MIT researchers have found that the pigments responsible for the blue-green stain of the mucus that clogs the lungs of cystic fibrosis (CF) patients are primarily signaling molecules that allow large clusters of the opportunistic infection agent, Pseudomonas aeruginosa, to organize themselves into structured communities.
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P. aeruginosa appears as a classic opportunistic infection, easily shrugged off by healthy people but a grave threat to those with CF, which chokes the lungs of its victims with sticky mucus.

“We have a long way to go before being able to test this idea, but the hope is that if survival in the lung is influenced by phenazine — or some other electron-shuttling molecule or molecules — tampering with phenazine trafficking might be a potential way to make antibiotics more effective,” said Newman, whose lab investigates how ancestral bacteria on the early Earth evolved the ability to metabolize minerals.

The retina, which is located in the back of the eye, has an outer layer of cells that detect light and translate it into electrical signals. It also has inner layers, which process the signals and send them to the brain.

In degenerative disorders like macular degeneration and retinitis pigmentosa, outer-layer cells, called photoreceptors, break down in the early stages of disease, leading to loss of vision. Extensive research has focused on replacing these cells, in an effort to restore sight. In people with advanced disease or blindness, however, the inner cell layers may also break down or become disorganized and need to be rebuilt, says Rose.

“The outer retina is like the CPU, and the inner retina is like the motherboard,” he says. “If I attach a new CPU to a dead motherboard, it won’t do any good, no matter how great a CPU it is.”
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In lower vertebrates like fish and chickens, retinal cells are known to generate new neurons in response to damage, often restoring sight. While mammals do not have the same self-healing capacity, some previous research has suggested that under particular circumstances, mammals’ retinas might be able to generate new neurons.

A new study by Harvard Medical School researchers reveals that the biochemical mechanism that makes yeast grow old has a surprising parallel in mice, suggesting it may be a universal cause of aging in all organisms.
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In young organisms, SIRT1 effectively doubles as a gene-expression regulator and a DNA repairer. But when DNA damage accumulates—as it does with age—SIRT1 becomes too busy fixing broken DNA to keep the expression of hundreds of genes in check. This process is so similar to what happens in aging yeast that its discoverers believe it may represent a universal mechanism of aging.

Aging may be a case of neglect — an absentee landlord at the cellular level that allows gene activity to go awry, according to a study published today.

Scientists have long known that aging causes gene expression to change, and DNA damage to accumulate. But now, research led by Harvard Medical School scientists explains the connection between the two processes in mammals.

The paper, published in the journal Cell, found that a multi-tasking protein called SIRT1 that normally acts as guardian of the genome gets dragged away to DNA fix-it jobs. When the protein abandons its normal post to work as a genetic handyman, order unravels elsewhere in the cell. Genes that are normally under its careful watch begin to flip on.

“What this paper actually implies is that aspects of aging may be reversible,” said David Sinclair, a Harvard Medical School biologist who led the research. “It sounds crazy, but in principle it should be possible to restore the youthful set of genes, the patterns that are on and off.”

The study is just the latest to draw yet more attention to sirtuins, proteins involved in the aging process

Humans have an innate defence system against deadly bacteria. However, how the step from gene to anti-bacterial effect occurs in the body is not yet known. To date, B. Pseudomallei, a bacterium suitable for bioweapons, had managed to elude medics. It can remain hidden in the human body for many years without being detected by the immune system. The bacteria can suddenly become activated and spread throughout the body, resulting in the patient dying from blood poisoning. AMC physician Joost Wiersinga and the Laboratory for Experimental Internal Medicine discovered which gene-protein combination renders the lethal bacteria B. pseudomallei harmless.

Wiersinga focussed on the so-called Toll-like receptors. These are the proteins that initiate the fight against pathogens. There are currently ten known Toll-like receptors which are located on the outside of immune cells, our body’s defence system. The toll-like receptors jointly function as a 10-figure alarm code. Upon coming into contact with the immune cell each bacterium enters its own Toll code. For known pathogens this sets off an alarm in the immune system and the defence mechanism is activated. Yet B. pseudomallei fools the system by entering the code of a harmless bacterium. As a result the body’s defence system remains on standby.

Yet some people are resistant: they become infected but not ill. Wiersinga found a genetic cause for this resistance. He discovered which toll receptor can fend off B. pseudomallei. He did this by rearing mice DNA in which the gene for Toll2 production was switched on and off. ‘The group where the gene for Toll2 was switched off, survived the bacterial infection’, says Wiersinga. ‘The other receptor that we investigated, Toll4, had no effect - even though for the past ten years medics had regarded this as the most important receptor.’ The ultimate aim of this study is to develop a vaccine.

Researchers now believe that some of the more entrenched elements of many athletes’ warm-up regimens are not only a waste of time but actually bad for you. The old presumption that holding a stretch for 20 to 30 seconds - known as static stretching - primes muscles for a workout is dead wrong. It actually weakens them.
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A well-designed warm-up starts by increasing body heat and blood flow.
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To raise the body’s temperature, a warm-up must begin with aerobic activity, usually light jogging. Most coaches and athletes have known this for years.
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Athletes who need to move rapidly in different directions, like soccer, tennis or basketball players, should do dynamic stretches that involve many parts of the body. “Spider-Man” is a particularly good drill: drop onto all fours and crawl the width of the court, as if you were climbing a wall.

Dieticians at Addenbrooke’s have said evidence suggested the yoghurt might cut the risk of contracting C.diff. Caroline Heyes, dietetic services manager at Addenbrooke’s hospital, said: “Probiotic yoghurts may play a role in preventing C.difficile infection so we have been running a pilot on three of the care of the elderly wards for six months.
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“We can’t say for sure how much of that benefit is down to the yoghurt and how much they are down to a whole range of infection control procedures that the hospital has in place such as the deep cleaning programme, the bare-below-the-elbow programme, and the increased isolation procedures,” Ms Heyes said.

Type 2 diabetes is up 90% since 1997. And that may be an underestimate because the numbers come from self-reported surveys conducted by the CDC in 1995-1997 and in 2005-2007. About a third of people with diabetes don’t yet know they have the dangerous disease.
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“The growth in diabetes prevalence has been concomitant with growth in obesity prevalence,”
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Obesity, the CDC says, is the major risk factor for diabetes. Yet it’s not necessary to become thin to avoid this debilitating disease. A study of people at high risk for diabetes shows you can cut your risk of diabetes by 58% in a three-year period by doing just two things:

* Lose 5% to 10% of your body weight.
* Five days a week, get 30 minutes of moderate physical activity.

A study found that copper fittings rapidly killed bugs on hospital wards, succeeding where other infection control measures failed.
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It is thought the metal ’suffocates’ germs, preventing them breathing. It may also stop them from feeding and destroy their DNA. Lab tests show that the metal kills off the deadly MRSA and C difficile superbugs. It also kills other dangerous germs, including the flu virus and the E coli food poisoning bug.
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Researcher Professor Peter Lambert, of Aston University, Birmingham, said: ‘The numbers decreased always on copper but not on the steel surfaces.’
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The healing power of copper has been recognised for thousands of years. More than 4,000 years ago, the Egyptians used it to sterilise wounds and drinking water and the Aztecs treated skin conditions with the metal. The ancient Greeks also knew of its benefits. Hippocrates, sometimes called ‘the father of medicine’, noted that it could be used to treat leg ulcers.

Canadian and U.S. researchers have found that the human rhinovirus, long blamed for causing the common cold, doesn’t actually cause those annoying sniffles, sneezes, and coughs.

Instead, the ubiquitous virus alters the activity of genes in the body, which then results in the misery that afflicts most people every year or so, according to a study in the first November issue of the American Journal of Respiratory and Critical Care Medicine.
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Human rhinovirus (HRV) causes some 30 percent to 50 percent of common colds and can also worsen more serious conditions, such as asthma.
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A “microarray analysis” of DNA showed no genetic changes eight hours after infection. But, after two days, about 6,500 genes had been affected, either with heightened activity or dampened activity.

The genes most affected by the presence of the virus were ones that make antiviral proteins and pro-inflammatory chemicals that contribute to airway inflammation, the researchers said.

The National Institutes of Health and some leading universities, such as Harvard and Stanford, have suffered black eyes this year because of revelations that researchers with federal grants failed to disclose secret payments that they took from pharmaceutical companies.

The NIH was warned about the dangers of the problem years ago by one of its own scientists, Ned Feder, who wrote letters to several publications suggesting that the agency require its grantees to publicly disclose money they earn from medical companies. Instead of heeding Dr. Feder’s advice, the agency punished him
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Dr. Feder went on to suggest that “the NIH could require grantees to make public disclosures of their paid arrangements with pharmaceutical, investment, and other companies, as well as their ownership of stock and stock options, as a condition of having their medical research funded by the government.”

The agency formally reprimanded Dr. Feder for writing to Nature and identifying himself in the letter as an employee of the NIH. Dr. Feder protested the reprimand, and it was subsequently removed, without explanation.
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“The NIH has shown no interest in reforming its policies unless they’re forced to do it,” said Dr. Feder, who is now staff scientist at the Project on Government Oversight.

It also makes perfect sense that our bodies evolved to store energy for worse times (and some of us have bodies better at doing that). Now we are in a new environment where (at least for many people alive today) finding enough calories is not going to be a problem so it would be nice if we could tell our bodies to get less efficient at storing fat

“MicroRNAs have been available to regulate and shape gene expression as far back as we can go in animal evolution—they might even predate animals,” says Bartel, a leader in the discovery and functional study of microRNAs. “They might have helped to usher in the era of multi-cellular animal life.”

First discovered in 1993, microRNAs are strands of RNA that are 21-24 nucleotides in length. They dampen gene expression by intercepting messenger RNA before it can turn the cellular crank that translates a gene into a protein. Earlier, Bartel’s research team showed that each microRNA can regulate the expression of hundreds of genes.

The ability of microRNAs to silence gene expression likely evolved from a more ancient defense against viruses, bacteria, and other mobile genetic elements that can mutate host DNA.
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The scientists determined that the starlet sea anemone has both microRNAs and piRNAs. In addition, the anemone makes proteins resembling those that interact with these small RNAs in humans. Both types of small RNA were also found in the sponge. The third target of their search, Trichoplax, did not contain any microRNAs, though Bartel suspects they may have existed in ancestral forms and later disappeared.

“Today the Broad Institute is the world’s leading genomics and biomedical institute, and we’re now making a $600 million bet that the Broad will be the place where the greatest scientific discoveries take place,” Eli Broad said at today’s ceremony.
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In its short history, the Broad Institute’s accomplishments include cataloging and identifying genetic risk factors for diseases such as type 2 diabetes and autism; discovering new therapeutic targets for cancer, malaria, and other diseases; and applying genomic tools to better understand and treat human pathogens like tuberculosis.
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The Broads’ gift is the largest to support biomedical research at a university anywhere in the world. The Broads initially invested $100 million in 2003 as a way to test the institute’s new approach to biomedical research. By 2005, the Broad Institute had already made significant accomplishments and progress, and the Broads invested a second $100 million. Their endowment of $400 million today will allow the Broad Institute to transition to a permanent, non-profit 501(c)(3) organization with both Harvard and MIT still at the heart of it, continuing to help govern the institute.

Four years ago we discovered that the Amish maintained super-low obesity levels despite eating a diet high in fat, calories and refined sugar. They key was their level of physical activity — men averaged 18,000 steps a day, women 14,000. That’s monumental compared to the paltry couple of thousand or so most of us eke out in a day.
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A recent study revealed even more about the Old Order Amish: They maintain low obesity levels despite having a gene variation that makes them susceptible to obesity. The secret here? You guessed it — lots of physical activity.

Study Conclusions: “Our results strongly suggest that the increased risk of obesity owing to genetic susceptibility by FTO variants can be blunted through physical activity. These findings emphasize the important role of physical activity in public health efforts to combat obesity, particularly in genetically susceptible individuals.”

Researchers at the Ohio State University Comprehensive Cancer Center examined the effect of freeze-dried black raspberries on genes altered by a chemical carcinogen in an animal model of esophageal cancer
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“We have clearly shown that berries, which contain a variety of anticancer compounds, have a genome-wide effect on the expression of genes involved in cancer development,” says principal investigator Gary D. Stoner
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Stoner notes that black raspberries have vitamins, minerals, phenols and phytosterols, many of which individually are known to prevent cancer in animals. “Freeze drying the berries concentrates these elements about ten times, giving us a power pack of chemoprevention agents that can influence the different signaling pathways that are deregulated in cancer,” he says.
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Their analyses included measuring the activity, or expression levels, of 41,000 genes. In the carcinogen-treated animals, 2,261 of these genes showed changes in activity of 50 percent or higher.