Hi speed camera may help early Cancer Testing

Snap Judgment: Ultrafast Camera Renews Promise of Blood Test for Early Cancer Detection: Scientific American
Scientific American by Larry Greenemeier


Cells that break away from a cancerous tumor and circulate in the bloodstream are a serious threat to helping cancer spread, or metastasize, throughout the body. Finding these circulating tumor cells (CTCs), however, can be like searching for a particular needle in a stack of needles. One milliliter of blood contains about five billion red blood cells, 10 million white blood cells and only 10 tumor cells.

Yet early cancer detection and treatment is a person's best chance of survival, And because metastasis is responsible for 90 percent of cancer deaths, researchers have spent decades trying to develop blood tests that can effectively spot CTCs before they can form new tumors. The biggest challenge has been quickly examining billions of rapidly moving blood cells in a sample at a resolution high enough to identify the cancerous intruders.

Researchers at the University of California, Los Angeles, (U.C.L.A.), are developing a system that combines an optical microscope with a device for counting and studying cells, along with a high-speed image processor they say can take blur-free images of fast-moving cells, a significant step toward catching CTCs in the act. The researchers described the system last month in Proceedings of the National Academy of Sciences (PNAS).

The heart of the U.C.L.A. system is an ultrafast microscopic camera the researchers introduced in 2009 that captures images at about six million frames per second. This "serial time-encoded amplified microscopy" (STEAM) camera creates each image using a very short laser pulse—a flash of light only a billionth of a second long. The STEAM camera's shutter speed is 27 picoseconds, about a million times faster than a current digital camera. (A picosecond it one trillionth of a second.)

An instrument must meet two major requirements to detect CTCs in a blood sample. Of course, it must have a high sensitivity or signal-to-noise ratio to identify the signals, says lead author Keisuke Goda, a U.C.L.A. program manager in electrical engineering and bioengineering. "And it must be high speed, otherwise it would take a ridiculously long time [to find a cancer cell] because the background cell count is huge." The STEAM flow analyzer is an automated microscope 100 times faster than the automated microscopes hospitals sometimes use for disease identification, he adds.

The U.C.L.A. camera converts each laser pulse into a data stream from which a high-speed image can be assembled. The team used this technology to identify breast cancer cells in a blood sample. "We look at the cell's shape, size and texture as well as its surface biochemistry," Goda explains. "We can tell through high-speed imaging that cancer cells tend to be larger than white or red blood cells. And we know that a cancer cell's shape is ill-defined compared to red and white blood cells."

The researchers are now doing clinical testing on breast, lung, stomach, prostate and intestinal cancer patients' blood samples. Longer term, they want to quickly diagnose additional cancer types, including ovarian and pancreatic cancers, which are fast-spreading and require early detection for a patient to survive, says Goda, who was recently appointed as a chemistry professor at the University of Tokyo but will continue his research with U.C.L.A. He adds that a relatively noninvasive blood test would encourage people to get screened frequently.

Such a blood test could provide a safer and more accurate alternative to mammographies and other imaging tests as well as painful biopsies. MRI and computed tomography (CT) scans can be effective in finding larger tumors, but a patient's prognosis is poor by the time a tumor is detected.

There is already one diagnostic tool on the market for identifying and counting CTCs in blood samples, but it is not optimized for early detection. The U.S. Food and Drug Administration (FDA) in 2004 approved the CellSearch system, made by Johnson & Johnson's Veridex unit, for identifying and counting CTCs in patients with metastatic breast cancer. The FDA has since cleared CellSearch to help guide treatment of metastatic forms of prostate and colorectal cancer as well. Last year Johnson & Johnson said it would invest $30 million in a partnership with Massachusetts General Hospital to further develop CellSearch.

Despite these planned upgrades, "the U.C.L.A. work has promise as an advance over what is currently available," says Leon Esterowitz, a program director at the National Science Foundation (NSF). CellSearch is used primarily to check the progress of cancer treatment, whereas U.C.L.A.'s imaging technology could find cancerous cells at an earlier stage, before they can form a new tumor. "They've greatly improved the sensitivity and speed of the techniques that are being used for instance by Johnson & Johnson," Esterowitz says.

Researchers at New York City's Weill Cornell Medical College and Cornell University College of Engineering in Ithaca are also developing a cancer blood test, although theirs uses a "geometrically enhanced differential immunocapture" (GEDI) silicon chip that can identify and collect cancer cells from a patient's blood sample. The chip works in a device that can determine when patients have a high concentration of rare cancer cells from metastatic prostate cancer, according to the researchers, who described their work in the April 2012 issue of PLoS ONE. GEDI, like CellSearch, would be used to determine the efficacy of the patients' chemotherapy rather than finding early-stage cancer cells.

Esterowitz notes that all these blood tests are effective only after cells have become cancerous. He points to a Northwestern University project that aims to illuminate precancerous cells. Northwestern researchers are analyzing tissue at the nano—as opposed to the micro—scale to root out cells whose nuclei have greatly expanded or otherwise show irregularities that could be signs of impending malignancy.

Northwestern's approach, led by biomedical engineer Vadim Backman, involves shining light on tissue either inside a patient's body or taken from it. The researchers use a combination of microscopy and spectroscopy to examine how that light is reflected. Fluctuations in the reflections indicate possible abnormalities in the sampled tissue's micromolecular density and may flag the presence of unhealthy cells, Backman says.

"Most effort in the past has been studying cancer cells and tumors themselves, but we're focusing on what precedes the tumor," Backman says. "The tumor is the tip of the iceberg. We want to look below the waterline."

Backman and his team claim to have already tested their technology on 2,000 patients with a high degree of accuracy. The next step is to develop a compact, easy-to-use version that could be commercialized, and then conduct additional tests to earn FDA approval for what could be an even more effective cancer early warning system.


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Nanotechnology Holds Promise for Heart Patients

Nanotechnology Holds Promise for Heart Patients - WSJ.com
The Wall Street Journal by GAUTAM NAIK


Scientists have used nanotechnology materials to repair vital tissues damaged by heart attacks in animals, suggesting a new way to treat the same ailment in people.

The experiments, done in rats and pigs, led to the growth of fresh blood vessels and improved heart function without harmful side effects, the scientists said Wednesday in the journal Science Translational Medicine.


“Currently, there are no approved therapies in regenerative medicine for heart failure,” said Karen Christman, assistant professor of bioengineering at the University of California, San Diego, who wasn’t involved in the latest experiments. “These results are quite exciting.”

The World Health Organization estimates that more than 17 million people died from cardiovascular diseases in 2008. In the U.S., about 785,000 people will have new heart attacks this year and 470,000 will suffer recurrent ones. While more patients are surviving such events, about two-thirds don’t make complete recoveries and are vulnerable to heart failure.

Some researchers hope to treat patients by transplanting cells into the heart to promote the growth of new tissues. Animal tests have yielded promising results, and large-scale human trials are expected to kick off in coming months. But some of the early data suggest this approach may yield only small improvements in cardiac function.

An alternative technique is to deliver a protein called vascular endothelial growth factor, or VEGF, to promote blood-vessel growth in the heart. This method hasn’t worked well so far because the heart’s blood circulation tends to rapidly wash away the VEGF.

In their newly published experiments, researchers described an engineering fix for the problem. They made fibers from bits of protein and then assembled them into a lattice-like structure. Each fiber is just five nanometers wide and 100 nanometers long. (A nanometer is the length of three to six atoms placed side by side.)

The lattice structure is in the form of a sticky gel. The scientists mixed it with the VEGF and injected the combination into the hearts of two groups of test animals, rats and pigs, in which they had induced heart attacks. (Pig hearts bear significant similarities to human ones.) In both cases, instead of being washed away, the VEGF stayed on the lattice and slowly got released over several weeks.

Bone-marrow stem cells normally circulate in the blood and are part of the “repair crew” for damaged tissue. In the animal experiments, when those cells sensed the release of VEGF, they relocated to the heart and began to grow tiny blood vessels known as capillaries.

“The nanofibers create a special microenvironment in the heart for recruiting stem cells,” said Patrick Hsieh, a cardiac surgeon at the National Cheng Kung University in Taiwan and lead author of the paper.

However, fresh capillary formation isn’t enough to help a failing heart. For regeneration to continue, stem cells from both the bone marrow and the heart itself must be coaxed to grow a second layer of tissue that is necessary for the formation of arteries, which are bigger and thicker than capillaries.

To the scientists’ surprise, the prolonged release of VEGF achieved that result.

“This is the most striking finding of our approach,” said Dr. Hsieh. “We saw more than fivefold artery growth compared with the controls,” which included one group of animals that only got VEGF and another that got the nanofibers without the VEGF. The new artery growth contributed to improved heart function in the animals, Dr. Hsieh said.

The researchers also detected the creation of fresh heart muscle. This, too, is significant because the “scarring” tissue that naturally forms after a heart attack is thin and can get stretched in ways that alter the shape of the heart. In the latest experiments, the nanofiber gel appeared to strengthen these weak areas of the heart.

While the beneficial results in pig hearts were particularly important due to their resemblance to human ones, two challenges remain before the same technique can be safely attempted in people.

“We need to determine the long-term effect in animals, and we need to determine the optimal time window” when the VEGF nanofibers need to be administered, said Dr. Hsieh.

The researchers said they treated the rats and pigs immediately after a heart attack. When it comes to people, said Dr. Hsieh, it might be similarly effective to give the therapy in the first week after a heart attack, when stem-cell activity is highest.

The exact timing will now have to be pinned down. “While this therapy is promising,” said Dr. Christman, “it is important to see if the positive effect on cardiac function is maintained over the long term.”



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See the magic a 3D printer can do for a youngster

Not only read this but watch the video

http://allthingsd.com/20120804/3-d-printer-brings-magic-arms-to-a-two-year-old/?mod=mailchimp


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A jelly fish may be a fix for damaged hearts?

Jellyfish Hints at Fix for Damaged Hearts - WSJ.com
The Wall Street Journal by GAUTAM NAIK



Researchers have designed a bioengineered jellyfish that can swim, an early step in scientists’ quest for a way to make fresh tissue for patients with damaged hearts.

Researchers have designed a bioengineered jellyfish that can swim, an early step toward potentially finding a way to make fresh tissue for patients with damaged hearts reports WSJ’s Gautam Naik.

The lab-made jellyfish is created with a mix of silicone and rat-heart cells. Although it isn’t a living organism, the robot’s muscular structure closely resembles that of a real jellyfish, enabling it to swim freely through water.

Scientists hope that such techniques will make it possible to harvest cells from one organism and then reorganize them in sophisticated ways to make a bioengineered system for human use, such as a heart pacemaker that wouldn’t require battery power.

Details of the experiment were published Sunday in the journal Nature Biotechnology.

“What we’re trying to do is become really good at building tissue” for medical use, said Kevin Kit Parker, a bioengineer at Harvard University and a co-author of the study. “This is just practice” in the quest to reverse-engineer entire organs, he added.

Tissue-engineering experiments often rely on trial and error. Dr. Parker said he wants to bring to the field the same quantitative rigor and precision that civil engineers use in building bridges.

Dr. Parker spent years searching for a good model for the human heart. While watching a jellyfish at Boston’s New England Aquarium, he was struck by how the creature used a muscle to pump its way through water, a mechanism similar to a beating heart.

His Harvard team linked up with researchers at the California Institute of Technology, and the two groups first embarked on a detailed study of jellyfish propulsion: the complex arrangement of muscles; the contracting and recoiling motion of the bodies; and the fluid dynamics resulting from their swimming motion.

The engineers used a silicone polymer to build a centimeter-long jellyfish consisting of a membrane with eight armlike appendages. They overlaid muscle cells, obtained from a rat heart, on this membrane in a particular pattern. “We coaxed them to self-organize so that they matched the [muscle] architecture of a jellyfish precisely,” Dr. Parker said.

The robot, named “Medusoid,” was placed in salty fluid that can conduct electrical currents. When the engineers oscillated the voltage in the fluid, the muscle-coated membrane began to contract in a synchronized manner. (By contrast, a real jellyfish obtains nutrients by feeding on plankton, eggs, larvae, small fish and other jellyfish, which then enables specialized tissue to electrically activate the muscular contraction.)

The muscular contraction creates vortices—doughnut-shaped rings of water—below the creature’s body. For jellyfish, vortices propel it forward and push food toward its mouth.

The main difference between the two creatures “is that the real jellyfish can go and get nutrients and ours can’t,” said John Dabiri, a co-author of the study and a bioengineer at Caltech.

The engineers now plan to design a jellyfish that can gather food on its own. They also want to include specialized tissue, so that the creature can activate the muscular contractions internally, as a real jellyfish does.

The current version of Medusoid moves in a simple manner and can’t really turn or maneuver. To achieve that, the engineers will have to include multiple cell types and devise a system that allows the lab-built creature to sense its environment and use an internal “decision-making circuit” to pick different behaviors.

While those challenges are significant, some practical benefits may be more easily attained. Drug companies often test new heart drugs on cardiac tissue, and the jellyfish—which mimics a beating human heart—could serve as an alternative model. “I could put your drug in the jellyfish and tell you if it’s going to work,” said Dr. Parker.

The study of vortices already has inspired some new areas for medical research. For example, when blood enters the left ventricle of the pumping heart, it creates a rotating fluid mass that is similar to the vortices created by a swimming jellyfish. The vortices in the heart can be measured with ultrasound.

In 2006, Dr. Dabiri co-authored a study, involving 120 participants, which suggested that the process of vortex-ring formation could offer important clues about cardiac health. “You can tell healthy from less-healthy hearts” by studying the vortices, Dr. Dabiri said.


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Keeping the flu away:

Keeping the flu away: Synthetic protein activates immune system within two hours
sciencedaily.com
ScienceDaily (July 6, 2012) — San Diego State University researchers at the Donald P. Shiley BioScience Center may have found the secret to helping the immune system fight off the flu before it gets you sick.

A new study published July 6 in the Public Library of Science journal PLoS ONE, finds that EP67, a powerful synthetic protein, is able to activate the innate immune system within just two hours of being administered.

Prior to this study, EP67 had been primarily used as an adjuvant for vaccines, something added to the vaccine to help activate the immune response. But Joy Phillips, Ph.D. a lead author of the study with her colleague Sam Sanderson, Ph.D. at the University of Nebraska Medical Center, saw potential for it to work on its own.

“The flu virus is very sneaky and actively keeps the immune system from detecting it for a few days until you are getting symptoms,” Phillips said. “Our research showed that by introducing EP67 into the body within 24 hours of exposure to the flu virus caused the immune system to react almost immediately to the threat, well before your body normally would.”

Because EP67 doesn’t work on the virus but on the immune system itself, it functions the same no matter the flu strain, unlike the influenza vaccine which has to exactly match the currently circulating strain.

Phillips said while this study focuses on the flu, EP67 has the potential to work on other respiratory diseases and fungal infections and could have huge potential for emergency therapeutics.

“When you find out you’ve been exposed to the flu, the only treatments available now target the virus directly but they are not reliable and often the virus develops a resistance against them,” Phillips said. “EP67 could potentially be a therapeutic that someone would take when they know they’ve been exposed that would help the body fight off the virus before you get sick.”

It could even be used in the event of a new strain of infectious disease, before the actual pathogen has been identified, as in SARS or the 2009 H1N1 influenza outbreak, Phillips said.

Right now, the testing has been done primarily in mice by infecting them with a flu virus. Those that were given a dose of EP67 within 24 hours of the infection didn’t get sick (or as sick) as those that were not treated with EP67.

The level of illness in mice is measured by weight loss. Typically, mice lose approximately 20 percent of their weight when they are infected with the flu but mice treated with EP67 lost an average of just six percent. More importantly, mice who were treated a day after being infected with a lethal dose of influenza did not die, Phillips said.

She said there are also huge implications for veterinary applications, since EP67 is active in animals, including birds.

Future research will examine the effect EP67 has in the presence of a number of other pathogens and to look closer at exactly how EP67 functions within different cells in the body.


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Take-Home HIV Test Approved By FDA

OraQuick: First Rapid, Take-Home HIV Test Approved By FDA
huffingtonpost.com


WASHINGTON — Americans will soon be able to test themselves in the privacy of their own homes for the virus that causes AIDS, now that the Food and Drug Administration has approved the first rapid, over-the-counter HIV test.

The OraQuick test detects the presence of HIV antibodies using a mouth swab and returns a result in 20 to 40 minutes.

Government officials estimate that about 240,000 people, or one-fifth of the roughly 1.2 million people carrying HIV in the U.S., don’t know they are infected. Testing is a chief means of slowing new infections, which have held steady at about 50,000 per year for two decades.

FDA officials said the test is designed for people who might not otherwise get tested.

“The availability of a home-use HIV test kit provides another option for individuals to get tested so that they can seek medical care, if appropriate,” said Dr. Karen Midthun, director of the FDA’s Center for Biologics Evaluation and Research.

Orasure plans to start selling the test in October, both online and through retailers like Walgreens, CVS and Walmart. It hasn’t set a price yet but expects the consumer version to cost less than $60 but more than the one marketed to health professionals, which costs about $17.50. CEO Doug Michels said the price increase will help pay for a toll-free call center to provide counseling and medical referrals to test users.

“Each of the call-center operators is bilingual in English and Spanish, they’ve gone through 160 hours of training on HIV counseling and testing,” Michels said in an interview with the Associated Press. “So they are highly trained professionals and they’ll be there to support the consumer.”

Michels said the company’s marketing efforts will focus on populations at greatest risk of being infected with HIV, including gay and bisexual men, African Americans and Hispanics.

FDA stressed in its approval announcement that the test is not 100 percent accurate in identifying people with the virus. A trial conducted by test maker Orasure showed OraQuick detected HIV in those carrying the virus only 92 percent of the time, though it was 99.9 percent accurate in ruling out HIV in patients not carrying the virus.

That means the test could miss one in 12 HIV-infected people who use it but would incorrectly identify only one patient as having HIV for every 5,000 HIV-negative people tested, the FDA said.

People who test negative should get re-tested after three months, because it can take several weeks for detectable antibodies to HIV to appear, according to Dr. Jonathan Mermin, director of the Centers for Disease Control and Prevention’s HIV unit.

The FDA has approved several other HIV test kits designed for home use, but they usually require a blood sample that must be sent to a laboratory for development.

HIV awareness groups hailed the approval as an important step in expanding testing for the virus.

“This test will allow anyone to empower themselves to know their HIV status when, how and with whom they want to,” said Tom Donohue, founding director of Who’s Positive.

Experts say it’s difficult to predict how widely the test will be used.

According to the Orasure’s study, 41 percent of people who discovered they were HIV-positive using OraQuick had never been tested. The company estimates that 9,000 new HIV carriers would be identified for every 1 million people who use the test.

Based in Bethlehem, Pa., Orasure has marketed a version of OraQuick to doctors, nurses and other health care practitioners since 2002. When used by professionals, the test is shown to accurately identify both carriers and non-carriers 99 percent of the time. It’s not clear why the test is less accurate in consumer trials, but researchers said they expected its sensitivity to drop when it was used by consumers.

HIV eventually develops into AIDS, unless treated with antiviral drugs. AIDS causes the body’s immune system to breakdown, leading to infections which become fatal.



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Rewiring DNA circuitry could help treat asthma

Rewiring DNA circuitry could help treat asthma
sciencedaily.com


ScienceDaily (July 5, 2012) — Reprogramming asthma-promoting immune cells in mice diminishes airway damage and inflammation, and could potentially lead to new treatments for people with asthma, researchers have found.

The researchers were able to reprogram the asthma-promoting cells (called Th2 (T-helper 2) cells) after identifying an enzyme that modifies the DNA of these cells. The enzyme could be a target for the development of new treatments for chronic inflammatory diseases, in particular allergic asthma, caused by an excess of Th2 cells.

Walter and Eliza Hall Institute researcher Dr Rhys Allan led the research while working at Institut Curie, Paris. The research team from Institut Curie, National Centre for Scientific Research (CNRS), France, National Institute of Health and Medical Research (INSERM), France, and Montpellier Cancer Research Institute published the study July 4 in the journal Nature.

Dr Allan said the research team discovered that the enzyme Suv39h1 could switch off genes to control the function of Th2 cells, which are key to the allergic response.

“Th2 cells have an important function in the immune response, but they also play a significant role in diseases such as allergic asthma,” Dr Allan said. “People with asthma have too many Th2 cells, which produce chemical signals that inflame and damage the upper airways. In this study, we discovered that the Suv39h1 enzyme plays a critical role in programming these asthma-promoting cells, making it a potential target for new therapies to treat asthma.”

More than two million Australians have asthma — approximately one in 10 people — and the disease is even more common among Indigenous Australians. The prevalence of asthma in children in Australia is among the highest in the world.

Dr Allan said the Suv39h1 enzyme was part of the ‘epigenetic circuitry’ of Th2 cells.

“Epigenetics refers to changes or modifications in the DNA that alter how genes are switched on and off, without changing the fundamental DNA sequence. Suv39h1 effectively ‘tags’ the DNA to tell the cells which genes they need to switch on or off to promote an allergic response.”

Using agents that inhibit Suv39h1 could destabilise Th2 cells in people who have an excess of these asthma-promoting cells so they no longer cause inflammation, Dr Allan said.

“We had the idea that erasing these epigenetic tags could ‘short-circuit’ the asthma-promoting Th2 cells and diminish the inflammatory immune response. And, in fact, in mouse models of allergic asthma, blocking this pathway with an inhibitory compound did reduce allergy-related airway damage. Ultimately, our results have identified a potential target for therapeutic intervention in asthma and potentially other Th2-mediated inflammatory diseases, which could improve outcomes for patients,” Dr Allan said.

Dr Allan is continuing to study the epigenetic circuitry of asthma-promoting immune cells in the institute’s Molecular Immunology division, with funding from the National Health and Medical Research Council of Australia (NHMRC).

The research was supported by Institut Curie, CNRS and INSERM. Dr Allan was funded by an INSERM-NHMRC exchange fellowship.

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The above story is reprinted from materials provided by Walter and Eliza Hall Institute.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Rhys S. Allan, Elina Zueva, Florence Cammas, Heidi A. Schreiber, Vanessa Masson, Gabrielle T. Belz, Danièle Roche, Christèle Maison, Jean-Pierre Quivy, Geneviève Almouzni, Sebastian Amigorena. An epigenetic silencing pathway controlling T helper 2 cell lineage commitment. Nature, 2012; DOI: 10.1038/nature11173
Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.



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