An analysis of the germs unleashed from a single commuter’s sneeze showed that within minutes they are being passed on via escalator handrails or seats on trains and underground carriages. At the busiest stations, one sneeze not smothered by a tissue or handkerchief will provide enough germs to infect another 150 commuters.
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A single sneeze expels 100,000 droplets of germs into the air at 90mph. Individual droplets get transferred to handles, rails and other areas frequently held or touched. Up to 10 per cent of all commuters will come into contact with an area infected by that one sneeze, Dr Henderson calculated.
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Researchers asked 1,300 workers about their health and found 99 per cent of commuters suffered at least one cold last winter. In contrast, just 58 per cent of those who work from home and 88 per cent of those who walk to work regularly caught a cold last winter.

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

“The drop in incidence seen in this year’s Annual Report is something we’ve been waiting to see for a long time,” said Otis W. Brawley, M.D., chief medical officer of the American Cancer Society (ACS). “However, we have to be somewhat cautious about how we interpret it, because changes in incidence can be caused not only by reductions in risk factors for cancer, but also by changes in screening practices. Regardless, the continuing drop in mortality is evidence once again of real progress made against cancer, reflecting real gains in prevention, early detection, and treatment.”
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According to a U.S. Surgeon General’s report, cigarette smoking accounts for approximately 30 percent of all cancer deaths, with lung cancer accounting for 80 percent of the smoking-attributable cancer deaths. Other cancers caused by smoking include cancers of the oral cavity, pharynx, larynx, esophagus, stomach, bladder, pancreas, liver, kidney, and uterine cervix and myeloid leukemia.

The analysis found that the overall incidence of cancer began inching down in 1999, but not until the data for 2005 were analyzed was it clear that a long-term decline was underway. “The take-home message is that many of the things we’ve been telling people to do to be healthy have finally reached the point where we can say that they are working,” Brawley said. “These things are really starting to pay off.”

Brawley and others cautioned, however, that part of the reduction could be the result of fewer people getting screened for prostate and breast cancers. In addition, the rates at which many other types of cancer are being diagnosed are still increasing
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Some experts said the drop was not surprising, noting that it was primarily the result of a fall in lung cancer because of declines in smoking that occurred decades ago. They criticized the ongoing focus on detecting and treating cancer and called for more focus on prevention.

“The whole cancer establishment has been focused on treatment, which has not been terribly productive,” said John C. Bailar III, who studies cancer trends at the National Academy of Sciences. “I think what people should conclude from this is we ought to be putting most of our resources where we know there has been progress, almost in spite of what we’ve done, and stop this single-minded focus on treatment.”

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.

During the 2007-2008 flu season, an early version of Google Flu Trends was used to share results each week with the Epidemiology and Prevention Branch of the Influenza Division at CDC. Across each of the nine surveillance regions of the United States, we were able to accurately estimate current flu levels one to two weeks faster than published CDC reports.
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So why bother with estimates from aggregated search queries? It turns out that traditional flu surveillance systems take 1-2 weeks to collect and release surveillance data, but Google search queries can be automatically counted very quickly. By making our flu estimates available each day, Google Flu Trends may provide an early-warning system for outbreaks of influenza.

For epidemiologists, this is an exciting development, because early detection of a disease outbreak can reduce the number of people affected. If a new strain of influenza virus emerges under certain conditions, a pandemic could emerge and cause millions of deaths (as happened, for example, in 1918). Our up-to-date influenza estimates may enable public health officials and health professionals to better respond to seasonal epidemics and — though we hope never to find out — pandemics.

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.

“We’re all sterile until we’re born,” says Glenn Gibson, a microbiologist at the University of Reading in Britain. “We haven’t got anything in us right up until the time we come into this big, bad, dirty world.”

But as soon as we pass out of the birth canal, when we are fetched by a doctor’s hands, placed in a hospital crib, put on our mother’s breast, when we drag a thumb across a blanket and stick that thumb in our mouths, when we swallow our first soft food, we are invaded by all sorts of bacteria. Once inside, they multiply - until the bacteria inside us outnumber our human cells.
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University of Chicago immunologist Alexander Chervonsky, with collaborators from Yale University, recently reported that doses of the right stomach bacteria can stop the development of type 1 diabetes in lab mice. “By changing who is living in our guts, we can prevent type 1 diabetes,” he told The Wall Street Journal.

The bottom line: We now have two sets of genes to think about - the ones we got from our parents and the ones of organisms living inside us. Our parents’ genes we can’t change, but the other set? Now that is one of the newest and most exciting fields in cell biology.

You could have two people sitting down to a bowl of cheerios, they could each eat the same number of cheerios but because of a difference in their gut bacteria one will get more calories than the other.

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.

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

Scientists estimate that 90 percent of the cells contained in the human body belong to nonhuman organisms - mostly bacteria, but also a smattering of fungi and other eensy entities. Some 100 trillion microbes nestle in niches from our teeth to our toes.

But what’s setting science on its heels these days is not the boggling numbers of bugs so much as the budding recognition that they are much more than casual hitchhikers capable of causing disease. They may be so essential to well-being that humans couldn’t live without them.

In this emerging view, humans and their microbes - or, as some biologists playfully put it, microbes and their attached humans - have evolved together to form an extraordinarily complex ecosystem.

“We can’t take nutrition properly without bacteria. We can’t fight bad germs without good germs,” he said. “It may turn out that secretions from bacteria affect not only long-term health, but hour-by-hour moods - could a person’s happiness depend on his or her bugs? It’s possible. Our existences are so incredibly intertwined.”

However, in the opinion of some researchers, this strange union may be headed for trouble because of profligate use of antibiotics and antiseptic lifestyles that deter the transfer of vital strains of bacteria that have swarmed in our systems at least since early humans ventured out of Africa.

Even as hospitals begin to get control of other drug-resistant infections such as MRSA, a form of staph, rates of C. diff are rising sharply, and a recent, more virulent strain of the bug is causing more severe complications. The Centers for Disease Control and Prevention estimates there are 500,000 cases of C. diff infection annually in the U.S., contributing to between 15,000 and 30,000 deaths. That’s up from roughly 150,000 cases in 2001.
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Many patients get C. diff infections as an unintended consequence of taking antibiotics for other illnesses. That’s because bacteria normally found in a person’s intestines help keep C. diff under control, allowing the bug to live in the gut without necessarily causing illness. But when a person takes antibiotics, both bad and good bacteria are suppressed, allowing drug-resistant C. diff to grow out of control.
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Only 3% to 5% of healthy, non-hospitalized adults carry C. diff in their gut, but that rate is much higher in hospitals and nursing homes, where carriers can spread the bacteria to others. Studies at several hospitals in recent years have shown that 20% or more of inpatients were colonized with C. diff, and a 2007 study of 73 long-term-care residents showed 55% were positive for C. diff. Even though the majority had no symptoms of disease, spores on the skin of asymptomatic patients were easily transferred to the investigators’ hands.

A new government study published Monday has found that the medicines most often prescribed for schizophrenia in children and adolescents are no more effective than older, less expensive drugs and are more likely to cause some harmful side effects. The standards for treating the disorder should be changed to include some older medications that have fallen out of use, the study’s authors said.
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“I think the reason the use of these newer drugs has gone up so fast is that there was this widespread assumption that they were safer and more effective than what we had before,” Dr. McClellan said. “Well, we’re seeing now that that’s not the whole story.”

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.”