithfully recapitulate AD neuropathology. Specifically, we found: increased abundance of cerebral intra- and extracellular soluble oligomeric and insoluble Aβ, decreased plasma soluble Aβ, increased abundance of microglial neurotoxic cytokines TNF-α and IL-1β, and neuronal loss in PSAPP/CD45−/− mice compared to CD45 sufficient PSAPP littermates. Upon CD45 ablation, in vitro and in vivo studies demonstrate an anti-Aβ phagocytic but pro-inflammatory microglial phenotype. This form of microglial activation occurs with elevated Aβ oligomers and neural injury and loss as determined by decreased ratio of anti-apoptotic Bcl-xL to pro-apoptotic Bax, increased activated caspase-3, mitochondrial dysfunction, and loss of cortical neurons in PSAPP/CD45−/− mice. These data show that deficiency in CD45 activity leads to brain accumulation of neurotoxic Aβ oligomers, and validate CD45-mediated microglial clearance of oligomeric Aβ as a novel AD therapeutic target.
As an extension of this work in a related neurodegenerative disease, HIV associated cognitive disorders (HAND), we investigated the possible role of CD45 in microglial responsiveness to HIV-1 Tat protein. We BV2 microglia when treated with phen and HIV-1 Tat protein (100 nm) become activated in a synergistic pro-inflammatory manner as supported by TNF-α and IL-1β release, both of which were dependent on p44/42 MAPK pathway activation. Stimulation of microglial CD45 by anti-CD45 antibody markedly inhibits these Tat or Tat/phen effects via inhibition of p44/42 MAPK, suggesting CD45 negatively regulates Tat mediated microglial activation. As a validation of these findings in vivo, brains from a transgenic mice deficient for CD45 demonstrate markedly increased production of TNF-α 24 hours after intracerebroventricular injection of Tat (500 ng/mouse) compared to control mice. This increased microglial activation was accompanied by astrogliosis and a significant loss of cortical neurons due to apoptosis in CD45 deficient animals. These results suggest therapeutic agents that activated CD45 PTP signaling may be effective in suppressing microglial activation associated with not only AD, but HAND as well.
Microglia in the Pathogenic Mechanisms Underlying Autism
Autism spectrum disorders (ASD) are part of neurodevelopmental abnormalities that have produced an important impact on the magnitude of neurological and developmental problems that affect the overall health of the pediatric population. Approximately 1 in 150 children in the United States is diagnosed with any of the autism spectrum disorders. Most of the neurobiological studies demonstrate that the main core of neuropathological abnormalities in ASD are characterized by disturbances in neuronal organization, such as an excessive number of neurons, simplification of dendritic organization and disorganization of cortical lamination. Studies from our laboratory and others have disclosed the role of microglia and neuroimmune responses in cortical regions of brains of children with ASD. These studies support the view that activation of neuroglia cells and neuroimmune mediators such as cytokines, chemokines and signaling pathways such as Toll-like receptors (TLRs) may influence neuronal and synaptic function and contribute to the pathogenic mechanisms and neurobehavioral processes present in ASD. Interestingly, the pattern of neuroglial and innate immune activation follows a pattern of selective involvement of areas of the cerebral cortex known to be dysfunctional in ASD such as the frontal and cingulategyri as well as cerebellum.
An imbalanced immuno-endocrine system will be described in patients with severe mental disorders, in individuals at risk for such disorders and in animal models of anxious and schizophrenia-like behavior. This imbalance consists for monocytes/macrophages of over and under expression of coherent sets of activating and suppressing genes (including the glucocorticoid receptor genes) and for the T cell system in raised numbers of both Th1, Th17 and Treg cells. At the level of the microglia such activation does also exist in both patients and animal models (particularly in the hippocampal area), evidence is given that such microglia activation impacts neuronal development and function. Measuring the immuno-endocrine imbalances make predictions for therapy outcome in patients possible.
Experimental research has demonstrated a prominent role of glial cells, activated by various brain injuries, in the mechanisms of neuronal damage, seizure precipitation and recurrence, as well as in some neurological dysfunctions often associated with neurodegenerative disorders and epilepsy. In particular, alterations in the phenotype and function of activated astrocytes and microglial cells have been described in experimental and human epileptic tissue, including induction of molecules involved in inflammatory processes. Brain injury can activate innate immune mechanisms involving microglia and astrocytes which in turn release a number of danger signals and proinflammatory mediators, thus initiating a cascade of inflammatory processes in brain tissue. Proinflammatory molecules can alter neuronal excitability and affect the physiological functions of glia by paracrine or autocrine actions, thus perturbing the glio-neuronal communications. In this context, understanding which are the soluble mediators and the molecular mechanisms crucially involved in glio-neuronal interactions is instrumental to shed light on how brain inflammation may contribute to neuronal hyperexcitability, cell loss and maladaptive plasticity in CNS disorders, thus highlighting possible novel therapeutic options.
Neuropathic pain after nerve injury is a growing heath problem. Increasing evidence suggests that peripheral nerve injury induces dramatic changes in spinal cord microglia, such as increased expression of microglia makers (eg., CD11b and Iba1), morphological changes of microglia (hypertrophy), and proliferation of microglia. In particular, nerve injury such as spinal nerve ligation induces dramatic activation (phosphorylation) of p38 MAP kinase selectively in spinal cord microglia. Further, spinal (intrathecal) injection of p38 inhibitor was shown to attenuate nerve injury-induced neuropathic pain symptom in rats and mice, such as mechanical allodynia, pain elicited by normally innocuous mechanical stimulus. Activation of p38 in microglial cells has been shown to induce the expression and release of the proinflammatory cytokines TNF-α and IL-1β and the neurotrophin BDNF. Spinal inhibition of TNF-α, IL-1β, or BDNF has been shown to reduce nerve injury-induced mechanical allodynia. Importantly, microglial mediators can powerfully modulate synaptic transmission in the spinal cord. Specifically, TNF-α, IL-1β, and BDNF can not only increase excitatory synaptic transmission but also decrease inhibitory synaptic transmission in the spinal cord. Thus, activation of spinal cord microglia contributes to the pathogenesis of neuropathic pain via neuron–glial interactions. Targeting microglia signaling may lead to new therapies for the management of devastating neuropathic pain. Finally, I will also discuss new strategies that can inhibit microglia and cytokine signaling for effective pain management.
* Additional abstracts coming soon.
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text:
Étienne Bézout, né à Nemours le  et mort aux Basses-Loges, dans la paroisse d'Avon, le , est un mathématicien français. Il est passé à la postérité pour le théorème de Bachet-Bézout en arithmétique, pour le Bézoutien, utilisé en algorithmique, et pour son  théorème sur le nombre de points d'intersection de deux courbes algébriques, résultat crucial en géométrie algébrique.

Biographie
Fils d'un magistrat de Nemours, Pierre Bézout, et de Jeanne-Hélène Filz, il est nommé par Étienne François de Choiseul en 1763 examinateur des gardes de la marine. Puis, il est chargé de la rédaction d'un cours de mathématiques qui conduira au Cours de mathématiques à l'usage des gardes du pavillon et de la marine. À la mort de Charles-Étienne Camus en 1768, il est nommé examinateur des élèves du corps de l'artillerie et rédige le Cours complet de mathématiques à l'usage de la marine et de l'artillerie, qui devient plus tard le livre de référence des candidats au concours d'entrée à l'École polytechnique.

Il est également l'auteur d'une Théorie générale des équations algébriques, publiée en 1779, consacrée à la théorie de l'élimination et aux fonctions symétriques des racines d'une équation algébrique : il utilise les déterminants dans un article de l'Histoire de l'Académie royale, parue en 1764, mais ne traite pas de la théorie générale.

Il est nommé adjoint mécanicien à l'Académie royale des sciences le , associé mécanicien-géomètre le , puis pensionnaire mécanicien surnuméraire le , enfin pensionnaire mécanicien le .

Il meurt prématurément le 27 septembre 1783, possiblement suite aux émanations de l'éruption catastrophique du volcan islandais Laki de 1783, qui a augmenté notablement le taux de mortalité en europe fin 1783, époque où sont mort également Euler et d'Alembert. Sa sépulture est dans l'église Saint-Pierre d'Avon.

Publications

 Cours de mathématiques à l'usage des gardes du pavillon et de la marine, première partie Éléments d'arithmétique, Imprimerie Ph.-D. Pierres, Paris, 1781 (lire en ligne)
 Cours de mathématiques à l'usage des gardes du pavillon et de la marine, seconde partie contenant les éléments de géométrie, la trigonométrie rectiligne & la trigonométrie sphérique, Imprimerie Ph.-D. Pierres, Paris, 1782 (lire en ligne)
 Cours de mathématiques à l'usage des gardes du pavillon et de la marine, troisième partie, contenant l'algèbre et l'application de cette science à l'arithmétique et la géométrie, chez J. B. G. Musier, Paris, 1766 (lire en ligne)
 Cours de mathématiques à l'usage des gardes du pavillon et de la marine, quatrième partie, contenant les principes généraux de la mécanique, précés des principes de calcul qui servent d'introduction aux sciences physico-mathématiques, imprimerie Baudelot et Eberhart, Paris, an IV (lire en ligne)
 Suite du cours de mathématiques à l'usage des gardes du pavillon et de la marine contenant le traité de navigation, chez J. B. G. Musier, Paris, 1769 (lire en ligne)
 Cours de mathématiques, à l'usage du corps de l'artillerie, tome 1, contenant l'arithmétique, la géométrie et la trigonométrie rectiligne, chez Richard, Caille et Ravier libraires, Paris, an VIII (lire en ligne)
 Cours de mathématiques, à l'usage du corps de l'artillerie, tome 2, contenant l'algèbre et l'application de l'algèbre à la géométrie, Imprimerie Ph.-D. Pierres, Paris, 1788 (lire en ligne)
 Cours de mathématiques, à l'usage du corps de l'artillerie, tome 3, contenant les principes généraux de la mécanique, & l'hydrostatique ; précédés des principes de calcul qui servent d'introduction aux sciences physico-mathématiques, Imprimerie Ph.-D. Pierres, Paris, 1788 (lire en ligne)
 Cours de mathématiques, à l'usage du corps de l'artillerie, tome 4, contenant l'application des principes généraux de la mécanique à différents cas de mouvement & d'équilibre, chez Richard, Caille et Ravier libraires, Paris, an VII (lire en ligne)
 Théorie générale des équations algébriques, Imprimerie Ph.-D. Pierres, Paris, 1779 (lire en ligne)
 Cours de mathématiques à l'usage des gardes du Pavillon et de la Marine. Impr. Baudelot & Eberhart, Paris, 1795. Texte disponible en ligne sur IRIS : 3ème partie ; 4ème partie ; Suite de la 4ème partie

Mémoires de l'Académie royale des sciences
 Mémoire sur les Courbes dont la rectification dépend d'une quantité donnée, 1758,  (lire en ligne)
 Mémoire sur plusieurs classes d'équations de tous les degrés qui admettent une solution algébrique ; 1762,  (lire en ligne)
 Recherches sur le degré des Équations résultantes de l'évanouissement des inconnues, & sur les moyens qu'il convient d'employer pour trouver ces équations, 1764,  (lire en ligne)
 Mémoire sur la résolution générale des équations de tous les degrés, 1765,  (lire en ligne)
 Formules calculées par Monsieur Bézout ajoutées au Mémoire sur quelques expériences relatives à la dioptrique par M. le Duc de Chaulnes, 1767,  (lire en ligne)
 Avec Lavoisier et Vandermonde, Expériences faites par ordre de l'Académie, sur le froid de l'année 1776, 1777,  (lire en ligne)

Mémoires de mathématique et de physique présentés à l'Académie royale des sciences
 Mémoire sur les quantités différencielles, qui n'étant point intégrables par elles-mêmes, le deviennent néanmoins quand on leur joint des quantités de même forme qu'elles, Imprimerie royale, Paris, 1760, tome 3,  (lire en ligne)

Annexes

Bibliographie
 Nicolas de Condorcet, Éloge de M. Bezout, dans Histoire de l'Académie royale des sciences - Année 1783, Imprimerie royale, Paris, 1786,  (lire en ligne)
 BEZOUT (M.), dans Table générale des matières contenues dans l'"Histoire" et dans les "Mémoires de l'Académie royale des sciences", chez Panckoucke, Paris, 1768, tome 7, 1751-1760,  (lire en ligne)
 BEZOUT (M.), dans Table générale des matières contenues dans l'"Histoire" et dans les "Mémoires de l'Académie royale des sciences", chez Panckoucke, Paris, 1774, tome 8, 1761-1770,  (lire en ligne)
 BEZOUT (M.), dans Table générale des matières contenues dans l'"Histoire" et dans les "Mémoires de l'Académie royale des sciences", Imprimerie de Moutard, Paris, 1786, tome 9, 1771-1780,  (lire en ligne)

Articles connexes
 Anneau de Bézout
 Liste des membres de l'Académie royale des sciences

 Méthode de Bézout
 Théorème de Bachet-Bézout
 Théorème de Bézout

Liens externes
 Académie des sciences : Les membres du passé dont le nom commence par B

Ouvrages de Bézout numérisés par le SCD de l'Université de Strasbourg
Texte de Bézout (1764) sur la résolution des équations algébriques, en ligne et commenté sur Bibnum
 Liliane Alfonsi, Un « savant » du siècle des Lumières : Étienne Bézout (1730-1783), mathématicien, académicien et enseignant (lire en ligne)

Bases de données et dictionnaires

Notes et références

Mathématicien français du XVIIIe siècle
Membre de l'Académie des sciences (France)
Membre de l'Académie de marine
Auteur de manuel scolaire
Éponyme d'un objet céleste
Naissance dans la province d'Île-de-France
Naissance à Nemours
Naissance en mars 1730
Décès en septembre 1783
Décès à 53 ans


text:
3 Tips for Creating an Office That Inspires Innovation
Ideas by We
This story was originally published on Ideas by We, WeWork's home for the latest on work strategy, lifestyle, and trends that go beyond business as usual. Check out the latest stories.
There's an immense amount of pressure on businesses to innovate ahead of the competition. It's that ability to stay two (or 10) steps ahead of the pack that allows for the biggest gains.
The path to innovation seems straightforward: It starts with hiring the best talent, who will think up new and novel solutions; putting them into action; learning and iterating. But in today's world, it doesn't end there.
Hiring top talent and then asking them to do their best work in a suboptimal office environment is a recipe for disaster. Have you experienced (or may be experiencing now) surroundings that remind you more of the movie Office Space than an innovation superhub?
"The world's most innovative companies optimize every aspect of their business—including their physical workspace."
The ability to think creatively, to imagine possibilities, to connect those dots that will drive business into the future can feel impossible when you spend your entire day in a windowless office with no natural light. Or when you feel chained to a desk. A depressing physical workspace may hinder even the most talented hire from thinking of their next big idea.
So, how should employers set the stage for innovation within their own workspaces? As part of the workplace strategy team here at WeWork, we've spent a lot of time optimizing the workplace experience so that employees can do their best work. Here are three ways you can rethink your workspace to encourage innovation among your own teams.
1. Make your workspace "hackable"
When teams are tasked with innovation, there's an expectation that employees will quickly be ideating, prototyping, and testing things out—so shouldn't their workspace be agile as well? In other words, shouldn't employees feel empowered to physically "hack" a conventional office setup?
What exactly does this mean? From desks to chairs, couches to tables, employees should have the ability to mold their workspace into what they need, rather than what the employer may have originally envisioned. For example, WeWork has made sure some of our furniture can be moved by adding handles and other visual cues. Employees can configure the space for their needs, whether it's a large group brainstorm or a comfortable place to work alone. In essence, we think of workspace as "software," or possessing the ability to be updated on-demand, rather than "hardware," which is static and unchanging. Employees should be encouraged to create an environment in which they feel comfortable and inspired—much like the feeling of a residential home.
A great example of this came from my recent visit to IDEO, an international design and consulting firm founded in Palo Alto, California. Their philosophy is that "hackable" workspace enables employees to make their actual work more scrappy and experimental. When imagining what it feels like to have a wall in certain space, for instance, IDEO employees put up cardboard walls and tested different arrangements to see how behaviors change within the space.
The result of all this space-hacking? A workspace environment in which people were enthusiastic about sharing ideas and solving problems. Moreover, employees in hackable spaces feel free to express their ideas and opinions without punishment; in other words, the employees feel psychologically safe to express themselves.
How important is psychological safety? In researching the dynamics of high-performing teams, Google's people operations department identified psychological safety as the first of five essential ingredients. Losing that fear of repercussion for trying something new makes employees feel empowered to take risks, have candid discussions, and brainstorm creative solutions. To them, failure is a learning experience, and confronting issues leads to positive outcomes. All of this can be fostered and encouraged by the right workspace.
2. Build a unique culture with rituals
All companies have rituals—from the mundane everyday routines (coffee breaks, tea time) to major, less frequent events like annual meetings and retirement parties. They're simple actions that connect us to ourselves, our place, and the moment. But did you know that workspace rituals can also have an effect on your employees when it comes to innovation?
Employees who are encouraged and empowered to initiate specific activities within their work environment tend to strengthen their sense of belonging within their team. In essence, rituals create a shared identity between people. Successful sports coaches, for example, typically use rituals to build social bonds between team members.
It's important to note the difference between a standard ritual and those rituals designed to encourage innovation. At WeWork, for example, we not only serve fresh coffee daily; we do so in a kitchen designed as a "center of gravity"—a place designed for people to naturally want to gather, chat, and share ideas. We don't just have a reception area; we have a whole community team whose job it is to make sure employees feel taken care of. And on Mondays, our team dinners are about more than food—they're about coming together after the weekend to connect and discuss the week ahead. All of these rituals contribute to employees feeling like they're part of a community, which contributes to the psychological safety needed to innovate.
In essence, workspace design can help create those rituals, but it's that layer of connection that really reinforces everyday activities with positive memories. Day after day, these rituals stimulate emotions and reduce anxiety, while increasing a sense of belonging and creating the right environment for innovation.
3. Add an element of play
Incorporating playfulness into everything we do is essential in developing the flexibility our brains need to access innovation and creativity (which decreases dramatically as we become older). According to Stuart Brown, M.D. and Christopher Vaughan, authors of Play: How It Shapes the Brain, Opens the Imagination, and Invigorates the Soul, play at its essence is the act of doing things "just because."
Play is:
Apparently purposeless
Inherent attraction
Freedom from time
Diminished consciousness of self
Improvisational potential
Continuation of desire
In the brain, play directly stimulates the neurotrophic factor (nerve growth), amygdala (emotion processing), and dorsolateral prefrontal cortex (executive decisions). Studies have shown, for example, that rats further develop their brains via a variety of stimuli while playing with toys and socializing with other rats.
Specifically, indicators for innovation can be found within emotionally charged early play memories, which become stronger in children as their brains develop. But in fact, when it comes to innovation, play shouldn't stop at childhood. If you incorporate more opportunities for playfulness into your workspace, you'll enable your employees to exercise their creative-thinking muscles on the way to their next innovative idea.
For example, try inviting your employees to brainstorm without a time limit (i.e., make sure no one feels guilty when hitting pause on their projects) for an afternoon to invite more playtime into their schedule. By encouraging this time, you're setting expectations with your employees that it's their job to be creative and drive innovation and your job as an employer to create an environment in which innovation happens.
Setting the stage for innovation
The world's most innovative companies optimize every aspect of their business—including their physical workspace. It's no longer enough just to hire the best of the best—to innovate at a competitive speed that talent needs a space in which to do their best work. This allows you to set the stage for innovative ideas that will drive your business forward.
WeWork offers companies of all sizes space solutions that help solve their biggest business challenges.


text:
puckstruck
the culture of hockey, and vice-versa
bookstruck
notes + sources
puckstruck sources
[p. 141] a slight sneer mantled joliat's lean bronze face
[p. 278] snubbing morenz
[p. 87] how to hook-check
[p. 327] like an orc chieftain
[p. 254] michael cusack
[p. 322] dave dryden
all (hockey) roads lead to peterborough
books for troubled times
gretzky's tears
gump worsley's pineapple squares
his name is orr
under review: no pink tea
oh, dear
the secret to hockey gold
unshaven
wet rice and hockey
wheel, knife, sher-wood, in that order
blow hard
goalie masquerade
habs 24/7
hockey smokers: dit clapper
hockey smokers: cal gardner
hc[in]hb: tommy ivan
hockey fashions: rod gilbert + bob nevin
hp@h: assist to béliveau
hp[in]hb: moose vasko
hockey players in hospital beds: terry sawchuk
leapin' lou
panoramic protection
smoothy smith
the great, once
a bunch of pukes
a red-hot bout with the grim reaper
are you afraid of anything?
ask the ref
billy burch took his skates to bed
detests helmets
hockey gods
it can do much harm
one slug
our best sticks were made of rock elm
the five truths of shovelling
the hot refresher
twenty-four ways of looking at guy lafleur
Tuukka Rask
one week and another: haven't really looked at it as a concussion
March 4, 2015 March 5, 2015 / puckstruck
In The Paint: Montreal's Classic Auctions closed out another big sale last week. Big-money items included a 1980 Miracle-On-Ice U.S.A. number-23 sweater worn by Rob McClanahan (sold for US$$86,220, including a buyer's premium); four different gold-and-diamond Stanley Cup rings of Billy Smith's (one of which went for US$ $36,563); a Herb Cain game-worn woolen number-four Bruins' sweater (US$25,937); and one of Andy Warhol's iconic 1984 "Wayne Gretzky #99" screenprints signed by both artist and subject (US$$8,249). Also on the block was this 1964 oil painting by brushtender Jacques Plante. Bidding started at US$300 with the final price climbing to US$2,014.
Carey Price is 6 foot 3, reported The Globe and Mail's Sean Gordon, and his thighs are as stout as 50-year-old timber.
From Stan Butler, who coaches the OHL's Brampton Battalion, came a tweet last week:
In hockey Choking equals Poor Preparation plus Low Self Confidence. #mentalpreparation
Evgeni Malkin told Sport Express about some of the keys to the success he's been enjoying in his ninth NHL season. Language was one of them: as soon as English ceased to be a problem, he said, came "looseness and confidence." Also, he has a good Russian cook now, who prepares soups and pancakes. His fridge, now, is filled with "tasty and familiar food, not the typical American chips and stuff."
"Thank God," said Malkin, "all is well and I am happy in life."
When, last week, Philadelphia GM Ron Hextall traded a defenceman, Kimmo Timonen, to Chicago's Blackhawks, he said that he was sending them not just a skilled and experienced player, "but a damn good person, too."
"I'm comfortable and strong," said Toronto captain Dion Phaneuf.
An entomologist who discovered a new species of wasp in Kenya's Teita Hills of Kenya, being a Bruins fans, named it Thaumatodryinus tuukkaraski, writes Carolyn Y. Johnson of The Boston Globe. And so Tuukka Rask —
who won the 2014 Vézina Trophy as the best goalie in the National Hockey League — will have the unusual honor of a callout in the scientific journal Acta Entomologica Musei Nationalis Pragae.
"This species is named after the acrobatic goaltender for the Finnish National ice hockey team and the Boston Bruins, whose glove hand is as tenacious as the raptorial fore tarsus of this dryinid species," the authors wrote in the paper, which has been accepted and will be published in April.
Robert S. Copeland, an entomologist at the International Centre of Insect Physiology and Ecology in Nairobi who grew up in Newton, said naming this particular wasp after Rask reflected his admiration for a player who has "had an outstanding career in one of the most difficult positions in sports."
The name also fit for other reasons. The project that led to the discovery of the species was underwritten by the government of Finland, Rask's home country. The wasp is yellowish and black, similar to the Bruins' colors. The grasping front legs of the female have claspers that look vaguely like goalie gloves.
Alert: if you happen to be browsing Player Bios filed by the Detroit Red Wings, and you come across captain Henrik Zetterberg's he does not, in fact, collect smoke-detectors. The actual wording is this:
OTHER: Hosts guests from local children's hospitals at DRW home games in his Zetterberg Foundation Suite… Serves as the team spokesperson for the annual smoke detector collection…Scored the Stanley Cup-clinching goal in 2008.
Last month, while Michal Neuvirth was still a goaltender for the Buffalo Sabres, he paid US$2,000 to dive and embellish his distress after Nashville's Mike Santorelli took a penalty for running into him. Neuvirth, who was trade on Monday to New York's Islanders, is the first goaltender to pay the price, apparently; he'll pay more if he does it again, says the NHL, up to a maximum of $5,000.
Headline on an NBC Sports item ahead of Detroit's game in Anaheim Monday last:
Zetterberg (Jamie Benn head punch) doubtful for tonight
Two days earlier in Dallas it happened, during the second period of a 7-6 win by the Red Wings. Benn took a roughing minor for the punch; Zetterberg played on until the end of the period and missed the third.
Of the game, Pavel Datsyuk said, "We play not really good today. We happy we win."
Regarding Zetterberg, reporters in a scrum that included Mike Heika of The Dallas Morning News asked coach Mike Babcock whether his captain might have a concussion. "Yeah," he said, "I don't really know that. I didn't talk to the guys. Let's just say he's got an upper-body injury and I don't know if he's fine tomorrow or not fine tomorrow, so we'll see him tomorrow. We'll practice tomorrow and then play the following day, so we'll see where he's at."
"You go through this whole range of feelings when things aren't going well," said Cam Neely, president of the Boston Bruins, for whom he once used to skate the wing. The team's season, if you haven't been paying attention, has been lacklustrous. "I've been frustrated. I've had some anger tossed in there. And now, for the first time, I've landed on disappointed."
Detroit GM Ken Holland: "He got punched in the head, didn't feel great after the game, so anytime you have any kind of head injury, you don't feel good and we're not going to put you in the lineup."
From Ken Dryden, writing in this month's Walrus about Scotland's referendum, tells of visiting the house in Harwick, in Scotland, that his ancestors left in 1834 to come to Canada. A man named Norman Huggan lives there now; afterwards, Dryden went to a local pub called the Waverley.
Longtime NHL referee (ret'd) Kerry Fraser wrote about Benn's punch in his column on TSN.ca, specifically the question of why wasn't the Stars' captain punished with more than the merest minor penalty.
Historically and currently a punching motion with the hand or fist, with or without the glove on the hand, normally directed at the head of an opponent is roughing. Roughing is a minor altercation that is not worthy of a major penalty to either participant. (An altercation is a situation involving two players with at least one to be penalized). A minor penalty shall be imposed on a player who strikes an opponent with his hand or fist. (Rule 51.1)
In reviewing this altercation that resulted from a Detroit end zone face-off, the initial push-off and subsequent glove punch that Jamie Benn administered to the head/helmet of Henrik Zetterberg fell completely within the parameters of this roughing rule. The altercation began as a result of Zetterberg tying up Benn with a stick between the legs and a left-hand shoulder wrap after the Stars captain won the draw back toward the top of the face-off circle.
Benn attempted a 'crow-hop' to break free from Zetterberg's restraint/interference to get to the front of the net without success. As the shot and eventual save was made by Jimmy Howard, Benn created separation with a forearm push and subsequent glove punch to the lower right side of Zetterberg's helmet. Unless there is a change in the rule and operating procedure, this play will continue to be enforced as a minor penalty for roughing. Continue reading →
this week + last: doesn't sound like a sutter
January 12, 2014 March 1, 2016 / puckstruck
After 45 games, the Leafs appeared to be hitting a wall.
Toronto's chances of making the playoffs, according to the SportsClubStats.com, now stand at 21 per cent.
"It doesn't take a rocket scientist to figure out that things aren't going anywhere near what our expectations are, that's for sure," coach Randy Carlyle said on Thursday.
Canadian GM Steve Yzerman announced the team he'll be taking to Sochi for the Olympics next month, which is when Michael Farber from Sports Illustrated took to Twitter: "My Canada includes Martin St. Louis."
But Wayne Gretzky, for one, approved of the players selected: "I really think he put together a good team," Gretzky told Pierre LeBrun of ESPN.com. "He's got skill, he's got size, he's got depth, he's got a good coaching staff, and they've done all their homework. They've done everything they can do. Now it's up to the players to play at the level that they need to play at to bring back the gold medal."
The Toronto Star's Damien Cox called the Winter Classic a gimmick ahead of the big New Year's Day game between Leafs and Red Wings in Ann Arbor, Michigan.
Farber: "No, I am not in Detroit. Since '03 Heritage Classic in Edmonton – Hype vs. Hypothermia – I have been strictly an indoor hockey writer."
Toronto's Phil Kessel: "She is gonna be chilly tm out on that ice"
On the day, Detroit's Pavel Datsyuk told his coach, Mike Babcock, "Well, we're being too careful with the puck. We gotta be because you're scared to turn it over. There's so much snow."
In front of a record-setting crowd of 105,491,tThe Leafs won, 3-2 in a shoot-out. Cox, post-game:
NHL gimmickry and ambition collided with frigid, blustery, irritable Mother Nature to produce a compelling outdoor game as a remarkable 82 TV cameras peered through an unceasing snow squall to broadcast every moment to 160 countries.
"I never talk to my team after we lose ever," Babcock said. "I did today. I said you should be proud. You have an off day tomorrow. Enjoy your family today."
"To me," said Babcock, "today was a home run for hockey,"
After bombs ripped through lives in Volgograd, in southern Russia, The Globe and Mail's Roy MacGregor listened to Alex Ovechkin's thoughts on the subject. "It's awful," he told reporters in Ottawa. "I don't know what people doing that kind of stuff for. I feel so sorry about the families and the people who were there."
When you hear this kind of situation happened, you think 'Oh my God!' You just feel bad. I don't know how to say it, but just say 'Why? Why you have to carry a bomb with you and push the button and destroy you and destroy everybody? If you want to do it, do it by yourself somewhere in a forest or in the mountains. Nobody is going to care about it. This is just stupid.
Boston's goalie, Tuukka Rask, talked about the danger of terrorist attacks at Sochi's Olympics, where he'll be defending Finnish nets: "You trust the system that nothing will happen. You can't live your life in fear." Continue reading →
From Greystone Books. Available in bookstores in Canada and the United States. 2014 Hockey Book of the Year, as per www.hockeybookreviews.com. "Funny, smart, unlike any hockey book I've read," Dave Bidini has said; "Joycean," Charles Foran called it. "It's rare to find a book that makes me proud to be Canadian," is what Michael Winter wrote: "A funny, myth-busting, life-loving read."
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Thankful that I never
played against
in an NHL playoff series;
I probably would have had to break his hand.
I would not have wanted to injure Gretzky, mind you;
I loved the guy.
I never touched him on the ice
in a regular season game.
I had too much respect
for how he played
and how he carried himself.
But I can say without question
I would have tried to hurt him
if we had been matched up
in the playoffs.
In my mind,
there are no friends
in a playoff series
I'm not talking about
elbowing someone in the head
or going after someone's knees.
I'm talking about a strategic slash.
To me, slashing someone's hand or breaking someone's fingers was nothing.
It was part of the game.
Broken hands heal.
Fingers heal.
The pain that comes from losing does not.
• from Overtime (2014) by Chris Chelios with Kevin Allen; excerpted, edited, and poemized.
"The first thing the student of Darwin learns is that what evolves does not necessarily improve — a truth that might just as well be sensed by considering the modern history of jazz or ice hockey."
• Adam Gopnik
ode to roy July 12, 2019
senior prank July 12, 2019
abandon cup: bad joe hall and the fatal stanley cup finals of 1919 June 30, 2019
rookie move June 28, 2019
george hainsworth: surely a well-driven puck would bowl him over like a ten-pin June 26, 2019


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Have you ever walked outside and discovered damage to your lawn, and you were not sure what is responsible or how to treat the problem? Is it an insect? Is it a mammal? Before you go into the garage to find whatever chemical you may have, let's pause. To correctly treat the problem, you must identify the culprit first, and then look for appropriate treatment options.
Here in the Piedmont of North Carolina, our most common lawn pests are grubs, moles, voles, fall armyworms, fire ants, spittlebugs, sugarcane beetle, mole crickets, and the occasional pesky raccoon.
Are you seeing raised tunnels in your lawn that sink in when stepped on? Sometimes there are cracks along the top of the tunnels? Moles and voles are responsible for this damage. There is a complex symbiotic relationship going on here. Moles are the excavators. They are subterranean mammals searching for grubs in your soil. They are not eating your plant roots. Voles are smaller, shrew-like opportunists using the mole tunnels to find plant roots to eat. Moles are meat eaters. Voles are vegetarians.
Controlling the moles and voles is most successful if you treat for the grubs. Start at the bottom of the food chain and the mammals will go elsewhere looking for food. Moles and voles are rodents, and they breed like rodents. Eliminating one may give you a feeling of satisfaction, but it does nothing to reduce the colony. There are a number of organic granular repellents with good results. Poison peanuts can be effective, but they pose a real danger to children and pets. The most effective option to reduce this rodent population is to close the barn door before the horse gets out. Eliminate their food source—grubs.
These grubs develop into Japanese beetles—an invasive non-native pest. They emerge from the lawn in June, eat your canna lilies, crepe myrtles and roses, and then lay their eggs below ground in July and die. The eggs hatch quickly, and then the larvae (grubs) are active below ground from August through May, eating grass roots starting in early spring. They can be controlled best at the grub stage. Organic methods include applying milky spore bacteria—a biological agent that feeds on the grubs and keeps them in check. It is slow to spread and takes up to three years to make a difference. A recommended chemical treatment for grubs uses Imidacloprid, found in the product Grub-No-More.
Fall armyworms can be a devastating pest. Some years they are not much of a concern. But when they appear en masse, they can destroy an entire lawn in days. If you notice your lawn dying in a steadily progressing line, you may have fall armyworms. The easiest way to check is with a soapy water flush. Put a good squirt of liquid dish soap in a bucket and fill the bucket with water. Dump that water along the leading edge of the damaged lawn. If you have fall armyworms, they will come wriggling up out of the lawn within minutes.
According to the NC State Turffiles, the fall armyworm is a sporadic but serious pest of turf grasses in North Carolina. The larva is the damaging stage of this pest and it is one inch to one and one-half inches long when fully grown. It can vary in color from green to brown, to almost black. There are four black dots on the dorsal side of each abdominal segment. It has a distinct inverted "Y" on the head.
Fall armyworms emerge from webby nests, often found on the foundation of the home. They do not nest in sod. Homeowners can treat with Talstar (Bifenthrin) if they have correctly identified fall armyworms as the pest. Always follow directions when applying pesticides.
Fire ants can be damaging to lawns, and are a danger to humans as well. Fire ants create large earthen mounds in lawns or garden beds. Often they are found in the lawn by the edge of the curb. If their nest is disturbed, they excrete an alarm pheromone that is a signal to attack. They will swarm the attacker with painful bites that can be very dangerous to people with allergies or young children. A pot full of boiling water poured into the mound is the cheapest and most organic way to kill a fire ant colony, but handle carefully. Talstar (Bifenthrin) is a common chemical pesticide for fire ants.
Spittlebugs are another common lawn pest here. Spittlebugs live inside masses of spittle or foamy froth, giving them their name. They lay orange eggs in hollow stems or lawn debris. The pale green nymphs hatch in about two weeks and begin to feed by sucking juices from Bermuda, centipede and zoysia grass. When you walk through the lawn, they will fly up and land on your legs. The best method of control is to dethatch your lawn, removing the nesting debris. Spittlebugs can be treated with Neem oil, Talstar or Grub-No-More.
Sugar cane beetles' preferred food is sugar cane, as their name suggests. But they are also fond of Bermuda grass and zoysia. They are one-half inch long and dull black in color with perforations along their abdomen forming stripes. They eat the roots and crowns of grasses, and can cause some tunneling damage. Talstar is the best control.
Mole crickets are becoming more pervasive here. They are one-inch long with shovel-like front legs for digging—hence the name. Mole crickets are gray to tan with large black eyes. They feed on grass roots and shoots, preferring Bermuda, centipede and zoysia grasses. Determine their presence with a soapy water flush in spring. You can control the nymphs with Grub-No-More in June to July. Adults are harder to control. Visible damage includes small mounds of soil scattered on the surface, or the lawn may feel spongy underfoot due to the insects' tunnels. The grass will turn brown and die in areas where mole crickets have tunneled.
And what if you have just laid fresh sod, but when you wake up in the morning it looks like someone rolled it all back? Could it be pesky neighborhood kids? Actually, the culprit is a raccoon looking for grubs and insects under that easily accessible layer of sod.
As Benjamin Franklin once said, an ounce of prevention is worth a pound of cure. A healthy lawn is less susceptible to injury from pests. Taking good care of your lawn by fertilizing or top-dressing with compost at the right time can give the lawn the nutrition it needs to be more vigorous and less susceptible to damage.


text:
← back to all news Orders up and good cash flow says Koenig & Bauer	Posted on Wednesday 7th November 2018 | 0 comments
Driven by strong security press business and growth in packaging printing markets, order intake in the Koenig & Bauer group rose by 4.4% over the previous year to €943.2m in the first nine months of 2018.
At the end of Q3, order backlog was up 25.5%, standing at €769.3m. Group revenue came to €788.8m but fell short of the previous year's figure of €847.7m due to the even greater accumulation of delivery dates requested by our customers in Q4 and bottlenecks in the parts availability. This was also reflected in EBIT, which at €28.6m was lower than in 2017 (€36.4m).
While the project situation is good, order intake, revenue and EBIT in the sheetfed segment were affected in particular by bottlenecks in the availability of parts.
President and CEO Claus Bolza-Schünemann: "The situation with respect to parts and the high order backlog dampen our new business due to longer delivery times. We are currently working intensely on optimising our entire supply chain to achieve a sustained reduction in delivery times."
Despite the growth in flexible packaging printing, order intake for Digital & Web was up only slightly on the previous year's figure due to fewer orders for newspaper and digital printing presses. Together with market-entry and growth-related expenses for corrugated board and flexible packaging, the lower revenue exerted pressure on EBIT in this segment.
Despite substantially higher orders, revenue in the Special segment was slightly below the previous year's figure. However, the EBIT margin remained stable in this segment. New orders for flexible packaging printing rose at a particularly gratifying rate, said K&B.
Financial and balance sheet profile strengthened
Cash flows from operating activities rose substantially over the previous year (–€24.6m) to €50.5m. Although free cash flow was burdened by the final payment instalment of €34.8m made in Q1 for the external funding of a part of the pension provisions, it also improved substantially.
In addition to net liquidity of €74.3m and securities of €15.7m that can be liquidated at any time, the group also has access to syndicated credit facilities. The equity ratio widened from 36.4% at the end of 2017 to 37.4%.
Group targets for 2018
Referring to the targets for 2018, CFO Mathias Dähn says: "The numerous press deliveries and service activities scheduled in the final months of the year will trigger a surge in revenue and earnings in Q4. In view of this business concentration, which is challenging due to the high capacity utilisation and the parts situation but not really unusual, we aim to achieve organic growth of around 4% in Group revenue for 2018.
"As things currently stand, we cannot rule out a shift of around €35m in revenue into 2019 as a result of delivery delays caused by bottlenecks in the parts availability. In terms of our earnings target for 2018, we are confident that we will achieve an EBIT margin of around 7% for the full year with higher revenue in view of the EBIT margin of 6.6% in the third quarter with low revenue.
"Global macroeconomic risks have increased due to trade conflicts and barriers, rising US interest rates and political uncertainties in Europe (Brexit, Italy) and in the emerging markets."
Medium-term goals until 2021
Depending on trends in the global economy, end markets and the necessary investments in growth, management is targeting a group-wide organic revenue growth rate of around 4% p.a. and an EBIT margin of between 4% and 9% by 2021.
The effects of the additional growth offensive to 2023 which the management board presented in conjunction with the announcement of the Q3 figures are not included in the medium-term targets, neither revenue nor costs.
Additional growth offensive 2023
Describing in greater detail the additional growth offensive to 2023, CFO Mathias Dähn says: "For a stronger profitable growth, we want to actively exploit the currently available market opportunities in corrugated board printing, flexible packaging and 2-piece can decorating alongside our service initiative.
"The same thing applies to marking & coding and postpress equipment such as rotary and flatbed die-cutters. Based on an addressed total market volume of currently around €2bn p.a. for machines, these business fields are expanding at annual rates of between 2% and 10% as they are benefiting from growth in consumer spending and demand for packaging around the world as well as long-term trends such as e-commerce, more sophisticated packaging and smaller sizes due to more single-person households.
"With newly developed products such as CorruCUT, CorruFLEX and CorruJET for corrugated board printing, CS MetalCan for 2-piece can decorating and the Rapida RDC 106 rotary die-cutter, we want to stand out from the competition with improved total cost of ownership, shorter make-ready times for ever more frequent job changes, greater ease of operation and high production output.
"The same thing also applies to our new and enhanced products for flexible packaging printing, flatbed die-cutters and marking & coding. Complex customer surveys and analysis always form the basis for our decisions. Our growth offensive 2023 necessitates additional experts and specialists in our global service and sales network as well as targeted portfolio additions based on platform concepts.
"We estimate the cumulative market-entry, growth-related and R&D expenses for 2019 to 2021 at around €50m. By 2023, we want to gradually generate additional revenue of around €200m in these addressed business areas. Given this favourable market environment with structural and above-average growth as well as less cyclical end markets such as food, beverages and pharmaceuticals, we want to gradually increase the EBIT margin from additional business to a double-digit figure at steady-state."
Management board change The supervisory board has appointed its member Dr Andreas Pleßke to the management board for five years with effect from 1 December 2018 for managing the Special segment. His area of responsibility also includes the optimisation of the internal production network.
Furthermore, the company has been able to find Prof Dr-Ing Raimund Klinkner as his successor to the supervisory board. Figures at a glance The financial statements can be downloaded as a PDF file from here.


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