Category Archives: Life Science

Using Bacteria to Power Microscopic Machines

Scientists at the U.S. Department of Energy’s (DOE) Argonne National Laboratory and Northwestern University have discovered that common bacteria can turn microgears when suspended in a solution, providing insights for designs of bio-inspired dynamically adaptive materials for energy.

“The ability to harness and control the power of bacterial motion is an important requirement for further development of hybrid biomechanical systems driven by microorganisms,” said Argonne physicist and principal investigator Igor Aronson. “In this system, the gears are a million times more massive than the bacteria.”

A few hundred bacteria work together in order to turn the gear. When multiple gears are placed in the solution with the spokes connected as in a clock, the bacteria will turn both gears in opposite directions, causing the gears to rotate in synchrony—even for long stretches of time.

“There exists a wide gap between man-made hard materials and living tissues; biological materials, unlike steel or plastics, are ‘alive,'” Aronson said. “Our discovery demonstrates how microscopic swimming agents, such as bacteria or man-made nanorobots, in combination with hard materials, can constitute a ‘smart material’ which can dynamically alter its microstructures, repair damage, or power microdevices.”

Researchers Find High-Fructose Corn Syrup Results in More Weight Gain

A Princeton University research team has demonstrated that rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same. In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides

Photo of Princeton University research team, including (from left) undergraduate Elyse Powell, psychology professor Bart Hoebel, visiting research associate Nicole Avena and graduate student Miriam Bocarsly, by Denise Applewhite

The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.

The second experiment — the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals — monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet. In humans, this would be equivalent to a 200-pound man gaining 96 pounds.

“These rats aren’t just getting fat; they’re demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides,” said Princeton graduate student Miriam Bocarsly. “In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes.” In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.

Taste Cells in the Stomach and Intestine

Stomach’s Sweet Tooth

Taste, scientists are discovering, is a whole-body sensation. There are taste cells in the stomach, intestine and, evidence suggests, the pancreas, colon and esophagus. These sensory cells are part of an ancient battalion tasked with guiding food choices
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Newly discovered taste cells in the gut appear to send a “prepare for fuel” message to the body, a finding that may explain a link between diet soda and diabetes risk.
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The gut’s taste cells appear to be built from the same machinery as the taste cells of the tongue, the structures of which scientists have only recently nailed down. Taste cells interact with what are called “tastants” via receptors, specialized proteins that protrude from cell walls and bind to specific molecules drifting by. When a tastant binds to a receptor, it signals other molecules that, in the mouth, immediately send an “accept” or “reject” message to the brain.
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Gut taste cells appear to regulate, in part, secretion of insulin, a hormone crucial for telling body tissues whether they should tap newly arrived glucose or valuable stored fat for energy.

Engineering Mosquitoes to be Flying Vaccinators

Mosquitoes Engineered Into Flying Vaccinators by Emily Singer

Researchers in Japan have transformed mosquitoes into vaccine-carrying syringes by genetically engineering the insects to express the vaccine for leishmaniasis–a parasitic disease transmitted by the sandfly–in their saliva. According to a study in Insect Molecular Biology, mice bitten by these mosquitoes produced antibodies against the parasite. It’s not yet clear whether the immune response was strong enough to protect against infection.

“Following bites, protective immune responses are induced, just like a conventional vaccination but with no pain and no cost,” said lead researcher Shigeto Yoshida, from the Jichi Medical University in JapanYoshida, in a press release from the journal. “What’s more continuous exposure to bites will maintain high levels of protective immunity, through natural boosting, for a life time. So the insect shifts from being a pest to being beneficial.”

Researchers consider the project more of a proof of principle experiment than a viable public health option, at least for now.

Very cool.

Invisible Worlds: Fastest Thing on the Planet

Fun with Fungi.

Statistical Errors in Medical Studies

I have written about statistics, and various traps people often fall into when examining data before (Statistics Insights for Scientists and Engineers, Data Can’t Lie – But People Can be Fooled, Correlation is Not Causation, Simpson’s Paradox). And also have posted about reasons for systemic reasons for medical studies presenting misleading results (Why Most Published Research Findings Are False, How to Deal with False Research Findings, Medical Study Integrity (or Lack Thereof), Surprising New Diabetes Data). This post collects some discussion on the topic from several blogs and studies.

HIV Vaccines, p values, and Proof by David Rind

if vaccine were no better than placebo we would expect to see a difference as large or larger than the one seen in this trial only 4 in 100 times. This is distinctly different from saying that there is a 96% chance that this result is correct, which is how many people wrongly interpret such a p value.
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So, the modestly positive result found in the trial must be weighed against our prior belief that such a vaccine would fail. Had the vaccine been dramatically protective, giving us much stronger evidence of efficacy, our prior doubts would be more likely to give way in the face of high quality evidence of benefit.
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While the actual analysis the investigators decided to make primary would be completely appropriate had it been specified up front, it now suffers under the concern of showing marginal significance after three bites at the statistical apple; these three bites have to adversely affect our belief in the importance of that p value. And, it’s not so obvious why they would have reported this result rather than excluding those 7 patients from the per protocol analysis and making that the primary analysis; there might have been yet a fourth analysis that could have been reported had it shown that all important p value below 0.05.

How to Avoid Commonly Encountered Limitations of Published Clinical Trials by Sanjay Kaul, MD and and George A. Diamond, MD

Trials often employ composite end points that, although they enable assessment of nonfatal events and improve trial efficiency and statistical precision, entail a number of shortcomings that can potentially undermine the scientific validity of the conclusions drawn from these trials. Finally, clinical trials often employ extensive subgroup analysis. However, lack of attention to proper methods can lead to chance findings that might misinform research and result in suboptimal practice.

Why Most Published Research Findings Are False by John P. A. Ioannidis
Continue reading →

Norway Reduces Infections by Reducing Antibiotic Use

Norway conquers infections by cutting use of antibiotics

Twenty-five years ago, Norwegians were also losing their lives to this bacteria. But Norway’s public health system fought back with an aggressive program that made it the most infection-free country in the world. A key part of that program was cutting back severely on the use of antibiotics.

Now a spate of new studies from around the world prove that Norway’s model can be replicated with extraordinary success, and public health experts are saying these deaths — 19,000 in the U.S. each year alone, more than from AIDS — are unnecessary.

“It’s a very sad situation that in some places so many are dying from this, because we have shown here in Norway that Methicillin-resistant Staphylococcus aureus [MRSA] can be controlled, and with not too much effort,” said Jan Hendrik-Binder, Oslo’s MRSA medical advisor. “But you have to take it seriously, you have to give it attention and you must not give up.”

The World Health Organization says antibiotic resistance is one of the leading public health threats on the planet. A six-month investigation by The Associated Press found overuse and misuse of medicines has led to mutations in once curable diseases like tuberculosis and malaria, making them harder and in some cases impossible to treat.

Now, in Norway’s simple solution, there’s a glimmer of hope.

Antibiotics Breed Superbugs Faster Than Expected

We continue to endanger ourselves by using antibiotics inappropriately. This is one of many things that happen when the public at large is ignorant about science and ignores scientific evidence. I don’t believe people want to put other people’s lives in danger. But our behavior in the face of the evidence has us doing just that. I believe because we don’t value science rather than because we don’t care about putting others (and ourselves) in danger. Antibiotics Breed Superbugs Faster Than Expected

Bacteria don’t just develop resistance to one drug at a time, but to many — and at accelerated rates. That’s because antibiotics boost bacterial production of free-radical oxygen molecules that damage bacterial DNA. Repairs to the DNA cause widespread mutations, giving bacteria more chances to randomly acquire drug-resistant traits.
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Drug resistance is a serious public health concern. According to the federal Centers for Disease Control and Prevention, 70 percent of 1.7 million infections acquired in hospitals every year are resistant to at least one drug. Those infections annually kill 99,000 Americans — more than double the number that die in car crashes.

Drugs that once destroyed almost any bacteria now kill only a few, or don’t work at all. In the case of some drugs, like Cipro, the decline is dramatic: Where in 1999 it worked against 95 percent of E. coli, it treated only 60 percent by 2006. Against lung infection-causing Acinobacter, its effectiveness fell by 70 percent in just four years.

Though drug resistance is ultimately inevitable, conventional wisdom holds that antibiotics consumed at suboptimum doses hasten the process. Bugs that would have succumbed to a larger dose live to multiply, pushing the strain as a whole closer to resistance. That happens when a prescription goes unfinished, or when antibiotics used on farms enter food and water at low levels.
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Of the 35 million pounds of antibiotics consumed annually in the United States, 80 percent goes to farm animals. Much of it is used to treat diseases spread by industrial husbandry practices, or simply to accelerate growth. As a result, farms have become giant petri dishes for superbugs, especially multidrug-resistant Staphylococcus aureus, or MRSA, which kills 20,000 Americans every year – more than AIDS.

Alarming cases of farm-based MRSA and other diseases led to a proposed Congressional law restricting the use of agricultural antibiotics. That bill, supported by the American Medical Association and American Public Health Association, is opposed by farm lobbyists and remains stuck in committee.

Researchers Explain How Rotifers Thrive Despite Forgoing Sex

Bdelloid rotifers haven’t had sex for at least thirty million years. Most asexual animals are doomed to extinction. The excellent show, Science Friday, looks at the extraordinary adaptations that allow rotifers to thrive sex-free.

For millions of years, the rotifers have reproduced asexually, flying in the face of an idea known as the Red Queen Hypothesis, which states that without the advantage of sexual reproduction, more-rapidly evolving parasites and predators will eventually doom the asexual species. Now, the researchers studying the tiny organism say that its ability to dry up and blow away to greener pastures may have given the rotifers a hidden tactical edge in this evolutionary war.

The webcast provides a nice overview of the research. Every week Science Friday provides many such interesting reviews of recent scientific research.

What Are Rotifers?

Rotifers are small, mostly freshwater animals, and are amongst the smallest members of the Metazoa — that group of multicellular animals which includes humans, and whose bodies are organized into systems of organs.
Most rotifers are about 0.5mm in length or less, and their bodies have a total of around a thousand cells. This means that their organ systems are a greatly simplified distillation of the organ systems found in the bodies of the higher animals.

A typical rotifer might have a brain of perhaps fifteen cells with associated nerves and ganglia, a stomach of much the same number, an excretory system of only a dozen or so cells, and a similarly fundamental reproductive system. They have no circulatory system. It is an anomaly that despite their complexity, many rotifers are much smaller than common single-celled organisms whose world they share.
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they are able to survive long periods — even perhaps hundreds of years — in a dried or frozen state, and will resume normal behaviour when rehydrated or thawed.
Secondly, they exhibit what biologists call cell constancy — they grow in size not by cell division, but by increase in the size of the cells which they already have.

Researchers Find Switch That Allows Cancer Cells to Spread

Researchers discovered of a specific protein called disabled-2 (Dab2) that switches on the process that releases cancer cells from the original tumor and allows the cells to spread and develop into new tumors in other parts of the body.

The process called epithelial-mesenchymal transdifferientiation (EMT) has been known to play a role in releasing cells (epithelial cells) on the surface of the solid tumor and transforming them into transient mesenchymal cell: cells with the ability to start to grow a new tumor.

This is often the fatal process in breast, ovarian, pancreatic and colon-rectal cancers.

Searching to understand how the EMT process begins, Ge Jin, who has joint appointments at the Case Western Reserve University School of Dental Medicine and the Lerner Research Institute at the Cleveland Clinic, began by working backwards from EMT to find its trigger. The researchers found that a compound called transforming growth factor-ÃŸ (TGF-ÃŸ) triggers the formation of the Dab2 protein. It was this protein, Dab2, that activated the EMT process.

He discovered that when the researchers knocked out Dab2, EMT was not triggered. “This is the major piece in cancer research that has been missing,” Jin said. Most tumors are epithelial in origin and have epithelial markers on their surface. The EMT process takes place when some of those cells dislodge from the surface and undergo a transformation into a fibrous mesenchymal cell maker with the ability to migrate.

“EMT is the most important step in this process,” said Jin. He was part of a six-member research team, led by Philip Howe from the Department of Cancer Biology at the Lerner Research Institute in a National Institute of Cancer-funded study. The research group studied the biological processes that initiated the cancer spread by using cancer cells in animal models.

“If we can understand the signaling pathway for modulating EMT, then we can design drugs to delay or halt EMT cells and control tumor progression,” Jin said. Beyond cancer, Jin said. “The process we discovered may lead to understanding how other diseases progress.”