President Obama Brings Hope to Future Space Exploration.

Monday, April 19, 2010

President Obama spoke at the Kennedy Space Center on April 15, 2010 about the new direction for NASA and America's Space Program.

Under Embargo Till: 16:00 UTC March 24, 2010
Posted: 16:00 UTC 03/24/2010

Emotions Key To Judging Others

Wednesday, March 24, 2010

A new study from MIT neuroscientists suggests that our ability to respond appropriately to intended harms — that is, with outrage toward the perpetrator — is seated in a brain region associated with regulating emotions.

Patients with damage to this brain area, known as the ventromedial prefrontal cortex (VMPC), are unable to conjure a normal emotional response to hypothetical situations in which a person tries, but fails, to kill another person. Therefore, they judge the situation based only on the outcome, and do not hold the attempted murderer morally responsible.

The finding offers a new piece to the puzzle of how the human brain constructs morality, says Liane Young, a postdoctoral associate in MIT’s Department of Brain and Cognitive Sciences and lead author of a paper describing the findings in the March 25 issue of the journal Neuron.

“We’re slowly chipping away at the structure of morality,” says Young. “We’re not the first to show that emotions matter for morality, but this is a more precise look at how emotions matter.”

Working with researchers at the University of Southern California, led by Antonio Damasio, Young studied a group of nine patients with damage (caused by aneurisms or tumors) to the VMPC, a plum-sized area located a few inches behind the eyes.

Such patients have difficulty processing social emotions such as empathy or embarrassment, but “they have a perfectly intact capacity for reasoning and other cognitive functions,” says Young.

The researchers gave the subjects a series of 24 hypothetical scenarios and asked for their reactions. The scenarios of most interest to the researchers were ones featuring a mismatch between the person’s intention and the outcome — either failed attempts to harm or accidental harms.

When confronted with failed attempts to harm, the patients had no problems understanding the perpetrator’s intentions, but they failed to hold them morally responsible. The patients even judged attempted harms as more permissible than accidental harms (such as accidentally poisoning someone) — a reversal of the pattern seen in normal adults.

“They can process what people are thinking and their intentions, but they just don’t respond emotionally to that information,” says Young. “They can read about a murder attempt and judge it as morally permissible because no harm was done.”

This supports the idea that making moral judgments requires at least two processes — a logical assessment of the intention, and an emotional reaction to it. The study also supports the theory that the emotional component is seated in the VMPC.

Young hopes to study patients who incurred damage to the VMPC when they were younger, to see if they have the same impaired judgment. She also plans to study patient reactions to situations where the harmful attempts may be directed at the patient and therefore are more personal.

Funded by the National Science Foundation, National Institute of Neurological Disorders and Stroke, National Institute on Drug Abuse, gifts from J. Epstein and S. Shuman.

New Method to Prevent Heart Attacks

Wednesday, March 17, 2010

Cardiovascular disease is by far the absolute most common national disease in Sweden and a little more than 26,000 people are treated every year at hospitals due to acute cardiac infarction, according to the Heart and Lung Foundation. KTH researcher Matilda Larsson at the School of technology and health at KTH has recently defended her thesis and her research aims at developing methods which can as early as possible assess the risk of cardiovascular disease.

The earlier the risk of cardiovascular disease can be identified, the easier it will be to avoid acute cardiac infarction which will save lives. But even if research and health care has been improved considerably over the past few years, cardiovascular disease even in the future will be one of the most common reasons for sickness and mortality in Sweden. That is why Matilda Larsson’s research is, to say the least, of vital importance.

“One of the problems that we face today is that the methods used for risk assessment are new, and they need to be fine-tuned. The people that use the technology that is available must have considerable experience in being able to interpret the data they receive,” says Matilda Larsson.

To rectify this problem, Matilda Larsson has developed the existing ultrasound technology so that the information is more easily accessible.

“By visualising the data, the doctor will find it easier to interpret the results,” says Matilda Larsson.

The usual method is that the doctor measures the heart’s blood flow and how the cardiac valves operate. With the Speckle tracking method, Matilda Larsson and her colleagues study how the ultrasound image’s greyscale pattern changes, and she can also measure the movement patterns and deformation of the heart and the vascular tissue.

“The long-term objective is to have access to a sensitive method which can predict myocardial infarction at an early stage,” says Matilda Larsson.
Her thesis is called “Quantification and visualisation of cardiovascular function using ultrasound” and she has applied for a patent for a method used within this area.

Matilda Larsson originally comes from Östervåla between Gävle and Uppsala, but she will not be returning there for quite some time.

“Now I will continue as a post doctoral student at the university in Leuven, Belgium, where I conducted some of my thesis work. We will study movements and deformation of the carotis,” says Matilda.

Fruit flies and test tubes open new window on Alzheimer’s disease

Tuesday, March 16, 2010

A team of scientists from Cambridge and Sweden have discovered a molecule that can prevent a toxic protein involved Alzheimer’s disease from building up in the brain. They found that in test tube studies the molecule not only prevents the protein from forming clumps but can also reverse this process. Then, using fruit flies with Alzheimer’s disease, they showed that the same molecule effectively “cures” the insects of the disease.

Alzheimer's disease is the most common neurodegenerative disorder and is linked to the misfolding and aggregation of a small protein known as the amyloid β (Aβ) peptide. Previous studies in animal models have shown that aggregation of Aβ damages neurones (brain cells) causing memory impairment and cognitive deficits similar to those seen in patients with Alzheimer's disease. The mechanisms underlying this damage are, however, still not understood.

The new molecule - designed by scientists in Sweden - is a small protein known as an Affibody (an engineered binding protein). In this new study, researchers at the University of Cambridge and the Swedish University of Agricultural Sciences found that in test-tube experiments this protein binds to the Aβ peptide, preventing it from forming clumps and breaking up any clumps already present.

In a second experiment, they studied the effect of this Affibody in a Drosophila (fruit fly) model of Alzheimer's disease previously developed at Cambridge.

Working with fruit flies that develop the fly equivalent of Alzheimer's because they have been genetically engineered to produce the Aβ protein, they crossed these flies with a second line of flies genetically engineered to produce the Affibody.

They found that offspring - despite producing the Aβ protein - did not develop the symptoms of Alzheimer's disease.

According to lead author Dr Leila Luheshi of the Department of Genetics at University of Cambridge: "When we examined these flies we found that the Affibody not only prevented and reversed the formation of Aβ clumps, it also promoted clearance of the toxic Aβ clumps from the flies' brains."

"Finding a way of preventing these clumps from forming in the brain, and being able to get rid of them, is a promising strategy for preventing Alzheimer's disease. Affibody proteins give us a window into the Alzheimer's brain: by helping us understand how these clumps damage brain cells, they should help us unravel the Alzheimer's disease process."

According to Professor Torleif Härd of the Swedish University of Agricultural Sciences and one of the senior authors of the study: "Our work shows that protein engineering could open up new possibilities in Alzheimer's therapy development."

Researchers Identify Gene that May Play Role in Atherosclerosis

Monday, March 15, 2010

To understand the role of inflammation in cardiovascular and other diseases, it is essential to identify and characterize genes that induce an inflammatory response in the body -- and the genes that regulate them.

A study published online this week in the journal Proceedings of the National Academy of Sciences suggests that a gene called Hu antigen R (HuR) plays a critical role in inducing and mediating an inflammatory response in cells experiencing mechanical and chemical stresses. The study was supported by the National Institutes of Health.

The findings may open up new possibilities for developing treatments of metabolic diseases associated with inflammation, such as atherosclerosis. Atherosclerosis typically occurs in branched or curved regions of arteries where plaques form because of cholesterol build-up. Inflammation can alter the structure of plaques so that they become more likely to rupture, causing a blood vessel blockage and leading to heart attack or stroke.

“This is the first systematic study showing that HuR not only responds to external stimuli as a stress-sensitive gene, but it also regulates other stress-sensitive genes,” said senior author Gang Bao, the Robert A. Milton Chair in Biomedical Engineering in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University.

The study results show that HuR promotes the expression of genes that support atherosclerosis and inhibits the expression of genes that combat atherosclerosis.

“We found that suppressing expression of HuR inhibited the inflammatory response of cells, which shows that designing drugs that block HuR function may reduce the risk of plaques rupturing,” explained Bao.

Bao guided Won Jong Rhee, a former postdoctoral fellow in his laboratory, to conduct a series of experiments investigating the biology, behavior and pathways of HuR.

The researchers first studied how the HuR gene responds to different flow environments and chemical treatments. They exposed human umbilical vein endothelial cells to disturbed flow -- which occurs in artery regions where plaques form -- and found that the cells expressed higher levels of HuR than when they experienced a static or laminar flow environment. This finding was validated in tissue experiments with results showing increased amounts of HuR in regions of a mouse aorta that were exposed to disturbed flow.

Then the researchers treated endothelial cells with statins, medications used to treat atherosclerosis by reducing the number of cholesterol-containing low-density lipoprotein (LDL) molecules in the blood and inhibiting inflammation. The results indicated a decreased level of HuR with statin treatment.

After establishing HuR as a stress-sensitive gene regulated by external stimuli, including flow and statin treatment, the researchers conducted experiments to determine whether HuR regulates the expression of other stress-sensitive genes. They found that reducing the level of HuR in cells increased the levels of two genes that combat atherosclerosis -- Kruppel-like factor 2 (Klf2) and endothelial nitric oxide synthase (eNOS). The reduction in HuR also decreased the expression of bone morphogenic protein-4 (BMP-4), a gene that supports atherosclerosis.

Reducing the level of HuR in cells also significantly inhibited many inflammatory responses of the endothelial cells, including the expression of two potential atherosclerosis drug targets: inter-cellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).

Though this study showed that HuR plays a critical role in inducing and mediating an inflammatory response in cells subjected to a stressful environment, the underlying mechanism for this regulation is still not known.

“HuR protein often binds to messenger RNAs to increase their stability and translation, but we found that regulation of other stress-sensitive genes by HuR was not due to changes in mRNA stability by direct protein binding,” explained Bao.

To uncover the pathways that lead to HuR’s stress sensitivity, the researchers conducted a series of studies to reveal that HuR functions by adding a phosphate group to the transcriptional factor nuclear factor kappa B (NFkB) and its inhibitor IkBa. Additional research is underway to reveal what mRNAs HuR binds to and the mechanisms used to respond to mechanical and chemical stresses. Identifying the triggers for inflammation and unraveling the details of inflammatory pathways may eventually furnish new therapeutic targets.

Hanjoong Jo, the Coulter Department’s Ada Lee and Pete Correll Professor in Biomedical Engineering, Kyunghwa Chang, graduate student Chih-Wen Ni and research scientist Zhilan Zheng also contributed to this research.

Under Embargo Till: 19:00 UTC March 15, 2010
Posted: 19:00 UTC 03/15/2010

Scientists Demonstrate Mammalian Regeneration Through a Single Gene Deletion

Monday, March 15, 2010

A quest that began over a decade ago with a chance observation has reached a milestone: the identification of a gene that may regulate regeneration in mammals. The absence of this single gene, called p21, confers a healing potential in mice long thought to have been lost through evolution and reserved for creatures like flatworms, sponges, and some species of salamander. In a report published today in the Proceedings of the National Academy of Sciences, researchers from The Wistar Institute demonstrate that mice that lack the p21 gene gain the ability to regenerate lost or damaged tissue.

Unlike typical mammals, which heal wounds by forming a scar, these mice begin by forming a blastema, a structure associated with rapid cell growth and de-differentiation as seen in amphibians. According to the Wistar researchers, the loss of p21 causes the cells of these mice to behave more like embryonic stem cells than adult mammalian cells, and their findings provide solid evidence to link tissue regeneration to the control of cell division.

“Much like a newt that has lost a limb, these mice will replace missing or damaged tissue with healthy tissue that lacks any sign of scarring,” said the project’s lead scientist Ellen Heber-Katz, Ph.D., a professor in Wistar’s Molecular and Cellular Oncogenesis program. “While we are just beginning to understand the repercussions of these findings, perhaps, one day we’ll be able to accelerate healing in humans by temporarily inactivating the p21 gene.”

Heber-Katz and her colleagues used a p21 knockout mouse to help solve a mystery first encountered in 1996 regarding another mouse strain in her laboratory. MRL mice, which were being tested in an autoimmunity experiment, had holes pierced in their ears to create a commonly used life-long identification marker. A few weeks later, investigators discovered that the earholes had closed without a trace. While the experiment was ruined, it left the researchers with a new question: Was the MRL mouse a window into mammalian regeneration?

The discovery set the Heber-Katz laboratory off on two parallel paths. Working with geneticists Elizabeth Blankenhorn, Ph.D., at Drexel University, and James Cheverud, Ph.D., at Washington University, the laboratory focused on mapping the critical genes that turn MRL mice into healers.

Meanwhile, cellular studies ongoing at Wistar revealed that MRL cells behaved very differently than cells from “non-healer” mouse strains in culture. Khamilia Bedebaeva, M.D., Ph.D., having studied genetic effects following the Chernobyl reactor radiation accident, noticed immediately that these cells were atypical, showing profound differences in cell cycle characteristics and DNA damage. This led Andrew Snyder, Ph.D., to explore the DNA damage pathway and its effects on cell cycle control.

Snyder found that p21, a cell cycle regulator, was consistently inactive in cells from the MRL mouse ear. P21 expression is tightly controlled by the tumor suppressor p53, another regulator of cell division and a known factor in many forms of cancer. The ultimate experiment was to show that a mouse lacking p21 would demonstrate a regenerative response similar to that seen in the MRL mouse. And this indeed was the case. As it turned out, p21 knockout mice had already been created, were readily available, and widely used in many studies. What had not been noted was that these mice could heal their ears.

“In normal cells, p21 acts like a brake to block cell cycle progression in the event of DNA damage, preventing the cells from dividing and potentially becoming cancerous,” Heber-Katz said. “In these mice without p21, we do see the expected increase in DNA damage, but surprisingly no increase in cancer has been reported.”

In fact, the researchers saw an increase in apoptosis in MRL mice – also known as programmed cell death – the cell’s self-destruct mechanism that is often switched on when DNA has been damaged. According to Heber-Katz, this is exactly the sort of behavior seen in naturally regenerative creatures.

“The combined effects of an increase in highly regenerative cells and apoptosis may allow the cells of these organisms to divide rapidly without going out of control and becoming cancerous,” Heber-Katz said. “In fact, it is similar to what is seen in mammalian embryos, where p21 also happens to be inactive after DNA damage. The down regulation of p21 promotes the induced pluripotent state in mammalian cells, highlighting a correlation between stem cells, tissue regeneration, and the cell cycle.”

The study was supported by grants from the Harold G. and Leila Y. Mathers Foundation, the F.M. Kirby Foundation, the W.W. Smith Foundation, the National Institute for General Medical Sciences and National Cancer Institute.

Study investigators also include Wistar researchers Paul M. Lieberman, Ph.D.; Dmitri Gourevitch M.D.; Lise Clark D.V.M., Ph.D.; Xiang-Ming Zhang; and John Leferovich. Snyder, formerly of the Lieberman laboratory at Wistar, and Bedebaeva are co-first authors on this paper. James Cheverud of Washington University is also a co-author on this paper.

The Wistar Institute is an international leader in biomedical research with special expertise in cancer research and vaccine development. Founded in 1892 as the first independent nonprofit biomedical research institute in the country, Wistar has long held the prestigious Cancer Center designation from the National Cancer Institute. The Institute works actively to ensure that research advances move from the laboratory to the clinic as quickly as possible.

Developing Weed Resistance in Corn Hybrids

Monday, March 15, 2010

Millions of people in the savannas of west and central Africa rely on maize (corn) as a staple crop, and as an “insurance” food crop at the beginning of the rainy season. A destructive parasitic weed, Striga hermonthica, poses a threat to this valuable crop. Almost 64% of cropland in this area of Africa is affected by the parasite, which causes an average grain yield loss of 68%. Farmers in Striga-infested areas have not yet adopted Striga-resistant hybrids.

Scientists at the International Institute of Tropical Agriculture (IITA) in partnership with scientists in the University of Ibadan in Nigeria and the National Institute of Agricultural Research in Benin Republic investigated the relationship between the genetic diversity of maize inbred lines having different levels of resistance to Striga and the performance of their hybrids under parasite infestation. The results are reported in the March-April 2010 edition of Crop Science, published by the Crop Science Society of America.

The study experimented on all combinations of ten lines of maize with varying levels of resistance to the parasitic weeds in different locations in Africa over three years. Hybrids from two resistant parental lines exhibited the highest level of field resistance, while hybrids from parents with low resistance fared the worst. Hybrids with only one parent with high Striga resistance showed moderate levels of field resistance.

Another important finding was that the genetic diversity of the parental lines did not affect grain yield or other traits among the hybrids. The researchers expect that genetically diverse, Striga-resistant maize crops will provide opportunities to further increase the levels of field resistance to S. hermonthica through breeding.

Such Striga resistant maize hybrids may encourage farmers that abandoned farms due to severe Striga infestation to go back into maize production. This would contribute to food security and provide income-generating opportunities to farmers that depend on maize as an important food crop in Striga infested areas.

Boeing A160T Proves Resupply Capability for US Marines

Monday, March 15, 2010

The Boeing [NYSE: BA] A160T Hummingbird has successfully completed a cargo delivery demonstration under a U.S. Marine Corps Warfighting Laboratory contract, proving the unmanned rotorcraft's ability to resupply frontline troops in rough terrain. The Hummingbird met or exceeded all of the demonstration requirements during the tests, conducted March 9 - March 11 at the U.S. Army's Dugway Proving Ground in Utah.

Boeing showed that the A160T can deliver at least 2,500 pounds of cargo from one simulated forward-operating base to another 75 nautical miles away in well under the required six hours. The simulated mission carried 1,250-pound sling loads over two 150-nautical-mile round trips, with the A160T operating autonomously on a preprogrammed mission.

"The Hummingbird's performance was outstanding, as we had expected," said Vic Sweberg, director of Unmanned Aerial Systems for Boeing Military Aircraft. "The A160T's capabilities can fulfill our customer's near-term need for 24/7, reliable cargo resupply. It also provides unmatched flexibility to carry out a variety of other missions, including intelligence, surveillance and reconnaissance; target acquisition; direct action; and communication relay."

The A160T completed seven test flights during the demonstration, including a two-minute hover at 12,000 feet with the 1,250-pound sling load, and a nighttime delivery to a simulated forward operating base. The A160T's ability to execute extremely accurate autonomous deliveries also was demonstrated.

The A160T has a 2,500-pound payload capacity. It features a unique optimum-speed-rotor technology that significantly improves overall performance efficiency by adjusting the rotor's speed at different altitudes, gross weights and cruise speeds. The autonomous unmanned aircraft, measuring 35 feet long with a 36-foot rotor diameter, has hovered at 20,000 feet and cruised at more than 140 knots. The A160T established a world endurance record in its class in 2008 with an 18.7-hour unrefueled flight.

A unit of The Boeing Company, Boeing Defense, Space & Security is one of the world's largest defense, space and security businesses specializing in innovative and capabilities-driven customer solutions, and the world's largest and most versatile manufacturer of military aircraft. Headquartered in St. Louis, Boeing Defense, Space & Security is a $34 billion business with 68,000 employees worldwide.

Under Embargo Till: 18:00 UTC March 14, 2010
Posted: 18:00 UTC 03/14/2010

New analysis of the structure of silks explains paradox of super-strength

Sunday, March 14, 2010

Spiders and silkworms are masters of materials science, but scientists are finally catching up. Silks are among the toughest materials known, stronger and less brittle, pound for pound, than steel. Now scientists at MIT have unraveled some of their deepest secrets in research that could lead the way to the creation of synthetic materials that duplicate, or even exceed, the extraordinary properties of natural silk.

Markus Buehler, the Esther and Harold E. Edgerton Associate Professor in MIT’s Department of Civil and Environmental Engineering, and his team study fundamental properties of materials and how those materials fail. With silk, that meant using computer models that can simulate not just the structures of the molecules but exactly how they move and interact in relation to each other. The models helped the researchers determine the molecular and atomic mechanisms responsible for the material’s remarkable mechanical properties.

Silk’s combination of strength and ductility — its ability to bend or stretch without breaking — results from an unusual arrangement of atomic bonds that are inherently very weak, Buehler and his team found. Doctoral student Sinan Keten, postdoctoral associate Zhiping Xu and undergraduate student Britni Ihle are co-authors of a paper on the research to be published on March 14 in the journal Nature Materials.

Silks are made from proteins, including some that form thin, planar crystals called beta-sheets. These sheets are connected to each other through hydrogen bonds — among the weakest types of chemical bonds, unlike, for example, the much stronger covalent bonds found in most organic molecules. Buehler’s team carried out a series of atomic-level computer simulations that investigated the molecular failure mechanisms in silk. “Small yet rigid crystals showed the ability to quickly re-form their broken bonds, and as a result fail ‘gracefully’ — that is, gradually rather than suddenly,” graduate student Keten explains.

“In most engineered materials” — ceramics, for instance — “high strength comes with brittleness,” Buehler says. “Once ductility is introduced, materials become weak.” But not silk, which has high strength despite being built from inherently weak building blocks. It turns out that’s because these building blocks — the tiny beta-sheet crystals, as well as filaments that join them — are arranged in a structure that resembles a tall stack of pancakes, but with the crystal structures within each pancake alternating in their orientation. This particular geometry of tiny silk nanocrystals allows hydrogen bonds to work cooperatively, reinforcing adjacent chains against external forces, which leads to the outstanding extensibility and strength of spider silk.

One surprising finding from the new work is that there is a critical dependence of the properties of silk on the exact size of these beta-sheet crystals within the fibers. When the crystal size is about three nanometers (billionths of a meter), the material has its ultra-strong and ductile characteristics. But let those crystals grow just beyond to five nanometers, and the material becomes weak and brittle.

Buehler says the work has implications far beyond just understanding silk. He notes that the findings could be applied to a broader class of biological materials, such as wood or plant fibers, and bio-inspired materials, such as novel fibers, yarns and fabrics or tissue replacement materials, to produce a variety of useful materials out of simple, commonplace elements. For example, he and his team are looking at the possibility of synthesizing materials that have a similar structure to silk, but using molecules that have inherently greater strength, such as carbon nanotubes.

The long-term impact of this research, Buehler says, will be the development of a new material design paradigm that enables the creation of highly functional materials out of abundant, inexpensive materials. This would be a departure from the current approach, where strong bonds, expensive constituents, and energy intensive processing (at high temperatures) are used to obtain high-performance materials.

Peter Fratzl, professor in the department of biomaterials in the Max Planck Institute of Colloids and Interfaces in Potsdam, Germany, who was not involved in this work, says that “the strength of this team is their pioneering multi-scale theoretical approach” to analyzing natural materials. He adds that this is “the first evidence from theoretical modeling of how hydrogen bonds, as weak as they might be, can provide high strength and toughness if arranged in a suitable way within the material.”

Professor of biomaterials Thomas Scheibel of the University of Bayreuth, Germany, who was also not involved in this work, says Buehler’s work is of the “highest caliber,” and will stimulate much further research. The MIT team’s approach, he says, “will provide a basis for better understanding of certain biological phenomena so far not understood.”

Funding for this work was supported by the Office of Naval Research, with additional funding from the National Science Foundation, the Army Research Office, the MIT Energy Initiative, and MIT’s UROP and MISTI-Germany programs.

Under Embargo Till: 18:00 UTC March 14, 2010
Posted: 18:00 UTC 03/14/2010

New microscopy technique offers close-up, real-time view of cellular phenomena

Sunday, March 14, 2010

For two decades, scientists have been pursuing a potential new way to treat bacterial infections, using naturally occurring proteins known as antimicrobial peptides (AMPs). Now, MIT scientists have recorded the first microscopic images showing the deadly effects of AMPs, most of which kill by poking holes in bacterial cell membranes.

Researchers in the laboratory of MIT Professor Angela Belcher modified an existing, extremely sensitive technique known as high-speed atomic force microscopy (AFM) to allow them to image the bacteria in real time. Their method, described in this Sunday’s online edition of Nature Nanotechnology, represents the first way to study living cells using high-resolution images recorded in rapid succession.

Using this type of high-speed AFM could allow scientists to study how cells respond to other drugs and to viral infection, says Belcher, the Germeshausen Professor of Materials Science and Engineering and Biological Engineering. The new work could also help researchers understand how some bacteria can become resistant to AMPs (none of which have been approved as drugs yet).

Atomic force microscopy, invented in 1986, is widely used to image nanoscale materials. Its resolution is similar to that of electron microscopy, but unlike electron microscopy, it does not require a vacuum and thus can be used with living samples. However, traditional AFM requires several minutes to produce one image, so it cannot record a sequence of rapidly occurring events.

In recent years, scientists have developed high-speed AFM techniques, but haven’t optimized them for living cells. That’s what the MIT team set out to do, building on the experience of lead author Georg Fantner, a postdoctoral associate in Belcher’s lab who had worked on high-speed AFM at the University of California at Santa Barbara.

How they did it: Atomic force microscopy makes use of a cantilever equipped with a probe tip that “feels” the surface of a sample. Forces between the tip and the sample can be measured as the probe moves across the sample, revealing the shape of the surface. The MIT team used a cantilever about 1,000 times smaller than those normally used for AFM, which enabled them to increase the imaging speed without harming the bacteria.

With the new setup, the team was able to take images every 13 seconds over a period of several minutes. They found that AMP-induced cell death appears to be a two-step process: a short incubation period followed by a rapid “execution.” They were surprised to see that the onset of the incubation period varied from 13 to 80 seconds.

“Not all of the cells started dying at the exact same time, even though they were genetically identical and were exposed to the peptide at the same time,” says Roberto Barbero, a graduate student in biological engineering and an author of the paper.

In the future, Belcher hopes to use atomic force microscopy to study other cellular phenomena, including the assembly of viruses in infected cells, and the effects of traditional antibiotics on bacterial cells. The technique may also prove useful in studying mammalian cells.

Funding provided by Erwin-Schrodinger Fellowship, National Institutes of Health, Army Research Office, Austrian Research Promotion Agency.