Nobel winner declares boycott of top science journals.


  • Randy Schekman
Randy Schekman, centre, at a Nobel prize ceremony in Stockholm. Photograph: Rob Schoenbaum/Zuma Press/Corbis

Leading academic journals are distorting the scientific process and represent a “tyranny” that must be broken, according to a Nobel prize winner who has declared a boycott on the publications.

Randy Schekman, a US biologist who won the Nobel prize in physiology or medicine this year and receives his prize in Stockholm on Tuesday, said his lab would no longer send research papers to the top-tier journals, Nature, Cell and Science.

Schekman said pressure to publish in “luxury” journals encouraged researchers to cut corners and pursue trendy fields of science instead of doing more important work. The problem was exacerbated, he said, by editors who were not active scientists but professionals who favoured studies that were likely to make a splash.

The prestige of appearing in the major journals has led the Chinese Academy of Sciences to pay successful authors the equivalent of $30,000 (£18,000). Some researchers made half of their income through such “bribes”, Schekman said in an interview.

Writing in the Guardian, Schekman raises serious concerns over the journals’ practices and calls on others in the scientific community to take action.

“I have published in the big brands, including papers that won me a Nobel prize. But no longer,” he writes. “Just as Wall Street needs to break the hold of bonus culture, so science must break the tyranny of the luxury journals.”

Schekman is the editor of eLife, an online journal set up by the Wellcome Trust. Articles submitted to the journal – a competitor to Nature, Cell and Science – are discussed by reviewers who are working scientists and accepted if all agree. The papers are free for anyone to read.

Schekman criticises Nature, Cell and Science for artificially restricting the number of papers they accept, a policy he says stokes demand “like fashion designers who create limited-edition handbags.” He also attacks a widespread metric called an “impact factor”, used by many top-tier journals in their marketing.

A journal’s impact factor is a measure of how often its papers are cited, and is used as a proxy for quality. But Schekman said it was “toxic influence” on science that “introduced a distortion”. He writes: “A paper can become highly cited because it is good science – or because it is eye-catching, provocative, or wrong.”

Daniel Sirkis, a postdoc in Schekman’s lab, said many scientists wasted a lot of time trying to get their work into Cell, Science and Nature. “It’s true I could have a harder time getting my foot in the door of certain elite institutions without papers in these journals during my postdoc, but I don’t think I’d want to do science at a place that had this as one of their most important criteria for hiring anyway,” he told the Guardian.

Sebastian Springer, a biochemist at Jacobs University in Bremen, who worked with Schekman at the University of California, Berkeley, said he agreed there were major problems in scientific publishing, but no better model yet existed. “The system is not meritocratic. You don’t necessarily see the best papers published in those journals. The editors are not professional scientists, they are journalists which isn’t necessarily the greatest problem, but they emphasise novelty over solid work,” he said.

Springer said it was not enough for individual scientists to take a stand. Scientists are hired and awarded grants and fellowships on the basis of which journals they publish in. “The hiring committees all around the world need to acknowledge this issue,” he said.

Philip Campbell, editor-in-chief at Nature, said the journal had worked with the scientific community for more than 140 years and the support it had from authors and reviewers was validation that it served their needs.

“We select research for publication in Nature on the basis of scientific significance. That in turn may lead to citation impact and media coverage, but Nature editors aren’t driven by those considerations, and couldn’t predict them even if they wished to do so,” he said.

“The research community tends towards an over-reliance in assessing research by the journal in which it appears, or the impact factor of that journal. In a survey Nature Publishing Group conducted this year of over 20,000 scientists, the three most important factors in choosing a journal to submit to were: the reputation of the journal; the relevance of the journal content to their discipline; and the journal’s impact factor. My colleagues and I have expressed concerns about over-reliance on impact factors many times over the years, both in the pages of Nature and elsewhere.”

Monica Bradford, executive editor at Science, said: “We have a large circulation and printing additional papers has a real economic cost … Our editorial staff is dedicated to ensuring a thorough and professional peer review upon which they determine which papers to select for inclusion in our journal. There is nothing artificial about the acceptance rate. It reflects the scope and mission of our journal.”

Emilie Marcus, editor of Cell, said: “Since its launch nearly 40 years ago, Cell has focused on providing strong editorial vision, best-in-class author service with informed and responsive professional editors, rapid and rigorous peer-review from leading academic researchers, and sophisticated production quality. Cell’s raison d’etre is to serve science and scientists and if we fail to offer value for both our authors and readers, the journal will not flourish; for us doing so is a founding principle, not a luxury.”

• This article was amended on 10 December 2013 to include a response from Cell editor Emilie Marcus, which arrived after the initial publication deadline.

Stem cell transplant repairs damaged gut in mouse model of inflammatory bowel disease.


A source of gut stem cells that can repair a type of inflammatory bowel disease when transplanted into mice has been identified by researchers at the Wellcome TrustMedical Research Council Cambridge Stem Cell Institute at the University of Cambridge and at BRIC, the University of Copenhagen, Denmark.

The findings pave the way for patient-specific regenerative therapies for inflammatory bowel diseases such as ulcerative colitis.

All tissues in our body contain specialised stem cells, which are responsible for the lifelong maintenance of the individual tissue and organ. Stem cells found in adults are restricted to their tissue of origin, for example, stem cells found in the  will be able to contribute to the replenishment of the gut whereas stem cells in the skin will only contribute to maintenance of the skin.

The team first looked at developing intestinal tissue in a mouse embryo and found a population of stem cells that were quite different to the  that have been described in the gut. The cells were very actively dividing and could be grown in the laboratory over a long period without becoming specialised into the adult counterpart. Under the correct growth conditions, however, the team could induce the cells to form mature intestinal tissue.

When the team transplanted these cells into mice with a form of , within three hours the stem cells had attached to the damaged areas of the mouse intestine and integrated with the gut cells, contributing to the repair of the damaged tissue.

Dr Kim Jensen, a Wellcome Trust researcher and Lundbeckfoundation fellow, who led the study, said: “We found that the cells formed a living plaster over the damaged gut. They seemed to respond to the environment they had been placed in and matured accordingly to repair the damage.

“One of the risks of  like this is that the cells will continue to expand and form a tumour, but we didn’t see any evidence of that with this immature stem cell population from the gut.”

Cells with similar characteristics were isolated from both mice and humans and the team were also able to generate similar cells by reprogramming adult human cells, so called induced Pluripotent Stem Cells (iPSCs), and growing them in the appropriate conditions.

“We’ve identified a source of gut  that can be easily expanded in the laboratory, which could have huge implications for treating human inflammatory bowel diseases. The next step will be to see whether the human cells behave in the same way in the mouse transplant system and then we can consider investigating their use in patients,” added Dr Jensen.

Toddler brain scan language insight.


Regions of the brain that show leftward asymmetry of myelin
The left hand side of the brain has more myelin

The brain has a critical window for language development between the ages of two and four, brain scans suggest.

Environmental influences have their biggest impact before the age of four, as the brain’s wiring develops to process new words, say UK and US scientists.

The research in The Journal of Neuroscience suggests disorders causing language delay should be tackled early.

It also explains why young children are good at learning two languages.

The scientists, based at King’s College London, and Brown University, Rhode Island, studied 108 children with normal brain development between the ages of one and six.

“Start Quote

Our work seems to indicate that brain circuits associated with language are more flexible before the age of 4, early intervention for children with delayed language attainment should be initiated before this critical age”

Dr Jonathan O’Muircheartaigh King’s College London

They used brain scans to look at myelin – the insulation that develops from birth within the circuitry of the brain.

To their surprise, they found the distribution of myelin is fixed from the age of four, suggesting the brain is most plastic in very early life.

Any environmental influences on brain development will be strongest in infanthood, they predict.

This explains why immersing children in a bilingual environment before the age of four gives them the best chance of becoming fluent in both languages, the research suggests.

It also suggests that there is a critical time during development when environmental influence on cognitive skills may be greatest.

Dr Jonathan O’Muircheartaigh, from King’s College London, led the study.

He told the BBC: “Since our work seems to indicate that brain circuits associated with language are more flexible before the age of four, early intervention for children with delayed language attainment should be initiated before this critical age.

“This may be relevant to many developmental disorders, such as autism, since delayed language is a common early trait.”

Growing vocabulary

Early childhood is a time when language skills develop very rapidly.

Babies have a vocabulary of up to 50 words at 12 months but by the age of six this has expanded to about 5,000 words.

Language skills are localised in the frontal areas of the left-hand side of the brain.

The researchers therefore expected more myelin to develop in the left-hand side of the brain, as the children learned more language.

In fact, they found it remained constant, but had a stronger influence on language ability before the age of four, suggesting there is a crucial window for interventions in developmental disorders.

“This work is important as it is the first to investigate the relationship between brain structure and language across early childhood and demonstrate how this relationship changes with age,” said Dr Sean Deoni from Brown University, a co-researcher on the study.

“This is important since language is commonly altered or delayed in many developmental disorders, such as autism.”

Commenting on the study, Prof Dorothy Bishop of the department of Developmental Neuropsychology at the University of Oxford said the research added important new information about early development of connections in brain regions important for cognitive functions.

“There is suggestive evidence of links with language development but it is too early to be confident about functional implications of the findings,” she said.

“Ideally we would need a longitudinal study following children over time to track how structural brain changes relate to language function.”

The study was funded by the National Institutes for Mental Health (US) and the Wellcome Trust (UK).

MS damage repair treatment looked at by Edinburgh researchers.


New treatments that could help slow the progression of multiple sclerosis could be a step closer due to research by Edinburgh University.

In MS patients the protective layer around nerve cells in the brain, known as myelin, is broken down.

Scientists have discovered that immune cells, known as macrophages, help trigger the regeneration of myelin.

The researchers hope their work could eventually lead to the development of new drugs.

The sheath around nerves cells, made of myelin, is destroyed in MS, leaving the nerves struggling to pass on messages.

_67989720_c0020395-synapses,_artwork-spl

This leads to problems with mobility, balance and vision. There is no cure but current treatments concentrate on limiting the damage to myelin.

‘Stripped away’

Now the team at Edinburgh University has found that the immune cells, known as macrophages, can release a compound called activin-A, which activates production of more myelin.

Dr Veronique Miron, from the Medical Research Council Centre for Regenerative Medicine at the university, said: “In multiple sclerosis patients, the protective layer surrounding nerve fibres is stripped away and the nerves are exposed and damaged.

 “Start Quote

We look forward to seeing this research develop further”

Dr Susan Kohlhaas MS Society

“Approved therapies for multiple sclerosis work by reducing the initial myelin injury – they do not promote myelin regeneration.

“This study could help find new drug targets to enhance myelin regeneration and help to restore lost function in patients with multiple sclerosis.”

The study, which looked at myelin regeneration in human tissue samples and in mice, was funded by the MS Society, the Wellcome Trust and the Multiple Sclerosis Society of Canada.

The findings are published in Nature Neuroscience.

Scientists now plan to start further research to look at how activin-A works and whether its effects can be enhanced.

Dr Susan Kohlhaas, head of biomedical research at the MS Society, said: “We urgently need therapies that can help slow the progression of MS and so we’re delighted researchers have identified a new, potential way to repair damage to myelin.

“We look forward to seeing this research develop further.”

Source:BBC

 

 

 

 

Study reveals why the body clock is slow to adjust to time changes.


New research in mice reveals why the body is so slow to recover from jet-lag and identifies a target for the development of drugs that could help us to adjust faster to changes in time zone.

With funding from the Wellcome Trust and F. Hoffmann La Roche, researchers at the University of Oxford, University of Notre Dame and F. Hoffmann La Roche have identified a mechanism that limits the ability of the body clock to adjust to changes in patterns of light and dark. And the team show that if you block the activity of this gene in mice, they recover faster from disturbances in their daily light/dark cycle that were designed to simulate jet-lag.

plane

Nearly all life on Earth has an internal circadian body clock that keeps us ticking on a 24-hour cycle, synchronising a variety of bodily functions such as sleeping and eating with the cycle of light and dark in a solar day. When we travel to a different time zone our body clock eventually adjusts to the local time. However this can take up to one day for every hour the clock is shifted, resulting in several days of fatigue and discombobulation.

In mammals, the circadian clock is controlled by an area of the brain called the suprachiasmatic nuclei (SCN) which pulls every cell in the body into the same biological rhythm. It receives information from a specialised system in the eyes, separate from the mechanisms we use to ‘see’, which senses the time of day by detecting environmental light, synchronising the clock to local time. Until now, little was known about the molecular mechanisms of how light affects activity in the SCN to ‘tune’ the clock and why it takes so long to adjust when the light cycle changes.

To investigate this, the Oxford University team led by Dr Stuart Peirson and Professor Russell Foster, used mice to examine the patterns of gene expression in the SCN following a pulse of light during the hours of darkness. They identified around 100 genes that were switched on in response to light, revealing a sequence of events that act to retune the circadian clock. Amongst these, they identified one molecule, SIK1, that terminates this response, acting as a brake to limit the effects of light on the clock. When they blocked the activity of SIK1, the mice adjusted faster to changes in light cycle.

Dr Peirson explains: “We’ve identified a system that actively prevents the body clock from re-adjusting. If you think about, it makes sense to have a buffering mechanism in place to provide some stability to the clock. The clock needs to be sure that it is getting a reliable signal, and if the signal occurs at the same time over several days it probably has biological relevance. But it is this same buffering mechanism that slows down our ability to adjust to a new time zone and causes jet lag.”

Disruptions in the circadian system have been linked to chronic diseases including cancer, diabetes, and heart disease, as well as weakened immunity to infections and impaired cognition. More recently, researchers are uncovering that circadian disturbances are a common feature of several mental illnesses, including schizophrenia and bipolar disorder.

Russell Foster, Director of the recently established Oxford University Sleep and Circadian Neuroscience Institute supported by the Wellcome Trust, said: “We’re still several years away from a cure for jet-lag but understanding the mechanisms that generate and regulate our circadian clock gives us targets to develop drugs to help bring our bodies in tune with the solar cycle.Such drugs could potentially have broader therapeutic value for people with mental health issues.”

Source: Cell.

 

 

African high-speed data network open to researchers.


A high-speed network that allows faster data transmission both among researchers in southern and eastern Africa and with scientists in Europe and other parts of the world has been launched.

The UbuntuNet network, unveiled in Dar es Salaam, Tanzania, last month, builds on links initially established between Europe and five African countries by the UbuntuNet Alliance, the regional research and education network for eastern and southern Africa.

The network provides a high-speed Internet connection between national research and education networks (NRENs) in the region and with the pan-European GÉANT network, giving access to 40 million users in 8,000 institutions.

It was developed under the AfricaConnect programme, which aims to provide researchers across Africa with access to faster data transmission facilities to encourage global research collaboration. The European Commission provides 80 per cent of the programme’s funding, with the rest coming from African governments out of their support for the NRENs.

European funding for AfricaConnect is due to last until 2015, after which the project is intended to be solely funded by its African partners.

Speaking last week at the 2012 Africa-European Union Cooperation Forum on ICT, held in Lisbon, Portugal, UbuntuNet Alliance project officer Tiwonge Msulira Banda said that African scientists in fields such as agriculture, management of natural resources, climate change and earth observation, will benefit from access to a world-class data transmission network.

“In all of these fields, UbuntuNet will open up opportunities for African researchers to get engaged in cutting-edge research at a global level,” he said.

One research area that was already benefiting from high-speed access, he added, was genomics, where the high-speed links are being used to exchange data between researchers in Malawi and Kenya and the Wellcome Trust‘s Sanger Institute in Cambridge, United Kingdom.

Banda said that UbuntuNet could even allow more Africans to become involved in particle physics experiments at the Large Hadron Collider at CERN (the European Organization for Nuclear Research).

Cathrin Stöver, chief international relations and communications manager of DANTE, the organisation that operates GÉANT and is coordinating AfricaConnect, emphasised that, although most of the initial funds were coming from Europe, “we will only do things that are agreed as beneficial by the African partners”.

She added that AfricaConnect is also committed to establishing close ties with regional research networks in west and central Africa.

Francis Tusubira, chief executive officer of the UbuntuNet Alliance, said that the organisation’s goal was to ensure that all countries in southern and eastern Africa had viable NRENs connected to the UbuntuNet network.

But he added that it was a major challenge to build the capacity to run the national networks effectively, partly because of the lack of graduates with relevant computer skills being produced by universities.

“We have thousands of engineering students coming out of universities, but put them in a working environment [involving computers] and they have no idea what to do,” he said.

Therefore one priority for the UbuntuNet Alliance under the AfricaConnect project is to establish programmes to boost the teaching of computer engineering skills in African universities over the next four years.

There was also a need to persuade African politicians of NRENs’ value so that they provide the funding required for their long-term operation, Tusubira said.

Tusubira announced that he had already received commitments of 60 per cent of the total African contributions required by the AfricaConnect project up to 2015, and that 40 per cent of this money had already been received.

Source:SciVx

9 genes found that affect bones.


Australian and UK scientists have shown that a large percentage of genes are likely to affect bone strength, potentially around 2,000 of the 21,000 genes in our bodies.

Identifying genes that lead to osteoporosis is an important first step in helping to treat this serious condition, which affects over 2 million Australians.

Out of 100 ‘knockout mice’, which have a gene disabled, the first generated on a ‘pipeline’ set up by the UK’s Wellcome Trust Sanger Institute (as part of a global effort to knockout every gene in the genome one by one) the scientists identified 9 genes that appear to weaken or strengthen bone.

Professor Peter Croucher from Sydney’s Garvan Institute of Medical Research, in collaboration with Dr Duncan Bassett and Professor Graham Williams from Imperial College London and colleagues at the Sanger Institute, used micro-CT and digital x-ray microradiography in combination with statistics and load bearing experiments to measure whether or not each of the first 100 genes impacted upon bone. Their results are published in PLoS Genetics, now online.

“We wanted to see what screening the first 100 knockout mice off the pipeline would tell us about the impact of these genes on bone, and whether or not our approach was an effective one,” said Professor Peter Croucher.

“The approach was successful in that we identified 9 genes that had not previously been described – each of which appeared to be important in regulating our skeleton. This suggests that roughly 8-10% of all genes may be involved in some way.”

“We believe a systematic screening of knockout mice in this way will give us the scale of data we need to define the structural and functional variations in genes that determine bone strength.”

CT scans and microradiography give us the structural information we need, and fracturing the bones afterwards tells us whether or not there is an increase or a decrease in the propensity to fracture. That’s the functional endpoint.”

“This has allowed us to describe four functional classifications of bone. Normal bone is strong and flexible, whereas abnormal bone can be strong but brittle, or weak and brittle, or weak but flexible.”

“At the moment, we’re trying to understand the potential role of the 9 genes we’ve just identified. Our results suggest that if you were to block some of them, it would result in higher bone mass and stronger bones. We’ll be making antibodies to those genes to test our results.”

“We believe that many genes will be individual players in complex pathways – so they will act as pointers to those pathways, and obviously some pathways will be much more important than others. It’s our aim to pinpoint the critical pathways.”

The study participants will be applying to The Wellcome Trust to fund the screening of the next 800-1000 genes off the Sanger Institute pipeline, over a period of 5 years.

Source: ttp://www.garvan.org.au