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Antibiotic use aids MRSA spread in hospital and infection control measures do little to prevent it, says hospital study

Written By Unknown on Kamis, 20 September 2012 | 07.43

ScienceDaily (Sep. 20, 2012) — The use of a commonly prescribed antibiotic is a major contributor to the spread of infection in hospitals by the 'superbug' MRSA, according to new research. The study also found that increasing measures to prevent infection -- such as improved hygiene and hand washing -- appeared to have only a small effect on reducing MRSA infection rates during the period studied.

MRSA -- methicillin-resistant Staphylococcus aureus -- is a bacteria that causes hospital-acquired infection and is resistant to all of the penicillin-type antibiotics frequently used in hospitals to prevent and treat infection. It can cause serious infections of the skin, blood, lungs and bones.

The researchers -- led by St George's, University of London -- tracked MRSA infection over 10 years from 1999 to 2009 at St George's Hospital, looking at how it has adapted to survive in a hospital environment and at factors that affected its prevalence. They found that a significant drop in MRSA rates coincided with a reduction in hospital prescriptions of ciprofloxacin, the most commonly prescribed antibiotic of the fluoroquinolone family.

Over a short period of the study, ciprofloxacin prescriptions fell from 70-100 daily doses for every thousand occupied beds to about 30 doses. In the same period, the number of patients identified by the laboratory to be infected with MRSA fell by half, from an average of about 120 a month to about 60. Following this, over the last two years of the study both the drug prescription level and MRSA rates remained at these reduced levels. Symptoms of MRSA infection can range from very mild to severe, but it is not known how many of the cases examined in the study were serious.

The study -- published in the Journal of Antimicrobial Chemotherapy -- looked at whether other factors such as improved infection control measures may have contributed to this decrease in infection. However, during a four-year period when more stringent infection control policies were introduced -- including improved cleaning and hand washing, and screening patients for MRSA on arrival at hospital -- the only major reduction in MRSA infection rates coincided with the reduction in ciprofloxacin prescriptions.

Lead author Dr Jodi Lindsay, a reader in microbial pathogenesis at St George's, University of London, said: "Surprisingly, it wasn't hygiene and hand washing that were the main factors responsible for the decrease in MRSA in the hospital. Rather, it seemed to be a change in the use of a particular group of antibiotics. Hand washing and infection control are important, but they were not enough to cause the decrease in MRSA we saw."

Dr Lindsay said the study suggested that MRSA relies on ciprofloxacin -- and fluoroquinolones in general -- to thrive in hospitals, as well as penicillin-type drugs, which was already assumed. The fluoroquinolone group of antibiotics have a similar enough mechanism of action to assume that the effect would be the same for them all.

She added that the findings suggest the most effective way to control MRSA and other hospital-based superbugs is to continue finding alternative ways to use antibiotics, rather than simply focusing on infection control techniques.

As well as identifying factors that influenced prevalence, the researchers identified the strain of MRSA that has become dominant. This strain -- CC22 -- has thrived by developing and maintaining multi-drug resistance, and becoming more fit to survive on hospital surfaces than other strains.

Dr Tim Planche, consultant microbiologist at St George's Healthcare NHS Trust and one of the co-authors of the study, said: "The Trust currently has infection rates among the lowest in London, having successfully driven acquisitions down over the past five or six years using a combination of both tough hygiene regimes and careful selective use of antibiotics. These findings, however, provide valuable insight and certainly warrant further investigation, which could lead to the development of even more effective infection control strategies in future."

Dr Lindsay said that studying the dynamic of how MRSA bacteria strains continue to evolve in hospitals in response to changing practice and interventions, such as infection control and antibiotic prescribing, will be essential to determine which interventions work, which are cost effective, and which are likely to have the best long-term outcomes.

She added: "But it seems that we now have an excellent opportunity to control superbugs in hospitals by re-examining how we prescribe antibiotics and ensuring we're using them in the most effective way possible."

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The above story is reprinted from materials provided by University of St George's London.

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Journal Reference:

  1. G. M. Knight, E. L. Budd, L. Whitney, A. Thornley, H. Al-Ghusein, T. Planche, J. A. Lindsay. Shift in dominant hospital-associated methicillin-resistant Staphylococcus aureus (HA-MRSA) clones over time. Journal of Antimicrobial Chemotherapy, 2012; 67 (10): 2514 DOI: 10.1093/jac/dks245

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Sudden cardiac death is associated with a thin placenta at birth, researchers find

ScienceDaily (Sep. 19, 2012) — Researchers studying the origins of sudden cardiac death have found that in both men and women a thin placenta at birth was associated with sudden cardiac death. A thin placenta may result in a reduced flow of nutrients from the mother to the fetus. The authors suggest that sudden cardiac death may be initiated by impaired development of the autonomic nervous system in the womb, as a result of fetal malnutrition.

The new study, published today in the International Journal of Epidemiology, also found that sudden death was associated independently with poor educational attainment. However, sudden cardiac death was not associated with maternal body size, fetal size at birth, or the length of gestation.

Professor David Barker and colleagues examined sudden death within the Helsinki Birth Cohort, which consists of 6075 men and 6370 women who were born in the city during 1934-1944 and attended child welfare clinics. Detailed information was recorded on the birth records of the group including the placental weight and the length and breadth of the placental surface as well as the child's weight, head circumference, and length.

Professor Barker, of the University of Southampton, comments that 'There is currently a growing body of research that shows that coronary heart disease is associated with alterations in prenatal growth and this has led to the hypothesis that coronary heart disease originates in the womb as a consequence of fetal malnutrition. In research recently carried out by myself and colleagues, we found that coronary heart disease among men was associated with altered shape and size of the placenta.'

'Our new research published today continues the investigation of the relationship between cardiac death and development within the womb. Our new findings suggest that sudden death may be initiated by the impaired development of the autonomic nervous system in the womb, due to placental thinness. A thin placenta may result in fetal malnutrition, due to a shallow invasion of the spiral arteries in the placenta which provide nutrients and blood to the baby. There is evidence that people who experience fetal malnutrition and who are small at birth have an increased sympopathoadrenal response to acute stress, which is known to be linked to death from cardiac arrest.'

Among women, sudden death was associated with a large placental area in comparison to the baby's weight. Placenta expansion in sheep is well documented and the findings in this study suggest that the placenta attempted to compensate for a thin surface by expanding the area of the surface. Professor Barker notes that 'there is evidence that compensatory placental expansion occurs in human and that this expansion may be beneficial in some circumstances. However, if the compensation is inadequate and the fetus continues to be under nourished then the need to share its nutrients with an enlarged placenta may become a metabolic burden and the quality of fetal development may be harmed. We believe that the female foetuses in our study compensated for placental thinness by expanding the placental surface.

Professor Barker and his team also found that sudden cardiac death was strongly associated with low socio-economic status and with low education attainment. He suggests that 'poor educational results may be due to a poor cognitive ability or other issues such as the inability to concentrate or maintain attention. We suggest that the association we have found between sudden death and poor educational attainment results from impaired prenatal development of the autonomic nervous system. These findings build upon a body of research that has consistently reported associations between sudden cardiac death and low socio-economic status.'

In the study, a total of one hundred and eighty-seven men (2.7%) and forty seven women (0.7%) suffered from sudden unexplained cardiac death outside of the hospital. The rate of sudden cardiac death among men and women increased with placental thinness, with a hazard ratio of 1.47. The authors restricted their analysis to deaths that occurred outside of hospital and were certified as coronary heart disease, with men and women who had never been admitted to hospital with coronary heart disease.

Professor Barker and his team do acknowledge that there are some limitations to the study. The placental measurements were made during routing obstetric practice 70 years ago and the quality of these measurements was not routinely checked and neither were other clinical measurements, such as blood pressure. The mean placental weight in this study was also more than the median recorded in a recent series of deliveries in Europe.

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The above story is reprinted from materials provided by Oxford University Press, via EurekAlert!, a service of AAAS.

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Journal Reference:

  1. David JP Barker, Gail Larsen, Clive Osmond, Kent L Thornburg, Eero Kajantie, and Johan G Eriksson. The placental origins of sudden cardiac death. International Journal of Epidemiology, 2012; DOI: 10.1093/ije/dys116

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Obese children have less sensitive taste-buds than those of normal weight

ScienceDaily (Sep. 19, 2012) — Obese kids have less sensitive taste-buds than kids of normal weight, indicates research published online in the Archives of Disease in Childhood.

This blunted ability to distinguish all five tastes of bitter, sweet, salty, sour, and umami (savoury) may prompt them to eat larger quantities of food in a bid to register the same taste sensation, suggest the authors.

They base their findings on 94 normal weight and 99 obese children aged between 6 and 18, who were in good health and not taking any medications known to affect taste and smell.

The taste sensitivity of every child was tested using 22 "taste strips" placed on the tongue, to include each of the five taste sensations, at four different levels of intensity, plus two blank strips.

Each child was asked to refrain from eating or drinking anything other than water and not to chew gum for at least an hour before they took the two tests, which involved identifying the different tastes and their intensity.

The sum of all five taste sensations at the four different intensities allowed for a maximum score of 20, with scores ranging from two to 19.

Girls and older children were better at picking out the right tastes.

Overall, the children were best able to differentiate between sweet and salty, but found it hardest to distinguish between salty and sour, and between salty and umami.

And obese children found it significantly more difficult to identify the different taste sensations, scoring an average of 12.6 compared with an average of just over 14 clocked up by children of normal weight.

Obese children were significantly less likely to identify the individual taste sensations correctly, particularly salty, umami, and bitter.

And while both obese and normal weight children correctly identified all the differing levels of sweetness, obese kids rated three out of the four intensity levels lower than kids of normal weight.

Similarly, children of normal weight were better able to distinguish the different taste sensations, the older they were, but this trend was not seen among the obese children.

Exactly why people have differing taste perceptions is unclear, but genes, hormones, acculturation and exposure to different tastes early in life are all thought to play a part, say the authors.

But previous research indicates that heightened sensitivity to different taste sensations may help to reduce the amount of food eaten as less is required to get the same "taste hit."

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The above story is reprinted from materials provided by BMJ-British Medical Journal.

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Journal Reference:

  1. Johanna Overberg, Thomas Hummel, Heiko Krude, Susanna Wiegand. Differences in taste sensitivity between obese and non-obese children and adolescents. Archives of Disease in Childhood, 2012; DOI: 10.1136/archdischild-2011-301189

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/DN4CU5hoO7Q/120919190924.htm
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Tissue around tumor holds key to fighting triple negative breast cancer

Written By Unknown on Rabu, 19 September 2012 | 17.57

ScienceDaily (Sep. 19, 2012) — A natural substance found in the surrounding tissue of a tumor may be a promising weapon to stop triple negative breast cancer from metastasizing.

A preclinical study published in PLOS ONE September 19 by Thomas Jefferson University researchers found that decorin, a well-studied protein known to help halt tumor growth, induces a series of tumor suppressor genes in the surrounding tissue in triple negative breast cancer tumors to help stop metastasis.

"These findings provide a new paradigm for decorin, with great implications for curbing tumor growth by inducing new tumor suppressor genes within the tumor microenvironment, and for the discovery of novel gene signatures that could eventually help clinical assessment and prognosis," said senior author Renato V. Iozzo, M.D., Professor of Pathology, Anatomy and Cell Biology, at Thomas Jefferson University.

Triple negative breast cancer is the most deadly of breast cancers, with fast-growing tumors, that disproportionately affect younger and African-American women. Today, no such marker is applied in care of triple negative breast cancer, and as a result, patients are all treated the same.

"Originally, we thought that decorin was affecting the tumor, but, surprisingly, decorin affects the so-called tumor microenvironment, where malignant cells grow and invade, igniting genes to stop such growth," said Dr. Iozzo, who is also a member of Jefferson's Kimmel Cancer Center. "Absence of decorin in the microenvironment could explain metastasis in some patients, where higher levels of the protein may keep cancer from spreading."

In the study, 357 genes were found to be induced by the increased presence of decorin, but more interestingly, the researchers discovered that three of these genes, which were previously unlinked to triple negative breast cancer, were tumor suppressor genes affecting the tumor microenvironment, including Bmp2K, Zc3hav1, and PEG3.

Decorin is a naturally occurring substance in the connective tissue where, among other roles, it helps regulate cell growth by interacting with growth factors and collagen. A decade ago, Dr. Iozzo and his team discovered that decorin, a cell protein, and specifically, a proteoglycan, is increased in the matrix surrounding tumor cells. They also discovered that decorin causes production of a protein, p21, which also can arrest cell growth. However, decorin's role in breast cancer and the mechanism behind its anti-tumor properties remained elusive.

For this study, researchers aimed to investigate the impact of decorin in triple negative breast cancer tumors using human cell lines in mice, as well analyze gene expression activity in the tumor microenvironment.

Tumors treated with decorin were found to have a decreased volume of up to 50 percent after 23 days. Using a sophisticated microarray technique, the researchers then analyzed the mouse tumor microenvironment, finding increased expression of 357 genes, three of which are the tumor suppressor genes of interest.

These results demonstrate a novel role for decorin in reduction or prevention of tumor metastases that could eventually lead to improved therapeutics for metastatic breast cancer.

"Here, we have a molecule that can turn a tumor microenvironment from a bad neighborhood to a clean neighborhood by inducing genes in that neighborhood to stop growth and prevent the tumor from metastasizing," said Dr. Iozzo.

This work was in part supported by the National Institutes of Health grants RO1CA39481, RO1CA47282 and RO1CA120975.

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The above story is reprinted from materials provided by Thomas Jefferson University, via Newswise.

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Journal Reference:

  1. Simone Buraschi, Thomas Neill, Rick T. Owens, Leonardo A. Iniguez, George Purkins, Rajanikanth Vadigepalli, Barry Evans, Liliana Schaefer, Stephen C. Peiper, Zi-Xuan Wang, Renato V. Iozzo. Decorin Protein Core Affects the Global Gene Expression Profile of the Tumor Microenvironment in a Triple-Negative Orthotopic Breast Carcinoma Xenograft Model. PLoS ONE, 2012; 7 (9): e45559 DOI: 10.1371/journal.pone.0045559

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Emotional neglect in children linked to increased stroke risk later in life

ScienceDaily (Sep. 19, 2012) — The results from a new study by neurological researchers from the Rush Alzheimer's Disease Center at Rush University Medical Center suggest that people who were emotionally neglected as children may have a higher risk of stroke in later adulthood.

"Studies have shown that children who were neglected emotionally in childhood are at an increased risk of a slew of psychiatric disorders. However, our study is one of few that looked at an association between emotional neglect and stroke," said study author Robert S. Wilson, PhD, a neuropsychologist at Rush.

The findings are published in the September 19, online issue of Neurology, the medical journal of the American Academy of Neurology.

For the study, 1,040 participants in the Memory and Aging Project who did not have dementia and were 55 years of age or older took a survey measuring physical and emotional abuse before the age of 18. The retrospective survey questions focused on whether the participant felt loved by their parents or caregiver when they were younger, were made to feel afraid or intimidated and whether they were punished with a belt or other object. Questions about parental divorce and the family's financial needs were also included.

Over a period of three and a half years, 257 people in the study died, of which 192 had a brain autopsy to look for signs of stroke. Forty of the participants had evidence of a stroke based on their medical history or an examination. A total of 89 people had signs of a stroke based on the autopsy results.

The study found that the risk of stroke was nearly three times higher in those people who reported a moderately high level of childhood emotional neglect than those who reported a moderately low level. The results stayed the same after considering factors such as diabetes, physical activity, smoking, anxiety and heart problems.

"Interestingly, the autopsy showed emotional neglect was associated with the presence of cerebral infarctions," said Dr. David A. Bennett, director of the Rush Alzheimer's Disease Center and co-author of the study. "The results add to a growing body of evidence suggesting that early life factors such as traumatic childhood experiences influence the development of physical illness and common chronic conditions of old age."

Wilson noted that a limitation of the study is that neglect was reported from memory many years after occurrence, so participants may not have remembered events accurately.

The study was supported by the National Institutes of Health and the Illinois Department of Public Health.

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The above story is reprinted from materials provided by Rush University Medical Center, via Newswise.

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Journal Reference:

  1. Robert S. Wilson, Patricia A. Boyle, Steven R. Levine, Lei Yu, Sophia E. Anagnos, Aron S. Buchman, Julie A. Schneider, and David A. Bennett. Emotional neglect in childhood and cerebral infarction in older age. Neurology, September 19, 2012 DOI: 10.1212/WNL.0b013e31826e25bd

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Test can help make diagnosis of Creutzfeldt-Jakob disease

ScienceDaily (Sep. 19, 2012) — A new guideline released by the American Academy of Neurology may help doctors in making the diagnosis of Creutzfeldt-Jakob disease. The guideline is published in the September 19, 2012, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Creutzfeldt-Jakob disease is a rare, always fatal brain disorder that involves quickly progressing dementia. New cases appear in about one person per million each year worldwide and confirming the diagnosis is challenging. People with the disease can have a wide range of symptoms. Many other conditions can cause similar symptoms, and with some of these conditions the dementia can be treated.

The guideline focused only on the diagnosis of sporadic Creutzfeldt-Jakob disease.

While several tests are available to help diagnose sporadic Creutzfeldt-Jakob disease, a brain biopsy is the most accurate test that can be performed on a person living with the disease. Brain biopsy is potentially dangerous.

The guideline examined the diagnostic accuracy of testing for a protein called 14-3-3 in the spinal fluid. The guideline authors reviewed all of the available evidence on the test, which included samples of 1,849 people with suspected sporadic Creutzfeldt-Jakob disease from nine studies.

They found that in cases where doctors strongly suspect Creutzfeldt-Jakob to be the cause of the dementia, the test can be helpful in reducing the uncertainty of the diagnosis. However, the test is not accurate enough to diagnose the disease with certainty or to rule it out completely. The test has a sensitivity of about 92 percent and a specificity of about 80 percent. Sensitivity is the percentage of patients with the disease who have a positive test result, and specificity is the percentage of patients who do not have the disease and who are correctly identified as having a negative test result.

The guideline determined that the 14-3-3 protein test can be useful when the probability of the person having Creutzfeldt-Jakob disease is between 20 percent and 90 percent.

"This means that if the physician considers the likelihood of Creutzfeldt-Jakob disease to be extremely low or extremely high, then testing for 14-3-3 protein would not be useful regardless of the result," said guideline author Taim Muayqil, MBBS, FRCPC, of King Saud University in Riyadh, Saudi Arabia, and a member of the American Academy of Neurology.

Muayqil noted that only doctors experienced in diagnosing dementia should determine whether the 14-3-3 protein test is needed and how results should be interpreted.

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The above story is reprinted from materials provided by American Academy of Neurology (AAN), via Newswise.

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Journal Reference:

  1. Taim Muayqil, Gary Gronseth, and Richard Camicioli. Evidence-based guideline: Diagnostic accuracy of CSF 14-3-3 protein in sporadic Creutzfeldt-Jakob disease: Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology, 2012 DOI: 10.1212/WNL.0b013e31826d5fc3

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Blind people develop accurate mental map by playing 'video' game

ScienceDaily (Sep. 19, 2012) — Researchers have developed a new "video" game for blind people that can help them learn about a new space using only audio cues, as reported Sept. 19 in the open access journal PLOS ONE.

The system, developed by a team led by Lotfi Merabet of Harvard Medical School and Jaime Sánchez of the University of Chile, is called the Audiobased Environment Simulator and uses only audio-based cues to allow blind users to learn about the layout of a previously unfamiliar building.

After playing the game, participants were better able to navigate a real-world version of the space explored in the virtual reality environment, confirming that the spatial information learned in the game was accurate and transferrable.

"Learning through such interactive games represents an innovative and motivating way to improve crucial skills that allow blind individuals to remain functionally independent," says Merabet.

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Journal Reference:

  1. Lotfi B. Merabet, Erin C. Connors, Mark A. Halko, Jaime Sánchez. Teaching the Blind to Find Their Way by Playing Video Games. PLoS ONE, 2012; 7 (9): e44958 DOI: 10.1371/journal.pone.0044958

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/uJnoApR41PY/120919190606.htm
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People change moral position without even realizing it

ScienceDaily (Sep. 19, 2012) — Shortly after expressing a moral view about a difficult topic, people may easily endorse the opposite view and remain blind to the psychological mismatch, according to research published Sept. 19 in the open access journal PLOS ONE.

In the study, led by Lars Hall of Lund University, Sweden, participants were presented with a survey about moral issues, including foundational principles and current hot topics with moral implications. To complete the survey they had to flip over the first page of questions, which was displayed on a clipboard, and this is where the researchers implemented a design usually used in performance magic: the back of the clipboard had a patch of glue that caught the top layer of the questions, so when the page was flipped back over, an opposite version of the original questions was revealed but the answers remained unchanged. In other words, the participants' responses were opposite to their originally declared positions (For a video illustration of the experiment, see http://www.lucs.lu.se/cbq/).

The researchers then discussed the participants' answers with them, and found that many participants supported their reported answers, even though the responses were opposite to what the individual had originally intended to express. The authors write that "participants often constructed coherent and unequivocal arguments supporting the opposite of their original position," suggesting "a dramatic potential for flexibility in our moral attitudes."

Commenting on their results, Lars Hall says, "It could have significant impact on research that uses self-reported questionnaires. Either we would have to conclude that many participants hold no real attitudes about the topics we investigate, or that standard survey scales fail to capture the complexity of the attitudes people actually hold."

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Journal Reference:

  1. Lars Hall, Petter Johansson, Thomas Strandberg. Lifting the Veil of Morality: Choice Blindness and Attitude Reversals on a Self-Transforming Survey. PLoS ONE, 2012; 7 (9): e45457 DOI: 10.1371/journal.pone.0045457

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Misinformation: Why it sticks and how to fix it

ScienceDaily (Sep. 19, 2012) — Childhood vaccines do not cause autism. Barack Obama was born in the United States. Global warming is confirmed by science. And yet, many people believe claims to the contrary.

Why does that kind of misinformation stick? A new report published in Psychological Science in the Public Interest, a journal of the Association for Psychological Science, explores this phenomenon. Psychological scientist Stephan Lewandowsky of the University of Western Australia and colleagues highlight the cognitive factors that make certain pieces of misinformation so "sticky" and identify some techniques that may be effective in debunking or counteracting erroneous beliefs.

The main reason that misinformation is sticky, according to the researchers, is that rejecting information actually requires cognitive effort. Weighing the plausibility and the source of a message is cognitively more difficult than simply accepting that the message is true -- it requires additional motivational and cognitive resources. If the topic isn't very important to you or you have other things on your mind, misinformation is more likely to take hold.

And when we do take the time to thoughtfully evaluate incoming information, there are only a few features that we are likely to pay attention to: Does the information fit with other things I believe in? Does it make a coherent story with what I already know? Does it come from a credible source? Do others believe it?

Misinformation is especially sticky when it conforms to our preexisting political, religious, or social point of view. Because of this, ideology and personal worldviews can be especially difficult obstacles to overcome.

Even worse, efforts to retract misinformation often backfire, paradoxically amplifying the effect of the erroneous belief.

"This persistence of misinformation has fairly alarming implications in a democracy because people may base decisions on information that, at some level, they know to be false," says Lewandowsky.

"At an individual level, misinformation about health issues -- for example, unwarranted fears regarding vaccinations or unwarranted trust in alternative medicine -- can do a lot of damage. At a societal level, persistent misinformation about political issues (e.g., Obama's health care reform) can create considerable harm. On a global scale, misinformation about climate change is currently delaying mitigative action."

Though misinformation may be difficult to correct, all is not lost. According to Lewandowsky, "psychological science has the potential to counteract all those harms by educating people and communicators about the power of misinformation and how to meet it."

In their report, Lewandowsky and colleagues offer some strategies for setting the record straight.

  • Provide people with a narrative that replaces the gap left by false information
  • Focus on the facts you want to highlight, rather than the myths
  • Make sure that the information you want people to take away is simple and brief
  • Consider your audience and the beliefs they are likely to hold
  • Strengthen your message through repetition

Research has shown that attempts at "debiasing" can be effective in the real world when based on these evidence-based strategies.

The report, "Misinformation and its Correction: Continued Influence and Successful Debiasing," is published in the September issue of Psychological Science in the Public Interest and is written by Stephan Lewandowsky and Ullrich Ecker of the University of Western Australia, Colleen Seifert and Norbert Schwarz of the University of Michigan, and John Cook of the University of Queensland and the University of Western Australia.

The report also features a commentary written by Edward Maibach of George Mason University.

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Journal Reference:

  1. S. Lewandowsky, U. K. H. Ecker, C. M. Seifert, N. Schwarz, J. Cook. Misinformation and Its Correction: Continued Influence and Successful Debiasing. Psychological Science in the Public Interest, 2012; 13 (3): 106 DOI: 10.1177/1529100612451018

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Promise of cell therapy for bowel disease

ScienceDaily (Sep. 19, 2012) — New research shows that a special population of stem cells found in cord blood has the innate ability to migrate to the intestine and contribute to the cell population there, suggesting the cells' potential to treat inflammatory bowel disease (IBD).

"These cells are involved in the formation of blood vessels and may prove to be a tool for improving the vessel abnormalities found in IBD," said lead author Graca Almeida-Porada, M.D., Ph.D., a professor at Wake Forest Baptist Medical Center's Institute for Regenerative Medicine. The research is published in the current print issue of the journal Hepatology.

Up to 1 million Americans have IBD, which is characterized by frequent diarrhea and abdominal pain. IBD actually refers to two conditions -- ulcerative colitis and Crohn's disease -- in which the intestines become red and swollen and develop ulcers. With IBD, blood vessels in the intestine leak and contribute to inflammation.

While there is currently no cure for IBD, there are drug therapies aimed at reducing inflammation and preventing the immune response. However, these therapies aren't always effective. The long-term aim of the research is to develop an injectable cell therapy to induce tissue recovery.

The work, performed while Almeida-Porada was at the University of Nevada, also involved colleagues from Indiana University School of Medicine. The researchers studied a special population of cells, known as endothelial colony-forming cells, found in cord blood, bone marrow and circulating blood. The finding in 1997 that the cells can contribute to blood vessel formation in adults, not just embryos, initiated the notion of using them for therapy. Studies in humans have validated the ability of these cells to improve reduced blood flow to the limbs and to treat heart diseases.

However, there have been few studies to explore the inherent biologic ability of these cells to home to different organs and contribute to tissue-specific cell populations. Evaluating their potential to migrate to the intestine was an obvious choice, said Almeida-Porada, because dysfunctional blood vessels are a hallmark of IBD. Not only are circulating levels of vessel-forming cells reduced in patients with IBD, but a key factor in IBD progression is the development of abnormal or immature blood vessels, which leads to chronic inflammation.

The cells were injected into fetal sheep at 59 to 65 days gestation. About 11 weeks later, intestinal tissue was analyzed to detect the presence of the human cells. The researchers found that the human cells had migrated to the intestine and contributed significantly to the cell population there.

"This study shows that the cells can migrate to and survive in a healthy intestine and have the potential to support vascular health," said Almeida-Porada. "Our next step will be to determine whether the cells can survive in the 'war' environment of an inflamed intestine."

The researchers also evaluated the ability of the cells to home to the liver. Smaller numbers of cells reached the liver than the intestine, suggesting that new strategies would be needed to enhance the therapeutic potential for this organ.

The research was supported by the National Heart, Lung, and Blood Institute grants HL097623 and HL073737.

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The above story is reprinted from materials provided by Wake Forest Baptist Medical Center, via Newswise.

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Journal Reference:

  1. Joshua A. Wood, Evan Colletti, Laura E. Mead, David Ingram, Christopher D. Porada, Esmail D. Zanjani, Mervin C. Yoder, Graça Almeida-Porada. Distinct contribution of human cord blood-derived endothelial colony forming cells to liver and gut in a fetal sheep model. Hepatology, 2012; 56 (3): 1086 DOI: 10.1002/hep.25753

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Possible key to slow progression toward AIDS found

ScienceDaily (Sep. 19, 2012) — One of the big mysteries of AIDS is why some HIV-positive people take more than a decade to progress to full-blown AIDS, if they progress at all.

Although the average time between HIV infection and AIDS in the absence of antiretroviral treatment is about 10 years, some individuals succumb within two years, while so-called slow progressors can stay healthy for 20 years or longer.

Researchers already know that many slow progressors carry a gene called HLA-B*57 (B57), an immune gene variant that is found in less than 5 percent of the general population but in 40 to 85 percent of slow progressors. Yet even among those with the B57 gene, the speed of disease progression can vary considerably.

Now, a group of investigators from the Multi-Center AIDS Cohort Study (MACS), housed within the UCLA AIDS Institute, may have uncovered the key to this variation. It is a killer T-cell immune response that occurs early on in HIV infection and targets a section -- or epitope -- of the HIV protein called IW9.

The novel findings are featured on the cover of the October issue of the Journal of Virology.

"Since the hope for a vaccine is that it would elicit immune control, the thought has been that understanding how B57 protection works would yield helpful lessons and principles for vaccine design," said Catherine Brennan, an assistant research scientist in the department of medicine at the David Geffen School of Medicine at UCLA and the study's lead author. "There have been a lot of efforts to understand how the immune response to HIV in B57 carriers is superior to the response in non-B57 carriers, but it has been hard to nail anything down conclusively."

HLA-B genes are known to work by activating killer T cells that recognize unique sections of proteins, or epitopes, but it has been a mystery which section or sections of HIV protein HLA-B57 and the killer T cells work through.

Previous research had largely focused on the killer T-cell response after several years of infection. However, Beth D. Jamieson, a professor of medicine at the Geffen School of Medicine and the study's principal investigator, believes that the most critical responses are likely to occur early during infection, when the T cells are still strong and can reduce the number of places where HIV hides out in the human body.

Researchers have studied the immune response in the early months of infection, but since it is not easy to predict at early stages which people will ultimately become slow progressors, correlating early immune responses with long-term outcomes has been difficult.

"What made this kind of study possible for us is the Multicenter AIDS Cohort Study, which is an incredible longitudinal study," Brennan said.

The MACS has been freezing blood samples every six months since 1984 from thousands of men either at risk of HIV infection or already infected.

"The size and duration of the study, along with the careful documentation of participant health and stewardship of frozen samples, allowed us to recover blood samples taken shortly after HIV infection from 14 HLA-B57 carriers with known infection dates and known long-term outcomes," Brennan said. "This allowed us to correlate early immune responses with long-term outcomes."

It was important to the researchers to compare only the killer T-cell responses among those with the B57 gene variant, instead of comparing the responses of those with and without B57. Although B57 carriers have, on average, much better prognoses than non-carriers, there is tremendous variability among the population, and not all do well, Jamieson said.

"Since possession of the B57 variant is not sufficient, we wanted to determine what specific immune events in B57 carriers are associated with immune control of the virus," she said. "We found that those who targeted the IW9 epitope early in infection had significantly longer times until onset of AIDS than those who did not. The finding that targeting of IW9 seems to be important is novel, as this epitope had been overlooked in many earlier studies of B57 and HIV."

The researchers cautioned that the study was based on a small sample of only 14 individuals and that a wider pool of subjects is needed to replicate their findings. Also, their results point to a correlation with -- not causation of -- slower disease progression among B57 carriers who target the IW9 epitope soon after HIV infection.

"This work, although not powered by a large cohort and necessarily exploratory in nature, does suggest that the role of IW9 targeting in B57-mediated protection merits closer attention," the researchers conclude. "Understanding the detailed mechanisms by which B57 is associated with slow progression to disease will reveal underlying principles of immune control of HIV-1, which is critical for the development of rational vaccine-design strategies."

Grants from the National Institutes of Health (R21 AG032942 and R21 AI60486), an IDEA award to C.A.B. from the California HIV/AIDS Research Program (ID10-LA-007), and the Multicenter AIDS Cohort Study (AI-35040) funded this research. The Multicenter AIDS Cohort Study is funded by the National Institute of Allergy and Infectious Diseases, with additional supplemental funding from National Cancer Institute grants UO1-AI-35042, UL1-RR025005 (GCRC), UO1-AI-35043, UO1-AI-35039, UO1-AI-35040 and UO1-AI-35041.

Other researchers on the study included F. Javier Ibarrondo, Catherine A. Sugar, Mary Ann Hausner, Roger Shih, Hwee L. Ng, Roger Detels and Otto O. Yang, all of UCLA; Joseph B. Margolick and Lisa P. Jacobson of Johns Hopkins University; Charles R. Rinaldo of the University of Pittsburgh; and John Phair of Northwestern University.

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The above story is reprinted from materials provided by University of California, Los Angeles. The original article was written by Enrique Rivero.

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Journal Reference:

  1. C. A. Brennan, F. J. Ibarrondo, C. A. Sugar, M. A. Hausner, R. Shih, H. L. Ng, R. Detels, J. B. Margolick, C. R. Rinaldo, J. Phair, L. P. Jacobson, O. O. Yang, B. D. Jamieson. Early HLA-B*57-Restricted CD8+ T Lymphocyte Responses Predict HIV-1 Disease Progression. Journal of Virology, 2012; 86 (19): 10505 DOI: 10.1128/JVI.00102-12

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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DNA barcoding can ID natural health products

ScienceDaily (Sep. 19, 2012) — DNA barcoding developed by University of Guelph researchers has proven up to 88 per cent effective in authenticating natural health products, according to a new U of G study.

The study appears in the latest issue of Food Research International. It's a crucial finding because the health product industry is under-regulated worldwide and mislabelling poses economic, health, legal and environmental implications, says study author Mehrdad Hajibabaei.

"Currently there is no other broadly applicable tool that can identify the species used in both animal and plant natural health products as rapidly and cost-effectively," said Hajibabaei, a U of G integrative biology professor and director of technology development for the Guelph-based Biodiversity Institute of Ontario (BIO).

Up to about 80 per cent of people in developed countries use natural health products, including vitamins, minerals and herbal remedies. In Canada, these products have been regulated since 2004. But regulators face a backlog of licence applications, and thousands of products on the market lack a full product licence. In the U.S. and the U.K., regulatory problems involving natural health products have affected consistency and safety.

Authenticating natural product capsules or tablets -- containing dried fragments rather than whole specimens -- poses challenges.

DNA barcoding allows scientists to use short standardized regions of genetic material to identify species and compare them to reference genetic sequences, said Hajibabaei.

The technique works for all life stages and even for fragments of organisms, allowing scientists to ID even dried contents of a small pill.

"DNA barcoding provides a simple and efficient method for accurate identification and can play a key role in developing a more robust protocol for their regulation," Hajibabaei said.

For the study, researchers tested 95 plant and animal products bought in Toronto and New York City. Samples included capsules, tablets, roots, extracts, teas and shredded products. The researchers also sampled for products containing widely used shark tissue or ginseng.

Fully 81 per cent of natural health products made from animals correctly matched their commercial label. The rest contained everything from cheaper alternatives to fragments of protected species. One product labelled as tiger shark fins actually contained a catfish species.

Several of the identified shark species are on the "red list" of the International Union for the Conservation of Nature.

Half of the plant products labelled as Korean ginseng -- which is more expensive and is sold for different medicinal benefits than other types -- were really American ginseng.

Besides Hajibabaei, the study was headed by Lauren Wallace, a former President's Scholar at U of G and now a doctoral student at McMaster University. Wallace received a summer research fellowship from the Ontario Genomics Institute in 2010 to work on the BIO project.

Other researchers were Stephanie Boilard, now a technician in Hajibabaei's lab; graduate students Shannon Eagle and Jennifer Spall; and post-doc Shadi Shokralla.

Three of the researchers were using DNA barcoding for the first time. "Ultimately, the study showcases the utility of DNA barcodes for use in the real world," Hajibabaei said.

The BIO is a hub for barcoding research worldwide and leads the International Barcode of Life (www.ibol.org) project to develop a DNA barcode reference library. Another project based at the institute is Biomonitoring 2.0 (www.biomonitoring2.org), which uses barcoding and DNA sequencing for large-scale environmental assessment.

This research has been funded by the federal government through Genome Canada and the Ontario Genomics Institute.

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The above story is reprinted from materials provided by University of Guelph.

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Journal Reference:

  1. Lauren J. Wallace, Stephanie M.A.L. Boilard, Shannon H.C. Eagle, Jennifer L. Spall, Shadi Shokralla, Mehrdad Hajibabaei. DNA barcodes for everyday life: Routine authentication of Natural Health Products. Food Research International, 2012; DOI: 10.1016/j.foodres.2012.07.048

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Efficacy of drugs boosted by using nanoparticles to target 'powerhouse of cells'

ScienceDaily (Sep. 19, 2012) — Nanoparticles have shown great promise in the targeted delivery of drugs to cells, but researchers at the University of Georgia have refined the drug delivery process further by using nanoparticles to deliver drugs to a specific organelle within cells.

By targeting mitochondria, often called "the powerhouse of cells," the researchers increased the effectiveness of mitochondria-acting therapeutics used to treat cancer, Alzheimer's disease and obesity in studies conducted with cultured cells.

"The mitochondrion is a complex organelle that is very difficult to reach, but these nanoparticles are engineered so that they do the right job in the right place," said senior author Shanta Dhar, an assistant professor of chemistry in the UGA Franklin College of Arts and Sciences.

Dhar and her co-author, doctoral student Sean Marrache, used a biodegradable, FDA-approved polymer to fabricate their nanoparticles and then used the particles to encapsulate and test drugs that treat a variety of conditions. Their results were published this week in early edition of the journal Proceedings of the National Academy of Sciences.

To test the effectiveness of their drug targeting system against cancer, they encapsulated the drug lonidamine, which works by inhibiting energy production in the mitochondria, and, separately, a form of the antioxidant vitamin E. They then treated cultured cancer cells and found that mitochondrial targeting increased the effectiveness of the drugs by more than 100 times when compared to the drugs alone and by five times when compared to the delivery of drugs with nanoparticles that target the outside of cells.

Similarly, the compound curcumin has shown promise in inhibiting formation of the amyloid plaques that are a hallmark of Alzheimer's disease, but it quickly degrades in the presence of light and is broken down rapidly by the body. By encapsulating curcumin in the mitochondria-targeting nanoparticles, however, the researchers were able to restore the ability of brain cells in culture to survive despite the presence of a compound that encourages plaque formation. Nearly 100 percent of the cells treated with the mitochondria-targeting nanoparticles survived in the presence of the plaque-inducing compound, compared to 67 percent of cells treated with free curcumin and 70 percent of cells treated with nanoparticles that target the outside of cells.

Finally, the researchers encapsulated the obesity drug 2,4-DNP -- which works by making energy production in the mitochondria less efficient -- in their nanoparticles and found that it reduced the production of fat by cultured cells known as preadipocytes by 67 percent compared to cells treated with the drug alone and by 61 percent of cells treated with nanoparticles that target the outside of cells.

"A lot of diseases are associated with dysfunctional mitochondria, but many of the drugs that act on the mitochondria can't get there," Marrache said. "Rather than try to alter the drugs, which can reduce their effectiveness, we encapsulate them in these nanoparticles and precisely deliver them to the mitochondria."

Dhar said that getting drugs to the mitochondria is no simple feat. Upon entering cells, nanoparticles enter a sorting center known as the endosome. The first thing Dhar and Marrache had to demonstrate was that the nanoparticles escape from the endosome and don't end up in the cells' disposal center, the lysosome.

The mitochondria itself is protected by two membranes separated by an interstitial space. The outer membrane only permits molecules of a certain size to pass through, while the inner membrane only permits molecules of a given range of charges to pass. The researchers constructed a library of nanoparticles and tested them until they identified the optimum size range -- 64 to 80 nanometers, or approximately 1,000 times finer than the width of a human hair -- and an optimum surface charge, plus 34 millivolts.

Dhar notes the components they used to create the nanoparticles are FDA approved and that their methods are highly reproducible and therefore have the potential to be translated into clinical settings. The researchers are currently testing their targeted delivery system in rodents and say that preliminary results are promising.

"Mitochondrial dysfunctions cause many disorders in humans," Dhar said, " so there are several potential applications for this delivery system."

The research was supported by National Institutes of Health startup grant P30 GM 092378 and by the UGA Office of the Vice President for Research.

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The above story is reprinted from materials provided by University of Georgia. The original article was written by Sam Fahmy.

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Journal Reference:

  1. S. Marrache, S. Dhar. Engineering of blended nanoparticle platform for delivery of mitochondria-acting therapeutics. Proceedings of the National Academy of Sciences, 2012; DOI: 10.1073/pnas.1210096109

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Autistic adults have unreliable neural responses, research team finds

ScienceDaily (Sep. 19, 2012) — Autism is a disorder well known for its complex changes in behavior -- including repeating actions over and over and having difficulty with social interactions and language. Current approaches to understanding what causes these atypical behaviors focus primarily on specific brain regions associated with these specific behaviors without necessarily linking back to fundamental properties of the brain's signaling abilities.

New research led by Carnegie Mellon University neuroscientists takes the first step toward deciphering the connection between general brain function and the emergent behavioral patterns in autism. Published in the journal Neuron, the study shows that autistic adults have unreliable neural sensory responses to visual, auditory and somatosensory, or touch, stimuli. This poor response reliability appears to be a fundamental neural characteristic of autism.

"Within the autism research community, most researchers are looking for the location in the brain where autism happens," said Ilan Dinstein, a postdoctoral researcher in Carnegie Mellon's Department of Psychology and lead author of the study. "We're taking a different approach and thinking about how a general characteristic of the brain could be different in autism -- and how that might lead to behavioral changes."

For the study, 14 adults with autism and 14 without -- all between the ages of 19 and 39 -- completed sensory experiments while inside a functional magnetic resonance imaging (fMRI) machine located at CMU's Scientific Imaging and Brain Research center. To test the visual system's neural response, participants were shown a pattern of moving dots. The auditory stimulation consisted of pure tones presented to both ears, and short air puffs were used to stimulate the somatosensory senses. The fMRI measured each individual's brain activity during the experiments.

In all of the primary cortices, visual, auditory and somatosensory, the within-individual response reliability was significantly lower -- by 30-40 percent -- in autism; meaning, there was not a typical, predictable response from trial to trial. Thus, in the individuals with autism, there was significant intra-individual variability, with responses varying from strong to weak. Non-autistic adults had replicable and consistent responses from trial to trial.

"This suggests that there is something very fundamental that is altered in the cortical responses in individual's with autism," said Marlene Behrmann, professor of psychology at CMU and a leading expert on using brain imaging to understand autism. "It also begins to build a bridge between the kind of genetic changes that might have given rise to autism in the first place -- and the kind of changes in the brain that are responsible for autistic behavioral patterns.

"And, what I think is so powerful is that we sampled visual, auditory and somatosensory senses. We were unbelievably thorough and attacked every sensory modality and showed the same pattern of unreliability across all three senses."

The study also presents the first time that researchers have investigated multiple sensory systems -- at a primary brain function level -- within the same autistic individual.

"One of the problems with autism is that there is considerable variability in symptoms across individuals," Dinstein said. "In this case, we have a tremendous amount of data on each individual and each of their three sensory systems. And, we see the same unreliability across all of them in autism relative to the controls."

While this study focused on adults, the team plans on taking the research further to study how the details of sensory unreliability play out in younger autistic groups.

"We are not suggesting that unreliable sensory -- visual, auditory, touch -- responses cause autism," said David Heeger, professor of psychology and neural science at New York University. "But rather that autism might be a consequence of unreliable activity throughout the brain during development. We've measured it in sensory areas of the brain but we hypothesize that the same kind of unreliability might be what's limiting the development of social and language abilities in the brain areas that subserve those functions."

In addition to expanding autism research to determine when and how basic neural processing affects autism, the research may have clinical implications.

"The poor cortical response reliability observed in the individuals with autism in this study may represent a biomarker which could contribute to better define Autism Spectrum Disorder (ASD) subtypes," said Pauline Chaste, a visiting research scholar at the University of Pittsburgh Medical Center who was not affiliated with the research but studies how genetic mutations affect psychiatric disorders. "This is very important because of the great heterogeneity of phenotype in ASD which makes the definition of subphenotypes critical for genetic studies as well as for treatment studies. Thus, the use of this biomarker may help to define new targets for treatment but also to assess efficacy. Moreover this study brings new insight into understanding atypical sensory sensitivity in autism, which is a major concern for a vast majority of patients and remains sorely underexplored."

Lauren Lorenzi, a research associate at Carnegie Mellon, Nancy Minshew from the Department of Neurology at the University of Pittsburgh and Rafael Malach, the Morris and Barbara Levinson Professor of Brain Research at the Weizmann Institute of Science, were also part of the research team.

The Simons Foundation, Pennsylvania Department of Health and the National Institute of Health and National Institute of Child and Human Development's Autism Center of Excellence at the University of Pittsburgh funded this research.

This study will appear as the cover story of the October 2012 print issue of Neuron. The issue's cover design was created by Carnegie Mellon's Communication Design team.

For more information, watch Dinstein and Behrmann discuss this study at http://youtu.be/0eSdOjMaGO8.

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The above story is reprinted from materials provided by Carnegie Mellon University.

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Journal Reference:

  1. Ilan Dinstein, David J. Heeger, Lauren Lorenzi, Nancy J. Minshew, Rafael Malach, Marlene Behrmann. Unreliable Evoked Responses in Autism. Neuron, 2012; 75 (6): 981 DOI: 10.1016/j.neuron.2012.07.026

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Dyslexia cause may be different than previously thought

ScienceDaily (Sep. 19, 2012) — Dyslexia may result from impairment of a different linguistic system than previously thought, according to research published Sep. 19 in the open access journal PLOS ONE.

Speech perception engages at least two linguistic systems: the phonetic system, which extracts discrete sound units from acoustic input, and the phonological system, which combines these units to form individual words. Previously, researchers generally believed that dyslexia was caused by phonological impairment, but results from the current study, led by Iris Berent of Northeastern University in Boston, suggest that the phonetic system may actually be the cause.

"Our findings confirm that dyslexia indeed compromises the language system, but the locus of the deficit is in the phonetic, not the phonological system, as had been previously assumed," says Berent.

In the study, Hebrew-speaking college students had difficulty discriminating between similar speech sounds, but had no problem tracking abstract phonological patterns, even for novel words, suggesting that the phonological system is intact but the phonetic system is compromised.

"Our research demonstrates that a closer analysis of the language system can radically alter our understanding of the disorder, and ultimately, its treatment," says Berent.

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Journal Reference:

  1. Iris Berent, Vered Vaknin-Nusbaum, Evan Balaban, Albert M. Galaburda. Dyslexia Impairs Speech Recognition but Can Spare Phonological Competence. PLoS ONE, 2012; 7 (9): e44875 DOI: 10.1371/journal.pone.0044875

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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New cranial neural crest cell line developed

ScienceDaily (Sep. 19, 2012) — Researchers have successfully developed a stable population of neural crest cells derived from mice that can be grown in large quantities in the laboratory and that demonstrates the potential to develop into many different cell types needed throughout the body.

This powerful new research tool for understanding stem cell biology and human development and disease is described in an article published in Stem Cells and Development.

Mamoru Ishii and colleagues from University of Southern California, Los Angeles, and California Institute of Technology, Pasadena, CA, present their work leading to the development of two neural crest cell lines with stem cell characteristics in the article "A Stable Cranial Neural Crest Cell Line from Mouse." The 09-1 cell line is capable of differentiating into four main cell types: bone, muscle, brain, and cartilage/connective tissue.

"This exciting report is the first to characterize cranial neural crest cell lines isolated from the mouse embryo, which definitively demonstrate multipotency and long-term propagation," says Editor-in-Chief Graham C. Parker, PhD, research professor, Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine.

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The above story is reprinted from materials provided by Mary Ann Liebert, Inc./Genetic Engineering News, via EurekAlert!, a service of AAAS.

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Journal Reference:

  1. Mamoru Ishii, Athena C Arias, Liqiong Liu, Yi-Bu Chen, Marianne Bronner, Robert E Maxson. A Stable Cranial Neural Crest Cell Line from Mouse. Stem Cells and Development, 2012; : 120813192836009 DOI: 10.1089/scd.2012.0155

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Medication effective in treating social withdrawal in Fragile X and potentially autism patients

ScienceDaily (Sep. 19, 2012) — An investigational compound that targets the core symptoms of fragile X syndrome is effective for addressing the social withdrawal and challenging behaviors characteristic of the condition, making it the first such discovery for fragile X syndrome and, potentially, the first for autism spectrum disorder, a study by researchers at Rush University Medical Center and the University of California, Davis MIND Institute has found.

The finding is the result of a clinical trial in adult and pediatric subjects with fragile X syndrome. It suggests, however, that the compound may have treatment implications for at least a portion of the growing population of individuals with autism spectrum disorder, as well as for those with other conditions defined by social deficits. The study is published online September 19 in the journal Science Translational Medicine.

"There are no FDA-approved treatments for fragile X syndrome, and the available options help secondary symptoms but do not effectively address the core impairments in fragile X syndrome," said Dr. Elizabeth Berry-Kravis, the lead author of the article. "This is the first large-scale study that is based on the molecular understanding of fragile X syndrome and, importantly, suggests that the core symptoms may be amenable to pharmacologic treatment." Berry-Kravis is professor of Pediatrics, Neurological Sciences, and Biochemistry at Rush.

The "first-in-patient" drug trial was led by Berry-Kravis and Dr. Randi Hagerman of the UC Davis MIND Institute. It examined the effects of the compound STX 209, also known by the name Arbaclofen. The study was conducted collaboratively with Seaside Theraputics, a Cambridge, Mass., pharmaceutical company, that is focused on translating bench research on fragile X and autism into therapeutic interventions. Seaside Therapeutics produces the compound.

"This study shows that STX 209 is an important part of the treatment for fragile X syndrome, because it improved symptoms in those with significant social deficits or autism as well as fragile X syndrome," said Hagerman, who is the medical director of the MIND Institute. "Additional studies also are suggesting that STX 209 can be helpful for autism without fragile X syndrome. Until now, there have been no targeted treatments available for autism. This appears to be the first."

Fragile X syndrome is the most common known cause of inherited intellectual impairment, formerly referred to as mental retardation, and the leading known single-gene cause of autism. Social impairment is one of the core deficits in both fragile X and autism. The U.S. Centers for Disease Control and Prevention (CDC) estimates that about 1 in 4,000 males and 1 in 6,000 to 8,000 females have the disorder. An estimated 1 in 88 children born today will be diagnosed with autism, according to the CDC.

"This study will help to signal the beginning of a new era of targeted treatments for genetic disorders that have historically been regarded as beyond the reach of pharmacotherapy," Berry-Kravis said. "It will be a model for treatment of autism, intellectual disability and developmental brain disorders based on understanding of dysfunction in brain pathways, as opposed to empiric treatment of symptoms. We hope mechanistically-based treatments like STX209 ultimately will be shown to improve cognitive functioning in longer-term trials."

Studies in mice genetically engineered to exhibit features of fragile X, including social impairment, have suggested that the behavioral abnormalities in fragile X result from deficiencies in the neurotransmitter gamma-amino butyric acid (GABA). Decreased GABA has been observed in a mouse model of fragile X in many areas of the brain including the hippocampus, and has been hypothesized to be a basis of the social anxiety and avoidance characteristic of fragile X sufferers, the study says.

Arbaclofen is an agonist for gamma-amino butyric acid type B, or GABA-B, receptors. An agonist is a chemical that effectively combines with a receptor on a synapse to effect a physiologic reaction typical of a naturally occurring substance. Anxiety-driven repetitive behavior and social avoidance have been reduced in fragile X-engineered mice treated with arbaclofen. The current, first-of-its-kind study investigated whether Arbaclofen would produce similar results in human subjects.

The double-blind, placebo-controlled clinical trial initially recruited 63 subjects at 12 sites across the United States for the research, conducted between December 2008 and March 2010. The participants ranged in age from 6 to 39 years. Of the initial participants, 56 completed the clinical trial. There were no withdrawals related to drug tolerability. The majority of the subjects were treated with what was assessed as the optimum tolerated dosage of the study drug, 10 milligrams twice a day in younger patients and three times a day in adults. Compliance was monitored by patient guardians, who filled out a dosing form on a daily basis.

The study subjects returned for evaluations at two- and four-week intervals after beginning the six-week-long treatment. The drug then was tapered down over a one- to two-week period. After a week, the subjects entered a second treatment period.

The effects of the medication were scored on variables of the Aberrant Behavior Checklist, a behavior-rating scale for the assessment of drug-treatment effects. The checklist includes variables for irritability, lethargy/withdrawal, stereotypic (repetitive) behavior and hyperactivity, among other factors.

The study found improvement for the full study population on the social-avoidance subscale, an analysis validated by secondary ratings from parent observation of improvement in subjects' three most problematic behaviors. It found that the medication was the same as placebo, however, on the subscale for irritability.

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The above story is reprinted from materials provided by Rush University Medical Center, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. E. M. Berry-Kravis, D. Hessl, B. Rathmell, P. Zarevics, M. Cherubini, K. Walton-Bowen, Y. Mu, D. V. Nguyen, J. Gonzalez-Heydrich, P. P. Wang, R. L. Carpenter, M. F. Bear, R. J. Hagerman. Effects of STX209 (Arbaclofen) on Neurobehavioral Function in Children and Adults with Fragile X Syndrome: A Randomized, Controlled, Phase 2 Trial. Science Translational Medicine, 2012; 4 (152): 152ra127 DOI: 10.1126/scitranslmed.3004214

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/6d7qyoaox4U/120919142140.htm
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Human brains share a consistent genetic blueprint and possess enormous biochemical complexity

ScienceDaily (Sep. 19, 2012) — Scientists at the Allen Institute for Brain Science reported in the latest issue of the journal Nature that human brains share a consistent genetic blueprint and possess enormous biochemical complexity. The findings stem from the first deep and large-scale analysis of the vast data set publicly available in the Allen Human Brain Atlas.

The results of this study are based on extensive analysis of the Allen Human Brain Atlas, specifically the detailed all-genes, all-structures survey of genes at work throughout the human brain. This dataset profiles 400 to 500 distinct brain areas per hemisphere using microarray technology and comprises more than 100 million gene expression measurements covering three individual human brains to date. Among other findings, these data show that 84% of all genes are expressed somewhere in the human brain and in patterns that are substantially similar from one brain to the next.

"This study demonstrates the value of a global analysis of gene expression throughout the entire brain and has implications for understanding brain function, development, evolution and disease," said Ed Lein, Ph.D., Associate Investigator at the Allen Institute for Brain Science and co-lead author on the paper. "These results only scratch the surface of what can be learned from this immense data set. We look forward to seeing what others will discover."

Key Findings

The results of this study show that, despite the myriad personalities and cognitive talents seen across the human population, our brains are more similar to one another than different. Individual human brains share the same basic molecular blueprint, and deeper analysis of this shared architecture reveals several further findings:

  • Neighboring regions of the brain's cortex -- the wrinkly outer rind -- are more biochemically similar to one another than to more distant brain regions, which has implications for understanding the development of the human brain, both during the lifespan and throughout evolution.
  • The right and left hemispheres show no significant differences in molecular architecture. This suggests that functions such as language, which are generally handled by one side of the brain, likely result from more subtle differences between hemispheres or structural variation in size or circuitry, but not from a deeper molecular basis.
  • Despite controlling a diversity of functions, ranging from visual perception to planning and problem-solving, the cortex is highly homogeneous relative to other brain regions. This suggests that the same basic functional elements are used throughout the cortex and that understanding how one area works in detail will uncover fundamentals that apply to the other areas, as well.

In addition to such global findings, the study provides new insights into the detailed inner workings of the brain at the molecular level -- the level at which diseases unfold and therapeutic drugs take action.

  • 84% of all genes are expressed, or turned on, somewhere in the human brain.
  • Many previously uncharacterized genes are turned on in specific brain regions and localize with known functional groups of genes, suggesting they play roles in particular brain functions.
  • Synapse-associated genes -- those related to cell-to-cell communication machinery in the brain -- are deployed in complex combinations throughout the brain, revealing a great diversity of synapse types and remarkable regional variation that likely underlies functional distinctions between brain regions.

"The tremendous variety of synapses we see in the human brain is quite striking," said Seth Grant, FRSE, Professor of Molecular Neuroscience at the University of Edinburgh and collaborating author on the study. "Mutations in synaptic genes are associated with numerous brain-related disorders, and thus understanding synapse diversity and organization in the brain is a key step toward understanding these diseases and developing specific and effective therapeutics to treat them."

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The above story is reprinted from materials provided by Allen Institute for Brain Science.

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Journal Reference:

  1. Michael J. Hawrylycz, Ed S. Lein, Angela L. Guillozet-Bongaarts, Elaine H. Shen, Lydia Ng, Jeremy A. Miller, Louie N. van de Lagemaat, Kimberly A. Smith, Amanda Ebbert, Zackery L. Riley, Chris Abajian, Christian F. Beckmann, Amy Bernard, Darren Bertagnolli, Andrew F. Boe, Preston M. Cartagena, M. Mallar Chakravarty, Mike Chapin, Jimmy Chong, Rachel A. Dalley, Barry David Daly, Chinh Dang, Suvro Datta, Nick Dee, Tim A. Dolbeare, Vance Faber, David Feng, David R. Fowler, Jeff Goldy, Benjamin W. Gregor, Zeb Haradon, David R. Haynor, John G. Hohmann, Steve Horvath, Robert E. Howard, Andreas Jeromin, Jayson M. Jochim, Marty Kinnunen, Christopher Lau, Evan T. Lazarz, Changkyu Lee, Tracy A. Lemon, Ling Li, Yang Li, John A. Morris, Caroline C. Overly, Patrick D. Parker, Sheana E. Parry, Melissa Reding, Joshua J. Royall, Jay Schulkin, Pedro Adolfo Sequeira, Clifford R. Slaughterbeck, Simon C. Smith, Andy J. Sodt, Susan M. Sunkin, Beryl E. Swanson, Marquis P. Vawter, Derric Williams, Paul Wohnoutka, H. Ronald Zielke, Daniel H. Geschwind, Patrick R. Hof, Stephen M. Smith, Christof Koch, Seth G. N. Grant, Allan R. Jones. An anatomically comprehensive atlas of the adult human brain transcriptome. Nature, 2012; 489 (7416): 391 DOI: 10.1038/nature11405

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/K9srO9CJZWo/120919135318.htm
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The more people rely on their intuitions, the more cooperative they become

ScienceDaily (Sep. 19, 2012) — It's an age old question: Why do we do good? What makes people sometimes willing to put "We" ahead of "Me?" Perhaps our first impulse is to be selfish, and cooperation is all about reining in greed. Or maybe cooperation happens spontaneously, and too much thinking gets in the way.

Harvard scientists are getting closer to an answer, showing that people's first response is to cooperate and that stopping to think encourages selfishness.

David Rand, a Post-Doctoral Fellow in Psychology, Joshua Greene, the John and Ruth Hazel Associate Professor of the Social Sciences in the Department of Psychology, and Martin Nowak, Professor of Mathematics and of Biology, and Director of the Program for Evolutionary Dynamics, have published their findings in the September 20 issue of Nature. They recruited thousands of participants to play a "public goods game" in which it's "Me" vs. "Us." Subjects were put into small groups and faced with a choice: Keep the money you've been given, or contribute it into a common pool that grows and benefits the whole group. Hold onto the money and you come out ahead, but the group does best when everyone contributes.

The researchers wanted to know whether people's first impulse is cooperative or selfish. To find out, they started by looking at how quickly different people made their choices, and found that faster deciders were more likely to contribute to the common good.

Next they forced people to go fast or to stop and think, and found the same thing: Faster deciders tended to be more cooperative, and the people who had to stop and think gave less.

Finally, the researchers tested their hypothesis by manipulating people's mindsets. They asked some people to think about the benefits of intuition before choosing how much to contribute. Others were asked to think about the virtues of careful reasoning. Once again, intuition promoted cooperation, and deliberation did the opposite.

While some might interpret the results as suggesting that cooperation is "innate" or "hard-wired," if anything they highlight the role of experience. People who had better opinions of those around them in everyday life showed more cooperative impulses in these experiments, and previous experience with these kinds of studies eroded those impulses.

"In daily life, it's generally in your interest to be cooperative," Rand said. "So we internalize cooperation as the right way to behave. Then when we come into unusual environments, where incentives like reputation and sanctions are removed, our first response is to keep behaving the way we do in normal life. When we think about it, however, we realize that this is one of those rare situations where we can be selfish and get away with it."

Unlike many psychology studies, which use small numbers of college students, these experiments tested thousands of people from around the world using Amazon Mechanical Turk, an online labor market that's becoming an increasingly popular tool for social science research.

According to Rand, the findings highlight an interesting and counterintuitive truth -- that careful thought and reflection have a dark side. But is reflection always bad?

"When it's 'Me' vs. 'Us,' our intuitions seem to work well. That's what's going on here," explains Joshua Greene. "But what happens when people have different moral intuitions, for example, about abortion or raising taxes? When intuitions clash -- when it's the values of 'Us' vs. 'Them' -- reasoning and reflection may be our best hope for reconciling our differences."

"Over millions of years we've evolved the capacity for cooperation," explains Martin Nowak. "These psychological experiments examine the causes of cooperation on a shorter timescale, on the order of seconds. Both perspectives are essential as we face global problems which require cooperation on a massive scale. We need to understand where cooperation comes from historically and how best to make it happen here and now."

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Story Source:

The above story is reprinted from materials provided by Harvard University, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. David G. Rand, Joshua D. Greene, Martin A. Nowak. Spontaneous giving and calculated greed. Nature, 2012; 489 (7416): 427 DOI: 10.1038/nature11467

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

20 Sep, 2012


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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/sQyIezy4Wss/120919142144.htm
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