Booster Shots

Oddities, musings and news from the health world

Category: Rodent

Rodent of the Week: Healing bones ultra fast

April 30, 2010 |  1:00 pm

Rodent_of_the_week Athletes would love this: a treatment to heal broken bones that works three times faster than normal. Researchers at Stanford have devised such a treatment that works in mice.

They injected a protein that plays a central role in bone development — called Wnt — and were able to stimulate rapid bone growth. Researchers have known the protein could be useful in humans, but it has been difficult to purify and dissolve, making the substance hard to apply. The Stanford team overcame this problem by using molecular bubbles called liposomes that could be suspended in liquid for delivery into the body.

In the experiment, the scientists drilled holes in the leg bones of mice with a dental drill (the mice were anesthetized and given painkillers). Some of the mice received injections of the Wnt-covered liposomes and others were injected with the Wnt protein without the liposome carrier. Within three days, the animals who received the Wnt-covered liposomes had 3.5 times more bone than the other mice. These animals were completely healed in 28 days, while the other mice were still in the process of repairing the injury.

It's possible that using Wnt to generate healing may also produce tissue that is more functional and lacks scars.

The study is published online this week in the journal Science Translational Medicine.

— Shari Roan

 Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: Women, estrogen and lung cancer

April 23, 2010 |  1:00 pm

Rodent Lung cancer is the leading cause of cancer deaths among women, with most cases linked to smoking. But not everyone who gets lung cancer smokes. Indeed, among nonsmokers, lung cancer is still the seventh most-common cause of cancer worldwide. Most of the lung cancer cases among nonsmokers are in women.

Researchers now have some clues about this mysterious connection. In a study presented earlier this week at the annual meeting of the American Assn. for Cancer Research, scientists found that smoke triggers changes in gene expression in the lungs of female mice. That's not surprising. But those changes include increasing the activity of genes involved in estrogen metabolism. Based on these data, the study's authors suggest that estrogen metabolism (the process by which estrogen becomes available for use) may contribute to lung cancer in nonsmoking women as well.

The researchers, at Fox Chase Cancer Center in Philadelphia, found 10 genes were expressed in the lungs of female mice exposed to smoke. The gene most affected by smoke was one that is a key enzyme for estrogen metabolism.

It's possible that estrogen plays a role in lung cancer in women in a similar way as it does in breast cancer. Other studies have shown women with lung cancer who take hormone replacement therapy (which replaces estrogen) have worse outcomes than do women who don't take hormone therapy.

— Shari Roan

Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: Antidepressants could lessen stroke severity

April 16, 2010 |  1:00 pm

Rodent_of_the_week Existing drugs used to treat depression and other mood disorders might be useful to limit brain damage following a stroke because they promote the growth of new nerve cells in the brain, according to a study in mice. The research is tantalizing because drugs that are known to spur nerve growth are already available and because there are few other options to mitigate the effects of stroke once brain damage has occurred.

Researchers at the Buck Institute for Age Research in Novato, Calif., compared stroke size and recovery in mice who were genetically altered and treated to either grow or not grow new neurons prior to stroke. The strokes in the animals that did not grow new neurons were 30% larger. The mice that did grow new neurons -- called neurogenesis -- showed improvement in motor function following the stroke.

It's not known exactly how new neurons improve stroke outcome. But the lead author of the study, Dr. David Greenberg, said in a news release: "Assuming that neurogenesis is also beneficial in humans, drugs approved by the FDA for other purposes and already shown to promote new neuron growth in rodents might be worth studying as a potential treatment for stroke in humans."

Studies still need to be conducted in humans. And, Greenberg cautions, people who have suffered strokes should not treat themselves with antidepressants or lithium without medical advice.

Further research will examine the effects of drugs that produce new nerve growth in other brain diseases, such as Parkinson's, Alzheimer's and Huntington's diseases.

The study is published online this week in the Proceedings of the National Academy of Sciences.

-- Shari Roan

Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: A nanovaccine reverses diabetes in mice

April 9, 2010 |  1:00 pm

Rodent Researchers are finding clever ways to explore nanotechnology for medical therapies. In a study published Thursday in the journal Immunity, researchers used a "nanovaccine" to reverse diabetes in mice with the disease.

Nanoparticles are spheres that are thousands of times smaller than any type of cell. Researchers at the University of Calgary, in Alberta, focused on correcting the autoimmune attack that occurs in diabetes.

In Type 1 diabetes, the insulin-producing pancreatic cells are destroyed by T-cells. T-cells are needed in many other functions in the body, however, to fight infections and foreign substances. In diabetes, good T-cells battle against other types of T-cells that cause the disease. The researchers created a vaccine consisting of nanoparticles coated with a protein to help the immune system stop the action of the aggressive T-cells. The diabetic mice receiving the vaccine eventually developed normal blood sugar levels.

Theoretically, this type of nanovaccine could be used on other autoimmune diseases to target the part of the immune system that needs to be corrected. Much work remains before this research translates to future use in humans. Among the questions: How safe are therapies consisting of nanoparticles?

-- Shari Roan

Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: What do animal studies tell us? [updated]

April 2, 2010 |  1:00 pm

Rodent_of_the_week Rodent of the Week is devoted to highlighting promising animal research. We shine this little spotlight on animal research because, typically, it's an area we tend to ignore. While often fascinating, animal studies are conducted at such an early stage in the research process that it's irresponsible to publicize the findings of most of these studies. Doing so can inadvertently raise hopes that the research is destined to translate into gains in human health.

A study published this week in the journal PLoS Biology speaks to this dilemma. [An earlier version of this post said the study was published in the journal PLoS Medicine.] Researchers analyzing animal research found that about one-third of animal studies led to human, randomized clinical trials. And only one in 10 of those human clinical trials resulted in therapies approved for use in humans.

The reasons animal research frequently looks good in animals but fails to pan out in humans are many. Sometimes, there are methodological flaws in the animal studies. In other words, what looked effective really wasn't. It's also possible that some things work in animals and not in humans because we are, after all, different species. Also, only animal studies that succeed may end up being published.

A good example of the problem with animal studies is in stroke research, the authors point out. In animal models, almost 500 therapies have been shown to be effective in protecting neurological functioning following a stroke. But only two treatments have been proven useful in humans.

This doesn't mean animal research is worthless. Indeed, animal research is often necessary. To minimize the number of animal-to-human research failures, however, the authors recommend that animal studies be conducted using the same high standards as those used in human trials. This means doing things like paying attention to the sample size in the study, conducting blinded experiments (when the researcher doesn't know which treatment the animal is receiving) and strict control of variables.

For the rest of us, it's helpful to remind ourselves that success in a 1-ounce, furry creature with red eyes and a tail doesn't mean we'll benefit, too.

-- Shari Roan

Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: Leptin's back

March 26, 2010 |  1:00 pm

Rodent_of_the_weekWhen leptin was discovered in 1994, there was considerable excitement that the hormone, which is made by fat tissue, could be manipulated and emerge as a treatment for obesity. Leptin plays a critical role in regulating appetite and in glucose and fat metabolism. Leptin research proved to be considerably complex, however, and there is little to show for the initial excitement.

That may soon change. Studies on leptin have continued and some potential therapies are emerging. Researchers reported Thursday that a Phase 1 study in mice showed that leptin can take the place of insulin in treating the symptoms of Type 1 diabetes.

Scientists at the University of Texas, Southwestern Medical Center administered leptin instead of insulin to diabetic mice and found the therapy was successful at managing blood-sugar levels. Insulin, of course, is the standard therapy for Type 1 diabetes and works quite well although people can experience wide swings in blood-sugar levels. Leptin, however, works in a different way and may prove to have additional benefit. The non-obese, diabetic mice ate less and developed more lean body mass.

"We hope the positive results we've had in animals can translate to people living with this disease," The lead author of the study, Dr. Roger Unger, said in a news release. "Insulin therapy has transformed a uniformly fatal disease into a livable one; however, the regimen for people with type 1 diabetes is onerous and symptoms aren't always well controlled. We hope that low-dose insulin combined with leptin will closely mimic the body's normal physiological process."

The study is published online in the Proceedings of the National Academy of Sciences.

-- Shari Roan

Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: Could patients with severe asthma benefit from bone marrow transplants?

March 19, 2010 |  7:00 am

Rodent Cases of severe, therapy-resistant asthma are on the rise worldwide, and new strategies are needed to treat the estimated 100,000 people who die of asthma every year. Researchers from the National Institutes of Health and their colleagues are exploring a radical solution – bone marrow transplants.

Scientists know the transplants have the potential to reset the immune system and calm an overactive inflammatory response. They’re already used to treat patients who develop acute graft-versus-host disease following an organ transplant. Asthma also involves excessive inflammation, prompting the airways to constrict and the lungs to secrete mucus. Why not reboot the immune systems with a bone marrow transplant?

To test their theory, the researchers gave the transplants to asthmatic mice that were allergic to ragweed. Then, when the mice were exposed to ragweed, their allergic and asthmatic symptoms (measured by chemical levels in their blood) decreased significantly. The scientists concluded that the bone marrow transplants helped the mice by restoring a healthy balance of immune system cells known as Th1 and Th2.

The results were published online this week in Proceedings of the National Academy of Sciences.

Dr. Eva Mezey, who heads the adult stem cell research section at the National Institute of Dental and Craniofacial Research in Bethesda, Md., told HealthDay that “it’s very likely that the intervention would work in humans.”

But she emphasized that more research is needed before bone marrow transplants could be tested in people with severe asthma. For instance, although the mice got their bone marrow through an intravenous injection, human patients might do better with an aerosol because it could deliver the cells directly to the lungs, she said.

— Karen Kaplan

Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: A new understanding of how prostate cancer treatment may backfire

March 12, 2010 |  7:00 am

Rodent The very therapy used to treat prostate cancer patients in the early stage of the disease actually promotes the second, more deadly wave of the disease, according to a new study.

Men with prostate cancer often take drugs to shut down the body’s production of testosterone, the hormone that feeds the initial tumors. But when those tumor cells die, they trigger an inflammatory response that draws in immune cells called B cells. Those B cells, in turn, secrete a molecule that paves the way for the growth of a second wave of deadlier prostate cancer cells that are resistant to the hormone therapy.

The researchers – from UC San Diego, Scripps Research Institute-Florida and the Engelhardt Institute of Molecular Biology in Moscow – pieced this together by studying the progression of prostate cancer in a variety of genetically modified mice. Here’s how they put it in their report, published in Thursday’s edition of the journal Nature:

“The inflammatory response elicited by the dying primary tumor contributes to the failure rather than the previously proposed success of anti-cancer therapy.” (emphasis added)

It sounds like bad news, but there may be a silver lining. Now that the mechanism is understood, the researchers say that any interference with this sequence of events ought to delay the onset of the dangerous secondary tumors.

In their experiments, such interventions reliably delayed those tumors by three to four weeks. Converting that from “mouse time” to “human time,” they calculated that equivalent interventions in people would slow the development of secondary prostate cancer tumors by 2.3 to 3.1 years.

— Karen Kaplan

Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: Another advantage to nursing the baby

March 5, 2010 |  1:02 pm

Rodent Newborn mice who receive their mother's milk experience a biological process that boosts their metabolism, possibly lowering the risk of obesity and diabetes in adulthood, according to a new study.

Breast-feeding confers several protective benefits in human babies. Some research suggests, for example, that breast-fed babies have a lower risk of obesity and diabetes later in life. The new study sheds light on a little-known process that takes place just after birth in mice. Researchers in Spain found that suckling the mother's milk prompts the newborn's liver to produce a molecule that then turns on heat-generating brown fat. That process helps the baby's body adapt to a lower environmental temperature than it experienced inside the mother's womb.

The protein that is released in response to suckling, called FGF21, also appears to be important in regulating metabolism. In the study, researchers injected the protein into fasting newborn mice and found that the treatment prompted heat generation within brown fat and boosted body temperature. These brown fat cells burned more energy and glucose. Recent studies in humans have found that greater activity in brown fat appears to protect against obesity.

"There are many evidences that alterations of dietary, genetic, environmental, or other origin in the metabolic performance during the fetal and early neonatal life can make an individual prone to develop diabetes and obesity in adulthood," the lead author of the study, Francesc Villarroya, of the University of Barcelona, said in a news release. "It will be important to know whether any disturbance in this naturally occurring event [the burst of FGF21] may have negative consequences in adulthood."

Researchers still don't know yet if this process observed in mice is similar in human newborns. The study is published in the journal Cell Metabolism.

— Shari Roan

Photo credit: Advanced Cell Technology Inc.

Rodent of the Week: A mouse with a human liver

February 26, 2010 |  1:00 pm

Rodent Animal studies are typically a key step in the scientific process, but some illnesses are especially challenging to study in this manner. For example, the liver diseases hepatitis B and hepatitis C can infect only humans and chimpanzees. Scientists also have had a hard time trying to study liver infections because human liver cells don't grow well in a lab culture.

That explains why researchers at the Salk Institute in La Jolla are particularly pleased with a new rodent resident in their labs -- a mouse with a human liver. The humanized mouse will make it possible to test new therapies for human liver diseases, such as hepatitis and malaria.

To create the model, researchers began with a special mouse with liver problems that could be treated with a particular drug. By taking away the drug, the researchers got human liver cells to take hold and populate the mouse liver. Tweaking the technique produced a mouse liver 95% composed of human liver cells. Studies showed the  mouse liver could be infected with hepatitis B and hepatitis C and that the standard treatment for hepatitis C effectively treated the infection.

"This robust model system opens the door to utilize human [liver cells] for purposes that were previously impossible," Inder Verma, the senior author of the study, said in a news release. "This chimeric mouse can be used for drug testing and gene therapy purposes, and in the future, may also be used to study liver cancers."

The paper was published online this week in the Journal of Clinical Investigation.

-- Shari Roan

Photo credit: Advanced Cell Technology Inc.


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