Press releases
As a free service to the journalism community and general public, EMBO reports provides its press releases online (after the embargo has been lifted) to help disseminate and explain the cutting edge, high-impact developments reported in its pages.
Journalists wishing to receive press releases while papers are still under embargo should contact press@nature.com for further information.
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Joe Bennett
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March 2008
Top of pageGene therapy alleviates neurodegenerative disease in mice
Mice with neurodegenerative diseases have been successfully treated with gene therapy, according to research published online in EMBO reports this week. Using lentivirus vectors, scientists were able to administer a therapeutic enzyme to treat spinocerebellar ataxia, a neurodegenerative disease that currently has no cure.
Mutations in the DNA sequence of several genes cause the proteins they encode to contain abnormally large amounts of the amino acid glutamine. Over time, the build up of polyglutamine aggregates leads to neurological degeneration and the onset of disease symptoms. Hirokazu Hirai and co-workers artificially overexpressed CRAG — the enzyme that naturally assists in breaking down the polyglutamine aggregates — in the affected mice, which where then able to clear the aggregates. Subsequently, neurons were rescued from degeneration and the disease symptoms markedly alleviated.
Polyglutamine diseases, such as spinocerebellar ataxia or Huntington's disease, are not fatal, but the symptoms and complications they cause result in a very poor quality of life and a reduced life expectancy for those affected. The team hopes that their work in mice can be developed into a clinical treatment for the nine types of polyglutamine disease that result from these kinds of genetic errors.
Author contact:
Hirokazu Hirai (Gunma University Graduate School of Medicine, Japan)
Tel: +81 27 220 7930; E-mail: hiraih@med.gunma-u.ac.jp
Editorial contact:
Nonia Pariente (EMBO reports, Heidelberg, Germany)
Tel: +49 622 188 91305; E-mail: pariente@embo.org
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
Science writing lacks human touch
Scientific literature could be more engaging — and better understood — if it activated our senses as well as our minds. A study in the latest issue of EMBO reports validates what many befuddled readers may instinctively know: whilst scientific literature is rich in vocabulary, it lacks words designed to produce an emotional response.
In the study, computational biologists Andrey Rzhetsky and colleagues used linguistic tools to compare scientific publications with the works of famous poets and playwrights, articles from the Reuters news service and the open access encyclopaedia Wikipedia. They analysed the frequencies of use of sensory words and time-related terms to reveal that, whilst biomedical text is rich in vocabulary, it lacks words associated with the five senses. They suggest that this ‘sensory deprived’ style of writing impedes comprehension and numbs the senses and mind of the reader.
‘Mapping abstract concepts back to objects with meaningful sensory properties serves as a stepping-stone to solving complex problems’, the authors write. ‘Without sensory language, scientific prose can read like a long journey through a colourless, flat terrain.’
The authors conclude that using sensory language could not only make abstracts more engaging, but more readily understood — and that has a benefit across the spectrum, for experts and laymen alike.
Author contact:
Hirokazu Hirai (Gunma University Graduate School of Medicine, Japan)
Tel: +81 27 220 7930; E-mail: hiraih@med.gunma-u.ac.jp
Editorial contact:
Holger Breithaupt (EMBO reports, Heidelberg, Germany)
Tel: +49 6221 8891 306; E-mail: Holger.Breithaupt@embo.org
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
Contribution of cholesterol transporter to vascular disease
Low-density lipoprotein (LDL), a transporter of cholesterol, may also contribute to vascular diseases by a previously unidentified mechanism, according to a report published online this week in EMBO reports. The study reveals a link between native LDL (nLDL) and the vascular endothelial growth factor receptor 1 (VEGFR1), which plays a central role in blood vessel formation.
LDL is responsible for transporting cholesterol from the liver to peripheral tissues. During transit in the blood, cholesterol can be deposited causing the formation of plaques that lead to hardening of the arteries. Vascular diseases such as thrombosis, stroke and heart attacks are associated with this condition, and are attributed to eleven deaths every hour in the UK alone.
Using cell lines and mouse models, Yoshiro Maru and colleagues found that when nLDL is bound to the LDL receptor, it can activate VEGFR1 and accelerate migration of macrophages, scavenger cells that accumulate in the plaques. Both effects could contribute to the progression of the plaques and blocking of the arteries. The authors hope that their discovery of the link between VEGFR1 and nLDL could be exploited as a potential therapeutic target for medical applications.
Ligand-independent activation of vascular endothelial growth factor receptor 1 by low-density lipoprotein. Ryosuke Usui, Masabumi Shibuya, Shun Ishibashi & Yoshiro Maru EMBO reports, doi: 10.1038/sj.embor.7401103, online publication 26th October 2007 View article
Author contact:
Andrey Rzhetsky (University of Chicago, IL, USA)
Tel: +1 773 834 7367; E-mail: arzhetsky@uchicago.edu
Editorial contact:
Barbara Pauly (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 109; E-mail: Pauly@embo.org
Esther Schnapp (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 502; E-mail: esther.schnapp@embo.org
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
October 2007
Top of pageEnzyme promotes fat formation
The enzyme TPPII may contribute to obesity by stimulating the formation of fat cells, suggests a study in EMBO reports this week. The enzyme, TPPII, has previously been linked to making people feel hungry, but Jonathan Graff and colleagues now show that it may be even more deeply involved in causing obesity.
The team found that TPPII actually stimulated the formation of fat cells in worms and mammalian cells and that by reducing it, fat stores decreased. Mice with lower levels of TPPII were thinner than their wild type littermates, although their food intake was comparable.
The authors hope that TPPII could be exploited as a drug target to help fight increasing levels of obesity; inhibiting the enzyme would both increase feelings of fullness after eating and decrease build up of fat cells.
Tripeptidyl peptidase II promotes fat formation in a conserved fashion. Renée M McKay, James P McKay, Jae Myoung Suh, Leon Avery & Jonathan M Graff EMBO reports, doi: 10.1038/sj.embor.7401086, online publication 12th October 2007 View article
Author contact:
Jonathan Graff (University of Texas Southwestern Medical Centre, Dallas, TX, USA)
Tel: +1 214 648 1481; E-mail: jon.graff@utsouthwestern.edu
Editorial contact:
Barbara Pauly (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 109; E-mail: Pauly@embo.org
Esther Schnapp (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 502; E-mail: esther.schnapp@embo.org
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
September 2007
Top of pageThe beat goes on with AKAP18
A protein, known as AKAP18, could help the heart to beat faster in response to adrenaline or noradrenaline, according to a study published online this week in EMBO reports.
The protein has a crucial role in correctly targeting protein kinase A (PKA) to a molecular complex that helps control the rate and strength of heart muscle contractions. This complex regulates the uptake of calcium into intracellular stores in the heart, allowing it to relax and prepare for its next contraction. PKA must be present for the complex to be activated and AKAP18 makes sure that it gets there.
Coronary artery disease leading to heart attacks, which can be acutely fatal or can induce heart failure resulting in death, is the biggest killer of men in the United States of America and Europe. With 10 million new cases of heart failure every year, approximately 30% of patients respond poorly to current treatments, with an ultimately fatal outcome. New drugs to improve survival from post-infarction heart failure are desperately needed. AKAP18 may prove to be an effective novel target in the fight to live beyond this deadly event.
Kjetil Taskén and co-workers hope that AKAP18 can be used as a potential drug target to improve the survival rate of patients with heart failure following heart-attacks, or sufferers of heritable heart disease. By targeting AKAP18, the team aims to specifically affect PKA and its regulatory complex when it is over-activated and help the heart to continue to function effectively.
AKAP complex regulates Ca2+ re-uptake into heart sarcoplasmic reticulum. Birgitte Lygren, Cathrine Rein Carlson, Katja Santamaria, Valentina Lissandron, Theresa McSorley, Jessica Litzenberg, Dorothea Lorenz, Burkhard Wiesner, Walter Rosenthal, Manuela Zaccolo, Kjetil Taskén & Enno Klussmann (2007) EMBO reports, doi: 10.1038/sj.embor.7401081, online publication 28th September 2007 View article
Author contact:
Kjetil Taskén (Biotechnology Centre of Oslo, Norway)
Tel: +47 2284 0505; Mobile: +47 9086 0759; E-mail: kjetil.tasken@biotek.uio.no
Editorial contact:
Barbara Pauly (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 109; E-mail: Pauly@embo.org
Esther Schnapp (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 502; E-mail: esther.schnapp@embo.org
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
March 2007
Top of pagePreventing cancer without killing cells
Inducing senescence in aged cells may be sufficient to guard against spontaneous cancer development, according to a paper published online this week in EMBO reports. It was previously unknown whether cellular senescence or programmed cell death – apoptosis – was the more important safeguard mechanism for suppressing tumours arising from dysfunctional telomeres.
Aged cells have abnormal chromosomes with dysfunctional telomeres – shorter ends – that can promote tumorigenesis in the absence of the tumour suppressor p53, and may be related to the higher incidence of cancer in older individuals. However, in the presence of p53, dysfunctional telomeres can induce a permanent arrest of cell growth, known as senescence. Sandy Chang and colleagues studied mutant mice with dysfunctional telomeres and copies of the p53 gene that cannot initiate p53-dependent apoptosis but can execute p53-mediated senescence.
The authors found that activating the senescence pathway was sufficient to suppress spontaneous tumorigenesis. Their findings suggest that, by halting cellular proliferation, p53-mediated senescence may act as an important tumour suppressor mechanism in aged cells.
Telomere dysfunction suppresses spontaneous tumorigenesis in vivo by initiating p53-dependent cellular senescence. Wilfredo Cosme-Blanco, Mei-Feng Shen, Alexander J F Lazar, Sen Pathak, Guillermina Lozano, Asha S Multani & Sandy Chang (2007) EMBO reports, doi: 10.1038/sj.embor.7400937, online publication 30 March 2007 View article
Author contact:
Sandy Chang (MD Anderson Cancer Center, Houston, TX, USA)
Tel: +1 713 834 6361; E-mail: schang@mdanderson.org
Editorial contact:
Barbara Pauly (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 109; E-mail: Pauly@embo.org
Esther Schnapp (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 502; E-mail: esther.schnapp@embo.org
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
Laying sleeping sickness to rest
The parasite that leads to sleeping sickness can be lulled to sleep itself using a newly discovered pathway, according to research published online this week in EMBO reports. Trypanosoma brucei is a parasite that causes sleeping sickness resulting in neurological damage and death.
Shulamit Michaeli and colleagues describe a pathway in T. brucei parasites that they named SLS (SL-RNA silencing). Triggering this pathway shuts down the synthesis of a crucial RNA molecule, which halts the production of messenger RNAs and leads to the parasite's death. Inducing SLS could therefore be a novel way to eradicate parasites and prevent sleeping sickness – trypanosomiasis. The researchers also believe this could have implications for related parasites and diseases, such as Leishmania and leishmaniasis and Trypanosoma cruzi and Chagas disease.
Sleeping sickness affects humans and livestock, and is endemic in sub-Saharan Africa where it is estimated to affect as many as 70,000 people. Leishmaniasis is estimated to affect millions of individuals throughout the world, and can lead to skin lesions, tissue damage, fever, blindness and death. Chagas disease affects 16–18 million people across the Americas, and can cause intestinal complications, neurological disorders, heart damage and death. Although drugs are available to treat these diseases, their use is hampered by toxicity and undesirable side effects, difficulties in administering treatment, an increase in drug resistance, and high costs.
Spliced-leader RNA silencing: a novel stress-induced mechanism in Trypanosoma brucei. Yaniv Lustig, Lilach Sheiner, Yaron Vagima, Hanoch Goldshmidt, Anish Das, Vivian Bellofatto & Shulamit Michaeli (2007) EMBO reports, doi: 10.1038/sj.embor.7400930, online publication 9 March 2007 View article
Author contact:
Shulamit Michaeli (Bar-Ilan University, Ramat-Gan, Israel)
Tel: +972 3 5318068; E-mail: michaes@mail.biu.ac.il
Editorial contact:
Barbara Pauly (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 109; E-mail: Pauly@embo.org
Esther Schnapp (EMBO reports, Germany)
Tel: +49 (0) 6221 8891 502; E-mail: esther.schnapp@embo.org
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
July 2006
Top of pageScience and Security in the 21st Century
Over the decades, physicists and chemists have got used to the concept of dual-use research and its implications – that knowledge, technologies and materials, which could be used to construct weapons of mass destructions, are tightly regulated for security purposes. Now, with the spectre of bioterrorism looming, biologists too will have to get to grips with potential limitations on their research.
The 2006 special issue of EMBO reports on Science & Security covers the social, economic and ethical impact of dual-use research in the life sciences on society and vice versa. It also reflects on the science and technology of identifying individuals using biometrics and DNA profiles and their implications on citizens' privacy. The special issue is based on a joint EMBO/EMBL conference, which took place in October 2005.
Jonathan Tucker and Craig Hooper point out that proteomics is a research field with great potential for abuse. Natural toxins such as ricin from castor beans or bacterial toxins would make very good bioweapons, particularly for clandestine or terrorist use: they are highly effective at very low doses, they are easy to produce and there is no unwanted risk of creating a pandemic unlike infectious bacteria or viruses. The authors propose various options that could reduce the potential misuse of this research.
In another article, Jan van Aken discusses whether the sequencing of the Spanish flu virus last year was an important experiment that will help scientists to understand why this virus was so deadly or an example of irresponsible and dangerous research, which reawakened one of the most deadly pathogens humankind as ever encountered?
In July 2001, the US government withdrew from negotiations to give the Biological and Toxin Weapons Convention (BTWC) "more teeth" in the form of on-site inspections or sanctions, citing military and economic reasons. Instead, US representatives stressed the need for a voluntary code of conduct for researchers in the life sciences to prevent the nefarious abuse of biological and medical knowledge. In her article in the special issue of EMBO reports on Science and Security, Filippa Corneliussen investigates the effect of such codes for research using recombinant DNA and comes to the conclusion that codes of conduct or non-binding reviews may not be sufficient to prevent abuse.
Early this year, advocates of civil liberties in the US were up in arms after it came to light that the US National Security Agency had amassed telecommunications data of American citizens without a warrant. Irving Louis Horowitz writes that it is not the fast pace of new technologies that is the main threat for privacy, but the responsibility to oneself and others that needs closer examination.
Author contacts:
Jan van Aken (University of Hamburg, Germany)
Tel: +49 40 431 88 001; E-mail: van.aken@t-online.de
Filippa Corneliussen (London School of Economics, UK)
Tel: +44 20 7107 5241; E-mail: f.corneliussen@lse.ac.uk
Jonathan Tucker (Center for Nonproliferation studies, Monterey, CA, USA)
Tel: +1 202 464 6000; E-mail: jtucker@miis.edu
Irving Louis Horowitz (The State University of New Jersey, New Brunswick, NJ, USA)
Tel: +1 732 445 4035; E-mail: ihorowitz@transactionpub.com
Editorial contact:
Holger Breithaupt (EMBO reports, Heidelberg, Germany)
Tel: +49 6221 8891 306; E-mail: Holger.Breithaupt@embo.org
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
July 2004
Top of pageA better way to copy DNA
Scientists have developed a new method for DNA amplification that could replace the polymerase chain reaction (PCR), a technique that is invaluable for both medical diagnostics and basic research but which is confined to the laboratory. In the August issue of EMBO reports, Huimin Kong and colleagues at New England Biolabs (Beverly, MA, USA) describe a way to copy mass amounts of DNA that overcomes some of the limitations of this earlier technique.
HDA (helicase-dependent amplification) is as simple as PCR, but has significant advantages. PCR requires thermocycling to heat and cool a sample of DNA, to allow denaturation (separating DNA into single strands) and synthesis (copying single strands to create new double-stranded DNA). HDA instead mimics nature's method of replicating DNA by using a helicase enzyme to denature the DNA. As a result, the entire HDA reaction can be performed at one temperature that is optimized for synthesis, eliminating the need for an expensive and power-hungry thermocycler.
HDA could expand the application of DNA amplification to situations in which the requirements for PCR have made it prohibitive. The costs are likely to be more modest and, most importantly, the simplicity of HDA makes it suitable for the development of hand-held DNA diagnostic devices that could be used to detect pathogens at the point-of-care or in the field.
Helicase-dependent isothermal DNA amplification
M Vincent et al. (2004) EMBO reports 5, 8, in press
doi:10.1038/sj.embor.7400200, online publication 9 July 2004
View article
Author contact:
Huimin Kong (New England Biolabs, Beverly, MA, USA)
Tel: +1 978 927 5054; E-mail: kong@neb.com
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
Ottawa's leadership in biomedical and health research has paid off: Renewed federal government support essential to future growth
Montreal – Canada is one of the world's top research nations, thanks to Ottawa's commitment to research and leadership role in funding biomedical and health research over the past 5 years, according to an article published today in the prestigious journal EMBO reports.
But to keep up the momentum and continue to grow in innovation and high-quality research, the federal government needs to develop new ambitious strategies to take full advantage of Canada's expertise and research infrastructure and capacity, according to authors Dr John Bergeron and Dr Sean Taylor of McGill University.
Funding for Canadian biomedical and health research grew from C$5.1 billion in 1999 to C$7.5 billion in 2003. The increased support was part of the federal government's plan to keep pace with international competition in countries like the United States and Japan and increase the capacities of universities to conduct high-quality research.
In a commitment to being one of the top five research nations in the world, the government created innovative new programs in the Canadian Institutes of Health Research (CIHR), Canada Foundation for Innovation (CFI), the Canada Research Chairs (CRC) and Genome Canada (GC) to support infrastructure, facilities and equipment, large scale institutional projects, attract thousands of new researchers and train postdoctoral fellows and students.
The injection of funding has had a measurable impact on economy and knowledge transfer. Since 1999, there has been a 50% increase in licenses and options, a 200% increase in income from licenses and a 40% increase in the number of new spin-off companies. Canadian scientists are also more present on the world scientific stage, with a 25% increase in the number of scientific articles produced by Canadian researchers.
"The progress has been phenomenal," said Dr Bergeron, Chair of the Department of Anatomy and Cell Biology at McGill University, Director of the Montreal Proteomics Network (RPMPN), and President of the Human Proteome Organization. "Today the atmosphere among biomedical researchers in Canada is full of the energy and excitement of being on the leading edge and this has also helped to attract and retain the best people."
Biomedical and health research and innovation are fundamental to the health of Canadians for the development of new technologies and treatments. They are also key components of the knowledge based societies/economies of the 21st century, he said.
"The commitment to large projects has been a tremendous boost and has made Canada a significant player," said Dr Taylor, Program Manager of the Montreal Proteomics Network. "Many of the projects (such as the RPMPN, www.rpmpn.mcgill.ca) funded by GC, CIHR and the CFI have attained international recognition and are participating in global projects and have been able to secure international funding."
"Canadian scientists are world leaders in essentially all aspects of health research, from proteomics, stem cells and model organisms genetics to clinical research, population health and research on the health system itself", said Dr Alan Bernstein, President of the Canadian Institutes of Health Research. "This excellence is essential if Canadians are to reap the health and economic benefits of the current revolution in health research."
The challenge for the new federal government is to develop and implement a mechanism to continue this commitment so that Canada can grow as a leader of international innovation and high-quality research. This is particularly critical for the approximately 79 large scale proteomics and genomics projects funded in Canada through a combination of GC, the CFI, the CRC and the CIHR. Funding programs for these projects are set to expire in March 2005.
For many of these projects, the past three years have been devoted to investing in equipment, facilities and people, Dr Taylor said. Most projects are now fully operational with a high level of productivity and are delivering tremendous results both in terms of publications and patentable intellectual property. Each project has the potential to pay huge dividends to the health and economy of Canada in terms of new insights into diseases and new economic growth. Continued investment in biomedical science is crucial, he said. The new government has an opportunity to put forward an ambitious vision of the future that will benefit all Canadians.
A national effort. Recent developments in Canadian biomedical and health research support
John J M Bergeron & Sean C Taylor. (2004) EMBO reports 5, 8, 742–766 (2004)
doi:10.1038/sj.embor.7400212, online publication 30 July 2004
View article
For further information:
Sandra McPherson, PhD (McGill University)
Tel: (514) 398-1902; E-mail: sandra.mcpherson@mcgill.ca
Media contact:
Ruth Francis (Nature, London)
Tel: + 44 207 843 4562; E-mail: r.francis@nature.com
