University of Adelaide

There’s some good news for parents of preterm babies – latest research from the University of Adelaide shows that by the time they become teenagers, the brains of many preterm children can perform almost as well as those born at term.

A study conducted by the University’s Robinson Research Institute has found that as long as the preterm child experiences no brain injury in early life, their cognitive abilities as a teenager can potentially be as good as their term-born peers.

However, the results of the study, published in this month’s issue of The Journal of Pediatrics, also highlight that the quality of the home environment at the time of the child’s birth plays an important role in their cognition later in life.

“Every year, 10% of Australian babies are born preterm, and many studies have shown that these children often have cognitive difficulties in childhood,” says one of the lead authors of the study, Dr Julia Pitcher from the University of Adelaide’s Robinson Research Institute.

“This new study has some positive news. We looked at the factors that determine cognitive abilities in early adolescence, and found that whether or not you were born preterm appears to play a relatively minor role. Of significantly more importance is the degree of social disadvantage you experienced in your early life after birth, although genetics is important,” Dr Pitcher says.

The study, conducted by Research Officer Dr Luke Schneider, assessed the cognitive abilities of 145 preterm and term-born young people now aged over 12. He also assessed data on social disadvantage at the time of birth and at the time of the cognitive assessment.

“The results of our study provide further proof that those born at term tend to have better cognitive abilities – such as working memory, brain processing efficiency and general intellectual ability. But the postnatal environment seems to be playing an important role in whether or not a preterm child is able to overcome that initial risk of reduced brain development,” Dr Schneider says.

“Reduced connectivity in the brain, associated with microstructural abnormalities from preterm birth, is likely contributing to the cognitive deficits in these children. But these abnormalities seem to be amenable to improvement depending on the environment the child grows up in, particularly as an infant, and might account for why some preterm children do better than others.”

Dr Pitcher says: “What we don’t yet know is how different factors in the home environment drive specific aspects of brain development. But early nutrition and enrichment through physical and intellectual stimulation are likely to have key roles.”

This research is supported by the National Health and Medical Research Council (NHMRC).

redOrbit Staff & Wire Reports – Your Universe Online

The US Surgeon General has issued a new warning against skin cancer, claiming that even though the condition is preventable in most cases, it is believed to have affected more Americans than breast, prostate, lung, colon and all other forms of cancer combined over the past three decades.

In a statement released by the Department of Health and Human Services, the Surgeon General reported that the rates of melanoma and other forms of skin cancer are on the rise. Nearly five million Americans are being treated for the condition every year at an average annual cost of over $8 billion, and it is one of the most common forms of cancer among teens and young adults in the US.

There are more than 63,000 new cases of melanoma, the deadliest form of skin cancer and the leading cause of death from skin disease, diagnosed in the US annually. While that represents just two percent of all skin cancer cases, it is also a 200 percent increase from 1973 to 2011, and is responsible for nearly 9,000 deaths each year.

“Until today, the surgeon general has never said, ‘UV radiation is bad for you; protect your skin,’” acting Surgeon General Dr. Boris Lushniak, who is a dermatologist by trade, told CNN.com on Wednesday. “We have to change the social norms about tanning. Tanned skin is damaged skin, and we need to shatter the myth that tanned skin is a sign of health.”

According to the Surgeon General’s report, more than 400,000 annual cases of skin cancer in the US (including 6,000 instances of melanoma) are believed to be linked to indoor tanning. As many as 44 states, as well as Washington DC, have already instituted some type of legislation or regulation related to indoor tanning, the advisory said, but nearly one-third of white females between the ages of 16 and 25 participate in the activity each year.

While health experts have long advised that people should take measures to protect themselves from the sun’s UV rays and refrain from using indoor tanning salons, Kim Painter of USA Today noted that this is the first time the Surgeon General’s office has weighed in on the issue.

The warning comes just two months after the Food and Drug Administration’s announcement that tanning beds and tanning lamps will soon have to include labels cautioning that they not be used by anyone under the age of 18, she added, and days after the House of Representatives passed the Sunscreen Innovation Act, which includes a review process for all manufacturers submitting new sunscreens to the FDA, according to CNN.

“While many other cancers, such as lung cancer, are decreasing, rates of melanoma – the deadliest form of skin cancer — are increasing,” Assistant Secretary for Health Dr. Howard K. Koh, a skin oncologist by trade, said in a statement. “Almost all of these cancers were caused by unnecessary ultraviolet radiation exposure, usually from excessive time in the sun or from the use of indoor tanning devices.”

“When people tan or get sunburned, they increase their risk of getting skin cancer later in life,” added Lushniak. “We want all Americans to lead healthy, active lives. We all need to take an active role to prevent skin cancer by protecting our skin while being outdoors and avoiding intentional sun exposure and indoor tanning.”

Read Further:

> ASA Responds to Surgeon General’s Call to Action Regarding UV Exposure

> Statement from Tim Turnham, Executive Director, Melanoma Research Foundation, Regarding Surgeon General’s Skin Cancer Call to Action

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April Flowers for redOrbit.com – Your Universe Online
It has been evident for a while that men and women react to diet differently. Men lose weight easier than women, men need more calories than women because of muscle mass, and there are even differences in eating styles.
Now, a new study led by The University of Texas at Austin reveals that even our gut microbes react differently to our diet, even if that diet is exactly the same.
The findings, published in Nature Communication, indicate that therapies designed to improve health and treat disease through nutrition need to be tailored for each gender.
The data for this study was collected from the gut microbes of mice and two species of fish. The team also performed an in-depth analysis of data collected on humans by previous research teams. In fish, and in humans, the researchers discovered that diet affected the microbiota of males and females in different manners. For example, in some instances, different species of microbes would dominate. In other instances, one sex would have a higher diversity of bacteria than the other.
Scientists have only recently begun to appreciate the vital role played by the human microbiome, which consists of all the bacteria that live in or on a person’s body. The gut microbiome alone is made up of hundreds, or perhaps thousands, of different species of microbes, each varying in abundance.
Human health can be affected in a very real way by the variety and number of microbes in the gut, which is determined by a mixture of genetics and diet. Researchers have been able to link obesity, diabetes and inflammatory bowel disease to low diversity of bacteria in the human gut.
A lot still needs to be understood about which species, or combination of species, is the best for human health. To gain this knowledge, scientists need to know how various combinations of diet, genetics and environment affect the microbes. Unfortunately, most studies focus on a single factor and do not account for how the variables interact.
“Our study asks not just how diet influences the microbiome, but it splits the hosts into males and females and asks, do males show the same diet effects as females?” said Daniel Bolnick, professor in The University of Texas at Austin’s College of Natural Sciences.
Despite identifying the gender differences in gut microbiota, the data used for this study does not lend itself to specific diet tips because it is organized into complex clusters of disparate factors.
“To guide people’s behavior, we need to know what microbes are desirable for people,” said Bolnick. “Diet and sex do interact to influence the microbes, but we don’t yet know what a desirable target for microbes is. Now we can go in with eyes open when we work on therapies for gut microbe problems, as many involve dietary changes. We can walk into those studies looking for something we weren’t aware of before. All along we treated diet as if it works the same for men and women. Now we’ll be approaching studies of therapies in a different way.”
It still isn’t clear why males and females would have different reactions to changes in diet, but a couple of possibilities present themselves. For one, the hormones associated with gender could influence gut microbes, pushing the body’s environment to favor one strain over another. Another explanation could be found in the fact that the sexes differ in how their immune systems function, which could change which microbes live and die in the gut microbiome.
Bolnick notes that the one exception in his study was in the mice. The researchers found a tiny difference between males and females, but for the most part, the gut microbiomes of both sexes responded to diet in the same manner. This finding, which raises questions about how well mice studies can be generalized to other species, could have a great impact on future studies, as most dietary research is conducted on mice.
“This means that most of the research that’s being done on lab mice — we need to treat that with kid gloves,” said Bolnick.
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By Juliana Bunim, University of California – San Francisco

A new study from UC San Francisco is the first to show that while the impact of life’s stressors accumulate overtime and accelerate cellular aging, these negative effects may be reduced by maintaining a healthy diet, exercising and sleeping well.

“The study participants who exercised, slept well and ate well had less telomere shortening than the ones who didn’t maintain healthy lifestyles, even when they had similar levels of stress,” said lead author Eli Puterman, PhD, assistant professor in the department of psychiatry at UCSF. “It’s very important that we promote healthy living, especially under circumstances of typical experiences of life stressors like death, caregiving and job loss.”

The paper will be published in Molecular Psychiatry, a peer-reviewed science journal by Nature Publishing Group.

Telomeres are the protective caps at the ends of chromosomes that affect how quickly cells age. They are combinations of DNA and proteins that protect the ends of chromosomes and help them remain stable. As they become shorter, and as their structural integrity weakens, the cells age and die quicker. Telomeres also get shorter with age.

In the study, researchers examined three healthy behaviors –physical activity, dietary intake and sleep quality – over the course of one year in 239 post-menopausal, non-smoking women. The women provided blood samples at the beginning and end of the year for telomere measurement and reported on stressful events that occurred during those 12 months. In women who engaged in lower levels of healthy behaviors, there was a significantly greater decline in telomere length in their immune cells for every major life stressor that occurred during the year. Yet women who maintained active lifestyles, healthy diets, and good quality sleep appeared protected when exposed to stress – accumulated life stressors did not appear to lead to greater shortening.

“This is the first study that supports the idea, at least observationally, that stressful events can accelerate immune cell aging in adults, even in the short period of one year. Exciting, though, is that these results further suggest that keeping active, and eating and sleeping well during periods of high stress are particularly important to attenuate the accelerated aging of our immune cells,” said Puterman.

In recent years, shorter telomeres have become associated with a broad range of aging-related diseases, including stroke, vascular dementia, cardiovascular disease, obesity, osteoporosis diabetes, and many forms of cancer.

Research on telomeres, and the enzyme that makes them, telomerase, was pioneered by three Americans, including UCSF molecular biologist and co-author Elizabeth Blackburn, PhD. Blackburn co-discovered the telomerase enzyme in 1985. The scientists received the Nobel Prize in Physiology or Medicine in 2009 for their work.

“These new results are exciting yet observational at this point. They do provide the impetus to move forward with interventions to modify lifestyle in those experiencing a lot of stress, to test whether telomere attrition can truly be slowed,” said Blackburn.

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Marla Vacek Broadfoot, Duke University

Microorganisms like bacteria and fungi can evade treatment by acquiring mutations in the genes targeted by antibiotics or antifungal drugs. These permanent mutations were once thought to be the only way for drug-resistant strains to evolve. Now a new study has shown that microorganisms can use a temporary silencing of drug targets — known as epimutations — to gain the benefits of drug resistance without the commitment.

Though the new mechanism was discovered in a fungus called Mucor circinelloides, it is likely to be employed by other fungi as well as bacteria, viruses and other organisms to withstand treatment with various drugs. The finding appears July 27, 2014, in Nature.

“This mechanism gives the organism more flexibility,” said Joseph Heitman, M.D., Ph.D., senior study author and professor and chair of molecular genetics and microbiology at Duke University School of Medicine. “A classic, Mendelian mutation is a more permanent binding decision, like a traditional marriage. These epimutations are reversible, more akin to moving in together. If conditions change, it is easier to revert to the way things were.”

The epimutations are so transient, in fact, that the researchers almost disregarded them. Cecelia Wall, a graduate student in Drs. Heitman and Maria Cardenas’ labs, had been looking for mutations that would make the human fungal pathogen M. circinelloides resistant to the antifungal drug FK506 (also known as tacrolimus). This pathogen causes the rare but lethal fungal infection mucormycosis, an emerging infectious disease that predominantly affects individuals with weakened immune systems.

As is typical for most drug resistance experiments, Wall first grew the pathogen in Petri dishes containing the antifungal drug. She found that the few organisms that survived treatment looked different, being smaller and less diffuse than their parent fungi. Wall then isolated those fungi and sequenced the gene FKBP12 — the target of FK506 — to look for mutations that would confer drug resistance.

However, she couldn’t detect any mutations in about a third of the isolates. What’s more, Wall found that many of the mutants kept “disappearing,” looking less like mutants and more like their parents after she took the drug away.

“This is an example of something you might find in the laboratory and just throw away,” said Silvia Calo, Ph.D., lead study author and postdoctoral fellow in the Heitman and Cardenas labs. “You look for mutants in one gene and when you don’t find a mutation in some of the isolates, you decide not to work on those anymore and instead focus on others. But we wanted to know what was going on.”

The researchers began to wonder whether a phenomenon known as RNA interference or RNAi could be the cause of this unstable drug resistance. RNAi uses bits of RNA — the chemical cousin of DNA — to silence specific genes. Though RNAi doesn’t exist in every organism, the researchers knew it was active in M. circinelloides because of the pioneering work of their collaborators Rosa Ruiz-Vazquez and Santiago Torres-Martinez, with whom Calo trained at the University of Murcia, Spain.

So Calo looked for the presence of small RNAs — a signature of RNAi — in the drug resistant isolates. She didn’t find small RNAs in the isolates that contained mutations in FKBP12, but she did find them in those lacking mutations. Importantly, Calo found that these small RNAs only silenced the FKBP12 gene and not any other loci in the genome. The results demonstrate that M. circinelloides can develop drug resistance two different ways, either stably through permanent mutations or transiently through reversible epimutations.

“This plasticity enables an organism to reverse epigenetic mutations when selective pressures are relaxed,” said Calo. “Otherwise, silencing a gene when it doesn’t need to be silenced would be a waste of energy.”

The researchers think these epimutations could be employed in a variety of situations, enabling an organism to adapt to an unfavorable environment and then adapt again when conditions improve. Though they have only shown epimutations in two species of M. circinelloides, they have already been approached by a number of other researchers who are interested in investigating similar unstable behavior in other organisms like Aspergillus and Neurospora.

“It could be like the discovery of other molecular phenomena like introns or microRNAs, where it all began with just one example,” said Heitman. “We think this discovery may turn out to be generalized fairly quickly.”

redOrbit Staff & Wire Reports – Your Universe Online

Having already waded knee-deep into the world of driverless cars, optical head-mounted displays and other wearable technology, Google is reportedly poised to tackle its biggest challenge yet – a perfectly healthy human body.

According to Alistair Barr of The Wall Street Journal, the Mountain View, California-based firm’s Baseline Study project will collect anonymous genetic and molecular information from 175 men and women in the hopes that it can allow experts to develop a detailed map of what the physiology of a healthy human being should look like.

Fifty-year-old molecular biologist Dr. Andrew Conrad, who helped develop inexpensive high-volume tests for HIV in blood-plasma donations, will be in charge of the early stages of the project, Barr said. Dr. Conrad joined the company’s Google X research branch in March 2013, and since then he has recruited between 70 and 100 physiology, biochemistry, optics, imaging and molecular biology experts to work alongside him.

As Fast Company’s Chris Gayomali explained, Google is not the only company to launch a mass molecular-level or genomic study, as the Human Genome Project was launched in 1990 and began to successfully sequence the human genetic code in 2003. However, Google is said to be one of the few companies on Earth with the resources and capabilities to conduct an in-depth study of the body’s proteins and enzymes.

“The hope is that this will help researchers detect killers such as heart disease and cancer far earlier, pushing medicine more toward prevention rather than the treatment of illness,” Barr said. “The project won’t be restricted to specific diseases, and it will collect hundreds of different samples using a wide variety of new diagnostic tools. Then Google will use its massive computing power to find patterns, or ‘biomarkers,’ buried in the information.”

“The hope is that these biomarkers can be used by medical researchers to detect any disease a lot earlier,” he added. “The study may, for instance, reveal a biomarker that helps some people break down fatty foods efficiently, helping them live a long time without high cholesterol and heart disease. Others may lack this trait and succumb to early heart attacks. Once Baseline has identified the biomarker, researchers could check if other people lack it and help them modify their behavior or develop a new treatment to help them break down fatty foods better.”

Earlier this month, it was announced that Google had licensed its smart contact lens technology to pharmaceutical giant Novartis, who plans to use it to develop lenses capable of helping diabetics monitor their blood sugar levels. The device, which consists of a wireless chip and miniaturized sensor embedded between two layers of soft contact lens material, would essentially provide 24-7 glucose monitoring by testing the tears of the person wearing them.

Google unveiled a prototype version of the lens earlier this year. At the time, it was capable of testing tears once per second, and was investigating the use of LED lights that could serve as an alternate early-warning system. Furthermore, Novartis officials said they believe the “smart lens” technology could be adapted to help people suffering from presbyopia, an age-related condition that robs the eye’s ability to focus naturally.

The Baseline Study is an even more ambitious project – one which Barr says will rely upon the company’s massive network of computers and data centers to store and analyze medical information and make it easier for researchers to access. Most biomarkers discovered to date are associated with late-stage diseases, since studies typically focus on ill patients, and efforts to use them to detect ailments earlier have met with mixed success.

Dr. Conrad told The Wall Street Journal that he expects progress to be made in “little increments,” and his Baseline colleague Dr. Sam Gambhir, who also chairs the Stanford University Medical School’s Department of Radiology, said that Dr. Conrad understands “that this is not a software project that will be done in one or two years. We used to talk about curing cancer and doing this in a few years. We’ve learned to not say those things anymore.”

Google has promised that the information collected for the Baseline Study will be anonymous, and that it will be used solely for medical and health-related purposes, Barr said – no information will be shared with insurance companies. However, he added that the fact that the company “would know the structure of thousands of people’s bodies – down to the molecules inside their cells – raises significant issues of privacy and fairness.”

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Richard C. Lewis, University of Iowa
Vaccine reduced lung inflammation to allergens in lab and animal tests
If you’re allergic to dust mites (and chances are you are), help may be on the way.
Researchers at the University of Iowa have developed a vaccine that can combat dust-mite allergies by naturally switching the body’s immune response. In animal tests, the nano-sized vaccine package lowered lung inflammation by 83 percent despite repeated exposure to the allergens, according to the paper, published in the AAPS (American Association of Pharmaceutical Scientists) Journal. One big reason why it works, the researchers contend, is because the vaccine package contains a booster that alters the body’s inflammatory response to dust-mite allergens.
“What is new about this is we have developed a vaccine against dust-mite allergens that hasn’t been used before,” says Aliasger Salem, professor in pharmaceutical sciences at the UI and a corresponding author on the paper.
Dust mites are ubiquitous, microscopic buggers who burrow in mattresses, sofas, and other homey spots. They are found in 84 percent of households in the United States, according to a published, national survey. Preying on skin cells on the body, the mites trigger allergies and breathing difficulties among 45 percent of those who suffer from asthma, according to some studies. Prolonged exposure can cause lung damage.
Treatment is limited to getting temporary relief from inhalers or undergoing regular exposure to build up tolerance, which is long term and holds no guarantee of success.
“Our research explores a novel approach to treating mite allergy in which specially-encapsulated miniscule particles are administered with sequences of bacterial DNA that direct the immune system to suppress allergic immune responses,” says Peter Thorne, public health professor at the UI and a contributing author on the paper. “This work suggests a way forward to alleviate mite-induced asthma in allergy sufferers.”
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The paper’s first author is Vijaya Joshi, a graduate fellow in pharmacy at the UI. Contributing authors, all from the UI, include Andrea Dodd, Xuefang Jing, Amaraporn Wongrakpanich and Katherine Gibson-Corley.
The National Institutes of Health (grant numbers: P30 ES005605, R21 CA1 13345-01, R21 CA1 28414-01), the American Cancer Society and the UI’s Lyle and Sharon Bighley professorship funded the research.

redOrbit Staff & Wire Reports – Your Universe Online

Despite the complex structure of the human genome, more than 90 percent of it has no important biological function, scientists from Oxford University report in research published in the July 24 edition of the journal PLOS Genetics.

In fact, according to the study authors, just 8.2 percent of the genome is actively operating to make us who we are and keep our cellular systems functioning. The rest, Telegraph science correspondent Sarah Knapton wrote on Friday, is a mixture of leftover material from our evolutionary past, or has no function whatsoever.

The new percentage is a far cry from previous claims, made by ENCODE (Encyclopedia of DNA Elements) project scientists in 2012, that 80 percent of the human genome possessed some type of biochemical function. The Oxford researchers noted that those controversial claims left many experts disputing the ENCODE’s team’s broad definition of function, and that it should be demonstrated that activity occurring on DNA has a reason for taking place.

In reaching the 8.2 percent figure, the authors of the PLOS Genetics study said they worked to identify how much of the genome has avoided changing or evolving over the past 100 million years, as this serves to indicate these pieces of genetic code possess some important function which needs to be preserved and maintained.

“This is in large part a matter of different definitions of what is ‘functional’ DNA,” joint senior author Professor Chris Pointing of Oxford’s MRC Functional Genomics Unit said in a statement. “We don’t think our figure is actually too different from what you would get looking at ENCODE’s bank of data using the same definition for functional DNA.”

“But this isn’t just an academic argument about the nebulous word ‘function’. These definitions matter,” he added. “When sequencing the genomes of patients, if our DNA was largely functional, we’d need to pay attention to every mutation. In contrast, with only 8 percent being functional, we have to work out the 8 percent of the mutations detected that might be important. From a medical point of view, this is essential to interpreting the role of human genetic variation in disease.”

Of the functional 8.2 percent, slightly more than one percent of human DNA accounts for the proteins required to carry out nearly all of the body’s essential biological processes, Knapton said. The other seven percent is believed to play a role in activating or deactivating genes that encode proteins in response to various factors, at different times and in different regions of the body. These are known as the control and regulation elements.

Researchers Chris Rands, Stephen Meader, Chris Ponting and Gerton Lunter used a computational approach to compare the complete DNA sequences of humans with those of other mammals, including mice, rabbits, dogs and horses. Their plan was to find where chunks of DNA were inserted into or deleted from the mammals’ genome, which occurred randomly except when natural selection acted in order to preserve DNA considered to be functional.

“We found that 8.2 percent of our human genome is functional,” concluded Dr. Gerton Lunter from the Wellcome Trust Centre for Human Genetics at Oxford. “We cannot tell where every bit of the 8.2 percent of functional DNA is in our genomes, but our approach is largely free from assumptions or hypotheses. For example, it is not dependent on what we know about the genome or what particular experiments are used to identify biological function.”

University of Cambridge

The age at which girls reach sexual maturity is influenced by ‘imprinted’ genes, a small sub-set of genes whose activity differs depending on which parent passes on that gene, according to new research published this week in the journal Nature.

The findings come from an international study of more than 180,000 women involving scientists from 166 institutions worldwide, including the University of Cambridge. The researchers identified 123 genetic variations that were associated with the timing of when girls experienced their first menstrual cycle by analyzing the DNA of 182,416 women of European descent from 57 studies. Six of these variants were found to be clustered within imprinted regions of the genome.

Lead author Dr. John Perry at the Medical Research Council (MRC) Epidemiology Unit, University of Cambridge says: “Normally, our inherited physical characteristics reflect a roughly average combination of our parents’ genomes, but imprinted genes place unequal weight on the influence of either the mother’s or the father’s genes. Our findings imply that in a family, one parent may more profoundly affect puberty timing in their daughters than the other parent.”

The activity of imprinted genes differs depending on which parent the gene is inherited from – some genes are only active when inherited from the mother, others are only active when inherited from the father. Both types of imprinted genes were identified as determining puberty timing in girls, indicating a possible biological conflict between the parents over their child’s rate of development. Further evidence for the parental imbalance in inheritance patterns was obtained by analyzing the association between these imprinted genes and timing of puberty in a study of over 35,000 women in Iceland, for whom detailed information on their family trees were available.

This is the first time that it has been shown that imprinted genes can control rate of development after birth.

Dr. Perry says: “We knew that some imprinted genes control antenatal growth and development – but there is increasing interest in the possibility that imprinted genes may also control childhood maturation and later life outcomes, including disease risks.”

Senior author and pediatrician Dr. Ken Ong at the MRC Epidemiology Unit says: “There is a remarkably wide diversity in puberty timing – some girls start at age 8 and others at 13. While lifestyle factors such as nutrition and physical activity do play a role, our findings reveal a wide and complex network of genetic factors. We are studying these factors to understand how early puberty in girls is linked to higher risks of developing diabetes, heart disease and breast cancer in later life – and to hopefully one day break this link.”

Dr. Anna Murray, a co-author from the University of Exeter Medical School, adds: “We found that there are hundreds of genes involved in puberty timing, including 29 involved in the production and functioning of hormones, which has increased our knowledge of the biological processes that are involved, in both girls and boys.”

The study was supported in the UK by the Medical Research Council and the Wellcome Trust.

April Flowers for redOrbit.com – Your Universe Online

It isn’t unusual to see articles in the newspaper and online showing which US cities have the best housing, which are best for retirees, and which are the friendliest for your pets. The newest in this trend is a study released by the US National Bureau of Economic Research which reveals the unhappiest cities in the country. Despite the unhappiness quotient of these cities, the researchers were surprised to find that young people were still willing to relocate to them for job opportunities or lower housing prices.

Professor Joshua Gottlieb of the University of British Columbia’s Vancouver School of Economics led the study, which relies on a large survey that queries respondents about life satisfaction. The survey data, collected from the General Social Survey (GSS), the National Survey of Families and Households (NSFH), and the US Centers for Disease Control and Prevention (CDC), show that New York City tops the list of unhappy cities. According to Time.com contributor Sam Frizell, this is despite the more than 1 million inhabitants being amongst the highest paid people in the country. The researchers postulated that people in unhappy cities are paid more “presumably as compensation for their misery.”

Gottlieb and his colleagues Edward Glaeser and Oren Ziv from Harvard University said that life satisfaction is often interpreted as a measure of happiness, and the seeming contradiction of choosing to live in a city that is unhappy indicates that some people are willing to trade life satisfaction and happiness for higher incomes or lower housing costs.

“Our research indicates that people care about more than happiness alone, so other factors may encourage them to stay in a city despite their unhappiness,” Gottlieb said. “This means that researchers and policy-makers should not consider an increase in reported happiness as an overriding objective.”

The Daily Mail reports that the researchers looked at urban decline as a possible source of the unhappiness. “Self-reported unhappiness is high in [many] declining cities, and this tendency persists even when we control for income, race and other personal characteristics,” the authors write. They report finding at least three examples in which urban decline is correlated with unhappiness.

“Differences in happiness and subjective well-being across space weakly support the view that the desires for happiness and life satisfaction do not uniquely drive human ambitions,” the authors write.

“If we choose only that which maximized our happiness, then individuals would presumably move to happier places until the point where rising rents and congestion eliminated the joys of that locale.”

The study findings included the four top ten lists: Happiest metropolitan areas with a population over 1 million, Unhappiest metropolitan areas with a population over 1 million, Happiest American regions, and Least happy American regions. The number one city in each category, respectively, are: Richmond-Petersburg, VA; New York City, NY; Charlottesville, VA; and Scranton, PA.

By Richard Harth, Arizona State University

On July 5, 2011, a massive wall of dust,  (“haboob,” in Arabic), blanketed Phoenix, Arizona, creating an awesome spectacle, (or stubborn nuisance, depending on your perspective). Dust storms are a common occurrence in the arid desert environments of the American Southwest.

But windborne dust can be a serious health risk, lofting spores of a sometimes-lethal fungus known as Coccidioides. The resulting ailment, known as coccidioidomycosis or Valley fever, has been perplexing researchers since it was first described in 1892. It is currently on an alarming ascent in the United States.

Dr. Stephen Albert Johnston, Krupa Navalkar and their colleagues at Arizona State University’s Biodesign Institute have been investigating Valley fever. Navalkar is the lead author of a new study describing a promising strategy known as immunosignaturing, which can provide clinicians with an accurate identification of Valley fever, a potentially serious affliction that is often misdiagnosed.

“The incidence of this disease is seemingly low due to non-sensitive diagnostic assays,” Navalkar says. As Johnston further notes, “immunosignatures could easily change those false assumptions if made available in the clinical setting.”

Navalkar is a researcher in Biodesign’s Center for Innovations in Medicine, under the direction of Stephen Albert Johnston, who is also a co-author of the new study.

The group’s findings appear in the current issue of the journal ASM Clinical and Vaccine Immunology.

Valley fever is a fungal respiratory infection. It can be acquired when microscopic spores of the soil-dwelling fungus are inhaled. Two forms of the fungus exist, Coccidioides immitis and Coccidioides posadasii. They are endemic to regions of Arizona, New Mexico, California, Nevada, Utah, Texas and northern Mexico.

During extended periods of dryness, the fungal spores remain dormant. With rainfall, the spores or arthroconidia develop elongated filaments, which break off and can be lofted into the air by soil disruption due to farming, construction, earthquakes or dust storms.

Most individuals inhaling Coccidioides particles are assumed to be able to naturally resolve the infection, developing immunity to future spore infections. Often such non-symptomatic individuals are unaware they have been exposed. Others are not so fortunate, however.

In around 40 percent of cases, Valley fever causes flu-like symptoms including cough, headache, muscle and joint pain and rash. For reasons still unclear, those of Filipino, African American and Native American descent are more vulnerable to the severe disseminated form of the infection. The disease is also more severe in people with weakened immune systems as well as pregnant women.

Infection with Coccidioides can progress through three stages of increasing severity. Valley fever is the acute form of the disease, which, if left untreated, can develop into a second-stage chronic infection, lasting months or years. This form affects roughly 40 percent of those exposed. The third stage of the disease, known as disseminated Coccidioides, occurs when the infection spreads throughout the body, affecting skin, bones and nervous system and causing skin ulcers, swollen joints and severe pain, abscesses, bone lesions, heart inflammation, urinary tract infection and (potentially lethal) meningitis. Disseminated Coccidioides affects 5-10 percent of those with chronic infection.

The rapid rise in Valley fever cases in the arid southwest has become a serious health concern, as human habitation has pushed further into desert areas where the soil spores are widespread. Currently, Valley fever affects an estimated 150,000 people a year, with most cases occurring in Arizona, California, Nevada, New Mexico and Utah. The disease has no cure at present and is notoriously tricky to diagnose. One reason is that Valley fever is readily confused with other community-acquired pneumonias.

Currently, diagnosis is carried out through a technique known as immunodiffusion, which tests the blood for antibodies against Coccidioidal antigens. As the authors note, such tests are less than satisfactory, with a false negative rate as high as 50-70 percent. Around 5 percent of symptomatic patients display no measurable antibody levels to Valley fever by immunodiffusion.

The current study describes an alternate method used to address the poor accuracy of immunodiffusion, applying an innovative new technique known as ‘Immunosignaturing’. The technique can produce a detailed profile of system-wide immune activity from a small droplet of blood—typically, less than a microliter.

To produce its detailed immune portrait or immunosignature, the technique uses a microarray platform. This consists of a glass slide imprinted with 10,000 peptides. Each peptide consists of a string of 20 amino acids, randomly arranged. The power of the technology resides in the fact that the randomly generated peptides are not based on natural antigens to Coccidioides or indeed, any disease. They are “unbiased”  to the nature of particular disease antibodies and can therefore act as a sort of universal diagnostic.

When a droplet of antibody-containing blood is smeared across the microarray, the random peptides behave like naturally occurring antigens, binding with blood antibodies in a specific pattern. Global analysis of the resulting immunosignature is used to establish disease-specific blueprints of immune activity.

The method potentially offers much higher resolution and sensitivity to disease, compared with diagnostic tests measuring a single antibody-antigen binding event or a small ensemble of molecules.

In the first round of experiments in the current study, the group used immunosignatures to determine if Valley fever infected individuals could be accurately distinguished from three other patient groups afflicted with bacterial or fungal infections.

Once an immunosignature for Valley fever was established using the 10K peptide microarray, a smaller diagnostic array was composed from relevant diagnostic peptides. This smaller 96-peptide array was then tested for accuracy against the current immunodiffusion diagnostic standard.

The 10K peptide array successfully distinguished Valley fever from 3 other infections, with 98 percent accuracy. Impressively, the method also was able to classify false negative Valley fever patients in a blinded test, with 100 percent accuracy, easily outpacing existing immunodiffusion methods, which could only identify 28 percent of false negatives.

The smaller, 96 peptide diagnostic array showed less specificity than the 10K peptide array in terms of identifying false negatives. The authors propose that the larger 10K peptide array be used in initial screenings, followed by subarrays with reduced complements of carefully selected peptides, used for clinical diagnosis.

Immunosignaturing holds the promise for rapid, cost-effective and highly accurate diagnosis of Valley fever. The versatile platform has the potential to separate Valley fever patients from those afflicted with other bacterial or fungal infections. Making use of the same microarray, researchers can also identify false negatives with 100 percent accuracy.

Professors Phillip Stafford and Neal Woodburry of the Biodesign Institute also contributed to this study along with Dr. John Galgiani from the Valley Fever Center for Excellence (VFCE).

redOrbit Staff & Wire Reports – Your Universe Online

Scientists have discovered more than 100 genetic risk factors associated with schizophrenia in research that could provide new insight into how the condition is caused and could be the catalyst for new treatment options.

Writing in the journal Nature, an international team of researchers led by Dr. Michael O’Donovan of the Cardiff University School of Medicine conducted what is being called the largest genomic study yet published on any type of psychiatric disorder.

Their efforts have revealed biological mechanisms and pathways that may be linked to schizophrenia, and could lead to the first significant new method of treating the disorder in more than six decades. The research was a multinational, collaborative effort involving over 300 scientists from 35 countries and several years of work.

According to Karen Weintraub of USA Today, the study confirmed that the genes which regulate the brain chemical dopamine were involved in schizophrenia, as experts had predicted. However, it also revealed that genes associated with the body’s immune system, as well as some linked with cigarette smoking, were also involved.

“Some are very familiar genes expressed in nerve cells, and some are results where you scratch your head and you know you have more work to do” in order to understand the role they play in the condition, researcher and Stanley Center for Psychiatric Research director Steven Hyman told Weintraub.

[ Watch the Video: Kick-Starting Schizophrenia Research At Cardiff University ]

He explained that the finding does not prove a causal relationship between schizophrenia and either smoking or inflammation, as genes could play one role in the immune system and a different one in the brain. In all, the genome-wide association study (GWAS) identified 108 specific locations in the human genome that was associated with an increased risk of schizophrenia – including 83 which had not previously been linked to the condition.

“Detecting biological risk factors on this scale shows that schizophrenia can be tackled by the same approaches that have already transformed outcomes for people with other diseases,” Sir Michael Owen, director of the university’s MRC Centre for Neuropsychiatric Genetics and Genomics, said in a statement. “We now believe they can also do so for schizophrenia which has, until now, been so poorly understood.”

“The fact that we were able to detect genetic risk factors on this massive scale shows that schizophrenia can be tackled by the same approaches that have already transformed our understanding of other diseases,” added Dr. O’Donovan in a separate statement. “The wealth of new findings has the potential to kick-start the development of new treatments in schizophrenia, a process which has stalled for the last 60 years.”

The research, which looked at 55 datasets from 40 contributors, also implicated genes active in pathways that control synaptic plasticity, which is a function essential to learning and memory, as well as those governing postsynaptic activity, including voltage-gated calcium channels (which play a role in signaling between cells in the brain).

Despite the promise the research holds, Dr. John Williams, head of neuroscience and mental health at the Wellcome Trust, wrote in The Telegraph that “it would be false to say that genomics work will lead to an imminent breakthrough in terms of a cure for mental illnesses.”

He added that the study reveals “how little we know about schizophrenia, and how far we are from biological tests and treatments for mental health disorders compared to other major diseases,” and that the answer to mental health illnesses such as schizophrenia would not be found solely in a genetic analysis.

“Understanding mental illness is about putting together a hugely complex jigsaw of different types of knowledge,” Dr. Williams concluded. “Gradually, as the picture we are forming becomes clearer, we can design interventions and therapy which will target individuals and their different matrix of symptoms more accurately.”

Rayshell Clapper for redOrbit.com – Your Universe Online

Probiotics work to manage gut flora by controlling the bad bacteria with good bacteria. WebMD reports that probiotics have even been linked to maintaining a strong immune system as well as these other ailments:

• Treating childhood diarrhea
• Treating ulcerative colitis
• Treating necrotizing enterocolitis
• Preventing antibiotic-associated diarrhea
• Preventing infectious diarrhea
• Preventing pouchitis
• Treating and preventing eczema associated with cow’s milk allergy

Probiotics serve many beneficial purposes. They help regulate the gut flora, primarily, but recent studies published in the American Health Association (AHA) journal Hypertension show that probiotics might also help lower and maintain blood pressure.

According to an AHA blog, “Probiotics are live microorganisms (naturally occurring bacteria in the gut) thought to have beneficial effects; common sources are yogurt or dietary supplements.” Many fermented foods such as fermented pickles, cabbage, and milk also contain probiotics. However, the most common ways that people ingest probiotics are through yogurt and dietary supplements.

The study, led by Dr. Jing Sun of the Griffith Health Institute and School of Medicine, Griffith University, Gold Coast, Queensland, Australia, analyzed nine other high-quality studies of 543 adults that examined the relationships between blood pressure and probiotics. Here is what the researchers found:

• Probiotic consumption lowered systolic blood pressure (the top number) by an average 3.56 millimeters of mercury (mm Hg) and diastolic blood pressure (the lower number) by an average 2.38 mm Hg, compared to adults who didn’t consume probiotics.

• The positive effects from probiotics on diastolic blood pressure were greatest in people whose blood pressure was equal to or greater than 130/85, which is considered elevated.

• Consuming probiotics for less than eight weeks didn’t lower systolic or diastolic blood pressure.

• Probiotic consumption with a daily bacteria volume of 109-10 12 colony-forming units (CFU) may improve blood pressure. Consumption with less than 109 CFU didn’t lower blood pressure. CFU is the amount of bacteria or the dose of probiotics in a product.

• Probiotics with multiple bacteria lowered blood pressure more than those with a single bacteria.

While these initial findings are quite positive, the results are not absolute and require more study and focus in order to truly understand the role that probiotics play in blood pressure. As Dr. Sun said, “We believe probiotics might help lower blood pressure by having other positive effects on health, including improving total cholesterol and low-density lipoprotein, or LDL, cholesterol; reducing blood glucose and insulin resistance; and by helping to regulate the hormone system that regulates blood pressure and fluid balance.”

Heart disease is the number one killer of men and women in America. According to the Mayo Clinic, high blood pressure is one form of heart disease and can lead to stroke, dementia, coronary artery disease, or even a heart attack. High blood pressure plays a role in circulation, eye damage, and kidney failure as well. As if these were not bad enough, high blood pressure may lead to sexual dysfunction, sleep problems, and bone loss. And the kicker is people can live with high blood pressure for quite some time without knowing it.

The findings in Dr. Sun’s study are worth looking into more seeing as heart disease plays such a tragic role in many American lives. For more information, see the current edition of the American Heart Association’s journal Hypertension.

> High blood pressure risk calculator

University of Chicago Press Journals

At some point, most kids will hear that drinking milk helps make their bones strong or that fish is food for the brain. But do these messages foster the idea that if something is good for us, it must surely taste bad? According to a new study in the Journal of Consumer Research, when children hear about the benefits of healthy food, they’re less likely to eat it.

“We predicted that when food is presented to children as making them strong or as a tool to achieve a goal such as learning how to read or count, they would conclude the food is not as tasty and therefore consume less of it,” write authors Michal Maimaran (Kellogg School of Management, Northwestern University) and Ayelet Fishbach (University of Chicago Booth School of Business).

To test this idea, the authors conducted five studies with children between the ages of three and five. In all of the studies, the children were read a picture book story about a girl who ate a snack of crackers or carrots. Depending on the experiment, the story either did or did not state the benefits of the snack (making the girl strong or helping her learn how to count). The children were then given the opportunity to eat the food featured in the story and the authors measured how much they ate. The children ate more when they did not receive any message about the foods making them strong or helping them learn how to count.

Brands marketing food items to parents and children can use these results to de-emphasize the benefits of healthy food and focus more on the positive experience of eating the food. These results also help to empower policy makers and medical institutions looking to combat childhood obesity and juvenile diabetes.

“Parents and caregivers who are struggling to get children to eat healthier may be better off simply serving the food without saying anything about it, or (if credible) emphasizing how yummy the food actually is,” the authors conclude.

Michal Maimaran and Ayelet Fishbach. “If It’s Useful and You Know It, Do You Eat? Preschoolers Refrain from Instrumental Food.” Journal of Consumer Research: October 2014.

University of Otago
The mystery of why mycobacteria—a family that includes the microbe that causes TB—are extraordinarily hardy organisms is being unraveled by University of Otago, New Zealand, research that offers new hope for developing a revolutionary class of antibiotics to tackle TB.
In collaboration with researchers in the US and Germany, Otago microbiologists have teased out the mechanisms by which the aerobic soil microbe Mycobacterium smegmatis is able to persist for extreme lengths of time in the absence, or near-absence, of oxygen.
Their findings, published this week in the prestigious US journal PNAS, show that hydrogen is a key factor that enables mycobacteria to survive oxygen-limitation over long periods.
The team, led by Professor Greg Cook, found that in such conditions the bacterium is able to quickly switch its cellular metabolism from a primarily oxygen-based one over to one that uses fermentation for energy production instead.
This metabolic mode depends on the production and recycling of molecular hydrogen, a high-energy fuel and diffusible gas. These cells produce hydrogen to ensure their survival until they once more have access to sufficient oxygen for growth.
Professor Cook says it had long been a puzzle how mycobacteria generate energy when in their oxygen-starved dormant states.
“Mycobacteria grow through combusting their preferred carbon-based fuel sources using oxygen. However, they can also somehow survive for months or years when their oxygen supply is exhausted.
“For example, in people with latent TB infections, Mycobacterium tuberculosis bacteria are walled in by clumps of immune and other body cells in what is thought to be an extremely low oxygen environment. However, such patients must be monitored for the rest of their lives in case the bacteria become active again,” he says.
Professor Cook’s team have established that Mycobacterium smegmatis metabolizes molecular hydrogen using three enzymes called hydrogenases. One hydrogenase produces hydrogen, whereas the other two consume it. These hydrogenases are activated under oxygen starvation by a master regulator called DosR.
The researchers found that strains of Mycobacterium smegmatis in which the genes for the hydrogenases or the regulator DosR had been ‘knocked out’ experienced a hundredfold reduction in the long-term survival compared to the normal bacterium, he says.
His team is currently testing whether these findings are extendable to Mycobacterium tuberculosis, which activates a further predicted hydrogenase under low oxygen conditions.
“If knocking out this other hydrogenase also drastically reduces long-term survival, the enzyme might end up being an excellent next-generation drug target in latent TB infections, which around one-third of the world’s population suffer.”
The Otago researchers’ studies on hydrogen fermentation in mycobacteria have been performed in collaboration with Professor William Jacobs Jr., a world-leading bacterial geneticist at the Albert Einstein College of Medicine in New York, who is known as the ‘TB terminator’.
One of the paper’s lead authors is Dr Michael Berney, a former research fellow in Professor Cook’s laboratory who is now an Assistant Professor associated with Professor Jacobs’ laboratory. The other co-authors include Professor Cook, Dr Chris Greening, who also co-led the study and recently completed his PhD studies in the Cook Laboratory, and Professor Dr Ralf Conrad, director of the Max-Planck Institute for Terrestrial Microbiology in Marburg, Germany.
The research was funded by the Royal Society of New Zealand’s Marsden Fund.

University of Colorado Denver

According to the Centers for Disease Control, approximately four out of five black women are overweight or obese and 36 percent meet physical activity objectives as determined by the CDC. That’s compared to 50 percent of white women meeting the same objectives.

A study conducted by the Center for African American Health and the University of Colorado School of Medicine’s Center for Women’s Health Research finds that African American women whose hairstyle is affected by perspiration may avoid physical activity altogether. Prior studies have found that between 29 percent and 48 percent of African American women say that their hairstyle was a factor in deciding whether or not to exercise. One key focus of this study was to learn more about cultural barriers to physical activity among African American women — including hairstyle-related factors. Some women involved in the study who experience hairstyle barriers to physical activity explained that it can take too much time or money to restyle their hair after exercise that causes perspiration. Although hairstyle maintenance barriers were reported less frequently than the most highly rated general barriers of “lacking self-discipline” and “lacking money”, they are important to understand in order to inform future interventions for the substantial number of sedentary AA women affected by hairstyle maintenance barriers.

What researchers found is that lower rates of exercise may be related to cultural barriers, including the costs and time required to restyle hair after exercise that causes perspiration. To reduce the time needed to restyle hair after exercise, some participants reported using “low-maintenance” hairstyles such as wearing braids or ponytails. In addition, some women described being cautious to do “safe” physical activities that do not cause perspiration, in order to overcome this barrier. This study found that 29 percent of African American women who did not exercise regularly experienced hairstyle barriers to exercise. In contrast, only 7 percent of African American women who exercised regularly reported their hair was a factor in deciding whether to exercise.

“After a couple of new health diagnoses, one of our study participants said she had to make a decision between her hair and her life,” said Lucille Johnson Campbell, MA, director of special initiatives for the Center for African-American Health and co-principal investigator for the study. “We want to find solutions so women in the African American community can get through these barriers and improve their health.”

Researchers assessed the health of participants and then used surveys and focus groups to identify hairstyle-related physical activity barriers and physical activity motivators. The study included 51 women from the Denver metro area ranging in age from 18 to 75 years. “The lifespan perspective from women of varying ages allowed for a greater range of discussion into understanding if hair influenced physical activity throughout generations,” said study investigator, Candace Brown, MAG, MEd, Doctoral Candidate at Virginia Commonwealth University.

The women were divided into two categories – “exercises” and “non-exercisers.” The “exercisers” reported at least 60 minutes of weekly activity and the “non-exercisers” reported less than 60 minutes. Both groups reported similar rates of diabetes, pre-diabetes, and arthritis.

“There is some exciting news from this study,” said Amy Huebschmann, MD, associate professor at CU School of Medicine and the Center for Women’s Health Research and co-principal Investigator for this study. “African American women want to overcome these barriers to exercise, and we studied many African American women who have already overcome these barriers by adjusting their hairstyles. The next step is to develop and test programs to overcome general barriers and hairstyle-related barriers.” Study participants suggested various activities to get them moving, including dance classes and other fun group activities. They also suggested other helpful strategies to overcome hairstyle-related barriers to physical activity: social support from other African American women and culturally relevant education about moisturizing hair products to combat the dry Colorado climate and “low-maintenance” hairstyles that are minimally affected by perspiration.

Huebschmann added that a recent societal culture shift may also help African American women to overcome hairstyle barriers to activity. “We had some women describe concerns of getting fired if they came to work with a low-maintenance hairstyle such as braids or natural hair, but we also heard women saying that they feel there is a growing cultural acceptance of these types of low-maintenance hairstyles.”

Rayshell Clapper for redOrbit.com – Your Universe Online
Picture this: You pick up your cell phone to call a close family member, someone you know well and speak with on the phone often. Every time, you physically enter the phone number; you know this number by heart and have for many years. Suddenly, though, you can’t remember the number to save your life. You stare at the phone, bewildered by the forgotten number. Frustration seeps in, and you feel your age.
Aging is not easy. First we notice wrinkles and skin issues. Then we move on to vision problems and aching bones and joints. Then the cognitive problems and issues begin. And the older we get, the worse many of these issues become. Most specifically, we struggle with cognitive processes and abilities, which is definitely the most frustrating. Things that were once easy to do and remember are no longer, all thanks to the aging process. But is there hope?
According to the Association for Psychological Science, the cognitive glass is not as half empty as once thought. In fact, it is definitely more half full. In a recent edition of Perspectives in Psychological Science, several articles identify three ways that cognitive aging is not as bleak as once thought.
1. Motivation, Motivation, Motivation
In the first article, motivation is key to keeping cognitive abilities sharp. In other words, the more motivated we are to challenge our cognition, the better off we will be. The study findings by North Carolina State University psychological scientist Thomas Hess show the following about motivation and cognitions:
“If the cognitive cost of engaging in difficult tasks increases as we age, older adults may be less motivated to expend limited cognitive resources on difficult tasks or on tasks that are not personally relevant to them. This selectivity, Hess argues, may allow older adults to improve performance on the tasks they do choose to engage in, thereby helping to account for inconsistencies between lab-based and real-world data.”
In other words, by picking and choosing what tasks to engage in, aging adults use their motivation to improve performances. We know that motivation is key in physical exercise, so it only stands to reason that it is also in mental exercise.
2. Bittersweet Memory
Memories are often flawed because we can’t remember things perfectly, exactly as the experiences happened. It turns out that prior knowledge (in other words memory) plays a difficult role in cognition. On the one hand, it fills in gaps when adults struggle with failure of episodic memory. However, on the other, it may also prevent learning and retaining new knowledge. The researchers, Sharda Umanath and Elizabeth Marsh of Duke University, state that more research is necessary to truly understand the roles that memory and prior knowledge play in cognitive abilities.
3. Fraud Alert
We hear on the news and from academics and professionals how older adults are prime victims of consumer fraud due to their aging cognition issues. However, another article states the following:
“Psychological scientists Michael Ross, Igor Grossmann, and Emily Schryer of the University of Waterloo in Canada review the available data to examine whether incidences of consumer fraud are actually higher among older adults. While there isn’t much research that directly answers this question, the research that does exist suggests that older adults may be less frequent victims than other age groups.”
These psychological scientists explain that older adults are no less vulnerable to fraud than others, or at least there is no evidence of this. Instead of focusing on scaring older adults, fraud prevention needs to be focused on consumers of all ages, and this only makes sense. Identity theft happens to people of all ages, young or old, child or adult.

University of Oxford
Cancer has left its ‘footprint’ on our evolution, according to a study which examined how the relics of ancient viruses are preserved in the genomes of 38 mammal species.
Viral relics are evidence of the ancient battles our genes have fought against infection. Occasionally the retroviruses that infect an animal get incorporated into that animal’s genome and sometimes these relics get passed down from generation to generation – termed ‘endogenous retroviruses’ (ERVs). Because ERVs may be copied to other parts of the genome they contribute to the risk of cancer-causing mutations.
Now a team from Oxford University, Plymouth University, and the University of Glasgow has identified 27,711 ERVs preserved in the genomes of 38 mammal species, including humans, over the last 10 million years. The team found that as animals increased in size they ‘edited out’ these potentially cancer-causing relics from their genomes so that mice have almost ten times as many ERVs as humans. The findings offer a clue as to why larger animals have a lower incidence of cancer than expected compared to smaller ones, and could help in the search for new anti-viral therapies.
A report of the research is published in the journal PLOS Pathogens.
“We set out to find as many of these viral relics as we could in everything from shrews and humans to elephants and dolphins,” said Dr Aris Katzourakis of Oxford University’s Department of Zoology, lead author of the report. “Viral relics are preserved in every cell of an animal: Because larger animals have many more cells they should have more of these endogenous retroviruses (ERVs) – and so be at greater risk of ERV-induced mutations – but we’ve found this isn’t the case. In fact larger animals have far fewer ERVs, so they must have found ways to remove them.”
A combination of mathematical modelling and genome research uncovered some striking differences between mammal genomes: mice (c.19 grams) have 3331 ERVs, humans (c.59 kilograms) have 348 ERVs, whilst dolphins (c.281 kilograms) have just 55 ERVs.
“This is the first time that anyone has shown that having a large number of ERVs in your genome must be harmful – otherwise larger animals wouldn’t have evolved ways of limiting their numbers,” said Dr Katzourakis. “Logically we think this is linked to the increased risk of ERV-based cancer-causing mutations and how mammals have evolved to combat this risk. So when we look at the pattern of ERV distribution across mammals it’s like looking at the ‘footprint’ cancer has left on our evolution.”
Dr Robert Belshaw of Plymouth University Peninsula Schools of Medicine and Dentistry, School of Biomedical and Healthcare Sciences, added: “Cancer is caused by errors occurring in cells as they divide, so bigger animals – with more cells – ought to suffer more from cancer. Put simply, the blue whale should not exist. However, larger animals are not more prone to cancer than smaller ones: this is known as Peto’s Paradox (named after Sir Richard Peto, the scientist credited with first spotting this). A team of scientists at Oxford, Plymouth and Glasgow Universities had been studying endogenous retroviruses, viruses like HIV but which have become part of their host’s genome and which in other animals can cause cancer. Surprisingly, they found that bigger mammals have fewer of these viruses in their genome. This suggests that similar mechanism might be involved in fighting both cancer and the spread of these viruses, and that these are better in bigger animals (like humans) than smaller ones (like laboratory mice).”
ERVs that are immediately harmful to an animal tend not be passed on, what makes them troublesome is that having arrived at one location in a genome the replication process means they can be copied across, ‘jumping’, to somewhere else. ERVs can, for example, ‘jump’ into the middle of gene machinery responsible for suppressing tumors, damaging it and ratcheting up the risk of mutations turning into cancer.
“We know that some cancers, such as t-cell leukaemia, are directly linked to retroviruses but a lot of the time ERVs contribute to the number of things that need to go wrong in cells for cancers to arise,” said Dr Katzourakis. “As animals get bigger so the number of cells increases and there are more opportunities for things to go wrong, so there is an evolutionary pressure for larger animals to reduce the number of ERVs.”
Dr Gkikas Magiorkinis of Oxford University’s Department of Zoology, an author of the report, said: “We know that taller people have higher risk for some cancers, which fits our study about ERVs posing evolutionary pressure through cancer. Yet we still have no evidence that ERVs might have causal links with cancer in humans, even though they clearly cause cancers in other animals such as mice. We need to search in a more systematic way to see if ERVs cause cancer in humans, and our study suggests that viral pathogenic mechanisms in larger animals like humans would be more complex than those observed in smaller animals.”
Dr Robert Belshaw of Plymouth University Peninsula Schools of Medicine and Dentistry, School of Biomedical and Healthcare Sciences, added: “Cancer is caused by errors occurring in cells as they divide, so bigger animals – with more cells – ought to suffer more from cancer. Put simply, the blue whale should not exist. However, larger animals are not more prone to cancer than smaller ones: this is known as Peto’s Paradox (named after Sir Richard Peto, the scientist credited with first spotting this). A team of scientists at Oxford, Plymouth and Glasgow Universities had been studying endogenous retroviruses, viruses like HIV but which have become part of their host’s genome and which in other animals can cause cancer. Surprisingly, they found that bigger mammals have fewer of these viruses in their genome. This suggests that similar mechanism might be involved in fighting both cancer and the spread of these viruses, and that these are better in bigger animals (like humans) than smaller ones (like laboratory mice).”
The research suggests that larger creatures must have more effective anti-viral genes and resources than smaller ones and, if these can be identified, in the future it may be possible to mimic these mechanisms to produce new anti-viral therapies.
The new study is relevant to Peto’s Paradox, an observation made by Sir Richard Peto that the incidence of cancer does not appear to correlate with the number of cells in an organism. “Our work doesn’t solve Peto’s paradox as a whole but is has solved it in respect of infection,” said Dr Katzourakis.

Michigan State University

Not unlike looking for the proverbial needle in a haystack, a team of Michigan State University researchers have found a gene that could be key to the development of stem cells – cells that can potentially save millions of lives by morphing into practically any cell in the body.

The gene, known as ASF1A, was not discovered by the team. However, it is at least one of the genes responsible for the mechanism of cellular reprogramming, a phenomenon that can turn one cell type into another, which is key to the making of stem cells.

In a paper published in the journal Science, the researchers describe how they analyzed more than 5,000 genes from a human egg, or oocyte, before determining that the ASF1A, along with another gene known as OCT4 and a helper soluble molecule, were the ones responsible for the reprogramming.

“This has the potential to be a major breakthrough in the way we look at how stem cells are developed,” said Elena Gonzalez-Munoz, a former MSU post-doctoral researcher and first author of the paper. “Researchers are just now figuring out how adult somatic cells such as skin cells can be turned into embryonic stem cells. Hopefully this will be the way to understand more about how that mechanism works.”

In 2006, an MSU team identified the thousands of genes that reside in the oocyte. It was from those, they concluded, that they could identify the genes responsible for cellular reprogramming.

In 2007, a team of Japanese researchers found that by introducing four other genes into cells, stem cells could be created without the use of a human egg. These cells are called induced pluripotent stem cells, or iPSCs.

“This is important because the iPSCs are derived directly from adult tissue and can be a perfect genetic match for a patient,” said Jose Cibelli, an MSU professor of animal science and a member of the team.

The researchers say that the genes ASF1A and OCT4 work in tandem with a ligand, a hormone-like substance that also is produced in the oocyte called GDF9, to facilitate the reprogramming process.

“We believe that ASF1A and GDF9 are two players among many others that remain to be discovered which are part of the cellular-reprogramming process,” Cibelli said.

“We hope that in the near future, with what we have learned here, we will be able to test new hypotheses that will reveal more secrets the oocyte is hiding from us,” he said. “In turn, we will be able to develop new and safer cell-therapy strategies.”

Hasan Otu of the University of Nebraska-Lincoln is also a member of the research team.

Kristen Kusek, Harvard University
New genome editing tool offers strategy to manage insect-borne disease
A cross-disciplinary team is calling for public discussion about a potential new way to solve longstanding global ecological problems by using an emerging technology called “gene drives.” The advance could potentially lead to powerful new ways of combating malaria and other insect-borne diseases, controlling invasive species and promoting sustainable agriculture.
Representing Harvard Medical School, the Wyss Institute for Biologically Inspired Engineering at Harvard University, Harvard School of Public Health, the Massachusetts Institute of Technology (MIT), Boston University, the Wilson Center, and Arizona State University, the team includes scientists working in disciplines ranging from genome engineering to public health and ecology, as well as risk and policy analysis.
Engineered gene drives are genetic systems that circumvent traditional rules of sexual reproduction and greatly increase the odds that the drive will be passed on to offspring. This enables the spread of specified genetic alterations through targeted wild populations over many generations. They represent a potentially powerful tool to confront regional or global challenges, including control of invasive species and eradication of insect-borne diseases such as malaria and dengue.
The idea is not new, but the Harvard-based researchers have now outlined a technically feasible way to build gene drives that potentially could spread almost any genomic change through populations of sexually reproducing species.
“We all rely on healthy ecosystems and share a responsibility to keep them intact for future generations,” said Kevin Esvelt, Wyss Institute Technology Development Fellow and lead author of two papers published last week. “Given the broad potential of gene drives to address ecological problems, we hope to initiate a transparent, inclusive and informed public discussion—well in advance of any testing—to collectively decide how we might use this technology for the betterment of humanity and the environment.”
Following discussion of the technology’s widespread implications at an NSF-sponsored workshop organized by the Woodrow Wilson Center and MIT in January 2014, the team wrote two related papers. The first, published in eLife, describes the proposed technical methods of building gene drives in different species, defines their theoretical capabilities and limitations, and outlines possible applications. The second, featured in Science, provides an initial assessment of potential environmental and security effects, an analysis of regulatory coverage and recommendations to ensure responsible development and testing prior to use. The authors also described key features of gene drives in a Scientific American blog post.
The new technical work in eLife builds upon research by Austin Burt of Imperial College London, who, more than a decade ago, first proposed using a type of gene drive based on cutting DNA to alter populations. The authors note that the versatile gene editing tool called CRISPR, which was recently co-developed by some of the same researchers at Harvard and the Wyss Institute and makes it possible to precisely insert, replace and regulate genes, now makes it feasible to create gene drives that work in many different species.
“Our proposal represents a potentially powerful ecosystem management tool for global sustainability, but one that carries with it new concerns, as with any emerging technology,” said George Church, professor of genetics at Harvard Medical School, Wyss Core Faculty member, and coauthor on both publications.
Esvelt noted that the genomic changes made by gene drives should be reversible. The team has outlined in the eLife publication numerous precautionary measures intended to guide the safe and responsible development of gene drives, many of which were not possible with earlier technologies.
“If the public ever considers making use of a gene drive, we will need to develop appropriate safeguards. Ensuring that we have a working reversal drive on hand to quickly undo the proposed genomic change would be one such precaution,” he said.
Because the drives can spread traits only over generations, they will be most effective in species that reproduce quickly or can be released in large numbers. For insects, it could take only a couple of years to see a desired change in the population at large, while slower-reproducing organisms would require much longer. Altering human populations is not feasible because it would require many centuries.
Gene drives could strike a powerful blow against malaria by altering mosquito populations so that they can no longer spread the disease, which kills 650,000 people every year and sickens hundreds of millions. They might also be used to rid local environments of invasive species or to pave the way toward more sustainable agriculture by reversing mutations that allow particular weed species, such as horseweed, to resist herbicides that are important for no-till farming.
The innovative nature of gene drives poses regulatory challenges. “Simply put, gene drives do not fit comfortably within existing U.S. regulations and international conventions,” said political scientist Kenneth Oye, author of the Science paper and director of the MIT Program on Emerging Technologies. “For example, animal applications of gene drives would be regulated by the FDA as veterinary medicines. Potential implications of gene drives fall beyond the purview of the lists of bacteriological and viral agents that now define security regimes. We’ll need both regulatory reform and public engagement before we can consider beneficial uses. That is why we are excited about getting the conversation on gene drives going early.”
“Many different groups and the interested public will need to come together to ensure that gene drives are developed and used responsibly,” said James P. Collins, an evolutionary ecologist at Arizona State University and senior author of the Science paper. Collins was formerly the assistant director for biological sciences at the National Science Foundation.
“Understanding how populations and ecosystems will respond to different alterations and addressing potential security concerns will require sustained multidisciplinary work by teams of biological engineers, ecologists, instrumentation specialists, social scientists and the public,” Collins said. “The eLife and Science articles provide a model for the next steps that need to be taken.”

Tracey Bryant, University of Delaware

University of Delaware researchers have identified a protein, hiding in plain sight, that acts like a bodyguard to help protect and stabilize another key protein, that when unstable, is involved in Crohn’s disease. The fundamental research points to a possible pathway for developing an effective therapy for the inflammatory bowel disease.

The research, by Catherine Leimkuhler Grimes, assistant professor of chemistry and biochemistry at UD, and Vishnu Mohanan, doctoral student in biological sciences, is published in the July 4 issue of the Journal of Biological Chemistry. The study was funded by a grant from the National Institutes of Health (NIH).

As the scientists point out, our immune system provides the first line of defense against invading pathogens, a task even more challenging in the human gut, where over a trillion commensal bacteria live — resident microorganisms that help convert food into protein, vitamins and minerals.

To distinguish “bad” versus “good” bacteria, our bodies rely on a complex network of receptors that can sense patterns that are unique to bacteria, such as small fragments of bacterial cell wall. The receptors recognize and bind to these fragments, triggering an immune response to take out the “bad guys” or control the growth of the “good guys.”

However, when one of these receptors breaks down, or mutates, an abnormal immune response can occur, causing the body to mount an immune response against the “good” bacteria. Chronic inflammatory disorders, such as Crohn’s disease, are hypothesized to arise as a result.

The UD team focused on a protein called NOD2 — nucleotide-binding oligomerization domain containing protein 2. More than 58 mutations in the NOD2 gene have been linked with various diseases, and 80 percent of these mutations are connected specifically to Crohn’s disease, according to Grimes.

In experiments to unveil NOD2’s signaling mechanisms and where they break down, “we stumbled on this chaperone molecule,” says Mohanan, who was the lead author of the scientific article.

The chaperone molecule was HSP70, which stands for “heat shock protein 70.” It assists with the folding of proteins into their correct three-dimensional shapes, even when cells are under stress from elevated body temperatures, such as a fever.

Grimes said she was a little skeptical at first about pursuing studies with HSP70 because it is a commonly known protein, but she found Mohanan’s initial data intriguing.

“Vishnu found that if we increased the expression level of HSP70, the NOD2 Crohn’s mutants were able to respond to bacterial cell wall fragments. A hallmark of the NOD2 mutations is inability to respond to these fragments. Essentially, Vishnu found a fix for NOD2, and we wanted to determine how we were fixing it.”

In further experiments, Mohanan created a tagged-wild-type NOD2 cell line in which NOD2 levels nearly matched the levels found in nature (versus “super” levels that might stimulate an artificial response) and found that NOD2 became more stabilized and degraded more slowly when treated with HSP70. In fact, HSP70 increased the half-life of NOD2 by more than four hours.

> Read More…

Sanford-Burnham Medical Research Institute
Study finds that the NBR1 protein plays a critical role in regulating obesity-induced inflammation that leads to metabolic disease
A new study by researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) has identified a new signal that triggers the events leading to insulin resistance in obesity. The signal causes inflammation in adipose tissue and leads to metabolic disease. The study, published July 17 in Cell Metabolism, suggests that blocking this signal may protect against the development of metabolic disease, type 2 diabetes, and other disorders caused by obesity-linked inflammation.
“We have uncovered a precise mechanism that explains how inflammation occurs in obesity,” said Jorge Moscat, Ph.D., professor and director of the Cell Death and Survival Networks Program at Sanford-Burnham. “The results are important because we know that inflammation of the fat tissue causes insulin resistance, a risk factor for metabolic syndrome and a primary feature of type 2 diabetes. If we can inhibit obesity-linked inflammation, we may be able to prevent the metabolic abnormalities, including type 2 diabetes, associated with obesity,” said Maria Diaz-Meco, Ph.D., from the same Program at Sanford-Burnham and co-director of this study.
NBR1 protein triggers inflammation
The researchers initiated their study by comparing levels of the NBR1 protein in healthy men and women with a wide range of body mass index (BMI) and fatness, to levels in men with metabolic syndrome. NBR1 is an inflammatory signaling molecule originally discovered in the labs of Moscat and Maria Diaz-Meco. Metabolic syndrome is a clinical classification of a combination of health problems—including insulin resistance—that are linked to an increased risk of diabetes and early heart disease.
The analysis found that men with metabolic syndrome had higher levels of NBR1 that correlated with metabolic alterations and markers of inflammation, providing the initial clue that NBR1 plays a role in obesity-linked inflammation and metabolic syndrome.
How NBR1 works
To understand how NRB1 works, the research team fed mice in which NBR1 was genetically inactivated a high-fat diet. Compared to normal mice, the mice without NBR1 had less inflammation and better glucose tolerance, suggesting that the protein was promoting inflammation and glucose intolerance.
The researchers went on to show that NBR1 mediates its effects by binding to a protein called MEKK3, and when NBR1 and MEKK3 interact, they cause adipose tissue inflammation.
“MEKK3 is a very attractive protein because it can be therapeutically targeted with small molecules that can lead to the generation of new drugs for insulin resistance, and potentially type 2 diabetes,” said Diaz-Meco.
“It’s estimated that over 35 percent of American adults are insulin resistant, and without an intervention, many of these cases will progress into type 2 diabetes. An important next step is to look for MEKK3-NBR1 inhibitors to reverse insulin resistance with the promise of new therapies for the treatment of type 2 diabetes,” added Steven R. Smith, M.D., professor in the Metabolic Disease Program at Sanford-Burnham, scientific director of the Translational Research Institute for Metabolism and Diabetes, chief scientific officer of Florida Hospital, and co-author of the study.

Cheryl Dybas, National Science Foundation (NSF)

Researchers discover natural clay deposits with antibacterial properties

Superbugs, they’re called: Pathogens, or disease-causing microorganisms, resistant to multiple antibiotics.

Such antibiotic resistance is now a major public health concern.

“This serious threat is no longer a prediction for the future,” states a 2014 World Health Organization report, “it’s happening right now in every region of the world and has the potential to affect anyone, of any age, in any country.”

Could the answer to this threat be hidden in clays formed in minerals deep in the Earth?

Biomedicine meets geochemistry

“As antibiotic-resistant bacterial strains emerge and pose increasing health risks,” says Lynda Williams, a biogeochemist at Arizona State University (ASU), “new antibacterial agents are urgently needed.”

To find answers, Williams and colleague Keith Morrison of ASU set out to identify naturally-occurring antibacterial clays effective at killing antibiotic-resistant bacteria.

The scientists headed to the field–the rock field. In a volcanic deposit near Crater Lake, Oregon, they hit pay dirt.

Back in the lab, the researchers incubated the pathogens Escherichia coli and Staphylococcus epidermidis, which breeds skin infections, with clays from different zones of the Oregon deposit.

They found that the clays’ rapid uptake of iron impaired bacterial metabolism. Cells were flooded with excess iron, which overwhelmed iron storage proteins and killed the bacteria.

“The ability of antibacterial clays to buffer pH also appears key to their healing potential and viability as alternatives to conventional antibiotics,” state the scientists in a paper recently published in the journal Environmental Geochemistry and Health.

“Minerals have long had a role in non-traditional medicine,” says Enriqueta Barrera, a program director in the National Science Foundation’s (NSF) Division of Earth Sciences, which funded the research.

“Yet there is often no understanding of the reaction between the minerals and the human body or agents that cause illness. This research explains the mechanism by which clay minerals interfere with the functioning of pathogenic bacteria. The results have the potential to lead to the wide use of clays in the pharmaceutical industry.”

Ancient remedies new again

Clay minerals, says Williams, have been sought for medicinal purposes for millennia.

Studies of French clays–green clays historically used in France in mineral baths–show that the clays have antibacterial properties. French green clays have been used to treat Mycobacterium ulcerans, the pathogen that causes Buruli ulcers.

Common in Africa, Buruli ulcers start as painful skin swellings. Then infection leads to the destruction of skin and large, open ulcers on arms or legs.

Delayed treatment–or treatment that doesn’t work–may cause irreversible deformities, restriction of joint movement, widespread skin lesions, and sometimes life-threatening secondary infections.

Treatment with daily applications of green clay poultices healed the infections. “These clays,” says Williams, “demonstrated a unique ability to kill bacteria while promoting skin cell growth.”

Unfortunately, the original French green clays were depleted. Later testing of newer samples didn’t show the same results.

Research on French green clays, however, spurred testing of other clays with likely antibacterial properties.

“To date,” says Williams, “the most effective antibacterial clays are those from the Oregon deposit.”

Samples from an area mined by Oregon Mineral Technologies (OMT) proved active against a broad spectrum of bacteria, including methicillin-resistant S. aureus (MRSA) and extended-spectrum beta-lactamase-resistant E. coli (ESBL).

What’s in those rocks?

Understanding the geologic environment that produces antibacterial minerals is important for identifying other promising locations, says Williams, “and for evaluating specific deposits with bactericidal activity.”

The OMT deposit was formed near volcanoes active over tens to hundreds of thousands of years. The Crater Lake region is blanketed with ash deposits from such volcanoes.

OMT clays may be 20 to 30 million years old. They were “born” eons before deposits from volcanoes such as Mt. Mazama, which erupted 7,700 years ago to form the Crater Lake caldera.

Volcanic eruptions over the past 70,000 or so years produced silica-rich magmas and hydrothermal waters that may have contributed to the Oregon deposit’s antibacterial properties.

To find out, Williams and Morrison took samples from the main OMT open pit. Four types of rocks were collected: two blue clays, and one white and one red “alteration zone” rock from the upper part of the deposit.

Blue clay to the rescue

The OMT blue samples were strongly bactericidal against E. coli and S. epidermidis. The OMT white sample reduced the population of E. coli and S. epidermidis by 56 percent and 29 percent, respectively, but the red sample didn’t show an antibacterial effect.

“We can use this information to propose the medicinal application of certain natural clays, especially in wound healing,” says Williams.

Chronic, non-healing wounds, adds Morrison, are usually more alkaline (vs. acidic) than healthy skin. The pH of normal skin is slightly acidic, which keeps numbers of bacteria low.

“Antibacterial clays can buffer wounds to a low [more acidic] pH,” says Williams, like other accepted chronic wound treatments, such as acidified nitrate. “The clays may shift the wound environment to a pH range that favors healing, while killing invading bacteria.”

The Oregon clays could lead to the discovery of new antibacterial mechanisms, she says, “which would benefit the health care industry and people in developing nations. A low-cost topical antibacterial agent is quickly needed.”

Answers to Buruli ulcers, MRSA and other antibiotic-resistant infections may lie not in a high-tech lab, but in ancient rocks forged in a hot zone: Oregon’s once–and perhaps future–volcanoes.

redOrbit Staff & Wire Reports – Your Universe Online

Adding alcoholic beverages to caffeinated energy drinks increases a person’s desire to continue consuming the beverages, according to research published online Thursday in the journal Alcoholism: Clinical & Experimental Research.

According to Lizzie Parry of the Daily Mail, researchers from the Australian National University looked at the effects of mixing energy drinks with vodka, and found that drinkers demonstrated an increased desire for alcohol when imbibing the mixture relative to drinking alcohol by itself.

“Based on our study, we can’t be certain whether it was the caffeine or the sugary additives that made the energy drink and vodka cocktail more appealing than drinking alcohol alone,” lead author Rebecca McKetin of the university’s Center for Research on Aging, Health and Well-being told HealthDay News reporter Alan Mozes. However, she did suggest one potential mechanism to explain the phenomenon.

“We normally think of alcohol as a depressant, but it also has a stimulant effect, and it is this stimulant effect that is most strongly related to how much we like alcohol, and whether we want to keep drinking,” McKetin added. “Caffeine, being a stimulant, tends to bring out the stimulant effects of alcohol intoxication. It may be this that causes energy drinks to increase the desire to keep drinking alcohol.”

In a statement, McKetin and colleague Alice Coen of the university’s School of Psychology recruited a total of 75 participants (29 male, 46 female) between the ages of 18 and 30. Those individuals were assigned to either an alcohol-only or an alcohol-and-energy drink (A+ED) condition in a double-blind randomized experiment.

Thirty-six of the study participants were given a cocktail containing 60ml of vodka and a Red Bull Silver Edition brand energy drink, while 39 others were asked to consume a mixture of 60ml of vodka with soda water. Both drinks also contained 200ml of fruit drink, and the subject completed the Alcohol Urge Questionnaire both prior to consuming the beverages and again 20 minutes following the completion of the test.

“We found that when people drink A+EDs that they have a stronger desire to keep drinking than if they drank alcohol on its own,” explained McKetin. “This would mean that someone who drinks A+EDs would want to keep drinking more than their friends who don’t. What we can’t say is whether this translates into people drinking more.”

“Obviously other factors would play a role there – people can over-ride their desires and many things play into a decision about whether someone would keep drinking or not,” she added. “However, if it did translate into greater alcohol consumption, we would expect to see people who drink A+EDs drinking more than their peers who don’t.”

“A greater urge to drink has substantial implications when we think about the nature of drinking episodes,” added Deakin University psychology professor Peter Miller. “As people become intoxicated, even at low levels, they show less inhibitions and are likely to drink more in a cycle of greater intoxication. Of course, the drunker you get, the more likely you are to get injured, be a victim or perpetrator of an assault, or even drive home while drunk, let alone making bad choices about the people you associate with and possible sexual behavior.”

McKetin said that the primarily implications of the study involved potential regulation of the sale of energy drinks alongside alcoholic beverages in night clubs or bars, as well as the overall availability of pre-mixed drinks featuring both caffeine and alcohol. However, the American Beverage Association noted that the research did not track whether or not additional alcohol was actually consumed – only that the desire to do so was there.

“As acknowledged by the authors, this study does not establish a link between energy drink consumption and increased alcohol consumption. Rather, it measures how people feel and not what they actually do,” the industry group said in a statement Thursday, according to Mozes. It added that its member companies “adhere to responsible labeling and marketing guidelines that do not allow energy drink labels to promote mixing with alcohol.”

redOrbit Staff & Wire Reports – Your Universe Online
Bacteria are frequently the cause of severe foodborne illnesses, but new research appearing in a recent edition of the journal Food Control reveals that a common cooking spice could effectively help combat pathogens such as E. coli.
In the study, scientists from Washington State University report that Cinnamomum cassia oil killed multiple strains of Shiga toxin-producing Escherichia coli (also known to the US Centers for Disease Control and Prevention (CDC) as non-O157 STEC). They believe their findings could improve food safety and reduce instances of food poisoning.
According to Lina Sheng, a graduate student in the WSU School of Food Science, the oil was found to be effective even in low concentrations. In fact, using a mixture of just 10 drops diluted in a liter of water, she and co-author Meijun Zhu, an assistant professor in the School of Food Science, were able to kill the bacteria in under 24 hours.
In a statement, Zhu explained that the increase of health-related concerns over chemical food additives has resulted in rising demand for natural additives, and that the focus of the study was “exploring plant-derived natural food bioactive compounds as antimicrobials to control foodborne pathogens, in order to ensure safety of fresh produce.”
Sheng noted that non-O157 STEC is responsible for more than 100,000 cases of illness each year, and that the US Department of Agriculture (USDA) Food Safety and Inspection Service has a “zero tolerance” policy for ground beef containing any of the six most common strands of the bacteria tested by the WSU researchers.
Cassia cinnamon, which is primarily produced in Indonesia, was selected for a stronger smell than the other common version of the spice, Ceylon cinnamon. Sheng explained that the oil “can be incorporated into films and coatings for packaging both meat and fresh produce” and could also be used when washing meat, fruits and vegetables.
The study authors are also investigating other natural methods of killing foodborne pathogens. Sheng and Zhu said that they will analyze the bacteria-inhibiting potential of dandelions when it comes to the condition known as bovine mastitis, which is a type of infection found in the mammary glands of dairy cows.
Earlier this month, researchers from Rush University Medical Center in Chicago reported that cinnamon could also help reverse brain damage caused by Parkinson’s disease in mice, and that the common spice was capable of treating biomechanical, cellular and anatomical changes in the brain.
“Cinnamon has been used widely as a spice throughout the world for centuries,” explained lead researcher and Rush University neurology professor Dr. Kalipada Pahan, noting that if the treatment method proves effective in humans, it “could potentially be one of the safest approaches to halt disease progression in Parkinson’s patients.”
“Cinnamon is metabolized in the liver to sodium benzoate” a common food preservative that is also “an FDA-approved drug used in the treatment for hepatic metabolic defects associated with hyperammonemia,” he added. While both common types of cinnamon are “metabolized into sodium benzoate,” Dr. Pahan said that the researchers found that Ceylon cinnamon was more effective because it does not contain the hepatotoxic molecule coumarin.
Image 2 (below): Cinnamomum cassia oil has been shown to kill certain strains of E. coli bacteria. Credit: Robert Hubner, WSU Photo Services

Brett Smith for redOrbit.com – Your Universe Online

Many mental health professionals look the other way when it comes to their patients smoking cigarettes, as they may appear to have a soothing effect. However, a new study has found that smoking cigarettes may have negative effects on mental health – in addition to the habit’s well-known physical effects.

In the study, researchers from Washington University School of Medicine and the University of Illinois took advantage of a natural sociological experiment – the skyrocketing taxation of cigarettes in the name of public health. The study team found that in states with greater taxes on cigarettes and more stringent policies to reduce smoking in public places, suicide rates dropped up to 15 percent, in relation to the national average, according to their report in the journal Nicotine & Tobacco Research.

“Our analysis showed that each dollar increase in cigarette taxes was associated with a 10 percent decrease in suicide risk,” said study author Richard A. Grucza, an associate professor of psychiatry at Washington University. “Indoor smoking bans also were associated with risk reductions.”

In the study, researchers examined information generated as individual states took distinct approaches to taxing and regulating cigarettes. From 1990 to 2004, states that implemented decisive tobacco-control policies saw their suicide rates lessen, compared to the national average.

The reverse was true in states with lesser taxes and relatively relaxed policies toward smoking in public. In those states, suicide rates boosted as high as 6 percent, in relation to the national average, during the same interval. From 1990 to 2004, the average yearly suicide rate was around 14 deaths per 100,000 people.

The researchers also categorized each suicide death by using the state where the person had lived, in addition to how decisive that state’s tobacco policies were during the study period. Using statistical procedures, the scientists determined if people who had committed suicide were regular smokers. They discovered that suicide risk among people who probably smoke was in fact connected with tobacco tax policies and state smoking laws.

“If you’re not a smoker, or not likely ever to become a smoker, then your suicide risk shouldn’t be influenced by tobacco policies,” Grucza said. “So the fact that we saw this influence among people who likely were smokers provides additional support for our idea that smoking itself is linked to suicide, rather than some other factor related to policy.”

The researchers speculated that smoking may boost the risk for psychiatric disorders, or make them more acute, which can impact suicide risk. They also warn about the potential negative health impacts of e-cigarettes, which are currently unregulated by the FDA.

“I think we really need to look more closely at the effects of smoking and nicotine, not just on physical health, but on mental health,” Grucza said. “We don’t know what’s happening between smoking and suicide, but it could be it’s increasing rates of depression among smokers, it could be that increases rates of addiction to other substances…”

“So it seems very plausible that smoking is hazardous for mental health as well as physical health,” he added.

UC Irvine
Conductivity could charge up futuristic disease treatments
The common pencil squid (Loliginidae) may hold the key to a new generation of medical technologies that could communicate more directly with the human body. UC Irvine materials science researchers have discovered that reflectin, a protein in the tentacled creature’s skin, can conduct positive electrical charges, or protons, making it a promising material for building biologically inspired devices.
Currently, products such as retinal implants, nerve stimulators and pacemakers rely on electrons – particles with negative charges – to transmit diagnosis data or to treat medical conditions. Living organisms use protons, with positive charges, or ions, which are atoms that contain both electrons and protons, to send such signals. The UCI discovery could lead to better ion- or proton-conducting materials: for instance, next-generation implants that could relay electrical messages to the nervous system to monitor or interfere with the progression of disease.
Alon Gorodetsky, assistant professor of chemical engineering & materials science at The Henry Samueli School of Engineering, led the research team. “Nature is really good at doing certain things that we sometimes find incredibly difficult,” he said. “Perhaps nature has already optimized reflectin to conduct protons, so we can learn from this protein and take advantage of natural design principles.”
He and his group have been studying reflectin to discern how it enables squid to change color and reflect light. They produced the squid protein in common bacteria and used it to make thin films on a silicon substrate. Via metal electrodes that contacted the film, the researchers observed the relationship between current and voltage under various conditions. Reflectin transported protons, they found, nearly as effectively as many of the best artificial materials.
Gorodetsky believes reflectin has several advantages for biological electronics. Because it’s a soft biomaterial, reflectin can conform to flexible surfaces, and it may be less likely to be rejected by the human body. In addition, protein engineering principles could be utilized to modify reflectin for very specific purposes and to allow the protein to decompose when no longer needed.
“We plan to use reflectin as a template for the development of improved ion- and proton-conducting materials,” Gorodetsky said. “We hope to evolve this protein for optimum functionality in specific devices – such as transistors used for interfacing with neural cells – similar to how proteins evolve for specific tasks in nature.”
The research is published in the July issue of Nature Chemistry. Co-authors are David Ordinario, Long Phan, Ward Walkup, Jonah-Micah Jocson, Emil Karshalev and Nina Husken of UCI.

Brett Smith for redOrbit.com – Your Universe Online

Managing Type 2 diabetes may include the need for daily medications or regular insulin injections, but a new study indicates that a protein called FGF1 could be the key to longer-lasting, more effective medications.

[ Watch the Video: Discovery Of Molecule’s Role May Lead To A Diabetes Cure ]

Published in the journal Nature, the new study discovered that treatment together with the protein doesn’t merely maintain blood sugar, but it also removes insulin insensitivity, the underlying biological cause of all forms of diabetes. The researchers added that the recently developed treatment method doesn’t lead to side effects typical to most current diabetes remedies.

“Controlling glucose is a dominant problem in our society,” said study author Ronald M. Evans, director of Salk Institute’s Gene Expression Laboratory, in a recent statement. “And FGF1 offers a new method to control glucose in a powerful and unexpected way.”

A condition that affects nearly 30 million Americans, Type 2 diabetes occurs when glucose increases in the circulatory system due to inadequate sugar-transporting insulin being made or due to the fact cells are getting to be insulin-resistant, disregarding signals to take in sugar. Being a chronic condition, diabetes might cause substantial health issues and has no cure. However, it can be managed through a blend of diet, regular exercise and medications.

Medications currently on the market try to boost levels of insulin and turn back insulin resistance by shifting expression of genes aimed at lessening glucose levels within the blood. However, some drugs boost the body’s generation of insulin to the point that glucose levels drop too low and lead to life-threatening hypoglycemia, and other side effects.

In 2012, Salk researchers noticed that mice without the growth factor FGF1 swiftly developed diabetes when given a high-fat diet, a finding which indicated FGF1 played a major role in controlling blood glucose levels. This led the scientists to consider if supplying extra FGF1 to diabetic mice could treat symptoms of the condition.

To test their theory, the scientists injected FGF1 into overweight mice with diabetes to gauge the protein’s prospective influence on metabolism. Scientists discovered that with a single dose, blood sugar levels rapidly dropped to normal levels in all the test subjects.

“Many previous studies that injected FGF1 showed no effect on healthy mice,” said study author Michael Downes, a senior staff scientist at Salk. “However, when we injected it into a diabetic mouse, we saw a dramatic improvement in glucose.”

The study revealed FGF1, even at large doses, did not cause side effects observed with traditional medications or cause blood sugar levels to drop to dangerously lower levels, a risk associated with numerous of glucose-lowering substances. Instead, the injections reconditioned the body’s own capacity to naturally normalize insulin and blood sugar levels, maintaining glucose amounts within a secure range. Essentially, FGF1 reversed the key symptoms of diabetes.

“With FGF1, we really haven’t seen hypoglycemia or other common side effects,” said Jae Myoung Suh, a co-author of the study and postdoctoral research fellow at Salk. “It may be that FGF1 leads to a more ‘normal’ type of response compared to other drugs because it metabolizes quickly in the body and targets certain cell types.”

The study team said they weren’t able to describe the exact mechanism behind the effects of FGF1 but said their work is the first step in using the protein to develop a therapeutic drug.

“We want to move this to people by developing a new generation of FGF1 variants that solely affect glucose and not cell growth,” Evans said. “If we can find the perfect variation, I think we will have on our hands a very new, very effective tool for glucose control.”

Nationwide Children’s Hospital

New research has identified a potential cause of and a better diagnostic method for preeclampsia, one of the most deadly and poorly understood pregnancy-related conditions in the world. The international team, led by researchers at Nationwide Children’s Hospital, discovered that the disease may result from a collection of protein mishaps like those associated with Alzheimer’s disease. Their findings, released today by Science Translational Medicine, have already led to an affordable, fast and accurate urine test that could revolutionize the diagnosis of preeclampsia in resource-poor nations.

“Preeclampsia is a very important health problem for women around the world, but for many years no one has understood why or how it happens,” said Irina A. Buhimschi, MD, director of the Center for Perinatal Research in The Research Institute at Nationwide Children’s and first author on the paper. “We were studying the urine of pregnant women with preeclampsia and noticed these improperly folded proteins, and that was the ‘Eureka!’ moment. It meant that preeclampsia could be similar to other protein misfolding diseases, such as Alzheimer’s and mad cow disease.”

Dr. Buhimschi’s team is the first to characterize the range of misfolded proteins found in the urine of pregnant women with preeclampsia.

Preeclampsia is the leading cause of preterm delivery in industrialized nations and accounts for up to 75,000 maternal deaths worldwide each year. It is characterized by protein in the urine and often-asymptomatic high blood pressure of no clear origin. When left untreated, the condition can progress to cause seizures, stroke, liver failure and death. Preeclampsia typically appears after the 20th week of pregnancy and only resolves upon delivery of the baby.

Dr. Buhimschi found that, in women with preeclampsia, the placenta was clogged with similar misfolded protein material to that found in the brains of people with Alzheimer’s. To carry out their functions properly, proteins must fold themselves into precise three-dimensional structures. But misfolded proteins, which fail to morph into their intended shape, are unable to function correctly. These and other proteins try to travel to and from the mother and baby on what is essentially a busy highway, Dr. Buhimschi explained, but the misfolded proteins build up in the mother’s body and in the placenta and cause a traffic jam.

To better understand the presence and importance of these proteins in the urine of pregnant women with preeclampsia, the team used a dye called Congo Red, which was known to bind proteins such as amyloid based on previous research done with other protein misfolding conditions. When this dye was used to test the urine of pregnant women, researchers found that it helped identify both the presence and future severity of preeclampsia.

The identified misfolded proteins include the amyloid precursor protein and enzymes and beta-amyloid, which are all associated with Alzheimer’s. Additional proteins found that often misfold include ceruloplasmin, immunoglobulin- free light chains and SERPINA1, which build up in toxic quantities in protein conformational disorders. Interferon-inducible protein 6-16 (IFI 6-16), a protein not previously known to be associated with other misfolding diseases but that was uniquely found misfolded in the urine of women with preeclampsia, is known to help prevent cell death and, in breast cancer cells, is responsible for resistance to treatment. The team used computer modeling to predict IFI 6-16’s involvement in preeclampsia aggregates and is continuing research to determine the mechanisms behind this and other proteins’ involvement in preeclampsia.

The studies resulting in this publication began seven years ago and have already led to a paper-based Congo Red Dot urine test for preeclampsia that won the international Grand Challenges for Development award, sponsored in part by the United States Agency for International Development. The project is now funded by a transition-to-scale grant from the Saving Lives at Birth consortium to determine whether the test improves preeclampsia diagnosis and reduces morbidity and mortality in resource-poor nations.

“In a way, we put the cart before the horse, getting the test in gear before we were able to formally publish all of the science behind it,” Dr. Buhimschi said. “It was just a great opportunity to really help people with a simple, cheap, non-invasive and very accurate test.”

The paper test currently being piloted is a more user-friendly version than the one in this publication, Dr. Buhimschi said, but it is based on the study’s results regarding the ability of Congo Red dye to bind with the misfolded proteins in women’s urine. “The test can help identify preeclampsia and predict its severity even before clinical symptoms appear,” she explained. “These proteins aren’t excreted in the urine of women who do not develop preeclampsia.”

While pilot testing continues around the world and at The Ohio State University Wexner Medical Center, Dr. Buhimschi and her collaborators are working to better understand the profile of misfolded proteins present in women with preeclampsia.

“In most protein conformational disorders, there is a particular protein that is the key culprit,” said Dr. Buhimschi, who also is a tenured professor at The Ohio State University College of Medicine. “If we can figure out which protein is the most critical actor in preeclampsia, we could potentially use drugs that target protein misassembly for that particular protein. This would allow us to treat or even prevent preeclampsia symptoms in women who test positive on the Congo Red Dot test.”

Understanding the range of mechanisms behind the pathophysiology of preeclampsia will be even more crucial to developing an effective treatment.

“The story is not over,” Dr. Buhimschi said. “Preeclampsia may be more than one disease. Particular types may be associated with certain subtypes of protein collections. We want to figure out exactly how each misfolded protein collection affects pregnant women and what we can do about it.”

University of Oxford

Taking B vitamins doesn’t slow mental decline as we age, nor is it likely to prevent Alzheimer’s disease, conclude Oxford University researchers who have assembled all the best clinical trial data involving 22,000 people to offer a final answer on this debate.

High levels in the blood of a compound called homocysteine have been found in people with Alzheimer’s disease, and people with higher levels of homocysteine have been shown to be at increased risk of Alzheimer’s disease. Taking folic acid and vitamin B-12 are known to lower levels of homocysteine in the body, so this gave rise to the ‘homocysteine hypothesis’ that taking B vitamins could reduce the risk of Alzheimer’s disease.

The new analysis was carried out by the B-Vitamin Treatment Trialists’ Collaboration, an international group of researchers led by the Clinical Trial Service Unit at the University of Oxford. The researchers brought together data from 11 randomized clinical trials involving 22,000 people which compared the effect of B vitamins on cognitive function in older people against placebo. Participants receiving B vitamins did see a reduction in the levels of homocysteine in their blood by around a quarter. However, this had no effect on their mental abilities.

When looking at measures of global cognitive function – or scores for specific mental processes such as memory, speed or executive function – there was no difference between those on B vitamins and those receiving placebo to a high degree of accuracy.

“It would have been very nice to have found something different,” says Dr. Robert Clarke of Oxford University, who led the work. “Our study draws a line under the debate: B vitamins don’t reduce cognitive decline as we age. Taking folic acid and vitamin B-12 is sadly not going to prevent Alzheimer’s disease.”

The study was funded by the British Heart Foundation, the UK Medical Research Council (MRC), Cancer Research UK, the UK Food Standards Agency and the Department of Health. The findings are published in the American Journal of Clinical Nutrition.

“Taking supplements like B vitamins doesn’t prevent heart disease, stroke or cognitive decline,” says Professor Clarke. “About 25% of the adult population take multi-vitamins, often with the idea that they are also good for the heart or the brain, but the evidence just isn’t there. Much better is to eat more fruit and vegetables, avoid too much red meat and too many calories, and have a balanced diet.”

Maternal folic acid intake before and during early pregnancy reduces a woman’s risk of having a neural tube defect birth defect and those thinking of having a baby are routinely advised to take folic acid supplements. Countries that have adopted mandatory population-wide folic acid fortification programs have also demonstrated reductions in neural-tube defect associated pregnancies without any adverse effects.

Dr. Simon Ridley, Head of Research at Alzheimer’s Research UK, said:

“Although one trial in 2010 showed that for people with high homocysteine, B vitamins had some beneficial effect on the rate of brain shrinkage, this comprehensive review of several trials shows that B vitamins have not been able to slow mental decline as we age, nor are they likely to prevent Alzheimer’s. While the outcome of this new and far reaching analysis is not what we hoped for, it does underline the need for larger studies to improve certainty around the effects of any treatment.

“Alzheimer’s is feared by many and it’s natural that people want to take action to try to prevent the disease, but people should always speak to their GP before changing their diet to include vitamin supplements. Research to understand how to prevent Alzheimer’s must continue, and in the meantime evidence shows that a number of simple lifestyle changes can help reduce the risk of the disease. Eating a healthy, balanced diet, taking regular exercise and keeping blood pressure and weight in check can all help lower the risk of Alzheimer’s.”

Dr. James Pickett, Head of Research at Alzheimer’s Society said:

“Given that many previous studies have shown that vitamin B doesn’t slow the progression of dementia or reduce risk, it’s not a huge surprise that a review of all of the evidence finds much the same. While taking B vitamins may not help everyone, they may have some benefits in specific groups of people with dementia. However, this study suggests that we need much more work to establish more evidence for this.

“One in three people over the age of 65 will develop dementia and yet research funding lags behind other conditions and we haven’t seen a new treatment made available in a decade. We need to see significantly more investment and recruit the next generation of leaders in research in order to deliver breakthroughs that could prove so vital to those affected by the condition.”

Hugh Perry, chair of the MRC Neurosciences and Mental Health Board, said:

“Science progresses through testing and re-testing previous research and sometimes overturning existing theories. Health advice always needs to be based on the best available data from the largest possible studies and this is even more important when the findings have implications for what we do or don’t eat and drink.”

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