Category Archives: Health Care

HHMI on Science 2.0: Information Revolution

The Howard Hughes Medical Institute does great things for science and for open science. They have an excellent article in their HHMI Bulletin – Science 2.0: You Say You Want a Revolution?

Cross-pollination among research disciplines is in fact at the core of many other popular science blogs. Michael Eisen, an HHMI investigator at the University of California, Berkeley, is an avid blog reader who particularly enjoys John Hawks’ site on paleoanthropology, genetics, and evolution. A recent post there discussed a new sequencing of Neanderthal mitochondrial DNA. “It’s like a conduit into another whole world,” says Eisen.
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The current extreme of collaboration via Science 2.0 is OpenWetWare.org. Begun in 2003 by Austin Che, who was then a computer science and biology graduate student at MIT, this biological-engineering Website uses the wiki model to showcase protocols and lab books: everything is open and can be edited by any of its 4,000 members.
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“Most publishers wish open access would go away,” says Brown. It won’t. Major research-funding organizations, including NIH, HHMI, and the Wellcome Trust, now require their grantees to post their findings on openaccess Websites such as PLoS or PubMed Central within 12 months of publication in traditional journals. Publishers are pushing back, however, and in September, the House Judiciary Committee began holding hearings on whether the federal government should be allowed to require grantees to submit accepted papers to a free archive.

How Cells Age

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.

Harvard researchers gain new insight into 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

Aging is fascinating. By and large people just accept it. We see it happen to those all around us, without exception. But what causes biological aging? It is an interesting area of research.

Rate of Cancer Detected and Death Rates Declines

Declines in Cancer Incidence and Death Rates in report from the National Cancer Institute and CDC:

“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.

Diagnoses Of Cancer Decline

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.”

Genes Counter a Bacterial Attack

Gene against bacterial attack unravelled

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.

PLoS paper: MyD88 Dependent Signaling Contributes to Protective Host Defense against Burkholderia pseudomallei

Google Flu Leading Indicator

Google Flu Trends

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.

This is an interesting example of finding new ways to quickly access what is happening in the world. Google must be doing significant amounts of similar things to see how usage patterns can server as a leading indicator.

Bacteria and Efficient Food Digestion

Gut Bacteria May Cause And Fight Disease, Obesity

“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.

Follow link with related podcast: Gut bacteria may cause and fight, disease, obesity. This whole area of the ecosystem within us and our health I find fascinating. And I fall for confirmation bias on things like becoming inefficient at converting food to energy as a way reduce obesity.

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.

They then gave an example of the difference being 95 calories versus 99 calories. Hardly seems huge but it would add up. Still that is a less amazing difference than I was expecting.

Diabetes Up 90% in USA Since 1997

Diabetes Up 90% in U.S.

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.

Copper Doorknobs and Faucets Kill 95% of Superbugs

Copper door handles and taps kill 95% of superbugs in hospitals

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.

NFL Stars no Match for Bacteria

NFL stars no match for bacteria

The problem came to the forefront last week with Cleveland Browns player Kellen Winslow, who recently had his second staph infection. He is reportedly the sixth player to acquire staph among the Browns in five years.
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Peyton Manning of the Indianapolis Colts was revealed to have a staph infection, the Indianapolis Star reported Friday. University of North Carolina-Asheville fans also recently learned that Kenny George, the 7-foot-7 center on the basketball team, had a staph infection complication that led to part of his foot being amputated. It’s unclear how these high-profile athletes acquired their infections, but locker rooms have been found to habor staph bacteria in previous outbreaks.
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A study on the St. Louis Rams published in the New England Journal of Medicine in 2003 found that during the 2003 football season, there were eight MRSA infections among five of the 58 Rams players.

Common Cold Alters the Activity of Genes

Scientists Come Closer to Unlocking Secrets of Common Cold

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.

Read: Learning How Viruses Evade the Immune System – Gene Carnival – Black Raspberries Alter Hundreds of Genes Slowing Cancer – Study Finds No Measurable Benefit to Flu Shots