20091030-7  —  The power of the imagination is well-known: it’s no surprise that scary music is scarier with your eyes closed. But now neuroscientist and psychiatrist Prof. Talma Hendler of Tel Aviv University’s Functional Brain Center says that this phenomenon may open the door to a new way of treating people with Alzheimer’s, Parkinson’s and other neurological diseases.

In her new study, Prof. Hendler found that the simple act of voluntarily closing one’s eyes – instead of listening to music and sounds in the dark – can elicit more intense physical responses in the brain itself. This finding may have therapeutic value in treating people with brain disorders. Her research was just published in PLoS One and builds on her 2007 study published in Cerebral Cortex.

Prof. Hendler’s research suggests that, when our eyes are closed, a region in our brain called the amygdala is fired up. The experience of scary music becomes more emotionally and physically intense. And the converse of the scary music effect may be true: happy music could produce a joyous effect when our eyes are shut as well.

Listening to sounds with our eyes closed seems to wire together a direct connection to the regions of our brains that process emotions, says Prof. Hendler. “Music is a relatively abstract emotional carrier,” says Prof. Hendler. “It can easily take one’s subjective personal experience and manipulate it. Our new findings, however, suggest that the effect is not only subjective. Using a functional MRI (fMRI), we can see that distinct changes in the brain are more pronounced when a person’s eyes are not being used.”

Alfred Hitchcock in the laboratory

Dr. Yulia Lerner, a post-doctoral fellow at Prof. Hendler’s lab, had 15 healthy volunteers listen to spooky Hitchcock-style music, and then neutral sounds with no musical melody. They listened to these twice, once with their eyes open and a second time with their eyes shut, as she monitored their brain activity with an fMRI. While volunteers were listening to the scary music, Dr. Lerner found that brain activity peaked when the subjects’ eyes were closed. This medical finding corresponded to volunteer feedback that the subjects felt more emotionally charged by the scary music.

The amygdala, the region of the brain in which emotions are located, was significantly more active when the subjects’ eyes were closed. “It’s possible that closing one’s eyes during an emotional stimulation, like in our research, may help people through a variety of mental states. It synchs connectivity in the brain,” Dr. Hendler says. “We don’t know exactly how or why this happens – it’s like a light switch gets turned off, allowing the brain to better integrate the highs and lows of the emotional experience when the eyes are shut.”

Music brings balance to the brain and more readily integrates the affective and cognitive centres of our mind. Music may help us think better and even improve our learning abilities. But, she warns, more studies are needed before you let your teen crank up the hip-hop music as a study aid.

Applications for dementia and systemic brain disorders

“This study is the first time scientists have looked inside the brain non-invasively, to examine what happens to the brain under these conditions,” says Prof. Hendler. Small physical behaviours can radically alter the balance and colour of emotions. Not long ago in U.S. classrooms, teachers found that hyperactive students learned better while standing, rather than sitting at their desks. Now, Prof. Hendler’s latest study with scary music is “just an example of how a small manipulation in one’s physical state such as eyes open or shut can change our mental experience,” she says.

The findings, researchers hope, can be applied to therapies that achieve more significant and longer-lasting effects without chemical intervention. While her study just touches on the connection of physical and emotional activity in the brain, Prof. Hendler doesn’t rule out music therapy in alleviating symptoms in chronic mental disorders such as depression, Schizophrenia and Parkinson’s, in the future.


Men & Women NOT Needed for First Step in Making Babies

20091030-5,, October 29, 2009, by Celeste M Ball  —  Scientists at Stanford University in California have found a way to take out the first step in making babies –by creating sperm and eggs from embryonic stem cells.

Researchers used stem cells taken from embryos in the first days of life… and hope to soon be able to repeat the process by using pieces of skin.

The science paves the way for men and women with fertility issues to have their own biological children.

The breakthrough raises a number of moral ethical questions -including the possibility of children being born through entirely artificial means.

The sperm had heads and short tails and are thought to have been mature enough to fertilize an egg.

The eggs were at a much earlier stage but were still much more developed than any created so far by other scientists.

The science also raises the possibility of ‘male eggs’ made from men’s skin and ‘female sperm’ from women’s skin.

Critics argue that it is wrong to tamper with the building blocks of life.

They also fear the advances would distort relations between family members.


Understanding the details of how sperm and egg cells grow will help scientists develop treatments. Photograph: Corbis

‘Hidden stage of human development’ is opened up by Stanford University scientists

Scientists have turned human stem cells into early-stage sperm and eggs in research that promises to give doctors an unprecedented insight into the causes of infertility.

The work will allow researchers to study human reproductive cells from the moment they are created in embryos through to fully-mature sperm and eggs.

Understanding the details of how sperm and egg cells grow will help scientists develop treatments for people who are left infertile when the process goes wrong. The research may also lead to treatments that can correct growth defects before a child is born.

Genetic glitches that happen early on in the growth of sperm and eggs are a major cause of infertility in men and women. The process has been practically impossible to study until now though, because the sex cells form early on, before an embryo is two weeks old.

“This achievement opens a new window into what was only recently a hidden stage of human development,” said Susan Shurin at the National Institute of Child Health and Human Development, which part funded the research.

A team led by Renee Reijo Pera at Stanford University in California developed a technique that turned human embryonic stem cells green when they started growing into sperm and eggs. After isolating the reproductive cells, the scientists worked out which genes made them grow properly by switching different genes on and off.

Writing in the journal Nature, the scientists describe how that one gene, called DAZL, is involved in the formation of sex cells from the start. Two related genes are switched on later to steer the cells to full maturity.

The main significance of the work is not to attempt to generate gametes for couples who do not produce them naturally. Rather, the work describes a system in which various aspects of germ cell development can be studied in a dish. In the current study, they have gained insight into the function of three genes in which they specialize.”

Darren Griffin, a geneticist at the University of Kent, said the work was important because it gave researchers a way to study human sperm and egg development in a dish, instead of having to rely on tissues taken from animals or “removing bits of people’s gonads”.

“In future, a range of genetic and environmental factors could be studied, including the effects of pollutants on our fertility. Only through understanding such factors at a basic scientific level can we hope to develop novel diagnoses and therapies. The potential is enormous,” he said.

Allan Pacey, an andrologist at Sheffield University, said: “Ultimately this may help us find a cure for male infertility. Not necessarily by making sperm in the laboratory – I personally think that it unlikely – but by identifying new targets for drugs or genes that may stimulate sperm production to occur naturally. This is a long way off, but it is a laudable dream.Bottom of Form


OVERTAKING CHRONIC FATIGUE: An electron micrograph shows the XMRV retrovrius in the blood of a patient with chronic fatigue syndrome.

Recently implicated in some severe prostate cancer patients, the retrovirus XMRV has now been found in many with chronic fatigue–changing the landscape for diagnosis and possible treatment

By Katherine Harmon, Scientific American, October 2009  —  More so than many illnesses, chronic fatigue syndrome (CFS) frustrates those who suffer from it and those close to them, due to its nebulous assembly of symptoms, along with continued controversies over its etiology, diagnosis, treatment and even its nomenclature. Now, the discovery of a familiar retrovirus in many CFS patients could bring new energy to the field-and fresh hope for more specific medical care.

Chronic fatigue is in part a misnomer. The syndrome often has more to do with immune system abnormalities than pervasive tiredness-although the two can go hand in hand. The symptoms range from exhaustion to muscle pain, giving CFS a reputation among some as a “wastebasket diagnosis”. The slipperiness of the syndrome is in part because “it’s diagnosed based on exclusion,” says Judy Mikovits, director of research at the Whittemore Peterson Institute for Neuro-Immune Disease in Reno, Nev., and co-author of research on the retrovirus findings published online today in Science. Doctors often apply the label if no other explanation can be found for a patient’s symptoms, which may be part of the reason it seems to pop up in everyone from overworked career women to continually sick children.

Roughly 17 million people worldwide are thought to have CFS, but given current diagnosis methods, the true number could be much higher or lower. Having a specific virus to look for would make for much more robust tests and possibly even be a step toward treatment. Mikovits’s team thinks they have found just such a candidate.

The xenotropic murine leukemia virus-related virus (XMRV), a type of gammaretrovirus, has recently been linked to strong cases of prostate cancer. Like CFS, this cancer involves changes in an antiviral enzyme (RNase L). The prostate cancer discovery, described last month by Ila Singh, an associate professor of pathology at the University of Utah in Salt Lake City, et al. in the Proceedings of the National Academy of Sciences (PNAS), along with a traditionally high incidence of cancer in CFS patients, got Mikovits and her team thinking: Would they find the same retrovirus in people with CFS?

After analyzing biological samples from more than 100 CFS patients for the retrovirus, two thirds of them were found to test positive for the virus-compared with 3.7 percent of 218 healthy volunteers who were screened.

To find the retrovirus, Mikovits and her team studied documented cases, such as CFS outbreaks in a symphony orchestra in North Carolina and in Incline Village, Nev. “We found the virus in the same proportion in every outbreak,” she says. But how are people getting this retrovirus? “Ila’s work shows that everyone’s susceptible,” Mikovits says of the PNAS paper by Singh that illustrates the link between prostate cancer and XMRV and shows that the virus is not linked to a genetic mutation.

Experiments in Mikovits’s lab proved that the retrovirus can be transmitted via blood by infecting healthy cells drawn from volunteers with material from XMRV-positive CFS patients. Mikovits hopes to soon have a better understanding of how the virus might be transferred in the real world, especially among families. If it, for instance, is like human T-lymphotropic virus type 1 (HTLV-1), it may be communicable through breast milk or if it’s like a herpes virus that is common in CFS, it may be passed along to offspring.

Precisely how this virus is related to chronic fatigue, however, remains a mystery. One of the problems with tracking down CFS is that it may not be a single ailment. “We think that the problem is that CFS is a collection of many, many different diseases even though it has similar symptoms,” says Brigitte Huber, a professor of pathology at Tufts University’s Sackler School of Graduate Biomedical Sciences in Boston. She and others suspect that the retrovirus may be unleashing other underlying conditions and viruses in the body.

“This new retrovirus may be able, through infecting human cells, [to] induce a transcription of an endogenous virus,” says Huber, who has been studying the presence of an ancient retrovirus (HERV-K18) dormant in most people but active in patients with CFS and multiple sclerosis. “We’ve already shown that Epstein-Barr virus can do exactly this.”

Even in their testing for the XMRV retrovirus, Mikovits says, “We could see a human endogenous virus at the same time” as XMRV. “There are a number of old diseases that seem to be rising at an infectious rate,” she says. Although this background noise of various viruses may be difficult to sort though, it brings clues to help researchers find the root cause of CFS. “It’s possible, downstream, that this will all feed into the same mechanism,” Huber says.

Even before the precise mechanisms are found, work toward finding treatment proceeds. Animal model testing is already underway, and Mikovits notes that her team is looking into some reverse transcriptase inhibitors that have already been approved by the U.S. Food and Drug Administration for other uses.

“Now we have a drug target and a marker,” Mikovits says. “If we treat them with a drug and they get better, we win.”

In the meantime, her team has been making quick strides toward a simple diagnostic test that doctors could use to check for the virus. Tests have been running smoothly in the lab, she notes, with some diagnostics companies already interested in the technology. She predicts a test will be available in less than six months. Mikovits adds that she is “excited that we will actually have some causes…rather than just building a better wheelchair.”

By Mariette DiChristina, Scientific American, October 29, 2009  —  J. Craig Venter, the genomic scientist and founder of the J. Craig Venter Institute, was speaking yesterday about the potential for techniques involved in the field of synthetic life to improve medicine, but his words could have been applied to the all the talks during the opening session of TED MED (“TED” is for technology, entertainment, design). The conference is running from October 27 through 30 at the Hotel Del Coronado in San Diego. Speakers also described advances in using stem cells for regenerative medicine and tissue engineering.

Venter reviewed recent advances in “software building its own hardware.” That is, by inserting DNA from one organism into another, scientists have been able to use existing cellular machinery to read that DNA-transforming one species to another. He mentioned Phase II clinical trials of a vaccine for meningitis developed with the technique.

Moving DNA into stem cells through therapeutic cloning could treat diseases such as amyotrophic lateral sclerosis, known as Lou Gehrig’s disease, said Daniel Kraft of the Stanford Institute for Stem Cell Biology and Regenerative Medicine. “You could bank them for the future, when you might need them,” he said.

Other researchers are seeding cells onto scaffolds with the hopes of eventually building replacement tissue and organs. “Every 30 seconds, a person dies of a disease that could have been solved with tissue replacement,” said Anthony Atala, director of the Wake Forest Institute for Regenerative Medicine and chair of urology at Wake Forest University. During the past decade, the number of patients waiting for organs has doubled while donations have remained flat, added Atala. Although stem cells are needed for such tissues as heart, liver and pancreas, he said, tissue-specific cells from the patient could be used to grow other new organs in the future.


Wednesday, October 28, 2009                

TEDMED 2009 – Day 1

Filed under: Medgadget Exclusive


A bladder grown at the Wake Forest Institute for Regenerative Medicine

Yesterday we settled into our hotel room in San Diego, grabbed a burger, and went straight to session one of TEDMED. The first set of speakers consisted of a beat poet and performance artist Sekou Andrews, synthetic geneticist  Craig Venter, regenerative medicine gurus Daniel Kraft, Anthony Atala, and Damien Bates, magician Eric Mead, ER and Law and Order SVU writer  Neal Baer, geographic medicine popularizer Bill Davenhall, and songwriter Jill Sobule.

Sekou Andrews kicked off the conference with an energetic, free-flowing poem of sorts about health care, rhyming a mash-up of medical terms and concepts to get the crowd excited for the conference at hand.

After him, Craig Venter took the stage and chatted about synthetic biology and how his team synthesized the entire bacterium of Mycoplasma genitalium from four bottles of nucleotides (for a good overview of synthetic biology, take a look at this New Yorker piece). The main idea that kept emerging in his talk is that the DNA of a life form is analogous to the software and then all of the hardware is sculpted upon its code. It intuitively made sense, but the team was surprised when they actually were able to transplant the DNA of one bacterium into another, which lead the recipient organism to undergo physiologic metamorphosis.

Next we heard from a series of speakers involved with regenerative medicine. Daniel Kraft (flashback: MarrowMiner) spoke of the role of stem cells in medicine and how he discovered a better way to harvest them from the pelvis.


Damien Bates, the chief medical officer of Organogenesis, the company behind biologic wound healing film Apligraf, passed around a sample of their wound healing tissue for people to feel as well as talked about how the skin heals and how it can be aided by regenerative biology.

Anthony Atala, from the Wake Forest Institute for Regenerative Medicine, talked about the various methods his research center is using to grow specific tissues and organs. He described much of the tissue creation process as sort of building the layers of a cake, with each tissue type placed one on top of the other. For linearly organized organs, such as arteries, this isn’t so much of a problem, because you can just grow layers upon layers of tissues. However, for the more complicated, highly solid organs with lots of blood vessels, this methodology breaks down, and the scientists have to either use some sort of pre-made matrix or need to harvest tissues from other sources and de-cellularize them, leaving behind only the collagen scaffold that can be populated by cells.

To wrap up the hard science part of things, Bill Davenhall talked about the importance of adding more environmental data to patients’ charts, under the hypothesis that living in some environments predisposes a person to certain diseases, and this sort of geo-medicine data might be useful to practicing clinicians.

Lastly, Neal Bear, writer and producer of ER and Law and Order SVU, discussed story telling in medicine, and Jill Sobule sang a lighthearted song about the apocalypse (surprisingly not as depressing as it sounds).

That’s all for today.

Study Shows Lifestyle Changes Are More Effective Than Drugs in Preventing Diabetes

By Salynn Boyles
WebMD Health News 

Reviewed by Brunilda Nazario, MD, Oct. 28, 2009 — Lifestyle changes resulting in long-term weight loss of just a few pounds proved to be roughly twice as effective as drug treatment for preventing type 2 diabetes in an ongoing government-sponsored trial.

Researchers followed almost 3,000 high-risk patients for a decade in one of the largest and longest  studies aimed at preventing diabetes ever conducted in the U.S.

Roughly a third of the participants were initially asked to eat a low-fat diet and engage in at least 30 minutes of moderate activity a minimum of five times a week, with the goal of losing 7% of their body weight within a year.

Another third were put on the diabetes drug metformin; the remaining patients initially received no intervention.

Many of the people in the lifestyle intervention group met the weight loss goal, losing an average of 15 pounds during the first year of the study.

While they regained, on average, 10 of those pounds during the next seven years, the lifestyle intervention group continued to have the lowest rates of diabetes.

“Weight loss is still the most important thing we have to recommend to overweight people at risk for type 2 diabetes,” William C. Knowler, MD, of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), tells WebMD. “This study shows that the benefits of even modest weight loss can persist for many years.”

Reduction in Diabetes Incidence

Three years into the trial, Knowler and colleagues reported that diabetes incidence was reduced by a whopping 58% in the lifestyle intervention group and 31% in the metformin group, compared to people who received no intervention.

This dramatic difference led the researchers to offer lifestyle intervention, in the form of group counseling and support sessions, to all three groups for the rest of the study.

The 10-year follow up analysis, which appears Thursday in TheLancet, shows that:

  • Compared to the non-intervention group, patients in the intensive lifestyle intervention group and metformin group, respectively, were 34% and 18% less likely to develop diabetes over 10 years.
  • Lifestyle intervention was found to delay the onset of diabetes by four years. Drug treatment delayed diabetes by two years.
  • The benefits of intensive lifestyle intervention were particularly strong in the elderly. Those aged 60 and older in the diet and exercise group lowered their rate of developing diabetes by half over 10 years.

“Lifestyle and metformin were both useful for delaying or preventing diabetes,” says endocrinologist and co-researcher Ronald Goldberg, MD.

The researchers will continue to follow the study participants for at least another five years. One goal of the continued follow-up is to determine the impact of the lifestyle and drug interventions on the development of diabetes complications, such as nerve damage and blindness.

Diabetes on the Rise

About one in 10 adults in the U.S. — roughly 24 million people — have diabetes, and an additional 57 million are at risk for developing the disease because they are overweight or obese and have impaired blood sugar control.

Goldberg says the study findings highlight the importance of making prevention and lifestyle interventions a focus of national health care reform. He is professor of medicine in the division of endocrinology, diabetes, and metabolism at the Diabetes Research Institute, University of Miami Miller School of Medicine.

“The biggest expense in diabetes comes from treating the complications of disease,” he says. “If we can show that these interventions keep people from developing these complications, this could have an enormous impact.”