Latest Science Updates

A major reform of the way that NHS hospitals pay for legal liability insurance has led to improvements in patient safety, according to research funded by the Economic and Social Research Council.

Offering discounts on insurance premiums to hospitals that meet certain targets has led to falls in MRSA infection rates.

A team of academics from Nottingham, Oxford and Surrey universities looked at how the NHS Litigation Authority (NHSLA), which was set up in 1995, had changed the way that hospitals paid into the Clinical Negligence Scheme for Trusts (CNST), which funds the cost of clinical negligence claims, and whether these changes had improved patient safety.

Since 2002 the NHSLA has funded the scheme through "pay-as-you-go" contributions from hospitals based on a biannual assessment of hospitals' risk management standards based on three levels.

Hospitals that pass their assessment receive a discount on their contribution to the CNST for the next two years, rising from 10% for Level 1, to 20% for Level 2 and 30% for Level 3. Given that the average CNST contribution by a hospital trust is £1.7m, compliance with the highest standards can deliver significant financial savings.

The researchers looked at the relationship between hospitals' risk management standards and levels of MRSA infection. They found that compliance with high level risk management standards led to lower rates of MRSA infections.

Professor Paul Fenn, of Nottingham University Business School, who led the research, said the story of the last decade had been one of a gradual shift away from the reliance by the NHSLA on risk-sharing towards a "constructive use" of financial incentives to implement good risk management practice.

"The results reported in this paper are indeed consistent with the implementation of improved risk management procedures having a positive effect on patient safety in terms of a reduction in the number of infections," he says.

"They show that negligence liability can be a powerful force for improvements in patient safety, even when they are filtered through liability insurance arrangements."

Professor Fenn says the findings will be directly relevant to evaluating the implementation and operation of the NHS Redress Scheme that aims to provide a speedier way to resolve negligence claims below £20,000 but whose details have still to be published.

"Once these are known and the nature of its funding is clarified, the issues explored in this study should be of direct relevance to monitoring and evaluating its operation," he says.

The findings have been presented to policymakers at HM Treasury, the Department of Health, the NHLSA, the Healthcare Commission and the National Patient Safety Agency.

Breast cancer, the leading cause of death among women in France, is the most commonly occurring cancer in women. Sporadic breast cancer, which is non-hereditary, turns out to be the most widespread, representing 85 to 90% of all cases, but remains the least well-known. Researchers at CNRS and CEA (1), working with a team from Hôpital Saint-Louis (2), have just discovered the cause of 50% of sporadic breast cancers.

The results should also explain epidemiological studies which suggest that hormone treatment predisposes patients to breast cancer. The work is published in 'Cancer Research'.

More than four out of five breast cancers are not related to hereditary factors. These cancers, which are called sporadic, are due to causes which were until recently considered complex and poorly understood. On the other hand, hereditary forms of cancer, which represent only 10 to 15% of breast cancers, have for years been the subjects of studies, work which has resulted in the identification of ten genes whose mutation increases the risk of cancer in an individual.

Among these genes, nine are involved in the DNA damage response system, which is the collection of cell mechanisms that optimize the repair of DNA. The tenth gene codes for a protein which inhibits the action of the AKT1 enzyme. And among these ten genes, two are responsible for 50% of hereditary breast cancers: BRCA1 and BRCA2. Researchers from the "Radiobiologie moléculaire et cellulaire" (CNRS / CEA) lab took these data on hereditary cancers as the starting point for their research into non-hereditary forms.

A link between hereditary and sporadic cancers It turns out that the AKT1 protein is over-expressed in 50% of sporadic breast cancers. Could this protein play a key role in predisposition to non hereditary breast cancer? The researchers, seeking an answer to this question, were able to show that activation of AKT1 leads to the sequestration of the BRCA1 protein in the cytoplasm. This makes it impossible for the protein to penetrate the nucleus, which prevents it from fulfilling its role in DNA repair. The cell then behaves as if it had no BRCA1 gene, without involving a mutation (unlike hereditary forms, where the BRCA1 gene undergoes an alteration). This phenomenon is observed in 50% of sporadic tumors. These results show a single, previously undetected, link between sporadic and hereditary cancers: the DNA damage response system.

The researchers have also suggested that hormone treatment may confer upon patients a predisposition to breast cancer. As AKT1 is activated by hormones, hormone treatment (3) could indeed, in some cases, result in the chronic activation of the molecule. If this is the case, it could lead to a deregulation of the BRCA1 gene, and, as a result, to breast cancer. These first results still need to be confirmed, something that the team led by Bernard Lopez (4) will do soon through further laboratory and clinical studies.

1. Institut de radiobiologie cellulaire et moléculaire, which is part of the Department of Life Sciences.
2. The team is led by Fabien Calvo, director of Inserm unit 716 "Cibles pharmacologiques dans les cancers"
3. Like for example estrogen treatment.
4. CNRS senior researcher and deputy director at the laboratory "Radiobiologie moléculaire et cellulaire"

A new method of characterizing breast lesions found during an MRI exam could result in fewer biopsies of benign tumors with the benefits of reduced pain and expense for patients and providers, according to a paper that will be presented Nov. 30 at the annual meeting of the Radiological Society of North America (RSNA).

Wendy DeMartini, M.D., and colleagues in the breast imaging department at the Seattle Cancer Care Alliance developed a preliminary statistical model that breast radiologists could use eventually when deciding whether a lesion found on breast MRI is likely to be malignant or benign. Their retrospective review of almost 2,600 breast MRI exams performed during a four-year period at the SCCA found three crucial patient and lesion characteristics that, when used in combination, could predict the likelihood of malignancy, including identifying some lesions with probabilities of cancer close to zero.

Such a model, if confirmed by more research, could be beneficial because MRI exams are so sensitive that they reveal cancerous and non-cancerous lesions that often look alike and behave similarly when contrast dye is injected into the patient. Biopsy is often necessary to determine whether a lesion is cancerous. Statistical models may improve the ability to distinguish between such lesions and avoid unnecessary biopsies.

The researchers looked at several patient and lesion characteristics that radiologists take into account now when deciding whether a biopsy is required for diagnosis. They found three categories of characteristics that, when taken together, were the best at predicting malignancy. These were the reason that the women was having a breast MRI, the size of the lesion, and the lesion enhancement pattern from the the MRI contrast dye.

Lesions found in women undergoing MRI to look for additional malignancy after new breast cancer diagnosis, lesions that were found to be larger than one centimeter, and those whose enhancement quickly faded (called washout) were the most likely to be malignant, according to DeMartini, who is an assistant professor in the University of Washington School of Medicine.

In contrast, breast lesions found in women being screened because they are considered to be at high risk for developing cancer, that were found to be small lesions and increased their enhancement over time were very likely to benign.

"If the lesions had those three characteristics, the likelihood of malignancy was 1 percent," said DeMartini. "This is so close to zeros that rather than doing a biopsy we could instead follow the patient by doing another MRI in a few months, or we may not need to do any additional testing."

DeMartini cautioned that more research is needed before this statistical model can be validated for use as standard practice.

"This is a preliminary model. Future work will look at additional patient and lesion features and in the longer term we need to examine lesions from multiple practice sites," she said. "Our goal is to identify a group of lesions that we currently recommend for additional tests where the likelihood of cancer is so low that we can safely avoid additional testing."

A new "barcode chip" developed by researchers at the California Institute of Technology (Caltech) promises to revolutionize diagnostic medical testing. In less than 10 minutes, and using just a pinprick's worth of blood, the chip can measure the concentrations of dozens of proteins, including those that herald the presence of diseases like cancer and heart disease.

An IBBC, described in a paper in the advance online edition of Nature Biotechnology, is about the size of a microscope slide and is made out of a glass substrate covered with silicone rubber. The chip's surface is molded to contain a microfluidics circuit--a system of microscopic channels through which the pinprick of blood is introduced, protein-rich blood plasma is separated from whole blood, and a panel of protein biomarkers is measured from the plasma.

The chip offers a significant improvement over the cost and speed of standard laboratory tests to analyze proteins in the blood. In traditional tests, one or more vials of blood are removed from a patient's arm and taken to a laboratory, where the blood is centrifuged to separate whole blood cells from the plasma. The plasma is then assayed for specific proteins. "The process is labor intensive, and even if the person doing the testing hurries, the tests will still take a few hours to complete," says Heath. A kit to test for a single diagnostic protein costs about $50.

"We wanted to dramatically lower the cost of such measurements, by orders of magnitude," he says. "We measure many proteins for the cost of one. Furthermore, if you reduce the time it takes for the test, the test is cheaper, since time is money. With our barcode chip, we can go from pinprick to results in less than 10 minutes."

A single chip can simultaneously test the blood from eight patients, and each test measures many proteins at once. The researchers reported on devices that could measure a dozen proteins from a fingerprick of blood, and their current assays are designed for significantly more proteins. "We are aiming to measure 100 proteins per fingerprick within a year or so. It's a pretty enabling technology," Heath says.

To perform the assay, a drop of blood is added to the IBBC's inlet, and then a slight pressure is applied, which forces the blood through a channel. As the blood flows, plasma is skimmed into narrow channels that branch off from the main channel. This part of the chip is designed as if it were a network of resistors, which optimizes plasma separation.

The plasma then flows across the "barcodes." The barcodes consist of a series of lines, each 20 micrometers across and patterned with a different antibody that allows it to capture a specific protein from the plasma passing over. When the barcode is "developed," the individual bars emit a red fluorescent glow, whose brightness depends upon the amount of protein captured.

In the Nature Biotechnology paper, the researchers used the chip to measure variations in the concentration of human chorionic gonadotropin (hCG), the hormone produced during pregnancy. "The concentration of this protein increases by about 100,000-fold as a woman goes through the pregnancy cycle, and we wanted to show that we could capture that whole concentration range through a single test," Heath says.

The scientists also used the barcode chip to analyze the blood of breast and prostate cancer patients for a number of proteins that serve as biomarkers for disease. The types and concentrations of the proteins vary from disease to disease and between different individuals. A woman with breast cancer, for example, will produce a different suite of biomarkers than will a man with prostate cancer, while a woman with an aggressive form of cancer may produce proteins that are different from a woman with a less-deadly cancer.

Those proteins can also change as a patient receives therapy. Thus, determining these biomarker profiles can allow doctors to create individualized treatment plans for their patients and improve outcomes. The ease and the speed with which results can be obtained using the IBBC also will potentially allow doctors to assess their patients' responses to drugs and to monitor how those responses evolve with time, much as a diabetic patient might use a blood glucose test to monitor insulin delivery.

The barcode chip is now being tested in human clinical trials on patients with glioblastoma, a common and aggressive form of brain tumor. The researchers are also using the chips in studies of healthy individuals, to determine how diet and exercise change the composition of the proteins in the blood.

Currently, the barcoded information is "read" with a common laboratory scanner that is also used for gene and protein expression studies. "But it should be very easy to design something like a supermarket UPC scanner to read the information," making the process even more user-friendly, says Fan, the first author on the paper.

"As personalized medicine develops, measurements of large panels of protein biomarkers are going to become important, but they are also going to have to be done very cheaply," Heath says. "It is our hope that these IBBCs will enable such inexpensive and multiplexed measurements."

The work was funded by the National Cancer Institute and by the Institute for Collaborative Biotechnologies through a grant from the United States Army Research Office.

Rises in the ambient temperature modify the behavior of dog ticks and increase their affinity for humans. There is thus a risk that episodes of global warming may be associated with epidemics of tick-borne diseases.

This work, carried out by the Unité de recherche sur les maladies infectieuses et tropicales émergentes (CNRS/ IRD/ Université de la Méditerranée) is headed by Didier Raoult.

Dog ticks are mainly prevalent during the spring. They do not usually bite humans. The few cases of such bites have been observed during the summer when the ticks were exposed to very high temperatures. These parasites are vectors of bacteria (rickettsioses) which are the agents for serious infectious diseases in humans such as Rickettsia conorii, or Mediterranean spotted fever.

The team led by Raoult in the Unité de recherche sur les maladies infectieuses et tropicales émergentes, has recently demonstrated the role of climate warming in the increase in tick-borne diseases. Their study showed that rickettsioses were more common and more severe during the very hot summers of 2003 and 2005, and that a minor epidemic developed in the spring of 2007, which was the warmest in 50 years.

The researchers thus developed an experimental model. One group of ticks was incubated for 24 hours at 40°C and another group at 25°C. Both groups were then put in contact with humans. The results were unquestionable: the affinity of dog ticks for humans was much greater after the parasites had been kept at a temperature of 40°. Thus the affinity of this group of ticks for humans was disturbed by the rise in temperature. Under the effect of warmth, it was as if the ticks had gone mad and started to bite humans.

These findings may explain the seasonal incidence of bites in high summer, and the increasing number of cases that occur during excessively hot periods. Episodes of global warming may therefore be associated with epidemics of diseases vectored by ticks whose behavior has been affected by the ambient temperature.

Robots that develop and display emotions as they interact with humans, and become attached to them, will be exhibited at the ICT’08 event organized by the European Commission in Lyon next week.

Dr Lola Cañamero, of the University of Hertfordshire’s School of Computer Science, is co-ordinating a European project which is developing robots that are capable of growing emotionally, responding to humans and of expressing their own emotional states as they interact with people.

Prototypes of some of these robots showing mid-term project results will be exhibited at ICT 2008, Europe's leading information and communication technologies event, which will take place in Lyon from 25-27 November 2008.

The project, FEELIX GROWING (FEEL, Interact, eXpress: a Global approach to development With Interdisciplinary Grounding; funded by the Sixth Framework Programme of the European Commission, aims to develop autonomous robots which will be capable of interacting with humans in everyday environments, and will learn and develop emotionally, socially and cognitively in accordance with the needs and personalities of the individuals with which they associate.

“The aim is to develop robots that grow up and adapt to humans in everyday environments,” said Dr Cañamero. “If robots are to be truly integrated in humans’ everyday lives as companions or carers, they cannot be just taken off the shelf and put into a real-life setting, they need to live and grow interacting with humans, to adapt to their environment.”

At ICT 2008, Dr Cañamero and the project’s international team of researchers will explain and demonstrate this approach using live interactive demonstrations and videos. Live demonstrations will include a baby pet robot learning to control its stress as it explores a new environment helped by a human caregiver, several robotic heads that show facial emotional responses to humans’ faces and voices, humanoid robots that learn to execute simple tasks by observing and imitating humans, and an interactive floor that responds to human touch and movement with different light and sound patterns. Videos and demonstrations will also show how non-human primates (chimpanzees) react to some of these robots.

The other players in the FEELIX GROWING project are: Centre National de la Recherche Scientifique, France; Université de Cergy Pontoise, France; Ecole Polytechnique Fédérale de Lausanne, Switzerland; University of Portsmouth, UK; Institute of Communication and Computer Systems, Greece; Entertainment Robotics, Denmark; and SAS Aldebaran Robotics, France.
Adapted from materials provided by University of Hertfordshire, via AlphaGalileo.

The 2008 Atlantic Hurricane Season officially comes to a close on November 30, marking the end of a season that produced a record number of consecutive storms to strike the United States and ranks as one of the more active seasons in the 64 years since comprehensive records began.

A total of 16 named storms formed this season, based on an operational estimate by NOAA's National Hurricane Center. The storms included eight hurricanes, five of which were major hurricanes at Category 3 strength or higher. These numbers fall within the ranges predicted in NOAA’s pre- and mid-season outlooks issued in May and August. The August outlook called for 14 to 18 named storms, seven to 10 hurricanes and three to six major hurricanes. An average season has 11 named storms, six hurricanes and two major hurricanes.

“This year’s hurricane season continues the current active hurricane era and is the tenth season to produce above-normal activity in the past 14 years,” said Gerry Bell, Ph.D., lead seasonal hurricane forecaster at NOAA's Climate Prediction Center.

Overall, the season is tied as the fourth most active in terms of named storms (16) and major hurricanes (five), and is tied as the fifth most active in terms of hurricanes (eight) since 1944, which was the first year aircraft missions flew into tropical storms and hurricanes.

For the first time on record, six consecutive tropical cyclones (Dolly, Edouard, Fay, Gustav, Hanna and Ike) made landfall on the U.S. mainland and a record three major hurricanes (Gustav, Ike and Paloma) struck Cuba. This is also the first Atlantic season to have a major hurricane (Category 3) form in five consecutive months (July: Bertha, August: Gustav, September: Ike, October: Omar, November: Paloma).

Bell attributes this year’s above-normal season to conditions that include:

• An ongoing multi-decadal signal. This combination of ocean and atmospheric conditions has spawned increased hurricane activity since 1995.
• Lingering La Niña effects. Although the La Niña that began in the Fall of 2007 ended in June, its influence of light wind shear lingered.
• Warmer tropical Atlantic Ocean temperatures. On average, the tropical Atlantic was about 1.0 degree Fahrenheit above normal during the peak of the season.

NOAA's National Hurricane Center is conducting comprehensive post-event assessments of each named storm of the season. Some of the early noteworthy findings include:

• Bertha was a tropical cyclone for 17 days (July 3-20), making it the longest-lived July storm on record in the Atlantic Basin.
• Fay is the only storm on record to make landfall four times in the state of Florida, and to prompt tropical storm and hurricane watches and warnings for the state’s entire coastline (at various times during its August lifespan).
• Paloma, reaching Category 4 status with top winds of 145 mph, is the second strongest November hurricane on record behind Lenny in 1999 with top winds of 155 mph).

Much of the storm-specific information is based on operational estimates and some changes could be made during the review process that is underway.

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One of the most important developments in human civilisation was the practice of sustainable agriculture. But we were not the first - ants have been doing it for over 50 million years. Just as farming helped humans become a dominant species, it has also helped leaf-cutter ants become dominant herbivores, and one of the most successful social insects in nature.

According to an article in the November issue of Microbiology Today, leaf-cutter ants have developed a system to try and keep their gardens pest-free; an impressive feat which has evaded even human agriculturalists.

Leaf-cutter ants put their freshly-cut leaves in gardens where they grow a special fungus that they eat. New material is continuously incorporated into the gardens to grow the fungus and old material is removed by the ants and placed in special refuse dumps away from the colony. The ants have also adopted the practice of weeding. When a microbial pest is detected by worker ants, there is an immediate flurry of activity as ants begin to comb through the garden. When they find the pathogenic 'weeds', the ants pull them out and discard them into their refuse dumps.

"Since the ant gardens are maintained in soil chambers, they are routinely exposed to a number of potential pathogens that could infect and overtake a garden. In fact, many of the ant colonies do become overgrown by fungal pathogens, often killing the colony," said Professor Cameron Currie from the University of Wisconsin-Madison, USA. "Scientists have shown that a specialized microfungal pathogen attacks the gardens of the fungus-growing ants. These fungi directly attack and kill the crop fungus, and can overrun the garden in a similar fashion to the way weeds and pests can ruin human gardens."

A curious observation was that some worker ants had a white wax-like substance across their bodies. When they looked at it under a microscope scientists discovered that this covering was not a wax, but a bacterium! These bacteria are part of the group actinobacteria, which produce over 80% of the antibiotics used by humans. The bacteria produce antifungal compounds that stop the microfungal pathogen from attacking the garden. This discovery was the first clearly demonstrated example of an animal, other than humans, that uses bacteria to produce antibiotics to deal with pathogens.

"Research in our laboratory has revealed a number of interesting properties between the bacteria and the pathogenic fungus. The bacteria appear to be specially suited to inhibiting the pathogenic fungi that infect the ants' fungus garden," said Professor Currie.

The interaction between the ants and their fungus crop, and the ants and the bacteria is known as a mutualistic relationship. In general a mutualism is established when both members of the interaction benefit from the relationship. In the ant–fungus mutualism, the ants get food from the fungus. This mutualism is so tight that if the fungus is lost, the entire colony may die. In return, the fungus receives a continuous supply of growing material, protection from the environment, and protection from disease-causing pests.

So what do the bacteria get out of producing pesticides for the ants? "For starters, they get food. Many species of fungus-growing ants have evolved special crypts on their bodies where the bacteria live and grow. Scientists believe that the ants feed the bacteria through glands connected to these crypts," said Dr Garret Suen, a post-doctoral fellow in Professor Currie's lab. "Also, the bacteria get a protected environment in which to grow, away from the intense competition they would face if they lived in other environments such as the soil."

"Interestingly, the tight association between ant, bacteria and pathogen will sometimes result in the pathogen winning. This interplay has been described as a chemical 'arms race' between the bacteria and fungus, with one side beating the other as new compounds are evolved," said Professor Currie. "At the moment, we are beginning to understand the chemical warfare at the genetic level, and it is likely that these types of interactions are more prevalent in nature than previously thought."

So how exactly does an ant go about forming partnerships with a fungus and a bacterium? No one really knows. With new advances in molecular and genetic technologies, such as whole-genome sequencing, Professor Currie and Dr Suen hope to discover how these associations were established, and to understand how these interactions resulted in the remarkable fungus-growing ability of the ants.

Source: Sciencedaily

Increasing the production of naturally occurring proteins that contain selenium in human blood cells slows down multiplication of the AIDS virus, according to biochemists.

"We have found that increasing the expression of proteins that contain selenium negatively affects the replication of HIV," said K. Sandeep Prabhu, Penn State assistant professor of immunology and molecular toxicology. "Our results suggest a reduction in viral replication by at least 10-fold."

Selenium is a micronutrient that the body needs to maintain normal metabolism. Unlike other nutrients, which bind to certain proteins and modulate the protein's activity, selenium gets incorporated into proteins in the form of an amino acid called selenocysteine.

These proteins – selenoproteins – are especially important in reducing the stress caused by an infection, thereby slowing its spread.

Upon infecting a person, the virus quickly degrades selenoproteins so that it can replicate efficiently. It is unclear just how the virus is able to silence these proteins but Prabhu and his colleagues believe that stress inflicted on cells by the rapidly dividing virus, which produces a key protein known as Tat, is the likely culprit.

Tat is one of about 14 odd proteins produced by HIV during the first stage of infection. The job of these proteins is to trigger the expression of all the other genes that the virus needs to sustain itself. In addition, Tat also plays a key role in helping the virus replicate.

One of the proteins that targets Tat is a selenoprotein known as TR1.

"Since HIV targets the selenoproteins, we thought that the logical way to deal with the virus is to increase the expression of such proteins in the body," explained Prabhu, whose team's findings are outlined this week (Nov. 28) in the Journal of Biological Chemistry.

Researchers first isolated blood cells from healthy human volunteers who did not have HIV, and infected those cells with the virus. Next, they added tiny amounts of a selenium compound – sodium selenite – into the cell culture to see the effect on viral replication.

Results from the tests indicate that the addition of selenium inhibits the replication of HIV at least 10-fold, compared to cell cultures in which no selenium is added. When the researchers selectively reduced production of the selenium containing TR1 protein, they observed a 3.5-fold increase in viral replication.

"This confirms that while increasing the expression of TR1 has a negative impact on the replication of HIV, reducing it helps the virus replicate more efficiently," explained Prabhu. He believes that TR1 works by upsetting the chemical structure of Tat, which in turn reduces the virus' ability to replicate.

"Once we fully understand the function of these selenium proteins, it will give us a handle to come up with more effective drugs," said Prabhu, whose work is partly funded by the National Institutes of Health.

Other researchers on the paper include Parisa Kalantari, post-doctoral scholar; Vivek Narayan, graduate student; Kambadur Muralidhar, visiting faculty; Ujjawal H. Gandhi, graduate student; and Hema Vunta, graduate student, all at Penn State; Satish K. Natarajan, research associate, University of Nebraska; and Andrew J. Henderson, associate professor of medicine and microbiology, Boston University.