Scientists wipe out malaria-carrying mosquitoes in the lab by creating male-only offspring

Scientists have modified mosquitoes to produce sperm that will only create males, pioneering a fresh approach to eradicating malaria.

In a study published in the journal Nature Communications, scientists from Imperial College London have tested a new genetic method that distorts the sex ratio of Anopheles gambiae mosquitoes, the main transmitters of the malaria parasite, so that the female mosquitoes that bite and pass the disease to humans are no longer produced.

In the first laboratory tests, the method created a fully fertile mosquito strain that produced 95 per cent male offspring.

Continue reading “Scientists wipe out malaria-carrying mosquitoes in the lab by creating male-only offspring”

Scientists discover how to turn light into matter after 80-year quest

Theories Describing Light and Matter Interactions

 

 

Imperial College London physicists have discovered how to create matter from light – a feat thought impossible when the idea was first theorised 80 years ago.

In just one day over several cups of coffee in a tiny office in Imperial’s Blackett Physics Laboratory, three physicists worked out a relatively simple way to physically prove a theory first devised by scientists Breit and Wheeler in 1934.

Breit and Wheeler suggested that it should be possible to turn light into matter by smashing together only two particles of light (photons), to create an electron and a positron – the simplest method of turning light into matter ever predicted. The calculation was found to be theoretically sound but Breit and Wheeler said that they never expected anybody to physically demonstrate their prediction. It has never been observed in the laboratory and past experiments to test it have required the addition of massive high-energy particles. Continue reading “Scientists discover how to turn light into matter after 80-year quest”

Parasite makes mice lose fear of cats permanently

Behavioural changes persist after Toxoplasma infection is cleared.

18 September 2013

Mice infected with toxoplasmosis lose their instinctive fear for the smell of cats — and the parasite’s effects may be permanent.

Wendy Ingram/Adrienne Greene

A parasite that infects up to one-third of people around the world may have the ability to permanently alter a specific brain function in mice, according to a study published in PLoS ONE today1.

Toxoplasma gondii is known to remove rodents’ innate fear of cats. The new research shows that even months after infection, when parasites are no longer detectable, the effect remains. This raises the possibility that the microbe causes a permanent structural change in the brain.

The microbe is a single-celled pathogen that infects most types of mammal and bird, causing a disease called toxoplasmosis. But its effects on rodents are unique; most flee cat odour, but infected ones are mildly attracted to it.

This is thought to be an evolutionary adaptation to help the parasite complete its life cycle: Toxoplasma can sexually reproduce only in the cat gut, and for it to get there, the pathogen’s rodent host must be eaten.

In humans, studies have linked Toxoplasma infection with behavioural changes and schizophrenia. One work found an increased risk of traffic accidents in people infected with the parasite2; another found changes in responses to cat odour3. People with schizophrenia are more likely than the general population to have been infected with Toxoplasma, and medications used to treat schizophrenia may work in part by inhibiting the pathogen’s replication.

Schizophrenia is thought to involve excess activity of the neurotransmitter dopamine in the brain. This has bolstered one possible explanation for Toxoplasma’s behavioural effect: the parasite establishes persistent infections by means of microscopic cysts that grow slowly in brain cells. It can increase those cells’ production of dopamine, which could significantly alter their function. Most other suggested mechanisms also rely on the presence of cysts.

Persistent trait

Research on Toxoplasma has mainly used the North American Type II strain. Wendy Ingram, a molecular cell biologist at the University of California, Berkeley, and her colleagues investigated the effects of two other major strains, Type I and Type III, on mouse behaviour. They found that within three weeks of infection with either strain, mice lost all fear of cat odour — showing that the behavioural shift is a general trait of Toxoplasma.

More surprising was the situation four months after infection. The Type I pathogen that the researchers used had been genetically modified to provoke an effective immune response, allowing the mice to overcome the infection. After four months, it was undetectable in the mouse brain, indicating that no more than 200 parasite cells remained. “We actually expected that Type I wouldn’t be able to form cysts, and therefore wouldn’t be able to cause the behaviour change,” explains Ingram.

But that was not the case: the mice remained as unperturbed by cat odour as they had been at three weeks. “Long after we lose the ability to see it in the brain, we still see its behavioural effect,” says geneticist Michael Eisen, also at Berkeley.

This suggests that the behavioural change could be due to a specific, hard-wired alteration in brain structure, which is generated before cysts form and cannot be reversed. The finding casts doubt on theories that cysts or dopamine cause the behavioural changes of Toxoplasma infections.

Mind and matter

Joanne Webster, a parasite epidemiologist at Imperial College London who co-discovered the fear-negating effects of Toxoplasma in rats4, highlights the worrying implication that if the behavioural changes of Toxoplasma-caused schizophrenia are fixed, treatments that are intended to target cysts might have no effect. However, she notes that mice are not the best model for Toxoplasma infection in humans, because they experience more severe symptoms and complications. Webster uses rats in her research.

Ingram says that her group is using mice because of the better genetic tools available to help to uncover the mechanism behind behavioural changes. However, she is not yet convinced of the link between Toxoplasma infections and schizophrenia. Her findings may actually weaken that link, because they seem to provide evidence against the dopamine hypothesis.

She notes that Toxoplasma infections are common around the world, but their prevalence varies by region, whereas schizophrenia rates are consistent at around 1% globally. Furthermore, it is possible that the increased rate of Toxoplasma infections among people with schizophrenia is caused by them being more likely to pick up the parasite, rather than by the parasite causing schizophrenia.

Journal name:
Nature
DOI:
doi:10.1038/nature.2013.13777

Exposed: Edward Erin, the doctor whose faked asthma drug test results proved fatal

Fabricated research was not discovered until Edward Erin tried to poison his girlfriend

John Lawless

Monday, 17 June 2013

A British doctor faked test results during clinical trials for an asthma drug in which one person died and others contracted cancer and pneumonia, The Independent has learnt.

Dr Edward Erin’s fabrications were not detected until he was arrested and jailed for six years for lacing his lover’s coffee with drugs in an attempt to have her miscarry.

His sentence was later extended by two years after it emerged that he had tried to persuade a former cellmate to kill the woman and their baby son, and he is still in prison.

The medical trial began in 2003, when a dozen researchers at Imperial College London began trialling a new drug on 38 asthma sufferers at St Mary’s Hospital, London, where Erin worked as a chest consultant. His faked research partly contributed to the trial being extended internationally before its deadly side-effects were discovered.

***

It began with good intentions, but turned into the medical experiment from hell: a search for a wonder cure for asthma attacks which left one man dead, 20 seriously ill with pneumonia and eight with cancer. But for Britain’s leading heart and lung scientists at Imperial College, London, it was to get even worse: a doctor on their 12-strong team had faked his research results.

What makes the disclosure of his crime even more extraordinary is the fact that Dr Edward Erin’s fabrications were not detected until he was arrested and jailed for six years for lacing his lover’s coffee with drugs so she would miscarry.

Only two of the scientists involved in the study were willing to talk to The Independent: Professor Peter Barnes, who for three decades has been the world’s most respected specialist in his field, and the US asthma specialist Dr Sally Wenzel.

The medical trials began in 2004, when researchers started testing 38 asthma sufferers at St Mary’s Hospital, London. They were trying to discover whether a new drug could prevent airways of asthma sufferers from becoming life-threateningly inflamed.

In Barnes, a professor of thoracic medicine and head of airway disease at the National Heart and Lung Institute, it had at its head a renowned name in respiratory medicine. Working alongside him was Professor Andrew Bush, Imperial College’s professor of paediatrics and professor of paediatric respirology, Dr Trevor Hansel, medical director of the Imperial Clinical Respiratory Research Unit, and Dr Onn Min Kon, consultant respiratory physician and lead clinician for tuberculosis services at St Mary’s and Hammersmith Hospitals.

The costs of the trial were part-funded by the American drugs company, Centocor, which manufactured the drug being tested. Success would mean that it owned a multibillion dollar medicine.

After the American Journal of Respiratory and Clinical Care (AMJCC) published a paper, prepared by the UK team, saying results of their clinical study of 38 asthmatics had been promising, it was extended from using modestly ill to severely asthmatic patients, in international experiment almost eight times as big.

But what the team did not realise was that the results had been partly based on bogus tests concocted by Erin, a chest consultant at St Mary’s. Although his findings did not directly contribute to the development of cancers in the asthma patients, his data was an important factor in extending what had been a limited UK experiment to a global search involving almost eight times as many – and much more seriously ill – asthma sufferers.

From 2004 to 2006, three-quarters of 309 patients with severe and uncontrolled asthma who had volunteered to take part were given the drug, known as Golimumab, in three different strengths; the rest were on placebos. Dr Sally Wenzel, professor of medicine and director of the Asthma Institute at Pittsburgh’s Montefiore Hospital, was put in charge of the new clinical trials in the US and several European countries, including the UK.

The scientists running the study were deliberately not allowed to see the results as they were compiled, so their judgements were not compromised until all the data had been collated up to the 24th week. It was not until 25 February 2007, when the data was unlocked, that the awful consequences of the drug were discovered.

“There were serious side effects,” Professor Barnes said. “Pneumonia and cancer.” Dr Wenzel added: “It is potentially one of the big finds if it works, but Golimumab had substantial side effects.”

The next day the US Food and Drug Administration ordered an immediate shut-down of the trials. But it was too late. “One death occurred in the 200mg group,” the AMJCC dispassionately reported. “This patient was hospitalised in an unresponsive state one week after receiving the fourth Golimumab dose. The patient’s respiratory status declined, requiring ventilatory support, and the patient died from septic shock following diagnosis of small-bowel pneumatosis.”

It continued: “Eight malignancies were reported in Golimumab-treated patients: breast cancer in the 50mg group; B-cell lymphoma and malignant melanoma in the 100mg group; and cervical carcinoma, renal cell carcinoma, colon cancer (stage 0), and two basal cell carcinomas in the 200mg group.” One female test subject had to have her breast removed, while another man had a fast-growing polyps.

What was not then known was that an analysis of one set of tests, which looked at the build up of mucus developing in the lungs of patients, was bogus. Those findings were the result of work done by Erin, whose name appeared first among all the study authors in four AMJCC reports monitoring its progress. In 2008 he was arrested on charges of having laced his lover’s drink with drugs to try to make her miscarry and was suspended from practising as a doctor. Professor Barnes immediately asked another member of their research team to check all of his findings, and discovered that a lot of his data had been fabricated. Some statistics had been inflated to several times their real value.

In 2009, Erin was given six years in jail for two counts of attempting to administer poison and ordered to pay £30,000 costs. Judge Richard Hone, QC, described him as an “egocentric” who had delusions of grandeur. “The trial process has exposed you,” he added, “stripped of your flummery, as a liar, a cheat and a predator.”

“Erin did not seem different to any to any other research fellow,” Professor Barnes said. “He worked there. Was always in and working.” He discovered that Erin had consistently changed results for about three years. “The judge was absolutely right about Erin,” he said. “He was a liar and a cheat. But psychopaths are very convincing. It could happen to anyone.”

He continued: “Before he was arrested, we had no suspicions. We only had concerns about Erin because he was arrested and convicted of a crime. The person in a related area was not getting similar results. We obtained the notebook which contained the original data that Erin had taken. He had systematically changed figures.”

Professor Barnes acknowledges that Erin, a 44-year-old father of two with a 20-year unblemished medical record, may have been driven by a desire to enhance his career. “It is very difficult to see why he would he did it. It is as if he had a compulsion to change things. These people lie about things they don’t need to lie about. We have never had anything like it in my 30 years.”

In September 2010 a letter, signed by Professor Barnes, Professor Andrew Bush, Dr Trevor Hansel and Dr Onn Min Kon was sent to AMJCC retracting the research. It cited, among other things, an example of the way Erin had altered his data. One figure had been changed from 3.81 to 23.81.

In 2012, Erin’s sentence was extended for a further two years after a former cellmate revealed that the doctor had asked him, as he was about to be released from prison, to kill his former mistress and their baby son, Ernie.

The plot: A deception that continued in jail

On the surface, Dr Edward Erin was a respected doctor and family man.  But the 47-year-old father of two was leading a double life. Dubbed “Dr Poison”, he was jailed in 2009 for trying to poison his secretary, Bella Prowse, when she became pregnant after an affair that began at a Christmas party.

He tried to lace two drinks – a coffee and an orange juice – with drugs that he hoped would induce a miscarriage. Noticing her drinks had been tampered with, Ms Prowse went to the police. A former consultant at St Mary’s Hospital in west London, Erin’s subsequent trial revealed a man described by Old Bailey judge Richard Hone, QC, as “a liar, a cheat and a predator” who exploited his position and his wealth to seduce women.

Even in prison, Erin continued to plot a web of deception that he hoped would clear his name. He convinced a fellow inmate, Joe Mallia, to steal Ms Prowse’s phone and to send a text from it “confessing” that she had made the whole thing up. But Mallia took his story to The Sun, who then secretly filmed Erin going over the plot with Mallia.

The video was used as evidence against the disgraced doctor and he was found guilty of perverting the course of justice.

The retraction: an extract from the letter

In September 2010, a letter was sent to the AMJCC, signed by Dr Hansel, Prof Bush, Dr Kon and Prof Barnes:

“In January 2008 we were presented with some individual immunoassay points provided by Dr Edward M. Erin. On 16th February 2008 another member of our research team highlighted serious concerns. This matter was immediately reported to the relevant authorities. Having reviewed all immunoassay data from relevant studies, the Committee confirmed there was an overwhelming case to answer.

In their report, the Committee stated that Dr Erin, the first author in these publications, is the most likely person to have been responsible for the inaccuracies in the date. The Committee noted Dr Erin has not provided a satisfactory explanation for any of the several hundred unambiguously detailed numerical faults identified, despite being given a chance to provide an explanation.

Dr Erin has denied any wrongdoing on his part in relation to the above clinical research matters, but we authors feel the strong need for withdrawal of the above paper due to the factual inaccuracies.

Study shows drinking one 12oz sugar-sweetened soft drink a day can increase the risk of type 2 diabetes by 22 percent

Contact: Sam Wong Press Office sam.wong@imperial.ac.uk 44-020-759-42198 Diabetologia

Drinking one (or one extra)* 12oz serving size of sugar-sweetened soft drink a day can be enough to increase the risk of developing type 2 diabetes by 22%, a new study suggests. The research is published in  Diabetologia (the journal of the European Association for the Study of Diabetes) and comes from data in the InterAct consortium**. The research is by Dr Dora Romaguera, Dr Petra Wark and Dr Teresa Norat, Imperial College London, UK, and colleagues.

Since most research in this area has been conducted in North American populations, the authors wanted to establish if a link between sweet beverage consumption and type 2 diabetes existed in Europe. They used data on consumption of juices and nectars, sugar-sweetened soft drinks and artificially sweetened soft drinks collected across eight European cohorts participating in the European Prospective Investigation into Cancer and Nutrition (EPIC study; UK, Germany, Denmark, Italy, Spain, Sweden, France, Italy, Netherlands)***, covering some 350,000 participants.

As part of the InterAct project, the researchers did a study which included 12,403 type 2 diabetes cases and a random sub-cohort of 16,154 identified within EPIC. The researchers found that, after adjusting for confounding factors, consumption of one 12oz (336ml) serving size of sugar-sweetened soft drink per day increased the risk of type 2 diabetes by 22%. This increased risk fell slightly to 18% when total energy intake and body-mass index (BMI) were accounted for**** (both factors that are thought to mediate the association between sugar-sweetened soft drink consumption and diabetes incidence). This could indicate that the effect of sugar-sweetened soft drink on diabetes goes beyond its effect on body weight.

The authors also observed a statistically significant increase in type 2 diabetes incidence related to artificially sweetened soft drink consumption, however this significant association disappeared after taking into account the BMI of participants; this probably indicates that the association was not causal but driven by the weight of participants (i.e. participants with a higher body weight tend to report higher consumption of artificially sweetened drinks, and are also more likely to develop diabetes). Pure fruit juice and nectar***** consumption was not significantly associated with diabetes incidence, however it was not possible using the data available to study separately the effect of 100% pure juices from those with added sugars.

The authors say the increased risk of diabetes among sugar-sweetened soft drink consumers in Europe is similar to that found in a meta-analysis of previous studies conducted mostly in North America (that found a 25% increased risk of type 2 diabetes associated with one 12 oz daily increment of sugar-sweetened beverage consumption).

Dr Romaguera concludes: “Given the increase in sweet beverage consumption in Europe, clear messages on the unhealthy effect of these drinks should be given to the population.”

###

Notes to editors:

*The increased risk of 22% is for each extra 12oz sugar sweetened drink, so would apply to someone who had 1 drink versus someone who had 0, or someone who had 2 drinks versus someone who had 1, etc.

**The InterACT consortium is investigating, among other things, nutritional factors and physical activity to study the association of nutritional, dietary and physical activity behaviours with incident diabetes in the nested case-cohort study and to contribute to the analysis of gene-lifestyle interaction. It is a sub-division of the EPIC study, which was designed to investigate the relationships between diet, nutritional status, lifestyle and environmental factors and the incidence of cancer and other chronic diseases.

***The centres involved were France, Italy, Spain, Denmark, UK (Oxford, Cambridge), Netherlands (Bilthoven, Utrecht), Germany (Heidelberg, Potsdam), Sweden (Umea, Malmo)

****Extra info from Dr Romaguera:  The 22% figure is used as the top line because it is widely accepted by the scientific community that these models should not be adjusted for BMI. In the meta-analysis comparison with other studies from the USA, the risk is those studies is NOT adjusted by BMI. That makes it possible to compare the two sets of results (25% increased risk in North American studies versus 22% in Europe).

*****nectars (UK and USA definition) are fruit juices that have been diluted to some extent and may contain additives (sugar or sweeteners)

Financial meltdown was caused by too many bankers taking cocaine, says former government drugs tsar Prof David Nutt

Academic, who was sacked for claiming that horse riding was as safe as taking ecstasy, said abuse of cocaine caused the financial meltdown.

Rob Williams

Monday, 15 April 2013

The former Government drugs tsar, Professor David Nutt, has said the financial crisis was caused by too many bankers taking cocaine.

The controversial academic, who was sacked for claiming that ecstasy was as safe as horse riding, told the Sunday Times that abuse of cocaine caused the financial meltdown.

“Bankers use cocaine and got us into this terrible mess,” he told the paper adding that the drug made them “overconfident” and led to them taking more risks.

Nutt, who is professor of neuropsychopharmacology at Imperial College, claimed that cocaine was perfect for a banking “culture of excitement and drive and more and more and more. It is a ‘more’ drug”.

He goes on to claim in the interview that abuse of cocaine led to the financial meltdown, “and the Barings crash”.

Prof Nutt was sacked from his role as the Government’s most senior drugs advisor in 2009 following the publication of a paper in which he argued there was “not much difference” between the harm caused by riding a horse and taking ecstasy. He also claimed that ecstasy and LSD were less harmful than alcohol.

His most recent foray into the drugs debate was equally controversial.

Last week he attacked the Government over the laws dealing with magic mushrooms, ecstasy and cannabis, which he claims hinder medical research. Magic mushrooms were banned in 2005.

Prof Nutt said he deems the laws surrounding mushrooms “absurd” and “insane” and says it makes it hard to procure one of their ingredients – psilocybin, which is used to treat depression.

The Home Office countered that there was no evidence that regulations were a barrier to research.

Prof Nutt told the BBC: “We have regulations which are 50 years old, have never been reviewed and they are holding us back, they’re stopping us doing the science and I think it’s a disgrace actually.”

 

http://www.independent.co.uk/news/uk/home-news/financial-meltdown-was-caused-by-too-many-bankers-taking-cocaine-says-former-government-drugs-tsar-prof-david-nutt-8572948.html#

Scientists described small genetic changes that enable the H5N1 bird flu virus to replicate more easily in the noses of mammals

 

Bird flu mutation study offers vaccine clue

by  Sam Wong   08 April 2013                   

main image

 

shadow Scientists have described small genetic changes that enable the H5N1 bird flu virus to replicate more easily in the noses of mammals.

So far there have only been isolated cases of bird flu in humans, and no widespread transmission as the H5N1 virus can’t replicate efficiently in the nose. The new study, using weakened viruses in the lab, supports the conclusions of controversial research published in 2012 which demonstrated that just a few genetic mutations could enable bird flu to spread between ferrets, which are used to model flu infection in humans.

Researchers say the new findings could help to develop more effective vaccines against new strains of bird flu that can spread between humans.

“Knowing why bird flu struggles to replicate in the nose and understanding the genetic mutations that would enable it to happen are vital for monitoring viruses circulating in birds and preparing for an outbreak in humans,” said Professor Wendy Barclay, from the Department of Medicine at Imperial College London, who led the study.

“The studies published last year pointed to a mechanism that restricts replication of H5N1 viruses in the nose. We’ve engineered a different mutation with the same effect into one of the virus proteins and achieved a similar outcome. This suggests that there is a common mechanism by which bird flu could evolve to spread between humans, but that a number of different specific mutations might mediate that.”

Bird flu only rarely infects humans because the human nose has different receptors to those of birds and is also more acidic. The Imperial team studied mutations in the gene for haemagglutinin, a protein on the surface of the virus that enables it to get into host cells. They carried out their experiments in a laboratory strain of flu with the same proteins on its surface as bird flu, but engineered so that it cannot cause serious illness.

The more we understand about the kinds of mutations that will enable them to transmit between humans, the better we can prepare for a possible pandemic.– Professor Wendy Barclay

Department of Medicine

The research found that mutations in the H5 haemagglutinin enabled the protein to tolerate higher levels of acidity. Viruses with these mutations and others that enabled them to bind to different receptors were able to replicate more efficiently in ferrets and spread from one animal to another.

The results have important implications for designing vaccines against potential pandemic strains of bird flu. Live attenuated flu vaccines (LAIV) might be used in a pandemic situation because it is possible to manufacture many more doses of this type of vaccine than of the killed virus vaccines used to protect against seasonal flu. LAIV are based on weakened viruses that don’t cause illness, but they still have to replicate in order to elicit a strong immune response. Viruses with modified haemagglutinin proteins induced strong antibody responses in ferrets in this study, suggesting that vaccines with similar modifications might prove more effective than those tested previously.

“We can’t predict how bird flu viruses will evolve in the wild, but the more we understand about the kinds of mutations that will enable them to transmit between humans, the better we can prepare for a possible pandemic,” said Professor Barclay.

The research was funded by the Medical Research Council and the Wellcome Trust and published in the Journal of General Virology.

Reference

H Shelton et al. ‘Mutations in hemagglutinin that affect receptor binding and pH stability increase replication of a PR8 influenza virus with H5 HA in the upper respiratory tract of ferrets and may contribute to transmissibility.’ Journal of General Virology (2013) doi:10.1099/vir.0.050526-0

http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_8-4-2013-12-47-4

 

Overeating now bigger global problem than lack of food

 

Not good for global health <i>(Image: Peter Reali/Plainpicture)</i>Not good for global health (Image: Peter Reali/Plainpicture)

The largest ever study into the state of the world’s health has revealed that, for the first time, the number of years of healthy living lost as a result of people eating too much outweigh the number lost by people eating too little.

The Global Burden of Disease report – a massive research effort involving almost 500 scientists in 50 countries – also concludes that we have finally got a handle on some common infectious diseases, helping to save millions of children from early deaths. But collectively we are spending more of our lives living in poor health and with disability.

“The Global Burden of Disease 2010 is the most comprehensive assessment of human health in the history of medicine,” says Richard Horton, editor of The Lancet, in which the report will be published. “It provides insights into human health that are comparable in scope and depth to the sequencing of the human genome.”

The report assessed the prevalence of diseases and causes of death across the globe in 2010, and compared these to data collected in 1990 to identify any trends.

For the first time on a global scale, being overweight has become more of a health problem than lack of nutrition. In 1990, undernutrition was the leading cause of disease burden, measured as the number of years of healthy life an average person could expect to lose as a result of illness or early death. Back then, a high body-mass index, or BMI, was ranked tenth. Now, undernutrition has dropped to eighth place, while BMI has risen to become the sixth leading cause of disease burden.

Too much to eat

“A greater amount of disease burden has occurred because people are fat and have too much to eat, as opposed to having too little to eat,” says Alan Lopez at the University of Queensland in Brisbane, Australia, who worked on the study.

Being overweight can hike a person’s blood pressure and cause stroke and heart disease; together, these two conditions are responsible for a quarter of all deaths. And the problem isn’t limited to the west – the Middle East is one region that is seeing significant increases in BMI.

But while more of us may be overweight, we are also living longer. In some countries, the change has been huge – the Maldives, for example, has seen an increase in life expectancy of almost 30 years since the 1970s. Rural health programmes have also contributed to big improvements in countries including Bangladesh and Iran.

“There has been a lot of progress,” says Majid Ezzati at Imperial College London, who led part of the study investigating the risk factors of disease. “These are countries that have implemented programmes in large regions and nationwide to get interventions to the people that really need them.”

Progress in eliminating the causes of early childhood death – mainly infections, diarrhoea and birth problems – has been astounding. The rate of death in the under-5s has dropped by 60 per cent since 1990.

High mortality

Sub-Saharan Africa is still experiencing high levels of mortality from infectious diseases such as HIV and malaria, yet globally deaths from infectious diseases have dropped. In fact, we are more likely to die from non-infectious diseases – especially those caused by being overweight.

Looking forward, obesity and the use of tobacco and alcohol are obvious targets for health policy change. But it is also important to focus on healthy ageing.

“The large burden [of disease] related to disability was a surprise,” says Christopher Murray at the University of Washington in Seattle. “There’s been a focus on mortality, but there’s a huge volume [of disease burden] related to things that don’t really kill you.”

Musculoskeletal disorders – such as neck and back pain – dominate this category, as do mental disorders and substance abuse.

There’s a need to improve awareness of these chronic conditions in the developing world, says Irene Agyepong at the University of Ghana in Accra, who was not involved in the study. “The kind of awareness we have in the western world is not there in the south,” she says. “We have to focus on it now rather than wait until it is upon us, like the HIV AIDS epidemic is on us.”

http://www.newscientist.com/article/dn23004-overeating-now-bigger-global-problem-than-lack-of-food.html?full=true&print=true

 

Free statins with fast food could neutralize heart risk, scientists say

2010 report posted for filing

Contact: Sam Wong sam.wong@imperial.ac.uk 44-020-759-42198 Imperial College London

Fast food outlets could provide statin drugs free of charge so that customers can neutralize the heart disease dangers of fatty food, researchers at Imperial College London suggest in a new study published this week

Fast food outlets could provide statin drugs free of charge so that customers can neutralise the heart disease dangers of fatty food, researchers at Imperial College London suggest in a new study published this week.

Statins reduce the amount of unhealthy “LDL” cholesterol in the blood. A wealth of trial data has proven them to be highly effective at lowering a person’s heart attack risk.

In a paper published in the Sunday 15 August issue of the American Journal of Cardiology, Dr Darrel Francis and colleagues calculate that the reduction in cardiovascular risk offered by a statin is enough to offset the increase in heart attack risk from eating a cheeseburger and a milkshake.

Dr Francis, from the National Heart and Lung Institute at Imperial College London, who is the senior author of the study, said: “Statins don’t cut out all of the unhealthy effects of burgers and fries. It’s better to avoid fatty food altogether. But we’ve worked out that in terms of your likelihood of having a heart attack, taking a statin can reduce your risk to more or less the same degree as a fast food meal increases it.”

One statin, simvastatin, is already available in low doses (10mg) over the counter at pharmacies without a prescription. Other statins are so far only prescribed by doctors, and limited by cost to patients at particular risk of heart attack or stroke. However, the cost of the tablets has fallen sharply in recent years (from ~£40/month to ~£1.50/month), such that the cost to the NHS of seeing a doctor is much greater than the cost of the tablet.

“It’s ironic that people are free to take as many unhealthy condiments in fast food outlets as they like, but statins, which are beneficial to heart health, have to be prescribed,” Dr Francis said.

Statins have among the best safety profiles of any medication. A very small proportion of regular statin users experience significant side effects, with problems in the liver and kidneys reported in between 1 in 1,000 and 1 in 10,000 people.

“Everybody knows that fast food is bad for you, but people continue to eat it because it tastes good. We’re genetically programmed to prefer high-calorie foods, and sadly fast food chains will continue to sell unhealthy foods because it earns them a living.

“It makes sense to make risk-reducing supplements available just as easily as the unhealthy condiments that are provided free of charge. It would cost less than 5p per customer – not much different to a sachet of ketchup.

“When people engage in risky behaviours like driving or smoking, they’re encouraged to take measures that minimise their risk, like wearing a seatbelt or choosing cigarettes with filters. Taking a statin is a rational way of lowering some of the risks of eating a fatty meal.”

Studies have shown a clear link between total fat intake and blood cholesterol, which is strongly linked to heart disease. Recent evidence suggests that trans fats, which are found in high levels in fast food, are the component of the Western diet that is most dangerous in terms of heart disease risk.

Dr Francis and his colleagues used data from a previous large cohort study to quantify how a person’s heart attack risk increases with their daily intake of total fat and trans fat. He compared this with the decrease in risk from various statins, based on a meta-analysis of seven randomised controlled trials.

The results showed that most statin regimes are able to compensate for the relative risk increase from eating a cheeseburger and a small milkshake.

The researchers note that studies should be conducted to assess the potential risks of allowing people to take statins freely, without medical supervision. They suggest that a warning on the packet should emphasise that no tablet can substitute for a healthy diet, and advise people to consult their doctor for more advice.

###

For more information, please contact:

Sam Wong Research Media Officer (Medicine) Imperial College London email: sam.wong@imperial.ac.uk Tel: +44(0)20 7594 2198 Out of hours duty press officer: +44(0)7803 886 248

Notes to editors:

1. E.A. Ferenczi et al. “Can a statin neutralise the cardiovascular risk of unhealthy dietary choices?” American Journal of Cardiology, Sunday 15 August 2010

Download the paper here: https://fileexchange.imperial.ac.uk/files/c7314c427/Statins%20AJC%20150810.PDF

2. For more information about statins, visit http://www.nhs.uk/Conditions/Cholesterol-lowering-medicines-statins/Pages/Introduction.aspx

3. About Imperial College London

Consistently rated amongst the world’s best universities, Imperial College London is a science-based institution with a reputation for excellence in teaching and research that attracts 14,000 students and 6,000 staff of the highest international quality. Innovative research at the College explores the interface between science, medicine, engineering and business, delivering practical solutions that improve quality of life and the environment – underpinned by a dynamic enterprise culture.

Since its foundation in 1907, Imperial’s contributions to society have included the discovery of penicillin, the development of holography and the foundations of fibre optics. This commitment to the application of research for the benefit of all continues today, with current focuses including interdisciplinary collaborations to improve global health, tackle climate change, develop sustainable sources of energy and address security challenges.

In 2007, Imperial College London and Imperial College Healthcare NHS Trust formed the UK’s first Academic Health Science Centre. This unique partnership aims to improve the quality of life of patients and populations by taking new discoveries and translating them into new therapies as quickly as possible.

Website: www.imperial.ac.uk

A vaccine-derived strain of poliovirus that has spread in recent years is serious but it can be tackled with an existing vaccine

2010 study posted for filing

Contact: Laura Gallagher l.gallagher@imperial.ac.uk 44-020-759-48432 Imperial College London

Polio research gives new insight into tackling vaccine-derived poliovirus

A vaccine-derived strain of poliovirus that has spread in recent years is serious but it can be tackled with an existing vaccine, according to a new study published today in the New England Journal of Medicine.

Vaccine-derived polioviruses can emerge on rare occasions in under-immunised populations, when the attenuated virus contained in a vaccine mutates and recombines with other viruses, to create a circulating vaccine-derived strain.

The researchers behind today’s study say their findings highlight the importance of completing polio eradication. They also say that should wild-type poliovirus be eradicated, routine vaccination with oral polio vaccines will need to cease, in order to prevent further vaccine-derived strains of the virus from emerging.

The study was carried out by researchers from the Medical Research Council Centre for Outbreak Analysis and Modelling at Imperial College London, working with the Government of Nigeria and the World Health Organization (WHO) research teams.

Poliovirus is highly infectious and primarily affects children under five years of age. Around one in 200 of the people infected with polio develop permanent paralysis, which can be fatal.

Polio was virtually wiped out by the early 2000s following a major vaccination drive by the Global Polio Eradication Initiative, but since then the number of cases of paralysis reported has plateaued, remaining roughly constant at between one and two thousand each year from 2003 to 2009, dropping only recently in 2010.

The first reported polio outbreak resulting from a circulating vaccine-derived poliovirus, known as a cVDPV, occurred in Hispaniola in 2000.  Prior to today’s study, there was little evidence available about the severity and potential impact of this kind of poliovirus.

Although billions of doses of oral vaccine have been distributed in the last decade, just 14 cVDPV outbreaks have been reported, affecting 15 countries. These outbreaks have usually been limited in size.

For the new study, researchers looked at the largest recorded outbreak of a cVDPV to date, which began to circulate in Nigeria in 2005. The authors examined data from 278 children paralysed by this cVDPV, and compared them with children paralysed by wild-type poliovirus in the country. Their analysis showed that this serotype 2 cVDPV is as easily transmitted and likely to cause severe disease as wild-type poliovirus of the same serotype.

The study also shows that vaccination with trivalent OPV, one of the main types of vaccine currently used to combat polio, is highly effective in preventing paralysis by this serotype 2 cVDPV.

The research shows that it is even more effective against cVDPV than against the wild-type polioviruses that are currently circulating, which can also be targeted with a different vaccine.

The new findings mean that it is particularly vital that efforts to vaccinate children with trivalent OPV continue in Nigeria and neighbouring countries, to protect children against all strains of polio. The scientists hope their findings will help countries to devise the right vaccine strategies to eradicate polio.

Helen Jenkins, the lead author of the study from the Medical Research Council Centre for Outbreak Analysis and Modelling at Imperial College London, said: “Our research shows that vaccine-derived polioviruses must be taken seriously and that we have the right tools to tackle them. We’ve had a lot of success against polio in the past and we’re optimistic that ultimately we should be able to eradicate it completely.

“However, our study shows that we can’t be complacent about the virus. It’s still vital for us to protect children from this dangerous and debilitating disease and we have to make sure we continue to vaccinate as many children as possible in affected countries for as long as wild-type poliovirus continues to circulate,” added Ms Jenkins.

Senior study author Dr Nicholas Grassly, also from the Medical Research Council Centre for Outbreak Analysis and Modelling at Imperial College London, added: “There has been some debate about the significance of circulating vaccine-derived polioviruses for the eradication initiative. Our research shows these viruses can be as pathogenic and transmissible as wild-type polioviruses and outbreaks must be responded to with just as much vigour.”

Dr Bruce Aylward, Director of the Global Polio Eradication Initiative at WHO, added:  “These new findings suggest that if cVDPVs are allowed to circulate for a long enough time, eventually they can regain a similar capacity to spread and paralyse as wild polioviruses.  This means that they should be subject to the same outbreak response measures as wild polioviruses.  These results also underscore the need to eventually stop all OPV use in routine immunization programmes after wild polioviruses have been eradicated, to ensure that all children are protected from all possible risks of polio in future.”

###

This study was funded by the Medical Research Council and the Royal Society.

For further information please contact:

Laura Gallagher Research Media Relations Manager Imperial College London email: l.gallagher@imperial.ac.uk Tel: +44(0)20 7594 8432 Out of hours duty press officer: +44(0)7803 886 248

Notes to editors:

1. “Implications of a circulating vaccine-derived poliovirus (cVDPV) in Nigeria for polio eradication” New England Journal of Medicine, Wednesday 23 June 2010

Lead author: Helen Jenkins, Imperial College London (for full list of authors please see paper) Download a proof copy of the study (strictly embargoed) using this link:  https://fileexchange.imperial.ac.uk/files/3eba66aa7b6/Nigeria%20cVDPV%20paper%20R2%20clean.doc

2. About the Global Polio Eradication Initiative (GPEI)

The GPEI is spearheaded by national governments, WHO, Rotary International, the US Centers for Disease Control and Prevention (CDC) and UNICEF. Since 1988 (the year the GPEI was launched), the incidence of polio has been reduced by more than 99%. In 1988, more than 350,000 children were paralyzed each year in more than 125 endemic countries. In 2010, 349 cases have been reported and four countries remain endemic: Nigeria, India, Pakistan and Afghanistan.

Further information can be found at www.polioeradication.org. A list of countries in which there have been cases of polio reported since 2009 can be found at http://www.polioeradication.org/casecount.asp

3. About Imperial College London

Consistently rated amongst the world’s best universities, Imperial College London is a science-based institution with a reputation for excellence in teaching and research that attracts 14,000 students and 6,000 staff of the highest international quality. Innovative research at the College explores the interface between science, medicine, engineering and business, delivering practical solutions that improve quality of life and the environment – underpinned by a dynamic enterprise culture.

Since its foundation in 1907, Imperial’s contributions to society have included the discovery of penicillin, the development of holography and the foundations of fibre optics. This commitment to the application of research for the benefit of all continues today, with current focuses including interdisciplinary collaborations to improve global health, tackle climate change, develop sustainable sources of energy and address security challenges.

In 2007, Imperial College London and Imperial College Healthcare NHS Trust formed the UK’s first Academic Health Science Centre. This unique partnership aims to improve the quality of life of patients and populations by taking new discoveries and translating them into new therapies as quickly as possible.

Website: www.imperial.ac.uk

4. For almost 100 years the Medical Research Council has improved the health of people in the UK and around the world by supporting the highest quality science. The MRC invests in world-class scientists. It has produced 29 Nobel Prize winners and sustains a flourishing environment for internationally recognised research. The MRC focuses on making an impact and provides the financial muscle and scientific expertise behind medical breakthroughs, including one of the first antibiotics penicillin, the structure of DNA and the lethal link between smoking and cancer. Today MRC funded scientists tackle research into the major health challenges of the 21st century. www.mrc.ac.uk

Study shows potential benefit of dark chocolate for liver disease patients

2010 study posted for filing

Contact: Isabelle Scali media.easl2010@cohnwolfe.com 44-771-743-5103 European Association for the Study of the Liver

Vienna, Austria, Thursday 15 April: Doctors could soon be prescribing a dose of dark chocolate to help patients suffering from liver cirrhosis and from dangerously high blood pressure in their abdomen, according to new research presented today at the International Liver CongressTM 2010, the Annual Meeting of the European Association for the Study of Liver in Vienna, Austria.

According to the Spanish research, eating dark chocolate reduces damage to the blood vessels of cirrhotic patients and also lowers blood pressure in the liver. Dark chocolate contains potent anti-oxidants which reduce the post-prandial (after-meal) blood pressure in the liver (or portal hypertension) associated with damaged liver blood vessels (endothelial dysfunction). The data also showed that eating dark chocolate may exert additional beneficial effects throughout the whole body. In comparison, white chocolate, which contains no beneficial ‘phytochemicals’, did not result in the same effects.

Professor Mark Thursz, MD FRCP, Vice Secretary of EASL and Professor of Hepatology, at Imperial College London said: “As well as advanced technologies and high science, it is important to explore the potential of alternative sources which can contribute to the overall wellbeing of a patient. This study shows a clear association between eating dark chocolate and portal hypertension and demonstrates the potential importance of improvements in the management of cirrhotic patients, to minimise the onset and impact of end stage liver disease and its associated mortality risks”.

Cirrhosis is scarring of the liver as a result of long-term, continuous damage to the liver . In cirrhosis, circulation in the liver is damaged by oxidative stress and reduced antioxidant systems. After eating, blood pressure in the abdominal veins usually increases due to increased blood flow to the liver.

This is particularly dangerous and damaging to cirrhotic patients as they already have increased blood pressure in the liver (portal hypertension) and elsewhere which, if severe, can cause blood vessel rupture. Thus, eating dark chocolate may ultimately prevent this potential threat to cirrhotic patients.

In this study 21 cirrhotic patients with end stage liver disease (child score 6.9±1.8;MELD 11±4; hepatic venous pressure gradient (HPVG*)16.6±3.8mmHg) were randomised to receive a standard liquid meal. Ten patients received the liquid meal containing dark chocolate (containing 85% cocoa, 0.55g of dark chocolate/Kg of body weight) while 11 patients received the liquid meal containing white chocolate which is devoid of cocoa flavonoids (anti-oxidant properties) according to body weight. HVPG, arterial pressure and portal blood flow (PBF)** were measured at baseline and 30 minutes after meal administration, using a US-Doppler.

Both meals caused a highly significant but similar increase in portal blood flow with a +24% increase in dark chocolate compared to +34% in those patients who received white chocolate. Interestingly, post-prandial hyperaemia*** was accompanied by an increase in HVPG resulting in a statistically significant increase (17.3±3.6mmHg to 19.1±2.6mmHg, p=0.07) for those patients eating dark chocolate and those receiving white chocolate (16.0±4.7mmHg to 19.7±4.1mmHg, p=0.003). Post-prandial increase in HVPG was markedly reduced in patients receiving dark chocolate (+10.3±16.3% Vs +26.3±12.7%, p=0.02).

###

*HVPG is blood pressure in the liver

**PBF refers to blood flow in the liver

***Hyperaemia refers to increase blood flow to tissues

 

About EASL

 

EASL is the leading European scientific society involved in promoting research and education in hepatology. EASL attracts the foremost hepatology experts as members and has an impressive track record in promoting research in liver disease, supporting wider education and promoting changes in European Liver policy.

EASL’s work continues throughout the year with numerous events and initiatives, including:

  • The International Liver CongressTM which lasts several days and attracts upwards of 7,500 participants
  • EASL meetings including Monothematic and Special conferences, Post Graduate courses and other EASL endorsed meetings that take place throughout the year
  • EASL Clinical and Basic Schools of Hepatology, a series of events covering different aspects in the field of hepatology
  • Journal of Hepatology published monthly with a readership of over 40,000
  • Presenting new initiatives for European liver policy change 

About The International Liver CongressTM 2010

 

The International Liver Congress™ 2010, the 45th annual meeting of the European Association for the study of the Liver, is being held at the Reed Messe Wien congress center, Vienna, Austria from April 14th-18th, 2010. The congress annually attracts over 7,500 clinicians and scientists from around the world and provides an opportunity to hear the latest research, perspectives and treatments of liver disease from principal experts in the field.

References:

 

1De Gottardi A. et al, Dark Chocolate attenuates the post –prandial increase in HVPG in patients with cirrhosis and portal hypertension. Abstract presented at The International Liver CongressTM 2010

2Cirrhosis Overview. NHS Choices. September 2009. http://www.nhs.uk/Conditions/Cirrhosis/Pages/Introduction.aspx accessed 19.03.10

Tenth of Quirky Creature’s Active Genes Are Foreign: Believed to ‘Ingest’ DNA from Other Simple Organisms

Bdelloid rotifer. Alan Tunnacliffe said: “We were thrilled when we discovered that nearly 10 per cent of bdelloids’ active genes are foreign, adding to the weirdness of an already odd little creature.” (Credit: Image courtesy of University of Cambridge)

ScienceDaily (Nov. 15, 2012) — Up to 10 per cent of the active genes of an organism that has survived 80 million years without sex are foreign, a new study from the University of Cambridge and Imperial College London reveals. The asexual organism, the bdelloid rotifer, has acquired a tenth of its active genes from bacteria and other simple organisms like fungi and algae.

The findings were reported Nov. 15 in the journal PLoS Genetics.

Bdelloid rotifers are best known for going 80 million years without sex, as they have evolved to reproduce successfully without males. Many asexual creatures go extinct without the benefit of traditional genetic evolution. However, bdelloids have flourished by developing ingenious ways of overcoming the limitations of being asexual.

Bdelloids have also developed the fascinating ability to withstand almost complete desiccation when the freshwater pools they typically live in dry up. They can survive in the dry state for many years only to revive with no ill effect once water becomes available again.

“We were thrilled when we discovered that nearly 10 per cent of bdelloids’ active genes are foreign, adding to the weirdness of an already odd little creature,” said Professor Alan Tunnacliffe, lead author of the study from the University of Cambridge. “We don’t know how the gene transfer occurs, but it almost certainly involves ingesting DNA in organic debris, which their environments are full of. Bdelloids will eat anything smaller than their heads!”

Because some of the foreign genes are activated when the bdelloids begin to dry out, the researchers believe that the genes play a role in bdelloids’ ability to survive desiccation.

Professor Tunnacliffe added: “Other researchers have shown that bdelloids contain powerful antioxidants, which help protect them from the toxic oxidising agents that are the by-products of desiccation. These antioxidants have not yet been identified, but we think that some of them result from foreign genes.”

For the study, the researchers extracted all of the messenger RNA (genetic code similar to DNA which provides a blueprint for the creation of proteins) from bdelloid rotifers and sequenced each message, creating a library of the animal’s active coding information. Using a supercomputer, they then compared these messages with all other known sequences and found that in many cases similar sequences had been found in other organisms.

Strangely, however, these other organisms were often not animals, but simple microbes. This means that bdelloids have genes that are not present in other animals, but have been acquired from micro-organisms and adapted for use in the rotifer.

The research was funded by the Biotechnology and the Biological Sciences Research Council (BBSRC) and the European Research Council.

http://www.sciencedaily.com/releases/2012/11/121115172032.htm

Human nose too cold for bird flu, says new study ( H5N1 )

2009 study posted for filing

Contact: Lucy Goodchild
lucy.goodchild@imperial.ac.uk
44-207-594-6702
Imperial College London

Avian influenza viruses do not thrive in humans because the temperature inside a person’s nose is too low, according to research published today in the journal PLoS Pathogens. The authors of the study, from Imperial College London and the University of North Carolina, say this may be one of the reasons why bird flu viruses do not cause pandemics in humans easily.

There are 16 subtypes of avian influenza and some can mutate into forms that can infect humans, by swapping proteins on their surface with proteins from human influenza viruses.

Today’s study shows that normal avian influenza viruses do not spread extensively in cells at 32 degrees Celsius, the temperature inside the human nose. The researchers say this is probably because the viruses usually infect the guts of birds, which are warmer, at 40 degrees Celsius. This means that avian flu viruses that have not mutated are less likely to infect people, because the first site of infection in humans is usually the nose. If a normal avian flu virus infected a human nose, the virus would not be able to grow and spread between cells, so it would be less likely to damage cells and cause respiratory illness.

The researchers also found that when they created a mutated human influenza virus by adding a protein from the surface of an avian influenza virus, this mutated virus struggled to thrive at 32 degrees Celsius. This suggests that if a new human influenza strain evolved by adopting proteins from an avian influenza virus, this would need to undergo further changes in order to adapt to the conditions in the human body.

The researchers reached their conclusions by growing cells from the human airway and infecting them with different human and avian influenza viruses, including H5N1, to see how well the viruses grew and spread. The human influenza viruses grew equally well in the cells whether they were maintained at 37 degrees Celsius, our core body temperature, or at 32 degrees Celsius, the temperature of the nose. In contrast, the four avian influenza viruses tested grew well at 37 degrees Celsius but grew very slowly at 32 degrees Celsius.

When the researchers added proteins from an avian influenza virus to a human influenza virus, the human influenza virus also grew slowly and struggled to replicate at 32 degrees Celsius.

As viruses kill the cells they infect, the researchers also measured the extent of cell death in the model. This showed that at 32 degrees Celsius, far fewer cells died as a result of infection with avian influenza compared with human influenza, supporting the idea that the avian virus could not thrive at that temperature.

Professor Wendy Barclay, one of the authors of the study from the Division of Investigative Science at Imperial College London, said: “Bird viruses are out there all the time but they can only cause pandemics when they undergo certain changes. Our study gives vital clues about what kinds of changes would be needed in order for them to mutate and infect humans, potentially helping us to identify which viruses could lead to a pandemic.

“It would be impossible to develop vaccines against all 16 subtypes of avian flu, so we need to prioritise. By studying a range of different viruses in systems like this one we can look for warnings that they are already beginning to make the kinds of genetic changes in nature that mean they could be poised to jump into humans; animal viruses that spread well at low temperatures in these cultures could be more likely to cause the next pandemic than those which are restricted,” added Professor Barclay.

 

###

 

The research was funded by the Medical Research Council in the UK and by the NIH in the USA.

World Health Organisation says has found new SARS-like virus

6:13pm EDT

By Kate Kelland

LONDON (Reuters) – A new virus belonging to the same family as the SARS virus that killed 800 people in 2002 has been identified in Britain in a man who had recently been in Saudi Arabia, the World Health Organisation (WHO) said on Sunday.

The United Nations health body, which issued a statement through its “global alert and response” system, said tests on the patient, a 49-year-old Qatari man, confirmed the presence of a new, or novel, coronavirus.

Coronaviruses are a large family of viruses which includes the common cold and SARS.

“Given that this is a novel coronavirus, WHO is currently in the process of obtaining further information to determine the public health implications,” the statement said.

SARS, or Severe Acute Respiratory Syndrome, appeared in China in 2002 and killed some 800 people globally before being brought under control.

Peter Openshaw, director of the Centre for Respiratory Infection at Imperial College London, said at this stage the novel virus looked unlikely to prove a concern, and may well only have been identified due to sophisticated testing techniques.

“For now, I would be watchful but not immediately concerned,” he told Reuters.

The WHO said the Qatari patient had first presented to doctors on September 3, 2012 with symptoms of an acute respiratory infection.

On September 7, he was admitted to an intensive care unit in Doha, Qatar, and on September 11, he was transferred to Britain by air ambulance from Qatar.

“The Health Protection Agency of the UK conducted laboratory testing and has confirmed the presence of a novel coronavirus,” the WHO said.

It said scientists at the HPA compared gene sequences of the virus from the Qatari patient with samples of virus sequenced by Dutch scientists from lung tissue of a fatal case earlier this year in a 60-year-old Saudi national.

The two were almost identical, it said.

Openshaw said the fact the two cases found so far are apparently unrelated suggests “that what has been picked up is just some rare event that in past times might have been undiagnosed”.

But he added: “Any evidence of sustained human-to-human transmission or of contact would be more worrying, raising the worry that another SARS-like agent could be emerging.”

The WHO said it was not recommending any travel restrictions but would be seeking further information on the virus.

(Reporting by Kate Kelland; Editing by Sophie Hares)

http://www.reuters.com/article/2012/09/23/us-virus-who-idUSBRE88M0FV20120923

Neural implants could spark better decisions

18:00 19 September 2012 by Douglas Heaven Magazine issue 2883.

Ever wish you could make better choices? That could one day be possible thanks to an electronic brain implant that can enhance short-term memory and decision-making in primates. The implant can also restore these functions in an animal model of Alzheimer’s disease and other types of brain damage, paving the way for the development of new treatments for people with these conditions.

Sam Deadwyler at Wake Forest University School of Medicine in Winston-Salem, North Carolina, and colleagues have previously shown that a neural implant can restore some motor and sensory functions in rats. Now they have used a similar implant to stimulate higher-level thinking in monkeys.

During normal brain function, neurons “fire” when they receive an input from another neuron via the connection between them, called a synapse. The spatial and temporal pattern of this activity  – where and when the neurons fire   – can be detected and recorded.

To find out if it is possible to hijack and then retune these patterns of activity, Deadwyler’s team first trained five rhesus macaques to perform a task that tests their attention, short-term memory and decision-making skills.

First, the monkeys were shown a random image from a pool of 5000. The image was then blanked out for an interval of 1 to 90 seconds, before reappearing in a different position, alongside up to seven other images. If the monkey selected the original image once it reappeared it was rewarded with juice.

After two years of training, the monkeys correctly matched the images 75 per cent of the time at the easier levels  – when the image was blanked out for a short period of time, and fewer images were displayed when it reappeared. Their success rate declined to 40 per cent in tasks with the longest interval and maximum amount of images to choose from.

The animals then had a device capable of recording and stimulating neuronal activity implanted into their prefrontal cortex, an area of the brain responsible for many facets of intelligence. Specifically, the implant was able to record neuronal communication in the so-called supra-granular layers (layers 2/3), part of the six layers that make up this part of the cortex, and both record from and stimulate neurons in layer 5 (see diagram). Layers 2/3 and 5 are around 1350 micrometres apart and differ in their predominant cell type and connectivity.

The challenge lay in working out which patterns of activity should be induced and when in order to enhance the monkeys’ performance in the task. To do so, the team recorded neuronal activity while the animals performed the task again. They then analysed the activity going into and out of the different layers and extracted patterns of neuronal firing that correlated with correct and incorrect decisions.

The team was then able to enhance the animals’ decision-making process by ensuring that the implant kicked in whenever the neuronal activity in layers 2/3 resembled that seen when an incorrect decision was being made. When it did, the implant stimulated a pattern of activity in layer 5 that replicated the activity recorded when a correct decision was made.

The implant was able to improve average performance in the task by 10 to 20 per cent. In the hardest versions of the task – such as when the original image reappeared alongside several other images  – the monkeys also significantly increased their speed, taking 2 rather than 3 seconds to correctly identify the image.

The team next tested the implant’s ability to restore cognitive function in monkeys that had been given cocaine. The drug is commonly used in animals to model the loss of synaptic connections seen in Alzheimer’s, dementia and other types of brain injury.

Without stimulation from the implant, the monkeys’ performance dropped by 10 per cent across all difficulty levels. When the implant was switched on, however, their performance was boosted to just below levels seen in monkeys who hadn’t been given cocaine or an implant.

“It’s a wonderful piece of work,” says Daniel Chew at the University of Cambridge, who was not involved in the study. He suggests that since the implant reduces the number of incorrect responses there may be an even greater degree of improvement on a more difficult task.

Simon Schultz at Imperial College London agrees that it is an impressive study, but says that it is not clear what exactly is going on. We understand the motor and sensory domains quite well, he says, but we still don’t know how the cortex works. These guys step around that, he says, by effectively recognising what a correct decision looks like, recording that pattern and playing it back.

In the study, the patterns of activity used to stimulate a correct answer were specific to each monkey. Would it be possible to use a pattern taken from one high-performing individual and use it to raise the game of others? According to team member Robert Hampson, giving one monkey a “correct” pattern of activity from another didn’t work, and in fact reduced performance, just as scrambled patterns did.

To apply this technology to people with conditions such as Alzheimer’s, this limitation would have to be overcome, either by learning much more about how a correct pattern is shaped from inputs into each area, or recording healthy brain activity before a person developed symptoms of brain damage.

A further problem is the invasive nature of implants. “It causes very acute inflammation and scarring,” says Chew. This can kill the neurons around the implant, insulating the electrodes and diminishing their effectiveness. Chew and his colleagues are trying to create biologically compatible electrodes to get around this problem.

Another possibility is bypassing the need for an implant entirely. Deadwyler and Hampson both point out that transcranial imaging and stimulation – the ability to visualise and stimulate activity in the brain non-invasively – is advancing quickly and that it may one day be possible to adapt their approach to work from outside the skull.

Regardless, the pair believe that human trials of the implant are in sight since similar hardware has already been approved by the US Food and Drug Administration for use in people with Parkinson’s. “[Human trials] may not be too far down the line,” says Deadwyler.

This is great news for people with brain deterioration  – the likely first participants of such a trial. But besides therapeutic treatment, the possibilities are endless. Imagine an implant in your visual cortex, says Schultz. This, he suggests, would make it possible to identify the pattern of activity that occurs when you imagine a number. When this pattern was recognised by the implant it could stimulate the pattern for a new number for you to picture. In theory, such an implant could be used to create a secure code for a cryptographic key based on values only you can access.

The problem with developing a prosthesis for cognitive enhancement rather than restoration is that it is harder to justify the trials. But, as Schultz jokes, “why stop at repair when you can enhance as well?” It’s a nice idea, but the ethical hurdles mean that developing a prosthesis for cognitive enhancement rather than restoration is not currently justifiable, he says. For the time being, at least, the focus will rightly be on ways to restore lost function in people with brain damage. And that’s surely a good decision.

Journal reference: Journal of Neural Engineering, doi.org/jcx

http://www.newscientist.com/article/dn22282-neural-implants-could-spark-better-decisions.html?full=true&print=true