Tag Archives: medical research

Gene Duplication and Evolution

Roughly 10 million years ago, a major genetic change occurred in a common ancestor of gorillas, chimpanzees, and humans. Segments of DNA in its genome began to form duplicate copies at a greater rate than in the past, creating an instability that persists in the genome of modern humans and contributes to diseases like autism and schizophrenia. But that gene duplication also may be responsible for a genetic flexibility that has resulted in some uniquely human characteristics.

“Because of the architecture of the human genome, genetic material is constantly being added and deleted in certain regions,” says Howard Hughes Medical Institute investigator and University of Washington geneticist Evan Eichler, who led the project that uncovered the new findings. “These are really like volcanoes in the genome, blowing out pieces of DNA.”

Eichler and his colleagues focused on the genomes of four different species: macaques, orangutans, chimpanzees, and humans. All are descended from a single ancestral species that lived about 25 million years ago. The line leading to macaques broke off first, so that macaques are the most distantly related to humans in evolutionary terms. Orangutans, chimpanzees, and humans share a common ancestor that lived 12-16 million years ago. Chimps and humans are descended from a common ancestral species that lived about 6 million years ago.

By comparing the DNA sequences of the four species, Eichler and his colleagues identified gene duplications in the lineages leading to these species since they shared a common ancestor. They also were able to estimate when a duplication occurred from the number of species sharing that duplication. For example, a duplication observed in orangutan, chimpanzees, and humans but not in macaques must have occurred sometime after 25 million years ago but before the orangutan lineage branched off.

Eichler’s research team found an especially high rate of duplications in the ancestral species leading to chimps and humans, even though other mutational processes, such as changes in single DNA letters, were slowing down during this period.

MRI That Can See Bacteria, Virus and Proteins

IBM team boosts MRI resolution

The researchers demonstrated this imaging at a resolution 100 million times finer than current MRI. The advance could lead to important medical applications and is powerful enough to see bacteria, viruses and proteins, say the researchers.

The researchers said it offered the ability to study complex 3D structures at the “nano” scale. The step forward was made possible by a technique called magnetic resonance force microscopy (MRFM), which relies on detecting very small magnetic forces.

In addition to its high resolution, MRFM has the further advantage that it is chemically specific, can “see” below surfaces and, unlike electron microscopy, does not destroy delicate biological materials.

Now, the IBM-led team has dramatically boosted the sensitivity of MRFM and combined it with an advanced 3D image reconstruction technique. This allowed them to demonstrate, for the first time, MRI on biological objects at the nanometre scale.

That is very cool.

Science Commons: Making Scientific Research Re-useful

Science Commons is a project of Creative Commons. Like other organizations trying to support the advancement of science with open access they deserve to be supported (PLoS and arXiv.org are other great organizations supporting science).

Science Commons has three interlocking initiatives designed to accelerate the research cycle – the continuous production and reuse of knowledge that is at the heart of the scientific method. Together, they form the building blocks of a new collaborative infrastructure to make scientific discovery easier by design.

Making scientific research re-useful, help people and organizations open and mark their research and data for reuse. Learn more.

Enabling one-click access to research materials, streamline the materials-transfer process so researchers can easily replicate, verify and extend research. Learn more.

Integrating fragmented information sources, help researchers find, analyze and use data from disparate sources by marking and integrating the information with a common, computer-readable language. Learn more.

NeuroCommons, is their proof-of-concept project within the field of neuroscience. The NeuroCommons is a beta open source knowledge management system for biomedical research that anyone can use, and anyone can build on.

Bacteria Offer Line of Attack on Cystic Fibrosis

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.

Regenerating Neurons in Eyes

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.

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.

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

Static Stretching Decreases Muscle Strength

Stretching: The Truth

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.

Yogurts Used to Combat Superbugs

Yoghurts used to combat superbugs

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.

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.